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Page 1: USMLE_01_1415_MANUAL_DM.pdf

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D e r m a

t o l o g y

American Manualof Examination

in Medicine

(2CK)

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No part of this book may be reproduced stored in a retrieval system or transmitted in any form or by any

means electronic mechanical photocopying recording or otherwise without prior permission of the

holders of the copyright

copy CTO EDITORIAL SL 2015

Design and layout CTO Editorial

C Francisco Silvela 106 28002 Madrid

Phone no (0034) 91 782 43 30 - Fax (0034) 91 782 43 43

E-mail address ctoeditorialctomedicinacom

Website wwwgrupoctoes

ISBN full edition 978-84-16276-21-9

DISCLAIMER

Medicine is a science subject to constant change As research and clinical experience widen our

knowledge treatments and pharmacotherapy changes are necessary The editors of this work have

verified their results against reliable sources in an effort to provide general and complete information

according to the accepted criteria at the time of publication Nevertheless given the fact that

human error may occur or that some changes may take place in medical sciences neither the editor

nor any of the contributors involved in the preparation ndashor publication- of this work can guaranteethat the content herein is accurate and complete in each and every aspect The editors and the

contributing sources cannot be held responsible for any errors omissions or the outcome derived from

the use of the information provided herein Therefore readers are recommended to verify the content

of this work against other sources As an example it is especially advisable to read the package insert

of any drug to be administered to ensure that the information furnished by this publication is accurate

and no modifications were made either to the recommended dose or to the contraindications for

administering said drug This recommendation is particularly significant in relation to new or seldom

used drugs Readers should also check with their own laboratory about normal values

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D e r m a

t o l o g y

American Manualof Examination

in Medicine

(2CK)

AuthorsDolores Mendoza

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Amer ican Manual of Examinat ion in Medicine (2CK)

01 Skin Layers 1

02 Terminology Elemental Cutaneous Lesions 1

21 Clinical Lesions 122 Histological Lesions 2

03 Allergic and Immune-mediated Diseases 2

31 Hypersensibility Reactions 2

32 Atopic Dermatitis 2

33 Contact Eczema 3

34 Seborrheic Dermatitis 3

35 Psoriasis 3

36 Urticaria 4

37 Toxicodermas 5

38 Multiform Erythema Stevens-Johnson Syndrome

and Toxic Epidermal Necrolysis 539 Erythema Nodosum6

310 Bullous Pemphigoid and Pemphigus Vulgaris 6

04 Infectious Diseases 8

41 Viral Infections 8

42 Bacterial Infections 10

43 Fungal Infections 12

44 Parasitic Infections14

45 Ischemia 1546 Miscellaneous 15

47 Neoplasias 17

Index

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Dermatology

Chapter 01

Skin

LayersThere are three skin layers epidermis dermis and subcutaneous cel-

lular tssue (Figure 1)

Reticular layer

Sebaceous(Oil) gland

Hair

follicle

Deep

arteriovenousplexusSweat

glandDermal Papillae

Super1047297cial arteriovenousplexus

Subcutaneoustissue

Dermis

Epidermis

Figure 1 Microscopic structure of normal skin

Chapter 02

TerminologyElemental

Cutaneous Lesions

21 Clinical Lesions

Primary Clinical Lesions bull Fluid-filled

Vesicle raised formaton less than 05 cm

Blister lesion equal or greater than 05 cm

Phlyctena large blister

Pustule vesicle of purulent content

Cyst encapsulated lesion of semi-solid or liquid content

bull Of solid consistency

Macule a patch of skin that changed color which is neither

raised nor depressed (non palpable)

When a macule is red in color it is described as erythematous If

it does not disappear afer a diascopy it is regarded as purpuric

(it translates the existence of extravasated blood)

In diff erental diagnosis of purpuric lesions senile purpura must

be taken into account which consists in the presence of viola-

ceous macules in areas exposed to trauma as a consequence

of capillary fragility Other cause for purpura is leukocytoclastc

vasculits which typically gives palpable purpuric papules but

not nodules

Papule small solid circumscribed elevaton of the skin of less

than 1 cm which resolves without leaving a scar It is called

plaque if it is equal or greater than 1 cm Unlike macule both

are palpable

Wheal erythematous edematous plate of dermal origin and of

fleetng evoluton (it disappears in less than 24 hours) It is char-

acteristc of urtcaria

Nodule circumscribed hypodermal lesion identfied by palpa-

ton It may or may not be raised (ldquoit is palpable rather than vis-

iblerdquo) Nodules are typical lesions of panniculits like the ery-

thema nodosum

Tubercle circumscribed infi

ltrated and raised nodule that usu-ally leaves a scar once it has resolved

Gumma granulomatous inflammaton that sofens and opens

gradually

Secondary Clinical Lesions

bull Secondary clinical lesions expected to disappear on their own

Scales plates in the stratum corneum which come off by them-

selves

Scab secreton or exudate or dried blood over the skin

Slough black necrotc plate of tssue with demarcated bor-

ders

bull Solutons of contnuity Erosion loss of epidermal substance that heals without leaving

a scar

Ulcer loss of epidermal and dermal substance that leaves a scar

afer healing

Excoriaton erosion secondary to scratching

Fissure crack that reaches high dermis as a result of hyperkera-

tosis

bull Others

Sclerosis skin induraton with elastcity loss due to fibrosis and

dermal collagenizaton

Scar fibrous tssue that replaces normal skin

Lichenifi

cat

on thickening of the epidermis with accentuat

on ofskin folds secondary to chronic scratching

Intertrigo cutaneous lesion located in skin folds

Telangiectasia arboriform erythematous macule secondary to

permanent dilaton of cutaneous vessels

Poikiloderma hypopigmented and hyperpigmented areas

with atrophy and telangiectasias Poikiloderma is unspecific

and it translates into the presence of chronic cutaneous dam-

age

As a summary Figure 2 lists the main cutaneous elemental lesions com-

mented on this item

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Amer ican Manual of Examinat ion in Medicine (2CK)

2

bull Type II is mediated by IgM and IgG G Cytotoxic Hemolytc anemia

bull Type I is mediated by immune complexes Toxicodermas

bull Type IV is mediated by T lymphocytes (cellular) Contact derma-

tts

32 Atopic Dermatitis

Atopic dermatts is an inflammatory disorder of the skin with chronic

and recurring presentaton which aff ects 12 - 15 of children popula-

ton Atopic dermatts manifests itself by dry skin and pruritus

Patents have more risk of bacterial secondary infectons (S aureus) and

viral infectons (simple herpes virus SHV or mollusca)

There is a variety of triggering factors or factors that maintain eczema

outbreaks aeroallergens (dust mites) bacterial antgens (S aureus)

food (ovoalbumin) and psychological stress among others

Clinical Presentation

Clinical presentaton is usually in the form of greasy erythematous

and desquamatve papules or plaques on the scalp (cradle cap in the

cases of newborns) central area of the face sternal region axilla and

or groin In newborns this presentaton can be generalized causing

Leinerrsquos erythroderma desquamatvum in adults it is likely to be re-

lated to blepharits

Diff erental diagnosis includes atopic eczema in children but diff eren-

tal diagnosis in adults reveals subacute erythematous lupus or pink

pityriasis when the trunk is involved and inverted psoriasis when skin

folds are aff ected

Remember

Letterer-Siwe disease can cause lesions similar to infantile seborrheicdermatitis However unlike infantile seborrheic dermatitis Letterer-Siwedisease is associated with lymphadenopathies and hepatosplenomegaly

Remember

Impetigo key words (yellowish scabs) should not be mistaken for seborrheicdermatitis key words (yellowish scales)

Diagnosis

Atopic dermatts has a clinical diagnosis Patents may present with eo-

sinophilia and increase of IgE values

Treatment

It is essental for the patent to follow certain rules in his lifestyle This

means the patent must avoid wearing perfumed products (like cologne

and cream) being exposed to extreme temperatures the use of fabric

sofeners and carpets or fluff y toys (because of possible sensitzaton of

dust mites) Besides the patent needs to wear 100 coon clothing

Macule Vesicle

Wheal Fissure

Papule Ulcer

Nodule Cyst

Figure 2 Cutaneous elemental lesions

22 Histological Lesions

The following are histological lesions of the skin

bull Hyperkeratosis increase in the stratum corneum (warts and psoriasis)

bull Hypergranulosis granular layer thickening

bull Acanthosis thickening of the stratum spinosum

bull Acantholysis rupture of intercellular bridges of the stratum spino-

sum (typical of pemphigus)

bull Spongiosis intercellular intraepidermal edema (characteristc of eczema)

bull Ballooning intracellular edema (herpes)

bull Parakeratosis presence of nuclei in the stratum corneum (typical

of psoriasis)

bull Dyskeratosis abnormal keratnizaton of individual cells of the stra-

tum spinosum (typical of Darierrsquos disease)

bull Papillomatosis lengthening of dermal papillae (psoriasis)

Chapter 03

Allergic and

Immune-mediated

Diseases

31 Hypersensibility Reactions

bull Type I is mediated by IgE It is the most rapid Anaphylaxis asthma

and urtcaria

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Dermatology

Precocious treatment is of the utmost importance

Topic cortcoids are the first line treatment

It is worth to remember that prolonged use of topic cortcoids can have

local and systemic secondary side eff ects

The second line of treatment involves immunomodulators (tacrolimus

and pimecrolimus) These can be used in children older than 2 years of

age

For acute outbreaks oral cortcoids are used in short cycles and not as

maintenance To stop medicaton suddenly may cause a rebound eff ect

33 Contact Eczema

The appearance of contact eczema is immunologically mediated (type

IV hypersensit

vity) against foreign agents acquired by percutaneouspenetraton Contact eczema requires prior sensitzaton to allergen

It is more common in adults than in children

Diagnosis

Diagnosis is established with clinical records and epicutaneous tests of

contact These tests are performed once lesions have been resolved by

applying patches with allergens on healthy skin leaving them in contact

with the skin during 48 hours They are read afer 48 and 96 hours The

intensity of reacton is measured qualitatvely negatve weak positve

(erythema) strong positve (papules-vesicles) or extreme positve (blis-

ters)

Treatment

Avoid contact with the allergen

Treatment of acute eczema implies applicaton of topic poultce (zinc

sulphate sodium borate) and cortcoids if lesions are limited and sys-

tem poultce if lesions are generalized

34 Seborrheic Dermatitis

Seborrheic Dermatts is a quite frequent disease It aff ects 4 - 5 of the

populaton Etology of seborrheic dermatts is unknown although it

has been related to an abnormal immunological response to a fungus

called Pityrosporum ovale Seborrheic dermatts is more frequent and

intense when associated to neurological processes alcoholism and im-

munodeficiencies

Clinical Presentation

According to patentrsquos age

a Seborrheic dermatts in infants Yellowish scales on scalp known

as cradle cab

b Seborrheic dermatts in adult erythematous desquamatng papu-

les or plates in fat areas of the facial region and scalp

Diagnosis

Diagnosis of this conditon is clinical

TreatmentTreatment involves antfungals associated with topic cortcoids Sebor-

rheic dermatts on the scalp is usually linked to a keratolytc agent like

the salicylic acid

35 Psoriasis

Psoriasis is a chronic inflammatory disease of the skin that presents

with outbreaks Psoriasis aff ects 1-2 of the populaton and can ap-

pear at any age with a maximum of incidence between 20 and 30 yearsof age There is a family history in a third of the patents

Plates are the characteristc erythematous desquamatng lesions well

delimited with a superficial thick and white-pearl scale

The most frequent clinical form is vulgar psoriasis or psoriasis in plates

Lesions are localized at extensor surfaces (elbows and knees) and the

scalp The umbilical and the lumbosacral areas are ofen aff ected

Nail involvement is frequent and is most common with a pi ng ap-

pearance This form is lile specific The forms that combine hyperkera-

tosis and distal onycholysis are more specific Oil spot is the most char-

acteristc sign (Figure 3)

Figure 3 Generalized pustular psoriasis

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Amer ican Manual of Examinat ion in Medicine (2CK)

4

Diagnosis

Diagnosis of this conditon is generally clinical

If there is no certainty a biopsy must be done which will reveal hyper-

keratosis acanthosis and parakeratosis

There is an increase in polymorphonuclears (sterile abscesses) in the

stratum corneum which are called Munro abscesses

Treatment (Table 1)

For moderate severe forms of psoriasis that do not respond to clas-

sical systemic treatments (see table) They are monoclonal antbod-

ies against proinflammatory substances that are high in patents with

psoriasis [alpha tumor necrosis factor (TNF) interleukin IL 12 and

23] Some of them are infliximab adalimumab ustekinumab and

etanercept

36 Urticaria

Urtcaria is an immunologic and inflammatory reacton of the skin

against diverse etological factors Independently of the cause release

of histamine and other inflammatory mediators occurs which cause va-

sodilaton and increase in capillary permeability producing an edema in

superficial dermis Urtcarias are divided in acute and chronic urtcarias

depending on whether outbreaks persist more or less than six weeks

About 60 of acute urtcarias are idiopathic Chronic urtcarias show a

higher percentage

Urtcarias of known origin are usually due to infectons drugs or food

Clinical Presentation

Clinical presentaton is characterized by the appearance of pruritc wheals

that last less than 24 hours and can be accompanied with angioedema

TREATMENT USES SIDE EFFECTS AND CONTRAINDICATIONS

Topic Mild-moderatepsoriasis

(lt 25 body

surface)

Emollients (urea glycerin) Moisturizing

Keratolytics (salicylic acid) Eliminate excess of scales

Reductants (dithranol) Hyperkeratotic plaques middot Stain skin and clothing

middot Irritating

middot Acneiform eruptions

Corticoids middot Stable psoriasis

in plates

middot The most used

middot Tachyphylaxis

middot Percutaneous absorption

middot Possible new outbreak after stopping medication

middot Avoid prolonged treatment

Vitamin D analogues

(calcitriol calcipotriol and

tacalcitol)

Stable psoriasis in plates middot Irritating in face and skin folds

middot Hypercalcemia

Systemic Moderate-

severe psoriasis

(gt 25 body

surface)

Psoralens plus ultraviolet

light of the A wavelength(PUVA)

Combinable with topics

and retinoids (RePUVA)

middot Cutaneous aging and carcinogenesis

middot Erythroderma and xerosis middot Immunosuppression

middot Hepatitis by psoralens

middot Not in children pregnancy patients with hepatic or renal

insuffi ciency photosensitivity or cutaneous precancerosis

middot Cataracts

middot It accumulates in the crystalline during 24 h (sunglasses)

Retinoids (acitretin) middot Severe psoriasis

pustular

or erythrodermic

middot It is not usually used

in women in fertile age

(see side effects)

middot Cutaneous dryness (the most frequent)

middot Hypertriglyceridemia

middot Hypercholesterolemia

middot Increase in transaminases

middot Diffuse alopecia

middot Vertebral hyperostosis ligamentous calci1047297cations

middot Teratogenicity avoid pregnancy until 2 years after

1047297nishing treatment

middot Avoid in children and patients with hepatic or renal failure

Cyclosporine A middot In1047298ammatory severe

psoriasis resistant to

other treatments

middot Rapid action

middot Rebound effect

middot Nephrotoxicity

middot High blood pressure (HBP)

middot Epitheliomas and lymphomas

middot Hypertrichosis

middot Gingival hyperplasia

middot Hyperuricemia

Methotrexate middot Severe psoriasis

resistant to other

treatments

middot Psoriatic arthropathy

middot Hepatotoxicity

middot Myelosuppression

middot Teratogenicity until 3 months after ending treatment

middot Photosensitivity

Table 1 Psoriasis treatment

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Dermatology

Vasculits urtcaria should be ruled out when lesions last more than 24 hours

and are accompanied with systemic clinical symptoms (ie arthralgias)

Treatment

Oral anthistamine therapy is the treatment of choice

Systemic cortcoids for severe or refractory cases

Adrenalin for severe cases with anaphylaxis

37 Toxicodermas

Toxicodermas are quite variable cutaneous reactons that appear afer

drug administraton They are one of the most frequent side eff ects of

drugs The causatve agents for many toxicodermas stll remains un-

known either immunological or not and clinical presentaton does not

facilitate agent dist

nct

on

Morbilliform exanthem is the most frequent A morbilliform exanthem

is a generalized erupton formed by symmetric and confluent macules

and papules that usually start by the trunk

They can appear one or two weeks afer taking the drug

A morbilliform exanthem can be associated with fever pruritus and eo-

sinophilia

The most frequent are non steroid ant-inflammatories antbiotcs (sul-

phamides and penicillins) antepileptcs allopurinol and N acetyl-cystene

DiagnosisDiagnosis is according to clinical presentaton

Treatment

Treatment implies withdrawal of potentally responsible drug Topic or

systemic anthistamines and cortcoids are given according to the extent

of symptoms (Figure 4)

Figure 4 Morbilliform exanthem due to amoxicillin

38 Multiform Erythema

Stevens-Johnson Syndrome

and Toxic Epidermal Necrolysis

Multform erythemas (ME) are of undetermined etopathogenesis

regarded as a cutaneous reacton against a diversity of stmuli Their

histologies show similarites what leads to consideraton of a common

pathogenesis

Clinical Presentation

Three diff erent groups have been described although many a tme their

clinical symptoms overlap

bull Erythema multforme minor is the most frequent with around 80

of the cases It usually precedes a symptomatc infecton by simple

herpes virus (60) or subclinical infecton about 15 days before

Erythema multforme minor manifests itself on extensor surfaces

at hands elbows and feet as a symmetric erupton of erythema-

tous edematous lesions with target-shape (herpes iris of Batemanor rosee-paerned lesion) with a violaceous sometmes bullous

center (Figure 5)

Mucosal aff ectaton is rare with small erosions in oral mucosa Erythe-

ma multforme minor tends to recurrence with subsequent outbreaks

of herpetc lesions

Figure 5 Erythema multiforme minor Herpes iris of Bateman

bull Erythema mult

forme major or Stevens-Johnson syndrome is therarest It normally has a prodromal period of untl 14 days with fe-

ver cough cephalea arthralgias and other symptoms Subsequent

to the prodromal period erythematous edematous plates appear

which are more extensive with a tendency to form blisters and

greater mucosal erosions (mouth genitals pharynx larynx and

conjunctve Figure 6) Systemic symptoms are normal and do not

tend to recurrence

The most frequent etological factors are drugs [sulphamides non

steroid ant-inflammatory drugs (NSAIDs) antconvulsants and an-

tbiotcs in decreasing order) Infectous agents have been also in-

volved mainly mycoplasma pneumoniae

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Amer ican Manual of Examinat ion in Medicine (2CK)

6

Figure 6 Exudative erythema multiforme major

bull Toxic epidermal necrolysis (TEN) many authors consider it the

most severe form of erythema multforme major arguing the same

pharmacological agents A morbilliform rash appears which is rap-idly confluent comprising almost the entre skin surface with flaccid

blisters that leave wide areas of denuded skin Involvement of sev-

eral mucosae is constant

Complicatons ofen occur (pneumonia digestve hemorrhage re-

nal failure and hemodynamic shock) with mortality rates close to

25 In children it must be performed a diff erental diagnosis with

staphylococcal scalded skin syndrome which does not aff ect mu-

cosae

Remember

Diseases that have the Nikolsky sign are TEN staphylococcal scalded skinsyndrome (SSSS) and pemphigus In TEN the whole epidermis comes off(bad prognosis) while in SSSS epidermal detachment occurs at the granularlayer

Histopathology

It must be highlighted the eff acement of dermoepidermal juncton by a

lymphohistocytc infiltrate and vacuolar degeneraton of the baseline lay-

er with necrotc keratnocytes In TEN keratnocytes necrosis is massive

Treatment

In ME minor only symptomat

c treatment is prescribed with topiccortcoids and oral anthistamines Treatment for herpes simplex virus

(HSV) infecton is useful to prevent ME lesions if patent is in the inital

stage of the viral infecton

ME major requires treatment of the underlying infecton or withdrawal

of implied drug and support measures The use of oral steroids accord-

ing to the patentrsquos general state is under discussion

A patent with TEN requires to be admied at the burn treatment room

with monitoring of hematocrit hydroelectrolytc balance and antbiotc

prophylaxis and support measures It is controversial the use of system-

ic cortcoids immunoglobulins andor cyclosporine

39 Erythema Nodosum

Erythema nodosum is the most frequent panniculits Painful erythema-

tous nodules occur mainly in the anterior side of legs with a self-limit-

ing course and predominantly aff ectng young women (Figure 7)

Figure 7 Erythema nodosum

They heal without leaving a scar within a period of four to six weeks

Erythema nodosum may be accompanied with fever deterioraton of

the general state and arthralgias

Patents with erythema nodosum may have a false positve VDRL

Etiology

This conditon is thought to be an immunological response triggered by

multple and diff erent stmuli bacterial fungal and viral infectons sys-temic diseases (sarcoidosis inflammatory intestnal disease Behcetrsquos

syndrome) neoplasias (lymphomas and leukemias) and drugs (oral

contraceptves sulphamides bromides and iodines)

Diagnosis

Erythema nodosum requires a deep biopsy to reveal septal panniculits

without vasculits

Complementary tests can be performed to rule out systemic involvement

for example chest X-ray Mantoux and antstreptolysin O antbody (ASLO)

Treatment Treatment entails eliminatng underlying cause if found then rest and

ant-inflammatories

310 Bullous Pemphigoid

and Pemphigus Vulgaris

See Table 2 and Figures 8 9 10 and 11

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Dermatology

Intercellular

substance ac

middot Pemphigus

Lineal

storage

in lucid

layer

-

Anti-Collagen Ac

Lucid

layer

Thick

layer

Basal

sublayer

Granular

storage

in papillary

dermis

middot Pemphigoid bullousmiddot Herpes gestationis

middot Acquired blistering epidermolysis

middot Dermatitis herpetiformis

Figure 8 Key points for histological diagnosis

of autoimmune blistering diseases

Figure 9 Pemphigus vulgaris

Figure 10 Pemphigus vulgaris with oral mucosa involvement with

erosions

Figure 11 Pemphigoid bullous Tense blisters No sign of Nikolsky

PEMPHIGUS VULGARISGENERALLY

IDIOPATHICHERPES GESTATIONIS

DERMATITIS

HERPETIFORMIS

Clinical presentation middot 40-50 years of age

middot They usually affect mucosae

middot No pruritus

middot Flaccid blister

middot Nikolsky

middot Elderly

middot Sometimes mucosae

middot With pruritus

middot Tense blister

middot No Nikolsky

middot Pregnant women

middot No mucosae

middot With pruritus

middot Herpetiform

middot No Nikolsky

middot 15-35 years of age

middot No mucosae

middot With pruritus

middot Herpetiform

middot No NikolskyDirect immuno1047298uorescence (DIF) IgG IgG IgG IgA

Histology middot INTRAepidermal blister

middot There is acantholysis

middot SUBepidermal blister

middot There are eosinophils

middot SUBepidermal blister

middot There are eosinophils

middot SUBepidermal blister

middot Neutrophils in dermis

Treatment Corticoids at high doses

immunosuppressants rituximab

and immunoglobulins

Corticoids Corticoids Diet +- dapsone

Remember Mortality rate 10 The most frequent Relapse if new

pregnancy

Associated to enteropathy

by gluten 90

Table 2 Autoimmune blistering diseases

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Amer ican Manual of Examinat ion in Medicine (2CK)

8

Chapter 04

Infectious Diseases

41 Viral Infections

Simple Herpes

Infection by Simple Herpes Virus

There are two types of simple herpes (Figure 12)

bull Type I is responsible for most extragenital herpes and 20 of the

genital herpes

bull Type II causes genital herpes and a small percentage of extragenital

herpes

Figure 12 Herpes simplex

Contagion is produced by direct contact though the carrier may be as-

ymptomatc Afer primary infecton virus remains silent in the sensi-

tve porton of cranial or spinal ganglia Immunosuppressed patents

endure the greatest severity of this conditon

Clinical Presentation

bull Extragenital simple herpes recurring orofacial herpes simplex is

the most frequent Most primary infect

ons are asymptomat

c Only5 manifest themselves in the form of herpetc gingivostomatts a

profile characterized by oral ulcers with cervical adenopathy and af-

fectaton of the patentrsquos general state (Figure 13) During relapses

clinical symptoms are milder with cluster vesicles on an erythema-

tous base Some factors facilitate relapses trauma sunlight cold

stress fever and the menstrual cycle

bull Genital simple herpes is the most common cause of genital ulcers

afer trauma Primary infecton is usually symptomatc and occurs

between 3 to 14 days afer sexual contact It causes clustered ulcers

in the balanopreputal sulcus or in the prepuce with painful inguinal

adenopathy Relapses are less severe than primary infecton and oc-

cur more frequently when genital herpes is due to HSV type II

Figure 13 Herpetic gingivostomatitis

bull Eczema herpetcum or Kaposi varicelliform erupton dissemina-

ton of herpetc infecton on pre-existng dermatosis (above all

atopic dermatt

s) bull Neonatal herpes is due to intrapartum contagion of HSV-II with

neurological involvement general deterioraton and skin vesicles or

ulcers

bull Other clinical forms are herpes gladiatorum herpetc whitlow and

keratoconjunctvits

Diagnosis

Diagnosis of this conditon is mainly clinical Virological culture is the

most reliable method of confirmaton The extent of a smear of the le-

sions (Tzanck cytodiagnosis) allows visualizaton of multnucleated cells

and intranuclear inclusions which become evident through histological

study

Treatment

Mild forms do not need treatment Treatment is required in the follow-

ing cases

bull Primary infecton

bull Severe or frequent relapses if they aff ect life quality

bull Complicatons like erythema multforme and eczema herpetcum

Drug of choice is oral acyclovir and its derivatves (valacyclovir famci-

clovir) Topic antvirals have not proven useful favoring maceraton of

lesions and thus over infecton It is not infrequent that topic antvirals

cause allergic contact dermatts due to hypersensitvity

Varicella-Zoster Virus

A primary infecton gives way to varicella (see Pediatrics secton) Afer

varicella the virus remains latent in the sensitve porton of the neural

ganglia and when relapse occurs it leads to zoster herpes

bull Varicella the following symptoms appear afer 15 days of incubaton

fever cephalea pruritus and polymorphic lesions in diff erent stages

macules papules vesicles (Figure 14) ulcers and scabs (starry sky

appearance) Mucosal (ulcers) and scalp involvement is characteristc

Manipulaton can leave scars Bacterial over infecton of lesions is the

most usual complicaton About 20 of adults suff er from varicella

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Dermatology

pneumonia radiologically demonstrable but clinical symptomatology is

only present in around 4 of the cases

Figure 14 Typical vesicles in patients with varicella

bull Zoster herpes thoracic zoster herpes is the most usual It sel-

dom occurs more than once throughout a personrsquos lifetime

It is characterized by vesicles on pre-existing erythema with

metameric distribution and lateral extension The most com-

mon complication is post herpetic neuralgia more frequent in

advanced age Carbamazepine or tricyclic antidepressants (Fig-

ure 15)

Figure 15 Zoster herpes

Special Clinical Forms

Special clinical forms are as follow

bull Ramsay-Hunt syndrome aff ectaton of geniculate ganglion of the

facial nerve

It produces vesicles in the outer ear external auditory canal and

pharynx homolateral facial paralysis deafness and vertgo

bull Ophthalmic involvement can result in severe keratts and requires ur-

gent referral to an ophthalmologist Suspicion should exist on patents

that present herpetc lesions on the tp of the nose) (Hutchinsonrsquos sign)

bull Disseminated zoster herpes several dermatomes are aff ected bilat-

erally Ramsay-Hunt syndrome is characteristc in the immunosup-

pressed

Remember

Affectation of the nose tip makes it necessary for ophthalmologicalexamination because the nose tip is innervated by the same nerve thatinnervates the cornea (1047297rst branch of the trigeminal nerve)

Treatment

Varicella without complicatons is treated symptomatcally Antvirals

are reserved for severe or complicated forms There is a commercial-

ized vaccine of live virus whose indicatons are stll under discussion

Zoster herpes must be treated with antvirals when detected during the

first 48-72 hours and aff ectng patents with

bull Immunosuppression

bull Age above 55

Special clinical forms previously cited

Drugs to be used are oral acyclovir and its derivatves (valacyclovir and

famciclovir) They accelerate the cure of lesions and decrease the inten-

sity of post herpetc neuralgia Patents with renal failure need a dose

adjustment as acyclovir is nephrotoxic These patents are adminis-

tered brivudine in a single daily dose

Molluscum ContagiosumDome shaped pink papules with central umbilicaton (Figure 16) Mol-

luscum contagiosum is typical of children that go to swimming pools It

is also present in the genital zone afer sexual contact and in immuno-

suppressed patents It is caused by Poxvirus

Figure 16 Molluscum contagiosum

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Amer ican Manual of Examinat ion in Medicine (2CK)

0

Lesions are asymptomatc

Diagnosis

Diagnosis is clinical Histology reveals characteristc inclusion bodies

Treatment

Lesions can resolve spontaneously

Cureage cryotherapy or local trichloroacetc acid are eff ectve meth-

ods to destroy lesions

Warts

Human papillomavirus can cause verruca vulgaris palmoplantar and

flat warts and condyloma accuminata Human papillomavirus is the

most frequent sexual transmied disease

Some subtypes of this virus (16 18) are of high risk and can cause epi-

dermoid carcinomas

Direct contact is the mechanism of contagion

Diagnosis

Diagnosis of this conditon is clinical

Staining with acetc acid can help visualize mucosal lesions

Treatment

Genital warts are treated with cryotherapy podophyllotoxin trichloro-

acetc acid imiquimod and 5-fluorouracil

Cervical lesions should be monitored by cytology and biopsy whenever

necessary to rule out cervical cancer (Figures 17 and 18)

Figure 17 Warts in HIV patient

Figure 18 Condyloma accuminata

42 Bacterial Infections

Impetigo

Impetgo is a very contagious superficial infecton without systemic re-

percussion and normally mixed etology by Gram positve cocci (strep-

tococci and staphylococci) Classically the most frequent accepted

cause was Streptococcus pyogenes However at present Staphylococcus

aureus stands out as the predominant cause

The most typical form is impetgo contagiosa (Figure 19) character-

ized by honey-colored (meliceric) scabs which normally appear on

the face and other exposed areas It is typical of children Although

infrequent poststreptococcal glomerulonephrits is a dreadful com-

plicaton

Figure 19 Impetigo contagiosa

On the contrary rheumatc fever shows no relaton to cutaneous strep-

tococcal infectons but only with pharyngeal infectons

There are other less habitual forms called bullous impetgo exclusively

of staphylococcal origin Clinical presentaton involves the presence of

blisters and erosions on the aff ected skin as a consequence of the epi-

dermolytc toxins that these bacteria contain Impetgo is treated with

topical mupirocin penicillin or oral fusidic acid

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Dermatology

Cellulitis

Cellulits is an infecton that aff ects deep dermis and subcutaneous cel-

lular tssues normally caused by streptococci (Streptococcus pyogenes

or of group A)

Community methicillin-resistant S aureus (CMRSA) is a triggering agent

that is becoming more and more frequent

Most common risk factors are diabetes chronic venous insuffi ciency

and immunosuppression

Clinical Presentation

Cellulits presents with erythematous plaques that are ill-defined pain-

ful and hot It is usually accompanied with fever and chills

Diagnosis

Diagnosis is clinical If there is an open door a culture of this area may

help see the source germ and resistance to ant

biot

cs

It is important to rule out abscesses osteomyelits and necrotzing fas-

ciits

If bacteremia is suspected blood cultures need to be performed

Treatment

Treatment implies oral antbiotcs for 7-10 days to cover Gram positve

cocci They are intravenously administered in case of lack of response

to oral treatment involvement of hands or periorbital zone diabetes or

extremes of age

Necrotizing FasciitisNecrotzing fasciits is a deep infecton up to muscular fascia that pro-

duces very intense pain and subsequent anesthesia

In 10 of the cases cellulits is due to an infecton by S pyogenes In the

remaining cases it occurs by a polymicrobial infecton caused by aerobes

and anaerobes including S aureus E coli and Clostridium perfringens

There may be prior history of trauma or surgery

Clinical Presentation

Clinical presentat

on involves pain of sudden onset and edema on theaff ected zone Pain may progress to anesthesia There appears subse-

quent erythema that progresses rapidly into necrosis

Characteristc clinical signs are tssue necrosis blisters intense pain

and gas producton

Diagnosis

Diagnosis is clinical and requires image testng X-rays or a computed

tomography CT

A biopsy of the border of the lesion helps achieve diagnosis

Treatment

Treatment entails precocious surgical debridement It is a surgical emer-

gency In additon to surgery broad-spectrum antbiotherapy will be

needed

Folliculitis

Folliculits is an infecton and inflammaton of one or several follicles

caused mainly by staphylococci

Clinical Presentation

Folliculits shows pustules with follicular distributon

When the infecton is deeper it is called furuncle

If several furuncles are infected a fluctuatng erythematous plaque forms

containing several points of suppuraton This plaque is labeled as anthrax

Diabet

c and immunosuppressed pat

ents are at higher risk

Characteristics of Folliculitis

1 Hot tub or swimming pool folliculits caused by Pseudomonas aeru-

ginosa

2 HIV associated pruritc folliculits or eosinophilic folliculits

Treatment

In mild cases treatment of choice comprises antseptcs and topic an-

tbiotcs

In more severe cases treatment of choice requires oral antbiotcs

Large sized lesions must be drained and a microbiological culture must be

performed to rule out methicillin-resistant Staphylococcus aureus MRSA

Acne Vulgaris

Acne is an inflammatory disease of the pilosebaceous follicle as a con-

sequence of an alteraton in follicular keratnizaton It aff ects adoles-

cents and young adults

Etology is multfactorial alteraton of keratnizaton of follicular infun-

dibulum quanttatve and qualitatve alteraton of sebum producton in

the sebaceous gland and alteratons of bacterial microflora (increase in

quant

ty of P acnes)

Aggravatng factors are stress androgenic oral contraceptves and the

use of cosmetc products that are not oil-free

Clinical Presentation

A comedo is the inital lesion which can be closed (whitehead) or open

(blackhead) and it evolves into inflammatory lesions that listed in as-

cending order of severity are papules pustules nodules and cysts

Lesions progress and leave scars Scars can be increased if lesions are

manipulated

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2

Diff erent lesions habitually combine simultaneously so acne becomes

polymorphic It is located in sebaceous areas face back shoulders and

the center thoracic region

Diagnosis

Diagnosis is clinical

Treatment

bull Comedonal acne is treated with topic retnoids and benzoyl peroxide

bull Inflammatory acne treatment requires benzoyl peroxide combined

with topic antbiotcs (erythromycin and clindamycin) Systemic

antbiotc treatment with oral tetracyclines will be prescribed if re-

sponse to topic antbiotc treatment fails

bull Severe nodular cystc acne treatment involves the use of isotret-

noin (13-cis-retnoic acid) It is a derivatve of vitamin A Isotretnoin

produces atrophy in the sebaceous gland and regulates keratniza-

ton The most frequent side eff ect is cutaneous and mucosal xero-

sis Triglycerides cholesterol and transaminases should be moni-

tored as their values may increasebull It can be associated with depression

bull It is teratogenic so pregnancy should be avoided during treatment

and untl a month afer treatment

Pilonidal Cysts

Pilonidal cysts are abscesses in the sacrococcygeal region

This type of cysts has predominance in men between 20 and 40 years

of age It is believed that repeated trauma on the aff ected area favors

their appearance

Clinical Presentation

Pilonidal cysts present with an indurated lesion that is fluctuatng hot

painful but non-adherent to deep planes in the sacrococcygeal region

Pilonidal cysts may or may not be associated to cellulits and purulent drain-

age

Diagnosis

Diagnosis is clinical and anal or perirectal abscesses should be dismissed

Treatment

Treatment implies an incision and surgical drainage

On some occasions a general surgery is required

43 Fungal Infections

Pityriasis Versicolor

Versicolor pityriasis is caused by commensal yeast called Pityrosporum

ovale which transforms into its pathogen form (Malassezia furfur) It

especially aff ects young patents (15 - 45 years of age) but it is rare

in childhood and advanced age Versicolor pityriasis relates to heat

humidity and sebaceous hypersecreton It is characterized by the ap-

pearance of hyperchromic or hypochromic macules that desquamate

on scratching (nail sign) if infecton is actve Macules usually appear on

the center thoracic region and on the back that is to say on seborrheic

zones Relapses are habitual despite treatment

Diagnosis

Diagnosis is normally clinical To that purpose the following serve as

support

bull Woodrsquos lamp emits yellow-orange fluorescence

bull Potassium hydroxide (KOH) test filaments and round elements can

be observed (ldquospaghe and meatball appearancerdquo Figure 20)

Treatment

Treatment is performed with topical azoles Oral administraton applies

for extensive cases or immunosuppressed patents Diff erental diagno-

sis includes pink pityriasis and eczemas (Figure 21)

Figure 20 Versicolor pityriasis Histological cut

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Dermatology

Figure 21 Versicolor pityriasis

Candidiasis

The most common triggering agent is Candida albicans It is normally sapro-

phyt

c although under certain condit

ons candidiasis may become patho-genic (immunosuppression humidity pregnancy and contraceptves)

Clinical Forms

bull Intertrigo erythematous plaque in cutaneous folds Atrophy and

fissures are typically deep in the skin fold as well as satellite and

peripheral lesions (papules andor pustules)

bull Mucosa involvement may cause diverse symptomatology like vul-

vovaginits glossits and white papules in the anterior region of the

oral mucosa Candidal balanits is characterized by the presence of

punctform erosions and pustules on gland and balanopreputal

sulcus Candidal balanits ofen appears afer sexual intercourse or

afer oral antbiotc intake

Remember

Almost a 100 of HIV patients suffer from muguet throughout their diseasecourse

bull Candidiasis of nail fold is usually associated with periungual inflam-

maton (perionixis) and inital proximal aff ectaton which diff erent-

ates it from tnea unguium (Figure 22)

Figure 22 Candidiasis of nail fold

Treatment

Oral Candidiasis fluconazole or nystatn

Candidiasis of the skin (intertrigo) apply topical antfungal medicaton

and keep zone clean and dry

Dermatophytosis or TineasDermatophyte infectons aff ect the skin and keratnized structures like

hair and nails (there is no mucosa involvement) Clinical diagnosis is

achieved afer performing a culture Woodrsquos lamp test normally turns

out to be negatve In general Trichophyton dermatophyte rubrum is

the most frequent dermatophyte

Non Inflammatory Tineas

Non inflammatory tneas do not produce irreversible scarring alope-

cia while inflammatory forms do Tineas are treated with azoles de-

rivatves

The types of tnea are the following

bull Ringworm of the scalp ( t nea capi t s or t nea tonsurans) is charac-

teristc of childhood It presents with alopecic plaques broken hair

and desquamaton Infectons tend to resolve spontaneously with-

out leaving scars at the onset

of puberty

bull Ringworm of the body (herpes

circinatus or t nea corporis) are

erythematous desquamatve

plaques (with more actve bor-

ders) which are also circinate

and normally pruritc (Figure

23) Plaques grow eccentrically

with less actvity in the centerand more in the borders

bull Ringworm of the foot ( t nea

pedis) the most frequent is the

ldquoathlete footrdquo with desquama-

ton in interdigital spaces

bull Tinea incognito refers to tnea

wrongly treated with cort-

coids what makes diagnosis

diffi cult as the lesion has been modified Figure 24)

Figure 24 Tinea incognito secondary to treatment with topical steroids

Figure 23 Herpes circinatus

(tinea corpis)

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Amer ican Manual of Examinat ion in Medicine (2CK)

4

bull Ringworm of the groin (t nea cruris or eczema marginatum von

hebra) formed by erythematous desquamatve plaque with more

actve borders (Figure 25)

Figure 25 Ringworm of the groin (tinea cruris)

bull Tinea unguium subungualhyperkeratosis with onychol-

ysis but without perionixis

(Figure 26)

Diagnosis

Clinical diagnosis is reached afer

performing a culture

Treatment

Treatment involves topical an-

tfungal medicaton in localized

areas

Oral antfungal medicaton is used in extensive forms nail fold or scalp

involvement

44 Parasitic Infections

Pediculosis

Pediculosis is transmied by direct contact or by contact with fomites

which release toxins that produce intense pruritus

Clinical Presentation

Pediculosis capi t s intense pruritus predominant in retroauricular and

occipital regions occasionally with excoriatons and impetginizaton

secondary to excoriatons

Pediculosis corporis intense pruritus in patents with poor hygiene or

who live in overcrowded conditons

Pediculosis pubis genital and pubic pruritus Brownish-grey macules

called maculae ceruleae are typical on underwear and skin These pig-

mentatons appear as a result of a reducton in hemoglobin by a para-

site enzyme

Diagnosis

Diagnosis is clinical and by direct visualizaton

Treatment

Pediculosis is treated with malathion lindane or topical permethrin

Scabies

Scabies is originated by an acarus known as Sarcoptes scabiei It has an

incubaton period of 1 month

Clinical Presentation

Scabies produces generalized pruritus more intense at night The pa-

tent usually catches the infestaton which is passed to the patentrsquos

relat

ves It is common tofi

nd that a recent trip to a tropical country hasbeen made Lesions appear between the fingers (Figure 27) in wrists

feet genitalia mammary areola and axilla but back and face are usu-

ally spared The most specific lesion is the acarine burrow in whose less

scaly end the advancing zone the mite lies Nodules are frequent in

axilla and genitals (nodular scabies)

bull Norwegian scabies is typical of the immunosuppressed Patents

present with generalized hyperkeratosis and scabs Norwegian sca-

bies produce lile pruritus but it is very contagious because there

are many acari

bull Nodular scabies involves the persistence of pruritc nodules despite

treatment Lesions usually appear in axilla and genitalia Pruritus is

due to a hypersensitvity phenomenon because of the acarus al-

ready dead Nodular scabies is treated with cortcoids

Figure 27 Scabies Acarine burrow

Treatment

bull Permethrin cream at 5 is the treatment of choice It is lile toxic

so it can be used in children and pregnant women

bull Topical lindane at 1 irritates and is neurotoxic therefore it is con-

traindicated in pregnant women and children

bull Oral ivermectn is utlized in cases of resistance to prior treatments

There is stll lile experience as to its use but in a first instance a

Figure 26 Tinea unguium

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Dermatology

single dose would be enough to cure scabies (already used by vet-

erinarians)

45 Ischemia

Decubitus Ulcers

Decubitus ulcers are the result of ischemic necrosis by contnuous pres-

sure on an area which restricts microcirculaton in that zone

Clinical Presentation

Decubitus ulcers are present in patents in bed with scarce mobilizaton

It is favored by bone prominences and lack of fat tssue If sensitvity

decreases there is more risk of formaton of decubitus ulcers

Diagnosis

Diagnosis is achieved based on medical records and clinical presentaton

Treatment

Preventon is of the utmost importance as well as frequent mobiliza-

ton of the patent in bed

Once ulcers have been established hydrocolloid dressings are used for

healing but sometmes surgical debridement is necessary

Gangrene

Gangrene means tssue necrosis

There are three types dry gangrene wet gangrene and gas gangrene

Clinical Presentation

Dry gangrene is due to ischemia generally secondary to atherosclero-

sis Clinical presentaton involves pain cold and paleness of extremi-

tes Once tssue is established it turns bluish-black in color and dry

Wet gangrene is owing to bacterial flora Tissue presents with an edem-

atous appearance either with blisters or pus

Gas gangrene caused by C perfringens It is normally located on re-

cent surgery Bacteria precociously destroyt

ssue producing gas It is amedical emergency

Diagnosis

Clinical diagnosis is obtained by microbiological culture

Treatment

Treatment requires surgical debridement with amputaton if necessary

and associaton of broad spectrum antbiotherapy

Gas gangrene is treated with hyperbaric oxygen

46 Miscellaneous

Acanthosis Nigricans

Acanthosis nigricans are vel-

vet-like papillomatous brown

plaques in neck axilla and groin

folds (Figure 28)

It is associated with diabetes

mellitus Cushingrsquos disease poly-

cystc ovarian syndrome and

obesity

The malignant form of acantho-

sis nigricans is a paraneoplastc

syndrome that diff erentates

from the benign form because

the laer has mucosal and pal-

moplantar involvement

Lichen Planus

Lichen planus is an inflammatory idiopathic disease that equally aff ects

both genders with higher frequency in middle age

Lichen planus has been related to diverse drugs like gold salts

anti-malarial medication and thiazides It has been also linked to

hepatitis C virus infection however this association is currently

doubtful

Clinical Presentation

Lichen planus presents with red-violaceous polygonal flat papulesquite pruritc which localizes on the flexor side of wrists forearms an-

kles and lumbosacral and flank regions On its surface a whitsh retcu-

late can be observed (Wickhamrsquos striae) About 60 - 70 of the cases

present with lesions in oral and genital mucosa oral which appear as

whitsh retculated lesions (Figures 29 and 30)

Figure 29 Lichen planus of oral mucosa with typical whitish

reticulate

Figure 28 Acanthosis nigricans

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Amer ican Manual of Examinat ion in Medicine (2CK)

6

Violaceous papules

with white stretch marks

Lichenoid lymphocyte

in1047297ltrate (band formation)

Destruction

of basal layer

Figure 30 Lymphocytic interface reaction (lichen planus)

Treatment

Mild forms are treated with topical cortcoids

Severe cases require oral cortcoids psoralens plus ultraviolet light of

the A wavelength (PUVA) or cyclosporine

Rosacea

Rosacea is a chronic disease of unknown pathogenesis characterized

by erythema and acneiform lesions on the face It aff ects middle aged

women (between 30 and 50 years of age) more

Rosacea etopathogenesis is unknown although there is involvement of

vasomotor lability infecton by Demodex folliculorum photo exposureand genetc predispositon

Clinical Presentation

Rosacea symptomatology comprises facial flushing episodes that end

up by provoking a persistent erythema telangiectasias and papulopus-

tular lesions without comedos Over tme ocular lesions and hyperpla-

sia of sof tssue may develop

Treatment

Avoid vasodilator stmuli

Mild cases require topical metronidazole or azelaic acid

Moderate cases need doxycycline or oral minocyclines

Severe cases are treated with oral isotretnoin at low doses

Pink Pityriasis

Gilbertrsquos pink pityriasis is an acute self-limitng dermatosis which main-

ly aff ects young adults It is of unknown origin although a viral etology

is suspected (there is some speculaton as to links with human herpes-

virus type 7)

Clinical Presentation

Erupton starts with an erythematous plaque between 2 and 5 cm of

diameter with a desquamatve central collaree ofen localized on the

trunk (heraldic mother patch Figure 31)

Figure 31 Pink pityriasis

Around a week later oval papules appear on the trunk and extremi-

tes These papules share similar characteristcs with the mother patch

though the first ones are smaller and distributed according to skin ten-

sion lines Pink pityriasis may be asymptomatc however it is some-

tmes linked to pruritus Lesions may last between 4 and 8 weeks and

disappear without leaving scars

Diagnosis and Treatment

Diagnosis is clinical Treatment is seldom needed and recommended

therapies in the past (PUVA erythromycin or oral antvirals) have not

shown clearly favorable results

Vitiligo

Vitligo is characterized by achromic macules by melanocyte destruc-

ton

Clinical Presentation

Vitligo shows achromic macules of chronic course and variable progres-

sion

Lesions are predominant on acral and periorificial areas They also show

the Koebner phenomenon

Patents may have markers of autoimmune diseases (ie antthyroid

antbodies and diabetes) but these diseases seldom manifest them-

selves

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Dermatology

Treatment

Localized lesions require topical cortcoids

Extensive or generalized lesions are treated with ultraviolet light B

(UVB) or PUVA

Strict solar photoprotecton is indispensable (Figure 32)

Figure 32 Vitiligo

47 Neoplasias

Seborrheic Keratosis

Seborrheic keratosis is the most frequent benign tumor in human be-

ings since it is part of cutaneous aging

Clinical Presentation

Seborrheic keratosis presents with hyperkeratosic papules with an oily

or velvet-like texture crests fissures and horny plugs on their surface

These papules are normally pigmented showing a brownish-black color

Treatment

No treatment is required as lesions do not become malignant

Seborrheic keratosis can be addressed with cureage or cryotherapy

Actinic keratosis

Actnic keratosis is the most common precancerous lesion and aff ects

almost a 100 of the populaton in sunny areas

Clinical Presentation

Actnic keratosis is characterized by erythematous and desquamatve

papules which are hyperkeratosic and rough on touch developing a

chronic course

Diagnosis

Diagnosis is clinical

Treatment

Treatment entails applicaton of topical 5-fluorouracil topical imiqui-

mod cryotherapy or surgery

If underlying carcinoma is suspected a biopsy must be performed to

rule out suspicion

Epidermoid Carcinoma

Epidermoid carcinoma is the second most frequent cutaneous tumor

Solar photo exposure is the main etological factor which is why epider-

moid carcinoma appears in zones of prolonged solar exposure like the

face Most carcinomas appear over premalignant lesions (actnic kera-

tosis and leukoplakia among others)

Clinical Presentation

Clinical presentaton reveals erythematous or erythematosquamous

plaques Over tme these plaques form papules and tumors which of-

ten become ulceratve and bleed

Diagnosis

Diagnosis is based on clinical suspicion and histopathological confirmaton

Treatment

Surgery with safety margins is the treatment of choice In carcinomas

in situ cryotherapy can be used as well as topical imiquimod electro-

coagulaton or CO2 laser techniques in destructon of tumors Radio-therapy may also be used in some cases

Basal Cellular Carcinoma

Basal cellular carcinoma is the most frequent cutaneous tumor Chronic so-

lar photo exposure is the main etological factor hence most of these car-

cinomas aff ect the facial zone in patents who are 40 years of age or older

Gorlinrsquos syndrome should be considered if multple basal cellular carci-

nomas are found in non photo exposed areas

Clinical Presentation

Basal cell carcinoma shows a pearly pink papule and superficial telan-

giectasias

It is localized over healthy skin and never aff ects mucosae

Treatment

Surgery is the treatment of choice Mohs surgery is performed in zones

where surrounding healthy tssue needs to be preserved Other alter-

natves are cryotherapy imiquimod electrocoagulaton radiotherapy

photodynamic therapy and intralesional interferon Prognosis is excel-

lent as growth is slow and metastasis exceptonal

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Amer ican Manual of Examinat ion in Medicine (2CK)

8

Melanoma

Melanoma is the most aggressive cutaneous tumor given its ability to

metastasize

Risk factors comprise solar photo exposure clear phototype the pres-

ence of dysplastc nevus or a high number of melanocytc nevi Fam-

ily history is quite important as some genetc mutatons determine a

higher risk of developing the disease

Clinical Forms

See Figure 33

Diagnosis

Precocious diagnosis is essental to perform precocious surgical extrpaton

The ABCDE criteria can help patents to see if they need to seek medical

consultaton (asymmetry of lesion uneven borders color and diameter

greater than 6 mm or abnormal evolut

on)

The Breslow index is the thickness of the lesion measured in millimeters

and is the main prognosis factor

Treatment

The base of treatment is precocious surgical extrpaton If the Breslow

index is less than 1 mm margins of 1 cm will be performed If Breslow

index is greater than 1 mm margins will be of 2 cm

For melanomas with a Breslow index greater than 1 mm the sentnel

ganglion must be located This is the first draining lymph node of the

territory where the tumor is localized If the ganglion is positve re-

gional lymphadenectomy will be performed along with interferon ad-ministraton (Figure 34)

In situ Extirpation 05 cm Follow-up

Breslow lt 1 mm Extirpation 1 cm Follow-up

Lymphadenectomy

Breslow gt 4 mm Interferon

Breslow ge 1 mm Extirpation 2 cm Sentinel ganglion

+

Figure 34 Melanoma treatment

Kaposirsquos sarcoma

Kaposirsquos sarcoma is the most common cutaneous tumor in HIV patents

Clinical presentation

Kaposirsquos sarcoma has a course with violaceous fusiform macules whichovertme may evolve into indurated nodules with blackberry appearance

This type of sarcoma has been linked to herpesvirus type 8 both in HIV

and seronegatve patents (Table 3)

EPIDERMAL KAPOSIrsquoS 983080HIV983081 CLASSIC KAPOSIrsquoS

Homosexual youth (95) The elderly

Diffuse and bilateral

(frequently in palate and face)

Unilateral plaques

(lower extremities)

Frequent mucosal and visceral involvement Not so frequent

middot Precocious lymphatic invasion

middot Aggressive

Not so precocious

Table 3 Differences between epidermal and classic Kaposirsquos sarcoma

Nodular melanoma

15

Middle-aged men

middot On healthy skin

middot Any zone

middot Sudden onset

middot Uniform black nodulemiddot Rapidly invasive (vertical growth without radial)middot Frequent ulceration and bleeding

Worst histological prognosis

Lentigo malignant melanoma

10

Elderly women

90 on facephotoexposedzones of aging skins(chronic exposure)

Spot that growsduring many years (gt 10)then progresses (nodule)

Better prognosis

Acral lentinginous melanoma

5ndash10 ( 60 black and Asian race)

Elderly men

middot Sole (ankle) handsmucosa ungual bed

middot No relation to photo exposure

middot Macule with mosaic appearance (spot that grows)middot Some amelanisticmiddot Bad prognosis due to late diagnosis

Melanoma of super1047297cial extension

70

Young women

middot 30 previous nervusmiddot Intermittent exposuremiddot Men back middot Women legs

More frequent

middot Macula with mosaic appearance in colors that grows 4-5 years and then in1047297ltrates (nodule)middot Metastasis 35 to 70

Figure 33 Clinical forms of malignant melanoma

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Dermatology

Diagnosis

Diagnosis relies on clinical suspicion and histopathological confirma-

ton

Treatment

Treatment of localized forms can include surgical extrpaton radiother-

apy or intralesional vinblastne

If the sarcoma is disseminated optons involve interferon or chemo-

therapy

Mycosis Fungoides

Mycosis fungoides is a T-cell lymphoma of low-grade malignancy Its

clinical course may be very slow and surpass 50 years Three stages are

clinically diff erentated

1 Eczematous or macular phase predominantly truncular erythema-

tous macules with years of evoluton They resemble a chromic ec-

zema Histology is unspecifi

c at this stage2 Infiltratve plaque phase infiltrated erythematous plaques appear

Histology is diagnostc at this stage A dermal infiltrate of atypical

lymphocytes band forms can be observed composed of CD+4 T

lymphocytes with cerebriform nuclei There is a marked epidermo-

tropism with the presence of clusters of intraepidermal lympho-

cytes called Pautrierrsquos microabscesses (Figure 35)

Figure 35 Mycosis fungoides Infiltrative plaque phase

3 Tumoral phase erythematous exophytc plaques start to appear

(tumors) with a tendency to ulceraton They can have a large size

Histology may become unspecific again as epidermotropism disap-

pears

In more advanced stages of the disease there is aff ectaton of extra-

cutaneous organs such as lymph nodes liver spleen lungs and bone

marrow Besides there may be blastc transformaton Other possible

complicaton is sepsis by Staphylococcus aureus

These three stages usually develop consecutvely nevertheless there

may patents whose debut starts directly with the tumoral stage

Remember

Microabscesses of mycosis fungoides are due to lymphocytes and are calledPautrierrsquos abscesses Psoriasis microabscesses result from neutrophils andare labeled as Munro-Sabouraud

Seacutezary Syndrome

Seacutezary syndrome can be considered as the leukemic phase of T-cell cu-

taneous lymphoma It is defined by the triad erythroderma (Figure 36

lymphadenopathies and the existence of more than 1000 Seacutezary cellsper milliliter in peripheral blood Seacutezary cells are atypical T- lymphocyte

with cerebriform nuclei

Very intense pruritus is characteristc For many authors Seacutezary syn-

drome is an aggressive clinical form and a bad prognosis of a mycosis

fungoides

Figure 36 Erythroderma due to Seacutezary syndrome

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No part of this book may be reproduced stored in a retrieval system or transmitted in any form or by any

means electronic mechanical photocopying recording or otherwise without prior permission of the

holders of the copyright

copy CTO EDITORIAL SL 2015

Design and layout CTO Editorial

C Francisco Silvela 106 28002 Madrid

Phone no (0034) 91 782 43 30 - Fax (0034) 91 782 43 43

E-mail address ctoeditorialctomedicinacom

Website wwwgrupoctoes

ISBN full edition 978-84-16276-21-9

DISCLAIMER

Medicine is a science subject to constant change As research and clinical experience widen our

knowledge treatments and pharmacotherapy changes are necessary The editors of this work have

verified their results against reliable sources in an effort to provide general and complete information

according to the accepted criteria at the time of publication Nevertheless given the fact that

human error may occur or that some changes may take place in medical sciences neither the editor

nor any of the contributors involved in the preparation ndashor publication- of this work can guaranteethat the content herein is accurate and complete in each and every aspect The editors and the

contributing sources cannot be held responsible for any errors omissions or the outcome derived from

the use of the information provided herein Therefore readers are recommended to verify the content

of this work against other sources As an example it is especially advisable to read the package insert

of any drug to be administered to ensure that the information furnished by this publication is accurate

and no modifications were made either to the recommended dose or to the contraindications for

administering said drug This recommendation is particularly significant in relation to new or seldom

used drugs Readers should also check with their own laboratory about normal values

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D e r m a

t o l o g y

American Manualof Examination

in Medicine

(2CK)

AuthorsDolores Mendoza

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Amer ican Manual of Examinat ion in Medicine (2CK)

01 Skin Layers 1

02 Terminology Elemental Cutaneous Lesions 1

21 Clinical Lesions 122 Histological Lesions 2

03 Allergic and Immune-mediated Diseases 2

31 Hypersensibility Reactions 2

32 Atopic Dermatitis 2

33 Contact Eczema 3

34 Seborrheic Dermatitis 3

35 Psoriasis 3

36 Urticaria 4

37 Toxicodermas 5

38 Multiform Erythema Stevens-Johnson Syndrome

and Toxic Epidermal Necrolysis 539 Erythema Nodosum6

310 Bullous Pemphigoid and Pemphigus Vulgaris 6

04 Infectious Diseases 8

41 Viral Infections 8

42 Bacterial Infections 10

43 Fungal Infections 12

44 Parasitic Infections14

45 Ischemia 1546 Miscellaneous 15

47 Neoplasias 17

Index

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Dermatology

Chapter 01

Skin

LayersThere are three skin layers epidermis dermis and subcutaneous cel-

lular tssue (Figure 1)

Reticular layer

Sebaceous(Oil) gland

Hair

follicle

Deep

arteriovenousplexusSweat

glandDermal Papillae

Super1047297cial arteriovenousplexus

Subcutaneoustissue

Dermis

Epidermis

Figure 1 Microscopic structure of normal skin

Chapter 02

TerminologyElemental

Cutaneous Lesions

21 Clinical Lesions

Primary Clinical Lesions bull Fluid-filled

Vesicle raised formaton less than 05 cm

Blister lesion equal or greater than 05 cm

Phlyctena large blister

Pustule vesicle of purulent content

Cyst encapsulated lesion of semi-solid or liquid content

bull Of solid consistency

Macule a patch of skin that changed color which is neither

raised nor depressed (non palpable)

When a macule is red in color it is described as erythematous If

it does not disappear afer a diascopy it is regarded as purpuric

(it translates the existence of extravasated blood)

In diff erental diagnosis of purpuric lesions senile purpura must

be taken into account which consists in the presence of viola-

ceous macules in areas exposed to trauma as a consequence

of capillary fragility Other cause for purpura is leukocytoclastc

vasculits which typically gives palpable purpuric papules but

not nodules

Papule small solid circumscribed elevaton of the skin of less

than 1 cm which resolves without leaving a scar It is called

plaque if it is equal or greater than 1 cm Unlike macule both

are palpable

Wheal erythematous edematous plate of dermal origin and of

fleetng evoluton (it disappears in less than 24 hours) It is char-

acteristc of urtcaria

Nodule circumscribed hypodermal lesion identfied by palpa-

ton It may or may not be raised (ldquoit is palpable rather than vis-

iblerdquo) Nodules are typical lesions of panniculits like the ery-

thema nodosum

Tubercle circumscribed infi

ltrated and raised nodule that usu-ally leaves a scar once it has resolved

Gumma granulomatous inflammaton that sofens and opens

gradually

Secondary Clinical Lesions

bull Secondary clinical lesions expected to disappear on their own

Scales plates in the stratum corneum which come off by them-

selves

Scab secreton or exudate or dried blood over the skin

Slough black necrotc plate of tssue with demarcated bor-

ders

bull Solutons of contnuity Erosion loss of epidermal substance that heals without leaving

a scar

Ulcer loss of epidermal and dermal substance that leaves a scar

afer healing

Excoriaton erosion secondary to scratching

Fissure crack that reaches high dermis as a result of hyperkera-

tosis

bull Others

Sclerosis skin induraton with elastcity loss due to fibrosis and

dermal collagenizaton

Scar fibrous tssue that replaces normal skin

Lichenifi

cat

on thickening of the epidermis with accentuat

on ofskin folds secondary to chronic scratching

Intertrigo cutaneous lesion located in skin folds

Telangiectasia arboriform erythematous macule secondary to

permanent dilaton of cutaneous vessels

Poikiloderma hypopigmented and hyperpigmented areas

with atrophy and telangiectasias Poikiloderma is unspecific

and it translates into the presence of chronic cutaneous dam-

age

As a summary Figure 2 lists the main cutaneous elemental lesions com-

mented on this item

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Amer ican Manual of Examinat ion in Medicine (2CK)

2

bull Type II is mediated by IgM and IgG G Cytotoxic Hemolytc anemia

bull Type I is mediated by immune complexes Toxicodermas

bull Type IV is mediated by T lymphocytes (cellular) Contact derma-

tts

32 Atopic Dermatitis

Atopic dermatts is an inflammatory disorder of the skin with chronic

and recurring presentaton which aff ects 12 - 15 of children popula-

ton Atopic dermatts manifests itself by dry skin and pruritus

Patents have more risk of bacterial secondary infectons (S aureus) and

viral infectons (simple herpes virus SHV or mollusca)

There is a variety of triggering factors or factors that maintain eczema

outbreaks aeroallergens (dust mites) bacterial antgens (S aureus)

food (ovoalbumin) and psychological stress among others

Clinical Presentation

Clinical presentaton is usually in the form of greasy erythematous

and desquamatve papules or plaques on the scalp (cradle cap in the

cases of newborns) central area of the face sternal region axilla and

or groin In newborns this presentaton can be generalized causing

Leinerrsquos erythroderma desquamatvum in adults it is likely to be re-

lated to blepharits

Diff erental diagnosis includes atopic eczema in children but diff eren-

tal diagnosis in adults reveals subacute erythematous lupus or pink

pityriasis when the trunk is involved and inverted psoriasis when skin

folds are aff ected

Remember

Letterer-Siwe disease can cause lesions similar to infantile seborrheicdermatitis However unlike infantile seborrheic dermatitis Letterer-Siwedisease is associated with lymphadenopathies and hepatosplenomegaly

Remember

Impetigo key words (yellowish scabs) should not be mistaken for seborrheicdermatitis key words (yellowish scales)

Diagnosis

Atopic dermatts has a clinical diagnosis Patents may present with eo-

sinophilia and increase of IgE values

Treatment

It is essental for the patent to follow certain rules in his lifestyle This

means the patent must avoid wearing perfumed products (like cologne

and cream) being exposed to extreme temperatures the use of fabric

sofeners and carpets or fluff y toys (because of possible sensitzaton of

dust mites) Besides the patent needs to wear 100 coon clothing

Macule Vesicle

Wheal Fissure

Papule Ulcer

Nodule Cyst

Figure 2 Cutaneous elemental lesions

22 Histological Lesions

The following are histological lesions of the skin

bull Hyperkeratosis increase in the stratum corneum (warts and psoriasis)

bull Hypergranulosis granular layer thickening

bull Acanthosis thickening of the stratum spinosum

bull Acantholysis rupture of intercellular bridges of the stratum spino-

sum (typical of pemphigus)

bull Spongiosis intercellular intraepidermal edema (characteristc of eczema)

bull Ballooning intracellular edema (herpes)

bull Parakeratosis presence of nuclei in the stratum corneum (typical

of psoriasis)

bull Dyskeratosis abnormal keratnizaton of individual cells of the stra-

tum spinosum (typical of Darierrsquos disease)

bull Papillomatosis lengthening of dermal papillae (psoriasis)

Chapter 03

Allergic and

Immune-mediated

Diseases

31 Hypersensibility Reactions

bull Type I is mediated by IgE It is the most rapid Anaphylaxis asthma

and urtcaria

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Dermatology

Precocious treatment is of the utmost importance

Topic cortcoids are the first line treatment

It is worth to remember that prolonged use of topic cortcoids can have

local and systemic secondary side eff ects

The second line of treatment involves immunomodulators (tacrolimus

and pimecrolimus) These can be used in children older than 2 years of

age

For acute outbreaks oral cortcoids are used in short cycles and not as

maintenance To stop medicaton suddenly may cause a rebound eff ect

33 Contact Eczema

The appearance of contact eczema is immunologically mediated (type

IV hypersensit

vity) against foreign agents acquired by percutaneouspenetraton Contact eczema requires prior sensitzaton to allergen

It is more common in adults than in children

Diagnosis

Diagnosis is established with clinical records and epicutaneous tests of

contact These tests are performed once lesions have been resolved by

applying patches with allergens on healthy skin leaving them in contact

with the skin during 48 hours They are read afer 48 and 96 hours The

intensity of reacton is measured qualitatvely negatve weak positve

(erythema) strong positve (papules-vesicles) or extreme positve (blis-

ters)

Treatment

Avoid contact with the allergen

Treatment of acute eczema implies applicaton of topic poultce (zinc

sulphate sodium borate) and cortcoids if lesions are limited and sys-

tem poultce if lesions are generalized

34 Seborrheic Dermatitis

Seborrheic Dermatts is a quite frequent disease It aff ects 4 - 5 of the

populaton Etology of seborrheic dermatts is unknown although it

has been related to an abnormal immunological response to a fungus

called Pityrosporum ovale Seborrheic dermatts is more frequent and

intense when associated to neurological processes alcoholism and im-

munodeficiencies

Clinical Presentation

According to patentrsquos age

a Seborrheic dermatts in infants Yellowish scales on scalp known

as cradle cab

b Seborrheic dermatts in adult erythematous desquamatng papu-

les or plates in fat areas of the facial region and scalp

Diagnosis

Diagnosis of this conditon is clinical

TreatmentTreatment involves antfungals associated with topic cortcoids Sebor-

rheic dermatts on the scalp is usually linked to a keratolytc agent like

the salicylic acid

35 Psoriasis

Psoriasis is a chronic inflammatory disease of the skin that presents

with outbreaks Psoriasis aff ects 1-2 of the populaton and can ap-

pear at any age with a maximum of incidence between 20 and 30 yearsof age There is a family history in a third of the patents

Plates are the characteristc erythematous desquamatng lesions well

delimited with a superficial thick and white-pearl scale

The most frequent clinical form is vulgar psoriasis or psoriasis in plates

Lesions are localized at extensor surfaces (elbows and knees) and the

scalp The umbilical and the lumbosacral areas are ofen aff ected

Nail involvement is frequent and is most common with a pi ng ap-

pearance This form is lile specific The forms that combine hyperkera-

tosis and distal onycholysis are more specific Oil spot is the most char-

acteristc sign (Figure 3)

Figure 3 Generalized pustular psoriasis

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Amer ican Manual of Examinat ion in Medicine (2CK)

4

Diagnosis

Diagnosis of this conditon is generally clinical

If there is no certainty a biopsy must be done which will reveal hyper-

keratosis acanthosis and parakeratosis

There is an increase in polymorphonuclears (sterile abscesses) in the

stratum corneum which are called Munro abscesses

Treatment (Table 1)

For moderate severe forms of psoriasis that do not respond to clas-

sical systemic treatments (see table) They are monoclonal antbod-

ies against proinflammatory substances that are high in patents with

psoriasis [alpha tumor necrosis factor (TNF) interleukin IL 12 and

23] Some of them are infliximab adalimumab ustekinumab and

etanercept

36 Urticaria

Urtcaria is an immunologic and inflammatory reacton of the skin

against diverse etological factors Independently of the cause release

of histamine and other inflammatory mediators occurs which cause va-

sodilaton and increase in capillary permeability producing an edema in

superficial dermis Urtcarias are divided in acute and chronic urtcarias

depending on whether outbreaks persist more or less than six weeks

About 60 of acute urtcarias are idiopathic Chronic urtcarias show a

higher percentage

Urtcarias of known origin are usually due to infectons drugs or food

Clinical Presentation

Clinical presentaton is characterized by the appearance of pruritc wheals

that last less than 24 hours and can be accompanied with angioedema

TREATMENT USES SIDE EFFECTS AND CONTRAINDICATIONS

Topic Mild-moderatepsoriasis

(lt 25 body

surface)

Emollients (urea glycerin) Moisturizing

Keratolytics (salicylic acid) Eliminate excess of scales

Reductants (dithranol) Hyperkeratotic plaques middot Stain skin and clothing

middot Irritating

middot Acneiform eruptions

Corticoids middot Stable psoriasis

in plates

middot The most used

middot Tachyphylaxis

middot Percutaneous absorption

middot Possible new outbreak after stopping medication

middot Avoid prolonged treatment

Vitamin D analogues

(calcitriol calcipotriol and

tacalcitol)

Stable psoriasis in plates middot Irritating in face and skin folds

middot Hypercalcemia

Systemic Moderate-

severe psoriasis

(gt 25 body

surface)

Psoralens plus ultraviolet

light of the A wavelength(PUVA)

Combinable with topics

and retinoids (RePUVA)

middot Cutaneous aging and carcinogenesis

middot Erythroderma and xerosis middot Immunosuppression

middot Hepatitis by psoralens

middot Not in children pregnancy patients with hepatic or renal

insuffi ciency photosensitivity or cutaneous precancerosis

middot Cataracts

middot It accumulates in the crystalline during 24 h (sunglasses)

Retinoids (acitretin) middot Severe psoriasis

pustular

or erythrodermic

middot It is not usually used

in women in fertile age

(see side effects)

middot Cutaneous dryness (the most frequent)

middot Hypertriglyceridemia

middot Hypercholesterolemia

middot Increase in transaminases

middot Diffuse alopecia

middot Vertebral hyperostosis ligamentous calci1047297cations

middot Teratogenicity avoid pregnancy until 2 years after

1047297nishing treatment

middot Avoid in children and patients with hepatic or renal failure

Cyclosporine A middot In1047298ammatory severe

psoriasis resistant to

other treatments

middot Rapid action

middot Rebound effect

middot Nephrotoxicity

middot High blood pressure (HBP)

middot Epitheliomas and lymphomas

middot Hypertrichosis

middot Gingival hyperplasia

middot Hyperuricemia

Methotrexate middot Severe psoriasis

resistant to other

treatments

middot Psoriatic arthropathy

middot Hepatotoxicity

middot Myelosuppression

middot Teratogenicity until 3 months after ending treatment

middot Photosensitivity

Table 1 Psoriasis treatment

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Dermatology

Vasculits urtcaria should be ruled out when lesions last more than 24 hours

and are accompanied with systemic clinical symptoms (ie arthralgias)

Treatment

Oral anthistamine therapy is the treatment of choice

Systemic cortcoids for severe or refractory cases

Adrenalin for severe cases with anaphylaxis

37 Toxicodermas

Toxicodermas are quite variable cutaneous reactons that appear afer

drug administraton They are one of the most frequent side eff ects of

drugs The causatve agents for many toxicodermas stll remains un-

known either immunological or not and clinical presentaton does not

facilitate agent dist

nct

on

Morbilliform exanthem is the most frequent A morbilliform exanthem

is a generalized erupton formed by symmetric and confluent macules

and papules that usually start by the trunk

They can appear one or two weeks afer taking the drug

A morbilliform exanthem can be associated with fever pruritus and eo-

sinophilia

The most frequent are non steroid ant-inflammatories antbiotcs (sul-

phamides and penicillins) antepileptcs allopurinol and N acetyl-cystene

DiagnosisDiagnosis is according to clinical presentaton

Treatment

Treatment implies withdrawal of potentally responsible drug Topic or

systemic anthistamines and cortcoids are given according to the extent

of symptoms (Figure 4)

Figure 4 Morbilliform exanthem due to amoxicillin

38 Multiform Erythema

Stevens-Johnson Syndrome

and Toxic Epidermal Necrolysis

Multform erythemas (ME) are of undetermined etopathogenesis

regarded as a cutaneous reacton against a diversity of stmuli Their

histologies show similarites what leads to consideraton of a common

pathogenesis

Clinical Presentation

Three diff erent groups have been described although many a tme their

clinical symptoms overlap

bull Erythema multforme minor is the most frequent with around 80

of the cases It usually precedes a symptomatc infecton by simple

herpes virus (60) or subclinical infecton about 15 days before

Erythema multforme minor manifests itself on extensor surfaces

at hands elbows and feet as a symmetric erupton of erythema-

tous edematous lesions with target-shape (herpes iris of Batemanor rosee-paerned lesion) with a violaceous sometmes bullous

center (Figure 5)

Mucosal aff ectaton is rare with small erosions in oral mucosa Erythe-

ma multforme minor tends to recurrence with subsequent outbreaks

of herpetc lesions

Figure 5 Erythema multiforme minor Herpes iris of Bateman

bull Erythema mult

forme major or Stevens-Johnson syndrome is therarest It normally has a prodromal period of untl 14 days with fe-

ver cough cephalea arthralgias and other symptoms Subsequent

to the prodromal period erythematous edematous plates appear

which are more extensive with a tendency to form blisters and

greater mucosal erosions (mouth genitals pharynx larynx and

conjunctve Figure 6) Systemic symptoms are normal and do not

tend to recurrence

The most frequent etological factors are drugs [sulphamides non

steroid ant-inflammatory drugs (NSAIDs) antconvulsants and an-

tbiotcs in decreasing order) Infectous agents have been also in-

volved mainly mycoplasma pneumoniae

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6

Figure 6 Exudative erythema multiforme major

bull Toxic epidermal necrolysis (TEN) many authors consider it the

most severe form of erythema multforme major arguing the same

pharmacological agents A morbilliform rash appears which is rap-idly confluent comprising almost the entre skin surface with flaccid

blisters that leave wide areas of denuded skin Involvement of sev-

eral mucosae is constant

Complicatons ofen occur (pneumonia digestve hemorrhage re-

nal failure and hemodynamic shock) with mortality rates close to

25 In children it must be performed a diff erental diagnosis with

staphylococcal scalded skin syndrome which does not aff ect mu-

cosae

Remember

Diseases that have the Nikolsky sign are TEN staphylococcal scalded skinsyndrome (SSSS) and pemphigus In TEN the whole epidermis comes off(bad prognosis) while in SSSS epidermal detachment occurs at the granularlayer

Histopathology

It must be highlighted the eff acement of dermoepidermal juncton by a

lymphohistocytc infiltrate and vacuolar degeneraton of the baseline lay-

er with necrotc keratnocytes In TEN keratnocytes necrosis is massive

Treatment

In ME minor only symptomat

c treatment is prescribed with topiccortcoids and oral anthistamines Treatment for herpes simplex virus

(HSV) infecton is useful to prevent ME lesions if patent is in the inital

stage of the viral infecton

ME major requires treatment of the underlying infecton or withdrawal

of implied drug and support measures The use of oral steroids accord-

ing to the patentrsquos general state is under discussion

A patent with TEN requires to be admied at the burn treatment room

with monitoring of hematocrit hydroelectrolytc balance and antbiotc

prophylaxis and support measures It is controversial the use of system-

ic cortcoids immunoglobulins andor cyclosporine

39 Erythema Nodosum

Erythema nodosum is the most frequent panniculits Painful erythema-

tous nodules occur mainly in the anterior side of legs with a self-limit-

ing course and predominantly aff ectng young women (Figure 7)

Figure 7 Erythema nodosum

They heal without leaving a scar within a period of four to six weeks

Erythema nodosum may be accompanied with fever deterioraton of

the general state and arthralgias

Patents with erythema nodosum may have a false positve VDRL

Etiology

This conditon is thought to be an immunological response triggered by

multple and diff erent stmuli bacterial fungal and viral infectons sys-temic diseases (sarcoidosis inflammatory intestnal disease Behcetrsquos

syndrome) neoplasias (lymphomas and leukemias) and drugs (oral

contraceptves sulphamides bromides and iodines)

Diagnosis

Erythema nodosum requires a deep biopsy to reveal septal panniculits

without vasculits

Complementary tests can be performed to rule out systemic involvement

for example chest X-ray Mantoux and antstreptolysin O antbody (ASLO)

Treatment Treatment entails eliminatng underlying cause if found then rest and

ant-inflammatories

310 Bullous Pemphigoid

and Pemphigus Vulgaris

See Table 2 and Figures 8 9 10 and 11

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Dermatology

Intercellular

substance ac

middot Pemphigus

Lineal

storage

in lucid

layer

-

Anti-Collagen Ac

Lucid

layer

Thick

layer

Basal

sublayer

Granular

storage

in papillary

dermis

middot Pemphigoid bullousmiddot Herpes gestationis

middot Acquired blistering epidermolysis

middot Dermatitis herpetiformis

Figure 8 Key points for histological diagnosis

of autoimmune blistering diseases

Figure 9 Pemphigus vulgaris

Figure 10 Pemphigus vulgaris with oral mucosa involvement with

erosions

Figure 11 Pemphigoid bullous Tense blisters No sign of Nikolsky

PEMPHIGUS VULGARISGENERALLY

IDIOPATHICHERPES GESTATIONIS

DERMATITIS

HERPETIFORMIS

Clinical presentation middot 40-50 years of age

middot They usually affect mucosae

middot No pruritus

middot Flaccid blister

middot Nikolsky

middot Elderly

middot Sometimes mucosae

middot With pruritus

middot Tense blister

middot No Nikolsky

middot Pregnant women

middot No mucosae

middot With pruritus

middot Herpetiform

middot No Nikolsky

middot 15-35 years of age

middot No mucosae

middot With pruritus

middot Herpetiform

middot No NikolskyDirect immuno1047298uorescence (DIF) IgG IgG IgG IgA

Histology middot INTRAepidermal blister

middot There is acantholysis

middot SUBepidermal blister

middot There are eosinophils

middot SUBepidermal blister

middot There are eosinophils

middot SUBepidermal blister

middot Neutrophils in dermis

Treatment Corticoids at high doses

immunosuppressants rituximab

and immunoglobulins

Corticoids Corticoids Diet +- dapsone

Remember Mortality rate 10 The most frequent Relapse if new

pregnancy

Associated to enteropathy

by gluten 90

Table 2 Autoimmune blistering diseases

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Amer ican Manual of Examinat ion in Medicine (2CK)

8

Chapter 04

Infectious Diseases

41 Viral Infections

Simple Herpes

Infection by Simple Herpes Virus

There are two types of simple herpes (Figure 12)

bull Type I is responsible for most extragenital herpes and 20 of the

genital herpes

bull Type II causes genital herpes and a small percentage of extragenital

herpes

Figure 12 Herpes simplex

Contagion is produced by direct contact though the carrier may be as-

ymptomatc Afer primary infecton virus remains silent in the sensi-

tve porton of cranial or spinal ganglia Immunosuppressed patents

endure the greatest severity of this conditon

Clinical Presentation

bull Extragenital simple herpes recurring orofacial herpes simplex is

the most frequent Most primary infect

ons are asymptomat

c Only5 manifest themselves in the form of herpetc gingivostomatts a

profile characterized by oral ulcers with cervical adenopathy and af-

fectaton of the patentrsquos general state (Figure 13) During relapses

clinical symptoms are milder with cluster vesicles on an erythema-

tous base Some factors facilitate relapses trauma sunlight cold

stress fever and the menstrual cycle

bull Genital simple herpes is the most common cause of genital ulcers

afer trauma Primary infecton is usually symptomatc and occurs

between 3 to 14 days afer sexual contact It causes clustered ulcers

in the balanopreputal sulcus or in the prepuce with painful inguinal

adenopathy Relapses are less severe than primary infecton and oc-

cur more frequently when genital herpes is due to HSV type II

Figure 13 Herpetic gingivostomatitis

bull Eczema herpetcum or Kaposi varicelliform erupton dissemina-

ton of herpetc infecton on pre-existng dermatosis (above all

atopic dermatt

s) bull Neonatal herpes is due to intrapartum contagion of HSV-II with

neurological involvement general deterioraton and skin vesicles or

ulcers

bull Other clinical forms are herpes gladiatorum herpetc whitlow and

keratoconjunctvits

Diagnosis

Diagnosis of this conditon is mainly clinical Virological culture is the

most reliable method of confirmaton The extent of a smear of the le-

sions (Tzanck cytodiagnosis) allows visualizaton of multnucleated cells

and intranuclear inclusions which become evident through histological

study

Treatment

Mild forms do not need treatment Treatment is required in the follow-

ing cases

bull Primary infecton

bull Severe or frequent relapses if they aff ect life quality

bull Complicatons like erythema multforme and eczema herpetcum

Drug of choice is oral acyclovir and its derivatves (valacyclovir famci-

clovir) Topic antvirals have not proven useful favoring maceraton of

lesions and thus over infecton It is not infrequent that topic antvirals

cause allergic contact dermatts due to hypersensitvity

Varicella-Zoster Virus

A primary infecton gives way to varicella (see Pediatrics secton) Afer

varicella the virus remains latent in the sensitve porton of the neural

ganglia and when relapse occurs it leads to zoster herpes

bull Varicella the following symptoms appear afer 15 days of incubaton

fever cephalea pruritus and polymorphic lesions in diff erent stages

macules papules vesicles (Figure 14) ulcers and scabs (starry sky

appearance) Mucosal (ulcers) and scalp involvement is characteristc

Manipulaton can leave scars Bacterial over infecton of lesions is the

most usual complicaton About 20 of adults suff er from varicella

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Dermatology

pneumonia radiologically demonstrable but clinical symptomatology is

only present in around 4 of the cases

Figure 14 Typical vesicles in patients with varicella

bull Zoster herpes thoracic zoster herpes is the most usual It sel-

dom occurs more than once throughout a personrsquos lifetime

It is characterized by vesicles on pre-existing erythema with

metameric distribution and lateral extension The most com-

mon complication is post herpetic neuralgia more frequent in

advanced age Carbamazepine or tricyclic antidepressants (Fig-

ure 15)

Figure 15 Zoster herpes

Special Clinical Forms

Special clinical forms are as follow

bull Ramsay-Hunt syndrome aff ectaton of geniculate ganglion of the

facial nerve

It produces vesicles in the outer ear external auditory canal and

pharynx homolateral facial paralysis deafness and vertgo

bull Ophthalmic involvement can result in severe keratts and requires ur-

gent referral to an ophthalmologist Suspicion should exist on patents

that present herpetc lesions on the tp of the nose) (Hutchinsonrsquos sign)

bull Disseminated zoster herpes several dermatomes are aff ected bilat-

erally Ramsay-Hunt syndrome is characteristc in the immunosup-

pressed

Remember

Affectation of the nose tip makes it necessary for ophthalmologicalexamination because the nose tip is innervated by the same nerve thatinnervates the cornea (1047297rst branch of the trigeminal nerve)

Treatment

Varicella without complicatons is treated symptomatcally Antvirals

are reserved for severe or complicated forms There is a commercial-

ized vaccine of live virus whose indicatons are stll under discussion

Zoster herpes must be treated with antvirals when detected during the

first 48-72 hours and aff ectng patents with

bull Immunosuppression

bull Age above 55

Special clinical forms previously cited

Drugs to be used are oral acyclovir and its derivatves (valacyclovir and

famciclovir) They accelerate the cure of lesions and decrease the inten-

sity of post herpetc neuralgia Patents with renal failure need a dose

adjustment as acyclovir is nephrotoxic These patents are adminis-

tered brivudine in a single daily dose

Molluscum ContagiosumDome shaped pink papules with central umbilicaton (Figure 16) Mol-

luscum contagiosum is typical of children that go to swimming pools It

is also present in the genital zone afer sexual contact and in immuno-

suppressed patents It is caused by Poxvirus

Figure 16 Molluscum contagiosum

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Amer ican Manual of Examinat ion in Medicine (2CK)

0

Lesions are asymptomatc

Diagnosis

Diagnosis is clinical Histology reveals characteristc inclusion bodies

Treatment

Lesions can resolve spontaneously

Cureage cryotherapy or local trichloroacetc acid are eff ectve meth-

ods to destroy lesions

Warts

Human papillomavirus can cause verruca vulgaris palmoplantar and

flat warts and condyloma accuminata Human papillomavirus is the

most frequent sexual transmied disease

Some subtypes of this virus (16 18) are of high risk and can cause epi-

dermoid carcinomas

Direct contact is the mechanism of contagion

Diagnosis

Diagnosis of this conditon is clinical

Staining with acetc acid can help visualize mucosal lesions

Treatment

Genital warts are treated with cryotherapy podophyllotoxin trichloro-

acetc acid imiquimod and 5-fluorouracil

Cervical lesions should be monitored by cytology and biopsy whenever

necessary to rule out cervical cancer (Figures 17 and 18)

Figure 17 Warts in HIV patient

Figure 18 Condyloma accuminata

42 Bacterial Infections

Impetigo

Impetgo is a very contagious superficial infecton without systemic re-

percussion and normally mixed etology by Gram positve cocci (strep-

tococci and staphylococci) Classically the most frequent accepted

cause was Streptococcus pyogenes However at present Staphylococcus

aureus stands out as the predominant cause

The most typical form is impetgo contagiosa (Figure 19) character-

ized by honey-colored (meliceric) scabs which normally appear on

the face and other exposed areas It is typical of children Although

infrequent poststreptococcal glomerulonephrits is a dreadful com-

plicaton

Figure 19 Impetigo contagiosa

On the contrary rheumatc fever shows no relaton to cutaneous strep-

tococcal infectons but only with pharyngeal infectons

There are other less habitual forms called bullous impetgo exclusively

of staphylococcal origin Clinical presentaton involves the presence of

blisters and erosions on the aff ected skin as a consequence of the epi-

dermolytc toxins that these bacteria contain Impetgo is treated with

topical mupirocin penicillin or oral fusidic acid

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Dermatology

Cellulitis

Cellulits is an infecton that aff ects deep dermis and subcutaneous cel-

lular tssues normally caused by streptococci (Streptococcus pyogenes

or of group A)

Community methicillin-resistant S aureus (CMRSA) is a triggering agent

that is becoming more and more frequent

Most common risk factors are diabetes chronic venous insuffi ciency

and immunosuppression

Clinical Presentation

Cellulits presents with erythematous plaques that are ill-defined pain-

ful and hot It is usually accompanied with fever and chills

Diagnosis

Diagnosis is clinical If there is an open door a culture of this area may

help see the source germ and resistance to ant

biot

cs

It is important to rule out abscesses osteomyelits and necrotzing fas-

ciits

If bacteremia is suspected blood cultures need to be performed

Treatment

Treatment implies oral antbiotcs for 7-10 days to cover Gram positve

cocci They are intravenously administered in case of lack of response

to oral treatment involvement of hands or periorbital zone diabetes or

extremes of age

Necrotizing FasciitisNecrotzing fasciits is a deep infecton up to muscular fascia that pro-

duces very intense pain and subsequent anesthesia

In 10 of the cases cellulits is due to an infecton by S pyogenes In the

remaining cases it occurs by a polymicrobial infecton caused by aerobes

and anaerobes including S aureus E coli and Clostridium perfringens

There may be prior history of trauma or surgery

Clinical Presentation

Clinical presentat

on involves pain of sudden onset and edema on theaff ected zone Pain may progress to anesthesia There appears subse-

quent erythema that progresses rapidly into necrosis

Characteristc clinical signs are tssue necrosis blisters intense pain

and gas producton

Diagnosis

Diagnosis is clinical and requires image testng X-rays or a computed

tomography CT

A biopsy of the border of the lesion helps achieve diagnosis

Treatment

Treatment entails precocious surgical debridement It is a surgical emer-

gency In additon to surgery broad-spectrum antbiotherapy will be

needed

Folliculitis

Folliculits is an infecton and inflammaton of one or several follicles

caused mainly by staphylococci

Clinical Presentation

Folliculits shows pustules with follicular distributon

When the infecton is deeper it is called furuncle

If several furuncles are infected a fluctuatng erythematous plaque forms

containing several points of suppuraton This plaque is labeled as anthrax

Diabet

c and immunosuppressed pat

ents are at higher risk

Characteristics of Folliculitis

1 Hot tub or swimming pool folliculits caused by Pseudomonas aeru-

ginosa

2 HIV associated pruritc folliculits or eosinophilic folliculits

Treatment

In mild cases treatment of choice comprises antseptcs and topic an-

tbiotcs

In more severe cases treatment of choice requires oral antbiotcs

Large sized lesions must be drained and a microbiological culture must be

performed to rule out methicillin-resistant Staphylococcus aureus MRSA

Acne Vulgaris

Acne is an inflammatory disease of the pilosebaceous follicle as a con-

sequence of an alteraton in follicular keratnizaton It aff ects adoles-

cents and young adults

Etology is multfactorial alteraton of keratnizaton of follicular infun-

dibulum quanttatve and qualitatve alteraton of sebum producton in

the sebaceous gland and alteratons of bacterial microflora (increase in

quant

ty of P acnes)

Aggravatng factors are stress androgenic oral contraceptves and the

use of cosmetc products that are not oil-free

Clinical Presentation

A comedo is the inital lesion which can be closed (whitehead) or open

(blackhead) and it evolves into inflammatory lesions that listed in as-

cending order of severity are papules pustules nodules and cysts

Lesions progress and leave scars Scars can be increased if lesions are

manipulated

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Amer ican Manual of Examinat ion in Medicine (2CK)

2

Diff erent lesions habitually combine simultaneously so acne becomes

polymorphic It is located in sebaceous areas face back shoulders and

the center thoracic region

Diagnosis

Diagnosis is clinical

Treatment

bull Comedonal acne is treated with topic retnoids and benzoyl peroxide

bull Inflammatory acne treatment requires benzoyl peroxide combined

with topic antbiotcs (erythromycin and clindamycin) Systemic

antbiotc treatment with oral tetracyclines will be prescribed if re-

sponse to topic antbiotc treatment fails

bull Severe nodular cystc acne treatment involves the use of isotret-

noin (13-cis-retnoic acid) It is a derivatve of vitamin A Isotretnoin

produces atrophy in the sebaceous gland and regulates keratniza-

ton The most frequent side eff ect is cutaneous and mucosal xero-

sis Triglycerides cholesterol and transaminases should be moni-

tored as their values may increasebull It can be associated with depression

bull It is teratogenic so pregnancy should be avoided during treatment

and untl a month afer treatment

Pilonidal Cysts

Pilonidal cysts are abscesses in the sacrococcygeal region

This type of cysts has predominance in men between 20 and 40 years

of age It is believed that repeated trauma on the aff ected area favors

their appearance

Clinical Presentation

Pilonidal cysts present with an indurated lesion that is fluctuatng hot

painful but non-adherent to deep planes in the sacrococcygeal region

Pilonidal cysts may or may not be associated to cellulits and purulent drain-

age

Diagnosis

Diagnosis is clinical and anal or perirectal abscesses should be dismissed

Treatment

Treatment implies an incision and surgical drainage

On some occasions a general surgery is required

43 Fungal Infections

Pityriasis Versicolor

Versicolor pityriasis is caused by commensal yeast called Pityrosporum

ovale which transforms into its pathogen form (Malassezia furfur) It

especially aff ects young patents (15 - 45 years of age) but it is rare

in childhood and advanced age Versicolor pityriasis relates to heat

humidity and sebaceous hypersecreton It is characterized by the ap-

pearance of hyperchromic or hypochromic macules that desquamate

on scratching (nail sign) if infecton is actve Macules usually appear on

the center thoracic region and on the back that is to say on seborrheic

zones Relapses are habitual despite treatment

Diagnosis

Diagnosis is normally clinical To that purpose the following serve as

support

bull Woodrsquos lamp emits yellow-orange fluorescence

bull Potassium hydroxide (KOH) test filaments and round elements can

be observed (ldquospaghe and meatball appearancerdquo Figure 20)

Treatment

Treatment is performed with topical azoles Oral administraton applies

for extensive cases or immunosuppressed patents Diff erental diagno-

sis includes pink pityriasis and eczemas (Figure 21)

Figure 20 Versicolor pityriasis Histological cut

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Dermatology

Figure 21 Versicolor pityriasis

Candidiasis

The most common triggering agent is Candida albicans It is normally sapro-

phyt

c although under certain condit

ons candidiasis may become patho-genic (immunosuppression humidity pregnancy and contraceptves)

Clinical Forms

bull Intertrigo erythematous plaque in cutaneous folds Atrophy and

fissures are typically deep in the skin fold as well as satellite and

peripheral lesions (papules andor pustules)

bull Mucosa involvement may cause diverse symptomatology like vul-

vovaginits glossits and white papules in the anterior region of the

oral mucosa Candidal balanits is characterized by the presence of

punctform erosions and pustules on gland and balanopreputal

sulcus Candidal balanits ofen appears afer sexual intercourse or

afer oral antbiotc intake

Remember

Almost a 100 of HIV patients suffer from muguet throughout their diseasecourse

bull Candidiasis of nail fold is usually associated with periungual inflam-

maton (perionixis) and inital proximal aff ectaton which diff erent-

ates it from tnea unguium (Figure 22)

Figure 22 Candidiasis of nail fold

Treatment

Oral Candidiasis fluconazole or nystatn

Candidiasis of the skin (intertrigo) apply topical antfungal medicaton

and keep zone clean and dry

Dermatophytosis or TineasDermatophyte infectons aff ect the skin and keratnized structures like

hair and nails (there is no mucosa involvement) Clinical diagnosis is

achieved afer performing a culture Woodrsquos lamp test normally turns

out to be negatve In general Trichophyton dermatophyte rubrum is

the most frequent dermatophyte

Non Inflammatory Tineas

Non inflammatory tneas do not produce irreversible scarring alope-

cia while inflammatory forms do Tineas are treated with azoles de-

rivatves

The types of tnea are the following

bull Ringworm of the scalp ( t nea capi t s or t nea tonsurans) is charac-

teristc of childhood It presents with alopecic plaques broken hair

and desquamaton Infectons tend to resolve spontaneously with-

out leaving scars at the onset

of puberty

bull Ringworm of the body (herpes

circinatus or t nea corporis) are

erythematous desquamatve

plaques (with more actve bor-

ders) which are also circinate

and normally pruritc (Figure

23) Plaques grow eccentrically

with less actvity in the centerand more in the borders

bull Ringworm of the foot ( t nea

pedis) the most frequent is the

ldquoathlete footrdquo with desquama-

ton in interdigital spaces

bull Tinea incognito refers to tnea

wrongly treated with cort-

coids what makes diagnosis

diffi cult as the lesion has been modified Figure 24)

Figure 24 Tinea incognito secondary to treatment with topical steroids

Figure 23 Herpes circinatus

(tinea corpis)

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Amer ican Manual of Examinat ion in Medicine (2CK)

4

bull Ringworm of the groin (t nea cruris or eczema marginatum von

hebra) formed by erythematous desquamatve plaque with more

actve borders (Figure 25)

Figure 25 Ringworm of the groin (tinea cruris)

bull Tinea unguium subungualhyperkeratosis with onychol-

ysis but without perionixis

(Figure 26)

Diagnosis

Clinical diagnosis is reached afer

performing a culture

Treatment

Treatment involves topical an-

tfungal medicaton in localized

areas

Oral antfungal medicaton is used in extensive forms nail fold or scalp

involvement

44 Parasitic Infections

Pediculosis

Pediculosis is transmied by direct contact or by contact with fomites

which release toxins that produce intense pruritus

Clinical Presentation

Pediculosis capi t s intense pruritus predominant in retroauricular and

occipital regions occasionally with excoriatons and impetginizaton

secondary to excoriatons

Pediculosis corporis intense pruritus in patents with poor hygiene or

who live in overcrowded conditons

Pediculosis pubis genital and pubic pruritus Brownish-grey macules

called maculae ceruleae are typical on underwear and skin These pig-

mentatons appear as a result of a reducton in hemoglobin by a para-

site enzyme

Diagnosis

Diagnosis is clinical and by direct visualizaton

Treatment

Pediculosis is treated with malathion lindane or topical permethrin

Scabies

Scabies is originated by an acarus known as Sarcoptes scabiei It has an

incubaton period of 1 month

Clinical Presentation

Scabies produces generalized pruritus more intense at night The pa-

tent usually catches the infestaton which is passed to the patentrsquos

relat

ves It is common tofi

nd that a recent trip to a tropical country hasbeen made Lesions appear between the fingers (Figure 27) in wrists

feet genitalia mammary areola and axilla but back and face are usu-

ally spared The most specific lesion is the acarine burrow in whose less

scaly end the advancing zone the mite lies Nodules are frequent in

axilla and genitals (nodular scabies)

bull Norwegian scabies is typical of the immunosuppressed Patents

present with generalized hyperkeratosis and scabs Norwegian sca-

bies produce lile pruritus but it is very contagious because there

are many acari

bull Nodular scabies involves the persistence of pruritc nodules despite

treatment Lesions usually appear in axilla and genitalia Pruritus is

due to a hypersensitvity phenomenon because of the acarus al-

ready dead Nodular scabies is treated with cortcoids

Figure 27 Scabies Acarine burrow

Treatment

bull Permethrin cream at 5 is the treatment of choice It is lile toxic

so it can be used in children and pregnant women

bull Topical lindane at 1 irritates and is neurotoxic therefore it is con-

traindicated in pregnant women and children

bull Oral ivermectn is utlized in cases of resistance to prior treatments

There is stll lile experience as to its use but in a first instance a

Figure 26 Tinea unguium

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Dermatology

single dose would be enough to cure scabies (already used by vet-

erinarians)

45 Ischemia

Decubitus Ulcers

Decubitus ulcers are the result of ischemic necrosis by contnuous pres-

sure on an area which restricts microcirculaton in that zone

Clinical Presentation

Decubitus ulcers are present in patents in bed with scarce mobilizaton

It is favored by bone prominences and lack of fat tssue If sensitvity

decreases there is more risk of formaton of decubitus ulcers

Diagnosis

Diagnosis is achieved based on medical records and clinical presentaton

Treatment

Preventon is of the utmost importance as well as frequent mobiliza-

ton of the patent in bed

Once ulcers have been established hydrocolloid dressings are used for

healing but sometmes surgical debridement is necessary

Gangrene

Gangrene means tssue necrosis

There are three types dry gangrene wet gangrene and gas gangrene

Clinical Presentation

Dry gangrene is due to ischemia generally secondary to atherosclero-

sis Clinical presentaton involves pain cold and paleness of extremi-

tes Once tssue is established it turns bluish-black in color and dry

Wet gangrene is owing to bacterial flora Tissue presents with an edem-

atous appearance either with blisters or pus

Gas gangrene caused by C perfringens It is normally located on re-

cent surgery Bacteria precociously destroyt

ssue producing gas It is amedical emergency

Diagnosis

Clinical diagnosis is obtained by microbiological culture

Treatment

Treatment requires surgical debridement with amputaton if necessary

and associaton of broad spectrum antbiotherapy

Gas gangrene is treated with hyperbaric oxygen

46 Miscellaneous

Acanthosis Nigricans

Acanthosis nigricans are vel-

vet-like papillomatous brown

plaques in neck axilla and groin

folds (Figure 28)

It is associated with diabetes

mellitus Cushingrsquos disease poly-

cystc ovarian syndrome and

obesity

The malignant form of acantho-

sis nigricans is a paraneoplastc

syndrome that diff erentates

from the benign form because

the laer has mucosal and pal-

moplantar involvement

Lichen Planus

Lichen planus is an inflammatory idiopathic disease that equally aff ects

both genders with higher frequency in middle age

Lichen planus has been related to diverse drugs like gold salts

anti-malarial medication and thiazides It has been also linked to

hepatitis C virus infection however this association is currently

doubtful

Clinical Presentation

Lichen planus presents with red-violaceous polygonal flat papulesquite pruritc which localizes on the flexor side of wrists forearms an-

kles and lumbosacral and flank regions On its surface a whitsh retcu-

late can be observed (Wickhamrsquos striae) About 60 - 70 of the cases

present with lesions in oral and genital mucosa oral which appear as

whitsh retculated lesions (Figures 29 and 30)

Figure 29 Lichen planus of oral mucosa with typical whitish

reticulate

Figure 28 Acanthosis nigricans

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Amer ican Manual of Examinat ion in Medicine (2CK)

6

Violaceous papules

with white stretch marks

Lichenoid lymphocyte

in1047297ltrate (band formation)

Destruction

of basal layer

Figure 30 Lymphocytic interface reaction (lichen planus)

Treatment

Mild forms are treated with topical cortcoids

Severe cases require oral cortcoids psoralens plus ultraviolet light of

the A wavelength (PUVA) or cyclosporine

Rosacea

Rosacea is a chronic disease of unknown pathogenesis characterized

by erythema and acneiform lesions on the face It aff ects middle aged

women (between 30 and 50 years of age) more

Rosacea etopathogenesis is unknown although there is involvement of

vasomotor lability infecton by Demodex folliculorum photo exposureand genetc predispositon

Clinical Presentation

Rosacea symptomatology comprises facial flushing episodes that end

up by provoking a persistent erythema telangiectasias and papulopus-

tular lesions without comedos Over tme ocular lesions and hyperpla-

sia of sof tssue may develop

Treatment

Avoid vasodilator stmuli

Mild cases require topical metronidazole or azelaic acid

Moderate cases need doxycycline or oral minocyclines

Severe cases are treated with oral isotretnoin at low doses

Pink Pityriasis

Gilbertrsquos pink pityriasis is an acute self-limitng dermatosis which main-

ly aff ects young adults It is of unknown origin although a viral etology

is suspected (there is some speculaton as to links with human herpes-

virus type 7)

Clinical Presentation

Erupton starts with an erythematous plaque between 2 and 5 cm of

diameter with a desquamatve central collaree ofen localized on the

trunk (heraldic mother patch Figure 31)

Figure 31 Pink pityriasis

Around a week later oval papules appear on the trunk and extremi-

tes These papules share similar characteristcs with the mother patch

though the first ones are smaller and distributed according to skin ten-

sion lines Pink pityriasis may be asymptomatc however it is some-

tmes linked to pruritus Lesions may last between 4 and 8 weeks and

disappear without leaving scars

Diagnosis and Treatment

Diagnosis is clinical Treatment is seldom needed and recommended

therapies in the past (PUVA erythromycin or oral antvirals) have not

shown clearly favorable results

Vitiligo

Vitligo is characterized by achromic macules by melanocyte destruc-

ton

Clinical Presentation

Vitligo shows achromic macules of chronic course and variable progres-

sion

Lesions are predominant on acral and periorificial areas They also show

the Koebner phenomenon

Patents may have markers of autoimmune diseases (ie antthyroid

antbodies and diabetes) but these diseases seldom manifest them-

selves

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Dermatology

Treatment

Localized lesions require topical cortcoids

Extensive or generalized lesions are treated with ultraviolet light B

(UVB) or PUVA

Strict solar photoprotecton is indispensable (Figure 32)

Figure 32 Vitiligo

47 Neoplasias

Seborrheic Keratosis

Seborrheic keratosis is the most frequent benign tumor in human be-

ings since it is part of cutaneous aging

Clinical Presentation

Seborrheic keratosis presents with hyperkeratosic papules with an oily

or velvet-like texture crests fissures and horny plugs on their surface

These papules are normally pigmented showing a brownish-black color

Treatment

No treatment is required as lesions do not become malignant

Seborrheic keratosis can be addressed with cureage or cryotherapy

Actinic keratosis

Actnic keratosis is the most common precancerous lesion and aff ects

almost a 100 of the populaton in sunny areas

Clinical Presentation

Actnic keratosis is characterized by erythematous and desquamatve

papules which are hyperkeratosic and rough on touch developing a

chronic course

Diagnosis

Diagnosis is clinical

Treatment

Treatment entails applicaton of topical 5-fluorouracil topical imiqui-

mod cryotherapy or surgery

If underlying carcinoma is suspected a biopsy must be performed to

rule out suspicion

Epidermoid Carcinoma

Epidermoid carcinoma is the second most frequent cutaneous tumor

Solar photo exposure is the main etological factor which is why epider-

moid carcinoma appears in zones of prolonged solar exposure like the

face Most carcinomas appear over premalignant lesions (actnic kera-

tosis and leukoplakia among others)

Clinical Presentation

Clinical presentaton reveals erythematous or erythematosquamous

plaques Over tme these plaques form papules and tumors which of-

ten become ulceratve and bleed

Diagnosis

Diagnosis is based on clinical suspicion and histopathological confirmaton

Treatment

Surgery with safety margins is the treatment of choice In carcinomas

in situ cryotherapy can be used as well as topical imiquimod electro-

coagulaton or CO2 laser techniques in destructon of tumors Radio-therapy may also be used in some cases

Basal Cellular Carcinoma

Basal cellular carcinoma is the most frequent cutaneous tumor Chronic so-

lar photo exposure is the main etological factor hence most of these car-

cinomas aff ect the facial zone in patents who are 40 years of age or older

Gorlinrsquos syndrome should be considered if multple basal cellular carci-

nomas are found in non photo exposed areas

Clinical Presentation

Basal cell carcinoma shows a pearly pink papule and superficial telan-

giectasias

It is localized over healthy skin and never aff ects mucosae

Treatment

Surgery is the treatment of choice Mohs surgery is performed in zones

where surrounding healthy tssue needs to be preserved Other alter-

natves are cryotherapy imiquimod electrocoagulaton radiotherapy

photodynamic therapy and intralesional interferon Prognosis is excel-

lent as growth is slow and metastasis exceptonal

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Amer ican Manual of Examinat ion in Medicine (2CK)

8

Melanoma

Melanoma is the most aggressive cutaneous tumor given its ability to

metastasize

Risk factors comprise solar photo exposure clear phototype the pres-

ence of dysplastc nevus or a high number of melanocytc nevi Fam-

ily history is quite important as some genetc mutatons determine a

higher risk of developing the disease

Clinical Forms

See Figure 33

Diagnosis

Precocious diagnosis is essental to perform precocious surgical extrpaton

The ABCDE criteria can help patents to see if they need to seek medical

consultaton (asymmetry of lesion uneven borders color and diameter

greater than 6 mm or abnormal evolut

on)

The Breslow index is the thickness of the lesion measured in millimeters

and is the main prognosis factor

Treatment

The base of treatment is precocious surgical extrpaton If the Breslow

index is less than 1 mm margins of 1 cm will be performed If Breslow

index is greater than 1 mm margins will be of 2 cm

For melanomas with a Breslow index greater than 1 mm the sentnel

ganglion must be located This is the first draining lymph node of the

territory where the tumor is localized If the ganglion is positve re-

gional lymphadenectomy will be performed along with interferon ad-ministraton (Figure 34)

In situ Extirpation 05 cm Follow-up

Breslow lt 1 mm Extirpation 1 cm Follow-up

Lymphadenectomy

Breslow gt 4 mm Interferon

Breslow ge 1 mm Extirpation 2 cm Sentinel ganglion

+

Figure 34 Melanoma treatment

Kaposirsquos sarcoma

Kaposirsquos sarcoma is the most common cutaneous tumor in HIV patents

Clinical presentation

Kaposirsquos sarcoma has a course with violaceous fusiform macules whichovertme may evolve into indurated nodules with blackberry appearance

This type of sarcoma has been linked to herpesvirus type 8 both in HIV

and seronegatve patents (Table 3)

EPIDERMAL KAPOSIrsquoS 983080HIV983081 CLASSIC KAPOSIrsquoS

Homosexual youth (95) The elderly

Diffuse and bilateral

(frequently in palate and face)

Unilateral plaques

(lower extremities)

Frequent mucosal and visceral involvement Not so frequent

middot Precocious lymphatic invasion

middot Aggressive

Not so precocious

Table 3 Differences between epidermal and classic Kaposirsquos sarcoma

Nodular melanoma

15

Middle-aged men

middot On healthy skin

middot Any zone

middot Sudden onset

middot Uniform black nodulemiddot Rapidly invasive (vertical growth without radial)middot Frequent ulceration and bleeding

Worst histological prognosis

Lentigo malignant melanoma

10

Elderly women

90 on facephotoexposedzones of aging skins(chronic exposure)

Spot that growsduring many years (gt 10)then progresses (nodule)

Better prognosis

Acral lentinginous melanoma

5ndash10 ( 60 black and Asian race)

Elderly men

middot Sole (ankle) handsmucosa ungual bed

middot No relation to photo exposure

middot Macule with mosaic appearance (spot that grows)middot Some amelanisticmiddot Bad prognosis due to late diagnosis

Melanoma of super1047297cial extension

70

Young women

middot 30 previous nervusmiddot Intermittent exposuremiddot Men back middot Women legs

More frequent

middot Macula with mosaic appearance in colors that grows 4-5 years and then in1047297ltrates (nodule)middot Metastasis 35 to 70

Figure 33 Clinical forms of malignant melanoma

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Dermatology

Diagnosis

Diagnosis relies on clinical suspicion and histopathological confirma-

ton

Treatment

Treatment of localized forms can include surgical extrpaton radiother-

apy or intralesional vinblastne

If the sarcoma is disseminated optons involve interferon or chemo-

therapy

Mycosis Fungoides

Mycosis fungoides is a T-cell lymphoma of low-grade malignancy Its

clinical course may be very slow and surpass 50 years Three stages are

clinically diff erentated

1 Eczematous or macular phase predominantly truncular erythema-

tous macules with years of evoluton They resemble a chromic ec-

zema Histology is unspecifi

c at this stage2 Infiltratve plaque phase infiltrated erythematous plaques appear

Histology is diagnostc at this stage A dermal infiltrate of atypical

lymphocytes band forms can be observed composed of CD+4 T

lymphocytes with cerebriform nuclei There is a marked epidermo-

tropism with the presence of clusters of intraepidermal lympho-

cytes called Pautrierrsquos microabscesses (Figure 35)

Figure 35 Mycosis fungoides Infiltrative plaque phase

3 Tumoral phase erythematous exophytc plaques start to appear

(tumors) with a tendency to ulceraton They can have a large size

Histology may become unspecific again as epidermotropism disap-

pears

In more advanced stages of the disease there is aff ectaton of extra-

cutaneous organs such as lymph nodes liver spleen lungs and bone

marrow Besides there may be blastc transformaton Other possible

complicaton is sepsis by Staphylococcus aureus

These three stages usually develop consecutvely nevertheless there

may patents whose debut starts directly with the tumoral stage

Remember

Microabscesses of mycosis fungoides are due to lymphocytes and are calledPautrierrsquos abscesses Psoriasis microabscesses result from neutrophils andare labeled as Munro-Sabouraud

Seacutezary Syndrome

Seacutezary syndrome can be considered as the leukemic phase of T-cell cu-

taneous lymphoma It is defined by the triad erythroderma (Figure 36

lymphadenopathies and the existence of more than 1000 Seacutezary cellsper milliliter in peripheral blood Seacutezary cells are atypical T- lymphocyte

with cerebriform nuclei

Very intense pruritus is characteristc For many authors Seacutezary syn-

drome is an aggressive clinical form and a bad prognosis of a mycosis

fungoides

Figure 36 Erythroderma due to Seacutezary syndrome

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D e r m a

t o l o g y

American Manualof Examination

in Medicine

(2CK)

AuthorsDolores Mendoza

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Amer ican Manual of Examinat ion in Medicine (2CK)

01 Skin Layers 1

02 Terminology Elemental Cutaneous Lesions 1

21 Clinical Lesions 122 Histological Lesions 2

03 Allergic and Immune-mediated Diseases 2

31 Hypersensibility Reactions 2

32 Atopic Dermatitis 2

33 Contact Eczema 3

34 Seborrheic Dermatitis 3

35 Psoriasis 3

36 Urticaria 4

37 Toxicodermas 5

38 Multiform Erythema Stevens-Johnson Syndrome

and Toxic Epidermal Necrolysis 539 Erythema Nodosum6

310 Bullous Pemphigoid and Pemphigus Vulgaris 6

04 Infectious Diseases 8

41 Viral Infections 8

42 Bacterial Infections 10

43 Fungal Infections 12

44 Parasitic Infections14

45 Ischemia 1546 Miscellaneous 15

47 Neoplasias 17

Index

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Dermatology

Chapter 01

Skin

LayersThere are three skin layers epidermis dermis and subcutaneous cel-

lular tssue (Figure 1)

Reticular layer

Sebaceous(Oil) gland

Hair

follicle

Deep

arteriovenousplexusSweat

glandDermal Papillae

Super1047297cial arteriovenousplexus

Subcutaneoustissue

Dermis

Epidermis

Figure 1 Microscopic structure of normal skin

Chapter 02

TerminologyElemental

Cutaneous Lesions

21 Clinical Lesions

Primary Clinical Lesions bull Fluid-filled

Vesicle raised formaton less than 05 cm

Blister lesion equal or greater than 05 cm

Phlyctena large blister

Pustule vesicle of purulent content

Cyst encapsulated lesion of semi-solid or liquid content

bull Of solid consistency

Macule a patch of skin that changed color which is neither

raised nor depressed (non palpable)

When a macule is red in color it is described as erythematous If

it does not disappear afer a diascopy it is regarded as purpuric

(it translates the existence of extravasated blood)

In diff erental diagnosis of purpuric lesions senile purpura must

be taken into account which consists in the presence of viola-

ceous macules in areas exposed to trauma as a consequence

of capillary fragility Other cause for purpura is leukocytoclastc

vasculits which typically gives palpable purpuric papules but

not nodules

Papule small solid circumscribed elevaton of the skin of less

than 1 cm which resolves without leaving a scar It is called

plaque if it is equal or greater than 1 cm Unlike macule both

are palpable

Wheal erythematous edematous plate of dermal origin and of

fleetng evoluton (it disappears in less than 24 hours) It is char-

acteristc of urtcaria

Nodule circumscribed hypodermal lesion identfied by palpa-

ton It may or may not be raised (ldquoit is palpable rather than vis-

iblerdquo) Nodules are typical lesions of panniculits like the ery-

thema nodosum

Tubercle circumscribed infi

ltrated and raised nodule that usu-ally leaves a scar once it has resolved

Gumma granulomatous inflammaton that sofens and opens

gradually

Secondary Clinical Lesions

bull Secondary clinical lesions expected to disappear on their own

Scales plates in the stratum corneum which come off by them-

selves

Scab secreton or exudate or dried blood over the skin

Slough black necrotc plate of tssue with demarcated bor-

ders

bull Solutons of contnuity Erosion loss of epidermal substance that heals without leaving

a scar

Ulcer loss of epidermal and dermal substance that leaves a scar

afer healing

Excoriaton erosion secondary to scratching

Fissure crack that reaches high dermis as a result of hyperkera-

tosis

bull Others

Sclerosis skin induraton with elastcity loss due to fibrosis and

dermal collagenizaton

Scar fibrous tssue that replaces normal skin

Lichenifi

cat

on thickening of the epidermis with accentuat

on ofskin folds secondary to chronic scratching

Intertrigo cutaneous lesion located in skin folds

Telangiectasia arboriform erythematous macule secondary to

permanent dilaton of cutaneous vessels

Poikiloderma hypopigmented and hyperpigmented areas

with atrophy and telangiectasias Poikiloderma is unspecific

and it translates into the presence of chronic cutaneous dam-

age

As a summary Figure 2 lists the main cutaneous elemental lesions com-

mented on this item

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Amer ican Manual of Examinat ion in Medicine (2CK)

2

bull Type II is mediated by IgM and IgG G Cytotoxic Hemolytc anemia

bull Type I is mediated by immune complexes Toxicodermas

bull Type IV is mediated by T lymphocytes (cellular) Contact derma-

tts

32 Atopic Dermatitis

Atopic dermatts is an inflammatory disorder of the skin with chronic

and recurring presentaton which aff ects 12 - 15 of children popula-

ton Atopic dermatts manifests itself by dry skin and pruritus

Patents have more risk of bacterial secondary infectons (S aureus) and

viral infectons (simple herpes virus SHV or mollusca)

There is a variety of triggering factors or factors that maintain eczema

outbreaks aeroallergens (dust mites) bacterial antgens (S aureus)

food (ovoalbumin) and psychological stress among others

Clinical Presentation

Clinical presentaton is usually in the form of greasy erythematous

and desquamatve papules or plaques on the scalp (cradle cap in the

cases of newborns) central area of the face sternal region axilla and

or groin In newborns this presentaton can be generalized causing

Leinerrsquos erythroderma desquamatvum in adults it is likely to be re-

lated to blepharits

Diff erental diagnosis includes atopic eczema in children but diff eren-

tal diagnosis in adults reveals subacute erythematous lupus or pink

pityriasis when the trunk is involved and inverted psoriasis when skin

folds are aff ected

Remember

Letterer-Siwe disease can cause lesions similar to infantile seborrheicdermatitis However unlike infantile seborrheic dermatitis Letterer-Siwedisease is associated with lymphadenopathies and hepatosplenomegaly

Remember

Impetigo key words (yellowish scabs) should not be mistaken for seborrheicdermatitis key words (yellowish scales)

Diagnosis

Atopic dermatts has a clinical diagnosis Patents may present with eo-

sinophilia and increase of IgE values

Treatment

It is essental for the patent to follow certain rules in his lifestyle This

means the patent must avoid wearing perfumed products (like cologne

and cream) being exposed to extreme temperatures the use of fabric

sofeners and carpets or fluff y toys (because of possible sensitzaton of

dust mites) Besides the patent needs to wear 100 coon clothing

Macule Vesicle

Wheal Fissure

Papule Ulcer

Nodule Cyst

Figure 2 Cutaneous elemental lesions

22 Histological Lesions

The following are histological lesions of the skin

bull Hyperkeratosis increase in the stratum corneum (warts and psoriasis)

bull Hypergranulosis granular layer thickening

bull Acanthosis thickening of the stratum spinosum

bull Acantholysis rupture of intercellular bridges of the stratum spino-

sum (typical of pemphigus)

bull Spongiosis intercellular intraepidermal edema (characteristc of eczema)

bull Ballooning intracellular edema (herpes)

bull Parakeratosis presence of nuclei in the stratum corneum (typical

of psoriasis)

bull Dyskeratosis abnormal keratnizaton of individual cells of the stra-

tum spinosum (typical of Darierrsquos disease)

bull Papillomatosis lengthening of dermal papillae (psoriasis)

Chapter 03

Allergic and

Immune-mediated

Diseases

31 Hypersensibility Reactions

bull Type I is mediated by IgE It is the most rapid Anaphylaxis asthma

and urtcaria

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Dermatology

Precocious treatment is of the utmost importance

Topic cortcoids are the first line treatment

It is worth to remember that prolonged use of topic cortcoids can have

local and systemic secondary side eff ects

The second line of treatment involves immunomodulators (tacrolimus

and pimecrolimus) These can be used in children older than 2 years of

age

For acute outbreaks oral cortcoids are used in short cycles and not as

maintenance To stop medicaton suddenly may cause a rebound eff ect

33 Contact Eczema

The appearance of contact eczema is immunologically mediated (type

IV hypersensit

vity) against foreign agents acquired by percutaneouspenetraton Contact eczema requires prior sensitzaton to allergen

It is more common in adults than in children

Diagnosis

Diagnosis is established with clinical records and epicutaneous tests of

contact These tests are performed once lesions have been resolved by

applying patches with allergens on healthy skin leaving them in contact

with the skin during 48 hours They are read afer 48 and 96 hours The

intensity of reacton is measured qualitatvely negatve weak positve

(erythema) strong positve (papules-vesicles) or extreme positve (blis-

ters)

Treatment

Avoid contact with the allergen

Treatment of acute eczema implies applicaton of topic poultce (zinc

sulphate sodium borate) and cortcoids if lesions are limited and sys-

tem poultce if lesions are generalized

34 Seborrheic Dermatitis

Seborrheic Dermatts is a quite frequent disease It aff ects 4 - 5 of the

populaton Etology of seborrheic dermatts is unknown although it

has been related to an abnormal immunological response to a fungus

called Pityrosporum ovale Seborrheic dermatts is more frequent and

intense when associated to neurological processes alcoholism and im-

munodeficiencies

Clinical Presentation

According to patentrsquos age

a Seborrheic dermatts in infants Yellowish scales on scalp known

as cradle cab

b Seborrheic dermatts in adult erythematous desquamatng papu-

les or plates in fat areas of the facial region and scalp

Diagnosis

Diagnosis of this conditon is clinical

TreatmentTreatment involves antfungals associated with topic cortcoids Sebor-

rheic dermatts on the scalp is usually linked to a keratolytc agent like

the salicylic acid

35 Psoriasis

Psoriasis is a chronic inflammatory disease of the skin that presents

with outbreaks Psoriasis aff ects 1-2 of the populaton and can ap-

pear at any age with a maximum of incidence between 20 and 30 yearsof age There is a family history in a third of the patents

Plates are the characteristc erythematous desquamatng lesions well

delimited with a superficial thick and white-pearl scale

The most frequent clinical form is vulgar psoriasis or psoriasis in plates

Lesions are localized at extensor surfaces (elbows and knees) and the

scalp The umbilical and the lumbosacral areas are ofen aff ected

Nail involvement is frequent and is most common with a pi ng ap-

pearance This form is lile specific The forms that combine hyperkera-

tosis and distal onycholysis are more specific Oil spot is the most char-

acteristc sign (Figure 3)

Figure 3 Generalized pustular psoriasis

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4

Diagnosis

Diagnosis of this conditon is generally clinical

If there is no certainty a biopsy must be done which will reveal hyper-

keratosis acanthosis and parakeratosis

There is an increase in polymorphonuclears (sterile abscesses) in the

stratum corneum which are called Munro abscesses

Treatment (Table 1)

For moderate severe forms of psoriasis that do not respond to clas-

sical systemic treatments (see table) They are monoclonal antbod-

ies against proinflammatory substances that are high in patents with

psoriasis [alpha tumor necrosis factor (TNF) interleukin IL 12 and

23] Some of them are infliximab adalimumab ustekinumab and

etanercept

36 Urticaria

Urtcaria is an immunologic and inflammatory reacton of the skin

against diverse etological factors Independently of the cause release

of histamine and other inflammatory mediators occurs which cause va-

sodilaton and increase in capillary permeability producing an edema in

superficial dermis Urtcarias are divided in acute and chronic urtcarias

depending on whether outbreaks persist more or less than six weeks

About 60 of acute urtcarias are idiopathic Chronic urtcarias show a

higher percentage

Urtcarias of known origin are usually due to infectons drugs or food

Clinical Presentation

Clinical presentaton is characterized by the appearance of pruritc wheals

that last less than 24 hours and can be accompanied with angioedema

TREATMENT USES SIDE EFFECTS AND CONTRAINDICATIONS

Topic Mild-moderatepsoriasis

(lt 25 body

surface)

Emollients (urea glycerin) Moisturizing

Keratolytics (salicylic acid) Eliminate excess of scales

Reductants (dithranol) Hyperkeratotic plaques middot Stain skin and clothing

middot Irritating

middot Acneiform eruptions

Corticoids middot Stable psoriasis

in plates

middot The most used

middot Tachyphylaxis

middot Percutaneous absorption

middot Possible new outbreak after stopping medication

middot Avoid prolonged treatment

Vitamin D analogues

(calcitriol calcipotriol and

tacalcitol)

Stable psoriasis in plates middot Irritating in face and skin folds

middot Hypercalcemia

Systemic Moderate-

severe psoriasis

(gt 25 body

surface)

Psoralens plus ultraviolet

light of the A wavelength(PUVA)

Combinable with topics

and retinoids (RePUVA)

middot Cutaneous aging and carcinogenesis

middot Erythroderma and xerosis middot Immunosuppression

middot Hepatitis by psoralens

middot Not in children pregnancy patients with hepatic or renal

insuffi ciency photosensitivity or cutaneous precancerosis

middot Cataracts

middot It accumulates in the crystalline during 24 h (sunglasses)

Retinoids (acitretin) middot Severe psoriasis

pustular

or erythrodermic

middot It is not usually used

in women in fertile age

(see side effects)

middot Cutaneous dryness (the most frequent)

middot Hypertriglyceridemia

middot Hypercholesterolemia

middot Increase in transaminases

middot Diffuse alopecia

middot Vertebral hyperostosis ligamentous calci1047297cations

middot Teratogenicity avoid pregnancy until 2 years after

1047297nishing treatment

middot Avoid in children and patients with hepatic or renal failure

Cyclosporine A middot In1047298ammatory severe

psoriasis resistant to

other treatments

middot Rapid action

middot Rebound effect

middot Nephrotoxicity

middot High blood pressure (HBP)

middot Epitheliomas and lymphomas

middot Hypertrichosis

middot Gingival hyperplasia

middot Hyperuricemia

Methotrexate middot Severe psoriasis

resistant to other

treatments

middot Psoriatic arthropathy

middot Hepatotoxicity

middot Myelosuppression

middot Teratogenicity until 3 months after ending treatment

middot Photosensitivity

Table 1 Psoriasis treatment

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Dermatology

Vasculits urtcaria should be ruled out when lesions last more than 24 hours

and are accompanied with systemic clinical symptoms (ie arthralgias)

Treatment

Oral anthistamine therapy is the treatment of choice

Systemic cortcoids for severe or refractory cases

Adrenalin for severe cases with anaphylaxis

37 Toxicodermas

Toxicodermas are quite variable cutaneous reactons that appear afer

drug administraton They are one of the most frequent side eff ects of

drugs The causatve agents for many toxicodermas stll remains un-

known either immunological or not and clinical presentaton does not

facilitate agent dist

nct

on

Morbilliform exanthem is the most frequent A morbilliform exanthem

is a generalized erupton formed by symmetric and confluent macules

and papules that usually start by the trunk

They can appear one or two weeks afer taking the drug

A morbilliform exanthem can be associated with fever pruritus and eo-

sinophilia

The most frequent are non steroid ant-inflammatories antbiotcs (sul-

phamides and penicillins) antepileptcs allopurinol and N acetyl-cystene

DiagnosisDiagnosis is according to clinical presentaton

Treatment

Treatment implies withdrawal of potentally responsible drug Topic or

systemic anthistamines and cortcoids are given according to the extent

of symptoms (Figure 4)

Figure 4 Morbilliform exanthem due to amoxicillin

38 Multiform Erythema

Stevens-Johnson Syndrome

and Toxic Epidermal Necrolysis

Multform erythemas (ME) are of undetermined etopathogenesis

regarded as a cutaneous reacton against a diversity of stmuli Their

histologies show similarites what leads to consideraton of a common

pathogenesis

Clinical Presentation

Three diff erent groups have been described although many a tme their

clinical symptoms overlap

bull Erythema multforme minor is the most frequent with around 80

of the cases It usually precedes a symptomatc infecton by simple

herpes virus (60) or subclinical infecton about 15 days before

Erythema multforme minor manifests itself on extensor surfaces

at hands elbows and feet as a symmetric erupton of erythema-

tous edematous lesions with target-shape (herpes iris of Batemanor rosee-paerned lesion) with a violaceous sometmes bullous

center (Figure 5)

Mucosal aff ectaton is rare with small erosions in oral mucosa Erythe-

ma multforme minor tends to recurrence with subsequent outbreaks

of herpetc lesions

Figure 5 Erythema multiforme minor Herpes iris of Bateman

bull Erythema mult

forme major or Stevens-Johnson syndrome is therarest It normally has a prodromal period of untl 14 days with fe-

ver cough cephalea arthralgias and other symptoms Subsequent

to the prodromal period erythematous edematous plates appear

which are more extensive with a tendency to form blisters and

greater mucosal erosions (mouth genitals pharynx larynx and

conjunctve Figure 6) Systemic symptoms are normal and do not

tend to recurrence

The most frequent etological factors are drugs [sulphamides non

steroid ant-inflammatory drugs (NSAIDs) antconvulsants and an-

tbiotcs in decreasing order) Infectous agents have been also in-

volved mainly mycoplasma pneumoniae

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6

Figure 6 Exudative erythema multiforme major

bull Toxic epidermal necrolysis (TEN) many authors consider it the

most severe form of erythema multforme major arguing the same

pharmacological agents A morbilliform rash appears which is rap-idly confluent comprising almost the entre skin surface with flaccid

blisters that leave wide areas of denuded skin Involvement of sev-

eral mucosae is constant

Complicatons ofen occur (pneumonia digestve hemorrhage re-

nal failure and hemodynamic shock) with mortality rates close to

25 In children it must be performed a diff erental diagnosis with

staphylococcal scalded skin syndrome which does not aff ect mu-

cosae

Remember

Diseases that have the Nikolsky sign are TEN staphylococcal scalded skinsyndrome (SSSS) and pemphigus In TEN the whole epidermis comes off(bad prognosis) while in SSSS epidermal detachment occurs at the granularlayer

Histopathology

It must be highlighted the eff acement of dermoepidermal juncton by a

lymphohistocytc infiltrate and vacuolar degeneraton of the baseline lay-

er with necrotc keratnocytes In TEN keratnocytes necrosis is massive

Treatment

In ME minor only symptomat

c treatment is prescribed with topiccortcoids and oral anthistamines Treatment for herpes simplex virus

(HSV) infecton is useful to prevent ME lesions if patent is in the inital

stage of the viral infecton

ME major requires treatment of the underlying infecton or withdrawal

of implied drug and support measures The use of oral steroids accord-

ing to the patentrsquos general state is under discussion

A patent with TEN requires to be admied at the burn treatment room

with monitoring of hematocrit hydroelectrolytc balance and antbiotc

prophylaxis and support measures It is controversial the use of system-

ic cortcoids immunoglobulins andor cyclosporine

39 Erythema Nodosum

Erythema nodosum is the most frequent panniculits Painful erythema-

tous nodules occur mainly in the anterior side of legs with a self-limit-

ing course and predominantly aff ectng young women (Figure 7)

Figure 7 Erythema nodosum

They heal without leaving a scar within a period of four to six weeks

Erythema nodosum may be accompanied with fever deterioraton of

the general state and arthralgias

Patents with erythema nodosum may have a false positve VDRL

Etiology

This conditon is thought to be an immunological response triggered by

multple and diff erent stmuli bacterial fungal and viral infectons sys-temic diseases (sarcoidosis inflammatory intestnal disease Behcetrsquos

syndrome) neoplasias (lymphomas and leukemias) and drugs (oral

contraceptves sulphamides bromides and iodines)

Diagnosis

Erythema nodosum requires a deep biopsy to reveal septal panniculits

without vasculits

Complementary tests can be performed to rule out systemic involvement

for example chest X-ray Mantoux and antstreptolysin O antbody (ASLO)

Treatment Treatment entails eliminatng underlying cause if found then rest and

ant-inflammatories

310 Bullous Pemphigoid

and Pemphigus Vulgaris

See Table 2 and Figures 8 9 10 and 11

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Dermatology

Intercellular

substance ac

middot Pemphigus

Lineal

storage

in lucid

layer

-

Anti-Collagen Ac

Lucid

layer

Thick

layer

Basal

sublayer

Granular

storage

in papillary

dermis

middot Pemphigoid bullousmiddot Herpes gestationis

middot Acquired blistering epidermolysis

middot Dermatitis herpetiformis

Figure 8 Key points for histological diagnosis

of autoimmune blistering diseases

Figure 9 Pemphigus vulgaris

Figure 10 Pemphigus vulgaris with oral mucosa involvement with

erosions

Figure 11 Pemphigoid bullous Tense blisters No sign of Nikolsky

PEMPHIGUS VULGARISGENERALLY

IDIOPATHICHERPES GESTATIONIS

DERMATITIS

HERPETIFORMIS

Clinical presentation middot 40-50 years of age

middot They usually affect mucosae

middot No pruritus

middot Flaccid blister

middot Nikolsky

middot Elderly

middot Sometimes mucosae

middot With pruritus

middot Tense blister

middot No Nikolsky

middot Pregnant women

middot No mucosae

middot With pruritus

middot Herpetiform

middot No Nikolsky

middot 15-35 years of age

middot No mucosae

middot With pruritus

middot Herpetiform

middot No NikolskyDirect immuno1047298uorescence (DIF) IgG IgG IgG IgA

Histology middot INTRAepidermal blister

middot There is acantholysis

middot SUBepidermal blister

middot There are eosinophils

middot SUBepidermal blister

middot There are eosinophils

middot SUBepidermal blister

middot Neutrophils in dermis

Treatment Corticoids at high doses

immunosuppressants rituximab

and immunoglobulins

Corticoids Corticoids Diet +- dapsone

Remember Mortality rate 10 The most frequent Relapse if new

pregnancy

Associated to enteropathy

by gluten 90

Table 2 Autoimmune blistering diseases

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Amer ican Manual of Examinat ion in Medicine (2CK)

8

Chapter 04

Infectious Diseases

41 Viral Infections

Simple Herpes

Infection by Simple Herpes Virus

There are two types of simple herpes (Figure 12)

bull Type I is responsible for most extragenital herpes and 20 of the

genital herpes

bull Type II causes genital herpes and a small percentage of extragenital

herpes

Figure 12 Herpes simplex

Contagion is produced by direct contact though the carrier may be as-

ymptomatc Afer primary infecton virus remains silent in the sensi-

tve porton of cranial or spinal ganglia Immunosuppressed patents

endure the greatest severity of this conditon

Clinical Presentation

bull Extragenital simple herpes recurring orofacial herpes simplex is

the most frequent Most primary infect

ons are asymptomat

c Only5 manifest themselves in the form of herpetc gingivostomatts a

profile characterized by oral ulcers with cervical adenopathy and af-

fectaton of the patentrsquos general state (Figure 13) During relapses

clinical symptoms are milder with cluster vesicles on an erythema-

tous base Some factors facilitate relapses trauma sunlight cold

stress fever and the menstrual cycle

bull Genital simple herpes is the most common cause of genital ulcers

afer trauma Primary infecton is usually symptomatc and occurs

between 3 to 14 days afer sexual contact It causes clustered ulcers

in the balanopreputal sulcus or in the prepuce with painful inguinal

adenopathy Relapses are less severe than primary infecton and oc-

cur more frequently when genital herpes is due to HSV type II

Figure 13 Herpetic gingivostomatitis

bull Eczema herpetcum or Kaposi varicelliform erupton dissemina-

ton of herpetc infecton on pre-existng dermatosis (above all

atopic dermatt

s) bull Neonatal herpes is due to intrapartum contagion of HSV-II with

neurological involvement general deterioraton and skin vesicles or

ulcers

bull Other clinical forms are herpes gladiatorum herpetc whitlow and

keratoconjunctvits

Diagnosis

Diagnosis of this conditon is mainly clinical Virological culture is the

most reliable method of confirmaton The extent of a smear of the le-

sions (Tzanck cytodiagnosis) allows visualizaton of multnucleated cells

and intranuclear inclusions which become evident through histological

study

Treatment

Mild forms do not need treatment Treatment is required in the follow-

ing cases

bull Primary infecton

bull Severe or frequent relapses if they aff ect life quality

bull Complicatons like erythema multforme and eczema herpetcum

Drug of choice is oral acyclovir and its derivatves (valacyclovir famci-

clovir) Topic antvirals have not proven useful favoring maceraton of

lesions and thus over infecton It is not infrequent that topic antvirals

cause allergic contact dermatts due to hypersensitvity

Varicella-Zoster Virus

A primary infecton gives way to varicella (see Pediatrics secton) Afer

varicella the virus remains latent in the sensitve porton of the neural

ganglia and when relapse occurs it leads to zoster herpes

bull Varicella the following symptoms appear afer 15 days of incubaton

fever cephalea pruritus and polymorphic lesions in diff erent stages

macules papules vesicles (Figure 14) ulcers and scabs (starry sky

appearance) Mucosal (ulcers) and scalp involvement is characteristc

Manipulaton can leave scars Bacterial over infecton of lesions is the

most usual complicaton About 20 of adults suff er from varicella

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Dermatology

pneumonia radiologically demonstrable but clinical symptomatology is

only present in around 4 of the cases

Figure 14 Typical vesicles in patients with varicella

bull Zoster herpes thoracic zoster herpes is the most usual It sel-

dom occurs more than once throughout a personrsquos lifetime

It is characterized by vesicles on pre-existing erythema with

metameric distribution and lateral extension The most com-

mon complication is post herpetic neuralgia more frequent in

advanced age Carbamazepine or tricyclic antidepressants (Fig-

ure 15)

Figure 15 Zoster herpes

Special Clinical Forms

Special clinical forms are as follow

bull Ramsay-Hunt syndrome aff ectaton of geniculate ganglion of the

facial nerve

It produces vesicles in the outer ear external auditory canal and

pharynx homolateral facial paralysis deafness and vertgo

bull Ophthalmic involvement can result in severe keratts and requires ur-

gent referral to an ophthalmologist Suspicion should exist on patents

that present herpetc lesions on the tp of the nose) (Hutchinsonrsquos sign)

bull Disseminated zoster herpes several dermatomes are aff ected bilat-

erally Ramsay-Hunt syndrome is characteristc in the immunosup-

pressed

Remember

Affectation of the nose tip makes it necessary for ophthalmologicalexamination because the nose tip is innervated by the same nerve thatinnervates the cornea (1047297rst branch of the trigeminal nerve)

Treatment

Varicella without complicatons is treated symptomatcally Antvirals

are reserved for severe or complicated forms There is a commercial-

ized vaccine of live virus whose indicatons are stll under discussion

Zoster herpes must be treated with antvirals when detected during the

first 48-72 hours and aff ectng patents with

bull Immunosuppression

bull Age above 55

Special clinical forms previously cited

Drugs to be used are oral acyclovir and its derivatves (valacyclovir and

famciclovir) They accelerate the cure of lesions and decrease the inten-

sity of post herpetc neuralgia Patents with renal failure need a dose

adjustment as acyclovir is nephrotoxic These patents are adminis-

tered brivudine in a single daily dose

Molluscum ContagiosumDome shaped pink papules with central umbilicaton (Figure 16) Mol-

luscum contagiosum is typical of children that go to swimming pools It

is also present in the genital zone afer sexual contact and in immuno-

suppressed patents It is caused by Poxvirus

Figure 16 Molluscum contagiosum

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Amer ican Manual of Examinat ion in Medicine (2CK)

0

Lesions are asymptomatc

Diagnosis

Diagnosis is clinical Histology reveals characteristc inclusion bodies

Treatment

Lesions can resolve spontaneously

Cureage cryotherapy or local trichloroacetc acid are eff ectve meth-

ods to destroy lesions

Warts

Human papillomavirus can cause verruca vulgaris palmoplantar and

flat warts and condyloma accuminata Human papillomavirus is the

most frequent sexual transmied disease

Some subtypes of this virus (16 18) are of high risk and can cause epi-

dermoid carcinomas

Direct contact is the mechanism of contagion

Diagnosis

Diagnosis of this conditon is clinical

Staining with acetc acid can help visualize mucosal lesions

Treatment

Genital warts are treated with cryotherapy podophyllotoxin trichloro-

acetc acid imiquimod and 5-fluorouracil

Cervical lesions should be monitored by cytology and biopsy whenever

necessary to rule out cervical cancer (Figures 17 and 18)

Figure 17 Warts in HIV patient

Figure 18 Condyloma accuminata

42 Bacterial Infections

Impetigo

Impetgo is a very contagious superficial infecton without systemic re-

percussion and normally mixed etology by Gram positve cocci (strep-

tococci and staphylococci) Classically the most frequent accepted

cause was Streptococcus pyogenes However at present Staphylococcus

aureus stands out as the predominant cause

The most typical form is impetgo contagiosa (Figure 19) character-

ized by honey-colored (meliceric) scabs which normally appear on

the face and other exposed areas It is typical of children Although

infrequent poststreptococcal glomerulonephrits is a dreadful com-

plicaton

Figure 19 Impetigo contagiosa

On the contrary rheumatc fever shows no relaton to cutaneous strep-

tococcal infectons but only with pharyngeal infectons

There are other less habitual forms called bullous impetgo exclusively

of staphylococcal origin Clinical presentaton involves the presence of

blisters and erosions on the aff ected skin as a consequence of the epi-

dermolytc toxins that these bacteria contain Impetgo is treated with

topical mupirocin penicillin or oral fusidic acid

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Dermatology

Cellulitis

Cellulits is an infecton that aff ects deep dermis and subcutaneous cel-

lular tssues normally caused by streptococci (Streptococcus pyogenes

or of group A)

Community methicillin-resistant S aureus (CMRSA) is a triggering agent

that is becoming more and more frequent

Most common risk factors are diabetes chronic venous insuffi ciency

and immunosuppression

Clinical Presentation

Cellulits presents with erythematous plaques that are ill-defined pain-

ful and hot It is usually accompanied with fever and chills

Diagnosis

Diagnosis is clinical If there is an open door a culture of this area may

help see the source germ and resistance to ant

biot

cs

It is important to rule out abscesses osteomyelits and necrotzing fas-

ciits

If bacteremia is suspected blood cultures need to be performed

Treatment

Treatment implies oral antbiotcs for 7-10 days to cover Gram positve

cocci They are intravenously administered in case of lack of response

to oral treatment involvement of hands or periorbital zone diabetes or

extremes of age

Necrotizing FasciitisNecrotzing fasciits is a deep infecton up to muscular fascia that pro-

duces very intense pain and subsequent anesthesia

In 10 of the cases cellulits is due to an infecton by S pyogenes In the

remaining cases it occurs by a polymicrobial infecton caused by aerobes

and anaerobes including S aureus E coli and Clostridium perfringens

There may be prior history of trauma or surgery

Clinical Presentation

Clinical presentat

on involves pain of sudden onset and edema on theaff ected zone Pain may progress to anesthesia There appears subse-

quent erythema that progresses rapidly into necrosis

Characteristc clinical signs are tssue necrosis blisters intense pain

and gas producton

Diagnosis

Diagnosis is clinical and requires image testng X-rays or a computed

tomography CT

A biopsy of the border of the lesion helps achieve diagnosis

Treatment

Treatment entails precocious surgical debridement It is a surgical emer-

gency In additon to surgery broad-spectrum antbiotherapy will be

needed

Folliculitis

Folliculits is an infecton and inflammaton of one or several follicles

caused mainly by staphylococci

Clinical Presentation

Folliculits shows pustules with follicular distributon

When the infecton is deeper it is called furuncle

If several furuncles are infected a fluctuatng erythematous plaque forms

containing several points of suppuraton This plaque is labeled as anthrax

Diabet

c and immunosuppressed pat

ents are at higher risk

Characteristics of Folliculitis

1 Hot tub or swimming pool folliculits caused by Pseudomonas aeru-

ginosa

2 HIV associated pruritc folliculits or eosinophilic folliculits

Treatment

In mild cases treatment of choice comprises antseptcs and topic an-

tbiotcs

In more severe cases treatment of choice requires oral antbiotcs

Large sized lesions must be drained and a microbiological culture must be

performed to rule out methicillin-resistant Staphylococcus aureus MRSA

Acne Vulgaris

Acne is an inflammatory disease of the pilosebaceous follicle as a con-

sequence of an alteraton in follicular keratnizaton It aff ects adoles-

cents and young adults

Etology is multfactorial alteraton of keratnizaton of follicular infun-

dibulum quanttatve and qualitatve alteraton of sebum producton in

the sebaceous gland and alteratons of bacterial microflora (increase in

quant

ty of P acnes)

Aggravatng factors are stress androgenic oral contraceptves and the

use of cosmetc products that are not oil-free

Clinical Presentation

A comedo is the inital lesion which can be closed (whitehead) or open

(blackhead) and it evolves into inflammatory lesions that listed in as-

cending order of severity are papules pustules nodules and cysts

Lesions progress and leave scars Scars can be increased if lesions are

manipulated

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2

Diff erent lesions habitually combine simultaneously so acne becomes

polymorphic It is located in sebaceous areas face back shoulders and

the center thoracic region

Diagnosis

Diagnosis is clinical

Treatment

bull Comedonal acne is treated with topic retnoids and benzoyl peroxide

bull Inflammatory acne treatment requires benzoyl peroxide combined

with topic antbiotcs (erythromycin and clindamycin) Systemic

antbiotc treatment with oral tetracyclines will be prescribed if re-

sponse to topic antbiotc treatment fails

bull Severe nodular cystc acne treatment involves the use of isotret-

noin (13-cis-retnoic acid) It is a derivatve of vitamin A Isotretnoin

produces atrophy in the sebaceous gland and regulates keratniza-

ton The most frequent side eff ect is cutaneous and mucosal xero-

sis Triglycerides cholesterol and transaminases should be moni-

tored as their values may increasebull It can be associated with depression

bull It is teratogenic so pregnancy should be avoided during treatment

and untl a month afer treatment

Pilonidal Cysts

Pilonidal cysts are abscesses in the sacrococcygeal region

This type of cysts has predominance in men between 20 and 40 years

of age It is believed that repeated trauma on the aff ected area favors

their appearance

Clinical Presentation

Pilonidal cysts present with an indurated lesion that is fluctuatng hot

painful but non-adherent to deep planes in the sacrococcygeal region

Pilonidal cysts may or may not be associated to cellulits and purulent drain-

age

Diagnosis

Diagnosis is clinical and anal or perirectal abscesses should be dismissed

Treatment

Treatment implies an incision and surgical drainage

On some occasions a general surgery is required

43 Fungal Infections

Pityriasis Versicolor

Versicolor pityriasis is caused by commensal yeast called Pityrosporum

ovale which transforms into its pathogen form (Malassezia furfur) It

especially aff ects young patents (15 - 45 years of age) but it is rare

in childhood and advanced age Versicolor pityriasis relates to heat

humidity and sebaceous hypersecreton It is characterized by the ap-

pearance of hyperchromic or hypochromic macules that desquamate

on scratching (nail sign) if infecton is actve Macules usually appear on

the center thoracic region and on the back that is to say on seborrheic

zones Relapses are habitual despite treatment

Diagnosis

Diagnosis is normally clinical To that purpose the following serve as

support

bull Woodrsquos lamp emits yellow-orange fluorescence

bull Potassium hydroxide (KOH) test filaments and round elements can

be observed (ldquospaghe and meatball appearancerdquo Figure 20)

Treatment

Treatment is performed with topical azoles Oral administraton applies

for extensive cases or immunosuppressed patents Diff erental diagno-

sis includes pink pityriasis and eczemas (Figure 21)

Figure 20 Versicolor pityriasis Histological cut

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Dermatology

Figure 21 Versicolor pityriasis

Candidiasis

The most common triggering agent is Candida albicans It is normally sapro-

phyt

c although under certain condit

ons candidiasis may become patho-genic (immunosuppression humidity pregnancy and contraceptves)

Clinical Forms

bull Intertrigo erythematous plaque in cutaneous folds Atrophy and

fissures are typically deep in the skin fold as well as satellite and

peripheral lesions (papules andor pustules)

bull Mucosa involvement may cause diverse symptomatology like vul-

vovaginits glossits and white papules in the anterior region of the

oral mucosa Candidal balanits is characterized by the presence of

punctform erosions and pustules on gland and balanopreputal

sulcus Candidal balanits ofen appears afer sexual intercourse or

afer oral antbiotc intake

Remember

Almost a 100 of HIV patients suffer from muguet throughout their diseasecourse

bull Candidiasis of nail fold is usually associated with periungual inflam-

maton (perionixis) and inital proximal aff ectaton which diff erent-

ates it from tnea unguium (Figure 22)

Figure 22 Candidiasis of nail fold

Treatment

Oral Candidiasis fluconazole or nystatn

Candidiasis of the skin (intertrigo) apply topical antfungal medicaton

and keep zone clean and dry

Dermatophytosis or TineasDermatophyte infectons aff ect the skin and keratnized structures like

hair and nails (there is no mucosa involvement) Clinical diagnosis is

achieved afer performing a culture Woodrsquos lamp test normally turns

out to be negatve In general Trichophyton dermatophyte rubrum is

the most frequent dermatophyte

Non Inflammatory Tineas

Non inflammatory tneas do not produce irreversible scarring alope-

cia while inflammatory forms do Tineas are treated with azoles de-

rivatves

The types of tnea are the following

bull Ringworm of the scalp ( t nea capi t s or t nea tonsurans) is charac-

teristc of childhood It presents with alopecic plaques broken hair

and desquamaton Infectons tend to resolve spontaneously with-

out leaving scars at the onset

of puberty

bull Ringworm of the body (herpes

circinatus or t nea corporis) are

erythematous desquamatve

plaques (with more actve bor-

ders) which are also circinate

and normally pruritc (Figure

23) Plaques grow eccentrically

with less actvity in the centerand more in the borders

bull Ringworm of the foot ( t nea

pedis) the most frequent is the

ldquoathlete footrdquo with desquama-

ton in interdigital spaces

bull Tinea incognito refers to tnea

wrongly treated with cort-

coids what makes diagnosis

diffi cult as the lesion has been modified Figure 24)

Figure 24 Tinea incognito secondary to treatment with topical steroids

Figure 23 Herpes circinatus

(tinea corpis)

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Amer ican Manual of Examinat ion in Medicine (2CK)

4

bull Ringworm of the groin (t nea cruris or eczema marginatum von

hebra) formed by erythematous desquamatve plaque with more

actve borders (Figure 25)

Figure 25 Ringworm of the groin (tinea cruris)

bull Tinea unguium subungualhyperkeratosis with onychol-

ysis but without perionixis

(Figure 26)

Diagnosis

Clinical diagnosis is reached afer

performing a culture

Treatment

Treatment involves topical an-

tfungal medicaton in localized

areas

Oral antfungal medicaton is used in extensive forms nail fold or scalp

involvement

44 Parasitic Infections

Pediculosis

Pediculosis is transmied by direct contact or by contact with fomites

which release toxins that produce intense pruritus

Clinical Presentation

Pediculosis capi t s intense pruritus predominant in retroauricular and

occipital regions occasionally with excoriatons and impetginizaton

secondary to excoriatons

Pediculosis corporis intense pruritus in patents with poor hygiene or

who live in overcrowded conditons

Pediculosis pubis genital and pubic pruritus Brownish-grey macules

called maculae ceruleae are typical on underwear and skin These pig-

mentatons appear as a result of a reducton in hemoglobin by a para-

site enzyme

Diagnosis

Diagnosis is clinical and by direct visualizaton

Treatment

Pediculosis is treated with malathion lindane or topical permethrin

Scabies

Scabies is originated by an acarus known as Sarcoptes scabiei It has an

incubaton period of 1 month

Clinical Presentation

Scabies produces generalized pruritus more intense at night The pa-

tent usually catches the infestaton which is passed to the patentrsquos

relat

ves It is common tofi

nd that a recent trip to a tropical country hasbeen made Lesions appear between the fingers (Figure 27) in wrists

feet genitalia mammary areola and axilla but back and face are usu-

ally spared The most specific lesion is the acarine burrow in whose less

scaly end the advancing zone the mite lies Nodules are frequent in

axilla and genitals (nodular scabies)

bull Norwegian scabies is typical of the immunosuppressed Patents

present with generalized hyperkeratosis and scabs Norwegian sca-

bies produce lile pruritus but it is very contagious because there

are many acari

bull Nodular scabies involves the persistence of pruritc nodules despite

treatment Lesions usually appear in axilla and genitalia Pruritus is

due to a hypersensitvity phenomenon because of the acarus al-

ready dead Nodular scabies is treated with cortcoids

Figure 27 Scabies Acarine burrow

Treatment

bull Permethrin cream at 5 is the treatment of choice It is lile toxic

so it can be used in children and pregnant women

bull Topical lindane at 1 irritates and is neurotoxic therefore it is con-

traindicated in pregnant women and children

bull Oral ivermectn is utlized in cases of resistance to prior treatments

There is stll lile experience as to its use but in a first instance a

Figure 26 Tinea unguium

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Dermatology

single dose would be enough to cure scabies (already used by vet-

erinarians)

45 Ischemia

Decubitus Ulcers

Decubitus ulcers are the result of ischemic necrosis by contnuous pres-

sure on an area which restricts microcirculaton in that zone

Clinical Presentation

Decubitus ulcers are present in patents in bed with scarce mobilizaton

It is favored by bone prominences and lack of fat tssue If sensitvity

decreases there is more risk of formaton of decubitus ulcers

Diagnosis

Diagnosis is achieved based on medical records and clinical presentaton

Treatment

Preventon is of the utmost importance as well as frequent mobiliza-

ton of the patent in bed

Once ulcers have been established hydrocolloid dressings are used for

healing but sometmes surgical debridement is necessary

Gangrene

Gangrene means tssue necrosis

There are three types dry gangrene wet gangrene and gas gangrene

Clinical Presentation

Dry gangrene is due to ischemia generally secondary to atherosclero-

sis Clinical presentaton involves pain cold and paleness of extremi-

tes Once tssue is established it turns bluish-black in color and dry

Wet gangrene is owing to bacterial flora Tissue presents with an edem-

atous appearance either with blisters or pus

Gas gangrene caused by C perfringens It is normally located on re-

cent surgery Bacteria precociously destroyt

ssue producing gas It is amedical emergency

Diagnosis

Clinical diagnosis is obtained by microbiological culture

Treatment

Treatment requires surgical debridement with amputaton if necessary

and associaton of broad spectrum antbiotherapy

Gas gangrene is treated with hyperbaric oxygen

46 Miscellaneous

Acanthosis Nigricans

Acanthosis nigricans are vel-

vet-like papillomatous brown

plaques in neck axilla and groin

folds (Figure 28)

It is associated with diabetes

mellitus Cushingrsquos disease poly-

cystc ovarian syndrome and

obesity

The malignant form of acantho-

sis nigricans is a paraneoplastc

syndrome that diff erentates

from the benign form because

the laer has mucosal and pal-

moplantar involvement

Lichen Planus

Lichen planus is an inflammatory idiopathic disease that equally aff ects

both genders with higher frequency in middle age

Lichen planus has been related to diverse drugs like gold salts

anti-malarial medication and thiazides It has been also linked to

hepatitis C virus infection however this association is currently

doubtful

Clinical Presentation

Lichen planus presents with red-violaceous polygonal flat papulesquite pruritc which localizes on the flexor side of wrists forearms an-

kles and lumbosacral and flank regions On its surface a whitsh retcu-

late can be observed (Wickhamrsquos striae) About 60 - 70 of the cases

present with lesions in oral and genital mucosa oral which appear as

whitsh retculated lesions (Figures 29 and 30)

Figure 29 Lichen planus of oral mucosa with typical whitish

reticulate

Figure 28 Acanthosis nigricans

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Amer ican Manual of Examinat ion in Medicine (2CK)

6

Violaceous papules

with white stretch marks

Lichenoid lymphocyte

in1047297ltrate (band formation)

Destruction

of basal layer

Figure 30 Lymphocytic interface reaction (lichen planus)

Treatment

Mild forms are treated with topical cortcoids

Severe cases require oral cortcoids psoralens plus ultraviolet light of

the A wavelength (PUVA) or cyclosporine

Rosacea

Rosacea is a chronic disease of unknown pathogenesis characterized

by erythema and acneiform lesions on the face It aff ects middle aged

women (between 30 and 50 years of age) more

Rosacea etopathogenesis is unknown although there is involvement of

vasomotor lability infecton by Demodex folliculorum photo exposureand genetc predispositon

Clinical Presentation

Rosacea symptomatology comprises facial flushing episodes that end

up by provoking a persistent erythema telangiectasias and papulopus-

tular lesions without comedos Over tme ocular lesions and hyperpla-

sia of sof tssue may develop

Treatment

Avoid vasodilator stmuli

Mild cases require topical metronidazole or azelaic acid

Moderate cases need doxycycline or oral minocyclines

Severe cases are treated with oral isotretnoin at low doses

Pink Pityriasis

Gilbertrsquos pink pityriasis is an acute self-limitng dermatosis which main-

ly aff ects young adults It is of unknown origin although a viral etology

is suspected (there is some speculaton as to links with human herpes-

virus type 7)

Clinical Presentation

Erupton starts with an erythematous plaque between 2 and 5 cm of

diameter with a desquamatve central collaree ofen localized on the

trunk (heraldic mother patch Figure 31)

Figure 31 Pink pityriasis

Around a week later oval papules appear on the trunk and extremi-

tes These papules share similar characteristcs with the mother patch

though the first ones are smaller and distributed according to skin ten-

sion lines Pink pityriasis may be asymptomatc however it is some-

tmes linked to pruritus Lesions may last between 4 and 8 weeks and

disappear without leaving scars

Diagnosis and Treatment

Diagnosis is clinical Treatment is seldom needed and recommended

therapies in the past (PUVA erythromycin or oral antvirals) have not

shown clearly favorable results

Vitiligo

Vitligo is characterized by achromic macules by melanocyte destruc-

ton

Clinical Presentation

Vitligo shows achromic macules of chronic course and variable progres-

sion

Lesions are predominant on acral and periorificial areas They also show

the Koebner phenomenon

Patents may have markers of autoimmune diseases (ie antthyroid

antbodies and diabetes) but these diseases seldom manifest them-

selves

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Dermatology

Treatment

Localized lesions require topical cortcoids

Extensive or generalized lesions are treated with ultraviolet light B

(UVB) or PUVA

Strict solar photoprotecton is indispensable (Figure 32)

Figure 32 Vitiligo

47 Neoplasias

Seborrheic Keratosis

Seborrheic keratosis is the most frequent benign tumor in human be-

ings since it is part of cutaneous aging

Clinical Presentation

Seborrheic keratosis presents with hyperkeratosic papules with an oily

or velvet-like texture crests fissures and horny plugs on their surface

These papules are normally pigmented showing a brownish-black color

Treatment

No treatment is required as lesions do not become malignant

Seborrheic keratosis can be addressed with cureage or cryotherapy

Actinic keratosis

Actnic keratosis is the most common precancerous lesion and aff ects

almost a 100 of the populaton in sunny areas

Clinical Presentation

Actnic keratosis is characterized by erythematous and desquamatve

papules which are hyperkeratosic and rough on touch developing a

chronic course

Diagnosis

Diagnosis is clinical

Treatment

Treatment entails applicaton of topical 5-fluorouracil topical imiqui-

mod cryotherapy or surgery

If underlying carcinoma is suspected a biopsy must be performed to

rule out suspicion

Epidermoid Carcinoma

Epidermoid carcinoma is the second most frequent cutaneous tumor

Solar photo exposure is the main etological factor which is why epider-

moid carcinoma appears in zones of prolonged solar exposure like the

face Most carcinomas appear over premalignant lesions (actnic kera-

tosis and leukoplakia among others)

Clinical Presentation

Clinical presentaton reveals erythematous or erythematosquamous

plaques Over tme these plaques form papules and tumors which of-

ten become ulceratve and bleed

Diagnosis

Diagnosis is based on clinical suspicion and histopathological confirmaton

Treatment

Surgery with safety margins is the treatment of choice In carcinomas

in situ cryotherapy can be used as well as topical imiquimod electro-

coagulaton or CO2 laser techniques in destructon of tumors Radio-therapy may also be used in some cases

Basal Cellular Carcinoma

Basal cellular carcinoma is the most frequent cutaneous tumor Chronic so-

lar photo exposure is the main etological factor hence most of these car-

cinomas aff ect the facial zone in patents who are 40 years of age or older

Gorlinrsquos syndrome should be considered if multple basal cellular carci-

nomas are found in non photo exposed areas

Clinical Presentation

Basal cell carcinoma shows a pearly pink papule and superficial telan-

giectasias

It is localized over healthy skin and never aff ects mucosae

Treatment

Surgery is the treatment of choice Mohs surgery is performed in zones

where surrounding healthy tssue needs to be preserved Other alter-

natves are cryotherapy imiquimod electrocoagulaton radiotherapy

photodynamic therapy and intralesional interferon Prognosis is excel-

lent as growth is slow and metastasis exceptonal

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Amer ican Manual of Examinat ion in Medicine (2CK)

8

Melanoma

Melanoma is the most aggressive cutaneous tumor given its ability to

metastasize

Risk factors comprise solar photo exposure clear phototype the pres-

ence of dysplastc nevus or a high number of melanocytc nevi Fam-

ily history is quite important as some genetc mutatons determine a

higher risk of developing the disease

Clinical Forms

See Figure 33

Diagnosis

Precocious diagnosis is essental to perform precocious surgical extrpaton

The ABCDE criteria can help patents to see if they need to seek medical

consultaton (asymmetry of lesion uneven borders color and diameter

greater than 6 mm or abnormal evolut

on)

The Breslow index is the thickness of the lesion measured in millimeters

and is the main prognosis factor

Treatment

The base of treatment is precocious surgical extrpaton If the Breslow

index is less than 1 mm margins of 1 cm will be performed If Breslow

index is greater than 1 mm margins will be of 2 cm

For melanomas with a Breslow index greater than 1 mm the sentnel

ganglion must be located This is the first draining lymph node of the

territory where the tumor is localized If the ganglion is positve re-

gional lymphadenectomy will be performed along with interferon ad-ministraton (Figure 34)

In situ Extirpation 05 cm Follow-up

Breslow lt 1 mm Extirpation 1 cm Follow-up

Lymphadenectomy

Breslow gt 4 mm Interferon

Breslow ge 1 mm Extirpation 2 cm Sentinel ganglion

+

Figure 34 Melanoma treatment

Kaposirsquos sarcoma

Kaposirsquos sarcoma is the most common cutaneous tumor in HIV patents

Clinical presentation

Kaposirsquos sarcoma has a course with violaceous fusiform macules whichovertme may evolve into indurated nodules with blackberry appearance

This type of sarcoma has been linked to herpesvirus type 8 both in HIV

and seronegatve patents (Table 3)

EPIDERMAL KAPOSIrsquoS 983080HIV983081 CLASSIC KAPOSIrsquoS

Homosexual youth (95) The elderly

Diffuse and bilateral

(frequently in palate and face)

Unilateral plaques

(lower extremities)

Frequent mucosal and visceral involvement Not so frequent

middot Precocious lymphatic invasion

middot Aggressive

Not so precocious

Table 3 Differences between epidermal and classic Kaposirsquos sarcoma

Nodular melanoma

15

Middle-aged men

middot On healthy skin

middot Any zone

middot Sudden onset

middot Uniform black nodulemiddot Rapidly invasive (vertical growth without radial)middot Frequent ulceration and bleeding

Worst histological prognosis

Lentigo malignant melanoma

10

Elderly women

90 on facephotoexposedzones of aging skins(chronic exposure)

Spot that growsduring many years (gt 10)then progresses (nodule)

Better prognosis

Acral lentinginous melanoma

5ndash10 ( 60 black and Asian race)

Elderly men

middot Sole (ankle) handsmucosa ungual bed

middot No relation to photo exposure

middot Macule with mosaic appearance (spot that grows)middot Some amelanisticmiddot Bad prognosis due to late diagnosis

Melanoma of super1047297cial extension

70

Young women

middot 30 previous nervusmiddot Intermittent exposuremiddot Men back middot Women legs

More frequent

middot Macula with mosaic appearance in colors that grows 4-5 years and then in1047297ltrates (nodule)middot Metastasis 35 to 70

Figure 33 Clinical forms of malignant melanoma

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Dermatology

Diagnosis

Diagnosis relies on clinical suspicion and histopathological confirma-

ton

Treatment

Treatment of localized forms can include surgical extrpaton radiother-

apy or intralesional vinblastne

If the sarcoma is disseminated optons involve interferon or chemo-

therapy

Mycosis Fungoides

Mycosis fungoides is a T-cell lymphoma of low-grade malignancy Its

clinical course may be very slow and surpass 50 years Three stages are

clinically diff erentated

1 Eczematous or macular phase predominantly truncular erythema-

tous macules with years of evoluton They resemble a chromic ec-

zema Histology is unspecifi

c at this stage2 Infiltratve plaque phase infiltrated erythematous plaques appear

Histology is diagnostc at this stage A dermal infiltrate of atypical

lymphocytes band forms can be observed composed of CD+4 T

lymphocytes with cerebriform nuclei There is a marked epidermo-

tropism with the presence of clusters of intraepidermal lympho-

cytes called Pautrierrsquos microabscesses (Figure 35)

Figure 35 Mycosis fungoides Infiltrative plaque phase

3 Tumoral phase erythematous exophytc plaques start to appear

(tumors) with a tendency to ulceraton They can have a large size

Histology may become unspecific again as epidermotropism disap-

pears

In more advanced stages of the disease there is aff ectaton of extra-

cutaneous organs such as lymph nodes liver spleen lungs and bone

marrow Besides there may be blastc transformaton Other possible

complicaton is sepsis by Staphylococcus aureus

These three stages usually develop consecutvely nevertheless there

may patents whose debut starts directly with the tumoral stage

Remember

Microabscesses of mycosis fungoides are due to lymphocytes and are calledPautrierrsquos abscesses Psoriasis microabscesses result from neutrophils andare labeled as Munro-Sabouraud

Seacutezary Syndrome

Seacutezary syndrome can be considered as the leukemic phase of T-cell cu-

taneous lymphoma It is defined by the triad erythroderma (Figure 36

lymphadenopathies and the existence of more than 1000 Seacutezary cellsper milliliter in peripheral blood Seacutezary cells are atypical T- lymphocyte

with cerebriform nuclei

Very intense pruritus is characteristc For many authors Seacutezary syn-

drome is an aggressive clinical form and a bad prognosis of a mycosis

fungoides

Figure 36 Erythroderma due to Seacutezary syndrome

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Amer ican Manual of Examinat ion in Medicine (2CK)

01 Skin Layers 1

02 Terminology Elemental Cutaneous Lesions 1

21 Clinical Lesions 122 Histological Lesions 2

03 Allergic and Immune-mediated Diseases 2

31 Hypersensibility Reactions 2

32 Atopic Dermatitis 2

33 Contact Eczema 3

34 Seborrheic Dermatitis 3

35 Psoriasis 3

36 Urticaria 4

37 Toxicodermas 5

38 Multiform Erythema Stevens-Johnson Syndrome

and Toxic Epidermal Necrolysis 539 Erythema Nodosum6

310 Bullous Pemphigoid and Pemphigus Vulgaris 6

04 Infectious Diseases 8

41 Viral Infections 8

42 Bacterial Infections 10

43 Fungal Infections 12

44 Parasitic Infections14

45 Ischemia 1546 Miscellaneous 15

47 Neoplasias 17

Index

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Dermatology

Chapter 01

Skin

LayersThere are three skin layers epidermis dermis and subcutaneous cel-

lular tssue (Figure 1)

Reticular layer

Sebaceous(Oil) gland

Hair

follicle

Deep

arteriovenousplexusSweat

glandDermal Papillae

Super1047297cial arteriovenousplexus

Subcutaneoustissue

Dermis

Epidermis

Figure 1 Microscopic structure of normal skin

Chapter 02

TerminologyElemental

Cutaneous Lesions

21 Clinical Lesions

Primary Clinical Lesions bull Fluid-filled

Vesicle raised formaton less than 05 cm

Blister lesion equal or greater than 05 cm

Phlyctena large blister

Pustule vesicle of purulent content

Cyst encapsulated lesion of semi-solid or liquid content

bull Of solid consistency

Macule a patch of skin that changed color which is neither

raised nor depressed (non palpable)

When a macule is red in color it is described as erythematous If

it does not disappear afer a diascopy it is regarded as purpuric

(it translates the existence of extravasated blood)

In diff erental diagnosis of purpuric lesions senile purpura must

be taken into account which consists in the presence of viola-

ceous macules in areas exposed to trauma as a consequence

of capillary fragility Other cause for purpura is leukocytoclastc

vasculits which typically gives palpable purpuric papules but

not nodules

Papule small solid circumscribed elevaton of the skin of less

than 1 cm which resolves without leaving a scar It is called

plaque if it is equal or greater than 1 cm Unlike macule both

are palpable

Wheal erythematous edematous plate of dermal origin and of

fleetng evoluton (it disappears in less than 24 hours) It is char-

acteristc of urtcaria

Nodule circumscribed hypodermal lesion identfied by palpa-

ton It may or may not be raised (ldquoit is palpable rather than vis-

iblerdquo) Nodules are typical lesions of panniculits like the ery-

thema nodosum

Tubercle circumscribed infi

ltrated and raised nodule that usu-ally leaves a scar once it has resolved

Gumma granulomatous inflammaton that sofens and opens

gradually

Secondary Clinical Lesions

bull Secondary clinical lesions expected to disappear on their own

Scales plates in the stratum corneum which come off by them-

selves

Scab secreton or exudate or dried blood over the skin

Slough black necrotc plate of tssue with demarcated bor-

ders

bull Solutons of contnuity Erosion loss of epidermal substance that heals without leaving

a scar

Ulcer loss of epidermal and dermal substance that leaves a scar

afer healing

Excoriaton erosion secondary to scratching

Fissure crack that reaches high dermis as a result of hyperkera-

tosis

bull Others

Sclerosis skin induraton with elastcity loss due to fibrosis and

dermal collagenizaton

Scar fibrous tssue that replaces normal skin

Lichenifi

cat

on thickening of the epidermis with accentuat

on ofskin folds secondary to chronic scratching

Intertrigo cutaneous lesion located in skin folds

Telangiectasia arboriform erythematous macule secondary to

permanent dilaton of cutaneous vessels

Poikiloderma hypopigmented and hyperpigmented areas

with atrophy and telangiectasias Poikiloderma is unspecific

and it translates into the presence of chronic cutaneous dam-

age

As a summary Figure 2 lists the main cutaneous elemental lesions com-

mented on this item

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Amer ican Manual of Examinat ion in Medicine (2CK)

2

bull Type II is mediated by IgM and IgG G Cytotoxic Hemolytc anemia

bull Type I is mediated by immune complexes Toxicodermas

bull Type IV is mediated by T lymphocytes (cellular) Contact derma-

tts

32 Atopic Dermatitis

Atopic dermatts is an inflammatory disorder of the skin with chronic

and recurring presentaton which aff ects 12 - 15 of children popula-

ton Atopic dermatts manifests itself by dry skin and pruritus

Patents have more risk of bacterial secondary infectons (S aureus) and

viral infectons (simple herpes virus SHV or mollusca)

There is a variety of triggering factors or factors that maintain eczema

outbreaks aeroallergens (dust mites) bacterial antgens (S aureus)

food (ovoalbumin) and psychological stress among others

Clinical Presentation

Clinical presentaton is usually in the form of greasy erythematous

and desquamatve papules or plaques on the scalp (cradle cap in the

cases of newborns) central area of the face sternal region axilla and

or groin In newborns this presentaton can be generalized causing

Leinerrsquos erythroderma desquamatvum in adults it is likely to be re-

lated to blepharits

Diff erental diagnosis includes atopic eczema in children but diff eren-

tal diagnosis in adults reveals subacute erythematous lupus or pink

pityriasis when the trunk is involved and inverted psoriasis when skin

folds are aff ected

Remember

Letterer-Siwe disease can cause lesions similar to infantile seborrheicdermatitis However unlike infantile seborrheic dermatitis Letterer-Siwedisease is associated with lymphadenopathies and hepatosplenomegaly

Remember

Impetigo key words (yellowish scabs) should not be mistaken for seborrheicdermatitis key words (yellowish scales)

Diagnosis

Atopic dermatts has a clinical diagnosis Patents may present with eo-

sinophilia and increase of IgE values

Treatment

It is essental for the patent to follow certain rules in his lifestyle This

means the patent must avoid wearing perfumed products (like cologne

and cream) being exposed to extreme temperatures the use of fabric

sofeners and carpets or fluff y toys (because of possible sensitzaton of

dust mites) Besides the patent needs to wear 100 coon clothing

Macule Vesicle

Wheal Fissure

Papule Ulcer

Nodule Cyst

Figure 2 Cutaneous elemental lesions

22 Histological Lesions

The following are histological lesions of the skin

bull Hyperkeratosis increase in the stratum corneum (warts and psoriasis)

bull Hypergranulosis granular layer thickening

bull Acanthosis thickening of the stratum spinosum

bull Acantholysis rupture of intercellular bridges of the stratum spino-

sum (typical of pemphigus)

bull Spongiosis intercellular intraepidermal edema (characteristc of eczema)

bull Ballooning intracellular edema (herpes)

bull Parakeratosis presence of nuclei in the stratum corneum (typical

of psoriasis)

bull Dyskeratosis abnormal keratnizaton of individual cells of the stra-

tum spinosum (typical of Darierrsquos disease)

bull Papillomatosis lengthening of dermal papillae (psoriasis)

Chapter 03

Allergic and

Immune-mediated

Diseases

31 Hypersensibility Reactions

bull Type I is mediated by IgE It is the most rapid Anaphylaxis asthma

and urtcaria

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Dermatology

Precocious treatment is of the utmost importance

Topic cortcoids are the first line treatment

It is worth to remember that prolonged use of topic cortcoids can have

local and systemic secondary side eff ects

The second line of treatment involves immunomodulators (tacrolimus

and pimecrolimus) These can be used in children older than 2 years of

age

For acute outbreaks oral cortcoids are used in short cycles and not as

maintenance To stop medicaton suddenly may cause a rebound eff ect

33 Contact Eczema

The appearance of contact eczema is immunologically mediated (type

IV hypersensit

vity) against foreign agents acquired by percutaneouspenetraton Contact eczema requires prior sensitzaton to allergen

It is more common in adults than in children

Diagnosis

Diagnosis is established with clinical records and epicutaneous tests of

contact These tests are performed once lesions have been resolved by

applying patches with allergens on healthy skin leaving them in contact

with the skin during 48 hours They are read afer 48 and 96 hours The

intensity of reacton is measured qualitatvely negatve weak positve

(erythema) strong positve (papules-vesicles) or extreme positve (blis-

ters)

Treatment

Avoid contact with the allergen

Treatment of acute eczema implies applicaton of topic poultce (zinc

sulphate sodium borate) and cortcoids if lesions are limited and sys-

tem poultce if lesions are generalized

34 Seborrheic Dermatitis

Seborrheic Dermatts is a quite frequent disease It aff ects 4 - 5 of the

populaton Etology of seborrheic dermatts is unknown although it

has been related to an abnormal immunological response to a fungus

called Pityrosporum ovale Seborrheic dermatts is more frequent and

intense when associated to neurological processes alcoholism and im-

munodeficiencies

Clinical Presentation

According to patentrsquos age

a Seborrheic dermatts in infants Yellowish scales on scalp known

as cradle cab

b Seborrheic dermatts in adult erythematous desquamatng papu-

les or plates in fat areas of the facial region and scalp

Diagnosis

Diagnosis of this conditon is clinical

TreatmentTreatment involves antfungals associated with topic cortcoids Sebor-

rheic dermatts on the scalp is usually linked to a keratolytc agent like

the salicylic acid

35 Psoriasis

Psoriasis is a chronic inflammatory disease of the skin that presents

with outbreaks Psoriasis aff ects 1-2 of the populaton and can ap-

pear at any age with a maximum of incidence between 20 and 30 yearsof age There is a family history in a third of the patents

Plates are the characteristc erythematous desquamatng lesions well

delimited with a superficial thick and white-pearl scale

The most frequent clinical form is vulgar psoriasis or psoriasis in plates

Lesions are localized at extensor surfaces (elbows and knees) and the

scalp The umbilical and the lumbosacral areas are ofen aff ected

Nail involvement is frequent and is most common with a pi ng ap-

pearance This form is lile specific The forms that combine hyperkera-

tosis and distal onycholysis are more specific Oil spot is the most char-

acteristc sign (Figure 3)

Figure 3 Generalized pustular psoriasis

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Amer ican Manual of Examinat ion in Medicine (2CK)

4

Diagnosis

Diagnosis of this conditon is generally clinical

If there is no certainty a biopsy must be done which will reveal hyper-

keratosis acanthosis and parakeratosis

There is an increase in polymorphonuclears (sterile abscesses) in the

stratum corneum which are called Munro abscesses

Treatment (Table 1)

For moderate severe forms of psoriasis that do not respond to clas-

sical systemic treatments (see table) They are monoclonal antbod-

ies against proinflammatory substances that are high in patents with

psoriasis [alpha tumor necrosis factor (TNF) interleukin IL 12 and

23] Some of them are infliximab adalimumab ustekinumab and

etanercept

36 Urticaria

Urtcaria is an immunologic and inflammatory reacton of the skin

against diverse etological factors Independently of the cause release

of histamine and other inflammatory mediators occurs which cause va-

sodilaton and increase in capillary permeability producing an edema in

superficial dermis Urtcarias are divided in acute and chronic urtcarias

depending on whether outbreaks persist more or less than six weeks

About 60 of acute urtcarias are idiopathic Chronic urtcarias show a

higher percentage

Urtcarias of known origin are usually due to infectons drugs or food

Clinical Presentation

Clinical presentaton is characterized by the appearance of pruritc wheals

that last less than 24 hours and can be accompanied with angioedema

TREATMENT USES SIDE EFFECTS AND CONTRAINDICATIONS

Topic Mild-moderatepsoriasis

(lt 25 body

surface)

Emollients (urea glycerin) Moisturizing

Keratolytics (salicylic acid) Eliminate excess of scales

Reductants (dithranol) Hyperkeratotic plaques middot Stain skin and clothing

middot Irritating

middot Acneiform eruptions

Corticoids middot Stable psoriasis

in plates

middot The most used

middot Tachyphylaxis

middot Percutaneous absorption

middot Possible new outbreak after stopping medication

middot Avoid prolonged treatment

Vitamin D analogues

(calcitriol calcipotriol and

tacalcitol)

Stable psoriasis in plates middot Irritating in face and skin folds

middot Hypercalcemia

Systemic Moderate-

severe psoriasis

(gt 25 body

surface)

Psoralens plus ultraviolet

light of the A wavelength(PUVA)

Combinable with topics

and retinoids (RePUVA)

middot Cutaneous aging and carcinogenesis

middot Erythroderma and xerosis middot Immunosuppression

middot Hepatitis by psoralens

middot Not in children pregnancy patients with hepatic or renal

insuffi ciency photosensitivity or cutaneous precancerosis

middot Cataracts

middot It accumulates in the crystalline during 24 h (sunglasses)

Retinoids (acitretin) middot Severe psoriasis

pustular

or erythrodermic

middot It is not usually used

in women in fertile age

(see side effects)

middot Cutaneous dryness (the most frequent)

middot Hypertriglyceridemia

middot Hypercholesterolemia

middot Increase in transaminases

middot Diffuse alopecia

middot Vertebral hyperostosis ligamentous calci1047297cations

middot Teratogenicity avoid pregnancy until 2 years after

1047297nishing treatment

middot Avoid in children and patients with hepatic or renal failure

Cyclosporine A middot In1047298ammatory severe

psoriasis resistant to

other treatments

middot Rapid action

middot Rebound effect

middot Nephrotoxicity

middot High blood pressure (HBP)

middot Epitheliomas and lymphomas

middot Hypertrichosis

middot Gingival hyperplasia

middot Hyperuricemia

Methotrexate middot Severe psoriasis

resistant to other

treatments

middot Psoriatic arthropathy

middot Hepatotoxicity

middot Myelosuppression

middot Teratogenicity until 3 months after ending treatment

middot Photosensitivity

Table 1 Psoriasis treatment

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Dermatology

Vasculits urtcaria should be ruled out when lesions last more than 24 hours

and are accompanied with systemic clinical symptoms (ie arthralgias)

Treatment

Oral anthistamine therapy is the treatment of choice

Systemic cortcoids for severe or refractory cases

Adrenalin for severe cases with anaphylaxis

37 Toxicodermas

Toxicodermas are quite variable cutaneous reactons that appear afer

drug administraton They are one of the most frequent side eff ects of

drugs The causatve agents for many toxicodermas stll remains un-

known either immunological or not and clinical presentaton does not

facilitate agent dist

nct

on

Morbilliform exanthem is the most frequent A morbilliform exanthem

is a generalized erupton formed by symmetric and confluent macules

and papules that usually start by the trunk

They can appear one or two weeks afer taking the drug

A morbilliform exanthem can be associated with fever pruritus and eo-

sinophilia

The most frequent are non steroid ant-inflammatories antbiotcs (sul-

phamides and penicillins) antepileptcs allopurinol and N acetyl-cystene

DiagnosisDiagnosis is according to clinical presentaton

Treatment

Treatment implies withdrawal of potentally responsible drug Topic or

systemic anthistamines and cortcoids are given according to the extent

of symptoms (Figure 4)

Figure 4 Morbilliform exanthem due to amoxicillin

38 Multiform Erythema

Stevens-Johnson Syndrome

and Toxic Epidermal Necrolysis

Multform erythemas (ME) are of undetermined etopathogenesis

regarded as a cutaneous reacton against a diversity of stmuli Their

histologies show similarites what leads to consideraton of a common

pathogenesis

Clinical Presentation

Three diff erent groups have been described although many a tme their

clinical symptoms overlap

bull Erythema multforme minor is the most frequent with around 80

of the cases It usually precedes a symptomatc infecton by simple

herpes virus (60) or subclinical infecton about 15 days before

Erythema multforme minor manifests itself on extensor surfaces

at hands elbows and feet as a symmetric erupton of erythema-

tous edematous lesions with target-shape (herpes iris of Batemanor rosee-paerned lesion) with a violaceous sometmes bullous

center (Figure 5)

Mucosal aff ectaton is rare with small erosions in oral mucosa Erythe-

ma multforme minor tends to recurrence with subsequent outbreaks

of herpetc lesions

Figure 5 Erythema multiforme minor Herpes iris of Bateman

bull Erythema mult

forme major or Stevens-Johnson syndrome is therarest It normally has a prodromal period of untl 14 days with fe-

ver cough cephalea arthralgias and other symptoms Subsequent

to the prodromal period erythematous edematous plates appear

which are more extensive with a tendency to form blisters and

greater mucosal erosions (mouth genitals pharynx larynx and

conjunctve Figure 6) Systemic symptoms are normal and do not

tend to recurrence

The most frequent etological factors are drugs [sulphamides non

steroid ant-inflammatory drugs (NSAIDs) antconvulsants and an-

tbiotcs in decreasing order) Infectous agents have been also in-

volved mainly mycoplasma pneumoniae

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6

Figure 6 Exudative erythema multiforme major

bull Toxic epidermal necrolysis (TEN) many authors consider it the

most severe form of erythema multforme major arguing the same

pharmacological agents A morbilliform rash appears which is rap-idly confluent comprising almost the entre skin surface with flaccid

blisters that leave wide areas of denuded skin Involvement of sev-

eral mucosae is constant

Complicatons ofen occur (pneumonia digestve hemorrhage re-

nal failure and hemodynamic shock) with mortality rates close to

25 In children it must be performed a diff erental diagnosis with

staphylococcal scalded skin syndrome which does not aff ect mu-

cosae

Remember

Diseases that have the Nikolsky sign are TEN staphylococcal scalded skinsyndrome (SSSS) and pemphigus In TEN the whole epidermis comes off(bad prognosis) while in SSSS epidermal detachment occurs at the granularlayer

Histopathology

It must be highlighted the eff acement of dermoepidermal juncton by a

lymphohistocytc infiltrate and vacuolar degeneraton of the baseline lay-

er with necrotc keratnocytes In TEN keratnocytes necrosis is massive

Treatment

In ME minor only symptomat

c treatment is prescribed with topiccortcoids and oral anthistamines Treatment for herpes simplex virus

(HSV) infecton is useful to prevent ME lesions if patent is in the inital

stage of the viral infecton

ME major requires treatment of the underlying infecton or withdrawal

of implied drug and support measures The use of oral steroids accord-

ing to the patentrsquos general state is under discussion

A patent with TEN requires to be admied at the burn treatment room

with monitoring of hematocrit hydroelectrolytc balance and antbiotc

prophylaxis and support measures It is controversial the use of system-

ic cortcoids immunoglobulins andor cyclosporine

39 Erythema Nodosum

Erythema nodosum is the most frequent panniculits Painful erythema-

tous nodules occur mainly in the anterior side of legs with a self-limit-

ing course and predominantly aff ectng young women (Figure 7)

Figure 7 Erythema nodosum

They heal without leaving a scar within a period of four to six weeks

Erythema nodosum may be accompanied with fever deterioraton of

the general state and arthralgias

Patents with erythema nodosum may have a false positve VDRL

Etiology

This conditon is thought to be an immunological response triggered by

multple and diff erent stmuli bacterial fungal and viral infectons sys-temic diseases (sarcoidosis inflammatory intestnal disease Behcetrsquos

syndrome) neoplasias (lymphomas and leukemias) and drugs (oral

contraceptves sulphamides bromides and iodines)

Diagnosis

Erythema nodosum requires a deep biopsy to reveal septal panniculits

without vasculits

Complementary tests can be performed to rule out systemic involvement

for example chest X-ray Mantoux and antstreptolysin O antbody (ASLO)

Treatment Treatment entails eliminatng underlying cause if found then rest and

ant-inflammatories

310 Bullous Pemphigoid

and Pemphigus Vulgaris

See Table 2 and Figures 8 9 10 and 11

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Dermatology

Intercellular

substance ac

middot Pemphigus

Lineal

storage

in lucid

layer

-

Anti-Collagen Ac

Lucid

layer

Thick

layer

Basal

sublayer

Granular

storage

in papillary

dermis

middot Pemphigoid bullousmiddot Herpes gestationis

middot Acquired blistering epidermolysis

middot Dermatitis herpetiformis

Figure 8 Key points for histological diagnosis

of autoimmune blistering diseases

Figure 9 Pemphigus vulgaris

Figure 10 Pemphigus vulgaris with oral mucosa involvement with

erosions

Figure 11 Pemphigoid bullous Tense blisters No sign of Nikolsky

PEMPHIGUS VULGARISGENERALLY

IDIOPATHICHERPES GESTATIONIS

DERMATITIS

HERPETIFORMIS

Clinical presentation middot 40-50 years of age

middot They usually affect mucosae

middot No pruritus

middot Flaccid blister

middot Nikolsky

middot Elderly

middot Sometimes mucosae

middot With pruritus

middot Tense blister

middot No Nikolsky

middot Pregnant women

middot No mucosae

middot With pruritus

middot Herpetiform

middot No Nikolsky

middot 15-35 years of age

middot No mucosae

middot With pruritus

middot Herpetiform

middot No NikolskyDirect immuno1047298uorescence (DIF) IgG IgG IgG IgA

Histology middot INTRAepidermal blister

middot There is acantholysis

middot SUBepidermal blister

middot There are eosinophils

middot SUBepidermal blister

middot There are eosinophils

middot SUBepidermal blister

middot Neutrophils in dermis

Treatment Corticoids at high doses

immunosuppressants rituximab

and immunoglobulins

Corticoids Corticoids Diet +- dapsone

Remember Mortality rate 10 The most frequent Relapse if new

pregnancy

Associated to enteropathy

by gluten 90

Table 2 Autoimmune blistering diseases

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Amer ican Manual of Examinat ion in Medicine (2CK)

8

Chapter 04

Infectious Diseases

41 Viral Infections

Simple Herpes

Infection by Simple Herpes Virus

There are two types of simple herpes (Figure 12)

bull Type I is responsible for most extragenital herpes and 20 of the

genital herpes

bull Type II causes genital herpes and a small percentage of extragenital

herpes

Figure 12 Herpes simplex

Contagion is produced by direct contact though the carrier may be as-

ymptomatc Afer primary infecton virus remains silent in the sensi-

tve porton of cranial or spinal ganglia Immunosuppressed patents

endure the greatest severity of this conditon

Clinical Presentation

bull Extragenital simple herpes recurring orofacial herpes simplex is

the most frequent Most primary infect

ons are asymptomat

c Only5 manifest themselves in the form of herpetc gingivostomatts a

profile characterized by oral ulcers with cervical adenopathy and af-

fectaton of the patentrsquos general state (Figure 13) During relapses

clinical symptoms are milder with cluster vesicles on an erythema-

tous base Some factors facilitate relapses trauma sunlight cold

stress fever and the menstrual cycle

bull Genital simple herpes is the most common cause of genital ulcers

afer trauma Primary infecton is usually symptomatc and occurs

between 3 to 14 days afer sexual contact It causes clustered ulcers

in the balanopreputal sulcus or in the prepuce with painful inguinal

adenopathy Relapses are less severe than primary infecton and oc-

cur more frequently when genital herpes is due to HSV type II

Figure 13 Herpetic gingivostomatitis

bull Eczema herpetcum or Kaposi varicelliform erupton dissemina-

ton of herpetc infecton on pre-existng dermatosis (above all

atopic dermatt

s) bull Neonatal herpes is due to intrapartum contagion of HSV-II with

neurological involvement general deterioraton and skin vesicles or

ulcers

bull Other clinical forms are herpes gladiatorum herpetc whitlow and

keratoconjunctvits

Diagnosis

Diagnosis of this conditon is mainly clinical Virological culture is the

most reliable method of confirmaton The extent of a smear of the le-

sions (Tzanck cytodiagnosis) allows visualizaton of multnucleated cells

and intranuclear inclusions which become evident through histological

study

Treatment

Mild forms do not need treatment Treatment is required in the follow-

ing cases

bull Primary infecton

bull Severe or frequent relapses if they aff ect life quality

bull Complicatons like erythema multforme and eczema herpetcum

Drug of choice is oral acyclovir and its derivatves (valacyclovir famci-

clovir) Topic antvirals have not proven useful favoring maceraton of

lesions and thus over infecton It is not infrequent that topic antvirals

cause allergic contact dermatts due to hypersensitvity

Varicella-Zoster Virus

A primary infecton gives way to varicella (see Pediatrics secton) Afer

varicella the virus remains latent in the sensitve porton of the neural

ganglia and when relapse occurs it leads to zoster herpes

bull Varicella the following symptoms appear afer 15 days of incubaton

fever cephalea pruritus and polymorphic lesions in diff erent stages

macules papules vesicles (Figure 14) ulcers and scabs (starry sky

appearance) Mucosal (ulcers) and scalp involvement is characteristc

Manipulaton can leave scars Bacterial over infecton of lesions is the

most usual complicaton About 20 of adults suff er from varicella

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Dermatology

pneumonia radiologically demonstrable but clinical symptomatology is

only present in around 4 of the cases

Figure 14 Typical vesicles in patients with varicella

bull Zoster herpes thoracic zoster herpes is the most usual It sel-

dom occurs more than once throughout a personrsquos lifetime

It is characterized by vesicles on pre-existing erythema with

metameric distribution and lateral extension The most com-

mon complication is post herpetic neuralgia more frequent in

advanced age Carbamazepine or tricyclic antidepressants (Fig-

ure 15)

Figure 15 Zoster herpes

Special Clinical Forms

Special clinical forms are as follow

bull Ramsay-Hunt syndrome aff ectaton of geniculate ganglion of the

facial nerve

It produces vesicles in the outer ear external auditory canal and

pharynx homolateral facial paralysis deafness and vertgo

bull Ophthalmic involvement can result in severe keratts and requires ur-

gent referral to an ophthalmologist Suspicion should exist on patents

that present herpetc lesions on the tp of the nose) (Hutchinsonrsquos sign)

bull Disseminated zoster herpes several dermatomes are aff ected bilat-

erally Ramsay-Hunt syndrome is characteristc in the immunosup-

pressed

Remember

Affectation of the nose tip makes it necessary for ophthalmologicalexamination because the nose tip is innervated by the same nerve thatinnervates the cornea (1047297rst branch of the trigeminal nerve)

Treatment

Varicella without complicatons is treated symptomatcally Antvirals

are reserved for severe or complicated forms There is a commercial-

ized vaccine of live virus whose indicatons are stll under discussion

Zoster herpes must be treated with antvirals when detected during the

first 48-72 hours and aff ectng patents with

bull Immunosuppression

bull Age above 55

Special clinical forms previously cited

Drugs to be used are oral acyclovir and its derivatves (valacyclovir and

famciclovir) They accelerate the cure of lesions and decrease the inten-

sity of post herpetc neuralgia Patents with renal failure need a dose

adjustment as acyclovir is nephrotoxic These patents are adminis-

tered brivudine in a single daily dose

Molluscum ContagiosumDome shaped pink papules with central umbilicaton (Figure 16) Mol-

luscum contagiosum is typical of children that go to swimming pools It

is also present in the genital zone afer sexual contact and in immuno-

suppressed patents It is caused by Poxvirus

Figure 16 Molluscum contagiosum

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Amer ican Manual of Examinat ion in Medicine (2CK)

0

Lesions are asymptomatc

Diagnosis

Diagnosis is clinical Histology reveals characteristc inclusion bodies

Treatment

Lesions can resolve spontaneously

Cureage cryotherapy or local trichloroacetc acid are eff ectve meth-

ods to destroy lesions

Warts

Human papillomavirus can cause verruca vulgaris palmoplantar and

flat warts and condyloma accuminata Human papillomavirus is the

most frequent sexual transmied disease

Some subtypes of this virus (16 18) are of high risk and can cause epi-

dermoid carcinomas

Direct contact is the mechanism of contagion

Diagnosis

Diagnosis of this conditon is clinical

Staining with acetc acid can help visualize mucosal lesions

Treatment

Genital warts are treated with cryotherapy podophyllotoxin trichloro-

acetc acid imiquimod and 5-fluorouracil

Cervical lesions should be monitored by cytology and biopsy whenever

necessary to rule out cervical cancer (Figures 17 and 18)

Figure 17 Warts in HIV patient

Figure 18 Condyloma accuminata

42 Bacterial Infections

Impetigo

Impetgo is a very contagious superficial infecton without systemic re-

percussion and normally mixed etology by Gram positve cocci (strep-

tococci and staphylococci) Classically the most frequent accepted

cause was Streptococcus pyogenes However at present Staphylococcus

aureus stands out as the predominant cause

The most typical form is impetgo contagiosa (Figure 19) character-

ized by honey-colored (meliceric) scabs which normally appear on

the face and other exposed areas It is typical of children Although

infrequent poststreptococcal glomerulonephrits is a dreadful com-

plicaton

Figure 19 Impetigo contagiosa

On the contrary rheumatc fever shows no relaton to cutaneous strep-

tococcal infectons but only with pharyngeal infectons

There are other less habitual forms called bullous impetgo exclusively

of staphylococcal origin Clinical presentaton involves the presence of

blisters and erosions on the aff ected skin as a consequence of the epi-

dermolytc toxins that these bacteria contain Impetgo is treated with

topical mupirocin penicillin or oral fusidic acid

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Dermatology

Cellulitis

Cellulits is an infecton that aff ects deep dermis and subcutaneous cel-

lular tssues normally caused by streptococci (Streptococcus pyogenes

or of group A)

Community methicillin-resistant S aureus (CMRSA) is a triggering agent

that is becoming more and more frequent

Most common risk factors are diabetes chronic venous insuffi ciency

and immunosuppression

Clinical Presentation

Cellulits presents with erythematous plaques that are ill-defined pain-

ful and hot It is usually accompanied with fever and chills

Diagnosis

Diagnosis is clinical If there is an open door a culture of this area may

help see the source germ and resistance to ant

biot

cs

It is important to rule out abscesses osteomyelits and necrotzing fas-

ciits

If bacteremia is suspected blood cultures need to be performed

Treatment

Treatment implies oral antbiotcs for 7-10 days to cover Gram positve

cocci They are intravenously administered in case of lack of response

to oral treatment involvement of hands or periorbital zone diabetes or

extremes of age

Necrotizing FasciitisNecrotzing fasciits is a deep infecton up to muscular fascia that pro-

duces very intense pain and subsequent anesthesia

In 10 of the cases cellulits is due to an infecton by S pyogenes In the

remaining cases it occurs by a polymicrobial infecton caused by aerobes

and anaerobes including S aureus E coli and Clostridium perfringens

There may be prior history of trauma or surgery

Clinical Presentation

Clinical presentat

on involves pain of sudden onset and edema on theaff ected zone Pain may progress to anesthesia There appears subse-

quent erythema that progresses rapidly into necrosis

Characteristc clinical signs are tssue necrosis blisters intense pain

and gas producton

Diagnosis

Diagnosis is clinical and requires image testng X-rays or a computed

tomography CT

A biopsy of the border of the lesion helps achieve diagnosis

Treatment

Treatment entails precocious surgical debridement It is a surgical emer-

gency In additon to surgery broad-spectrum antbiotherapy will be

needed

Folliculitis

Folliculits is an infecton and inflammaton of one or several follicles

caused mainly by staphylococci

Clinical Presentation

Folliculits shows pustules with follicular distributon

When the infecton is deeper it is called furuncle

If several furuncles are infected a fluctuatng erythematous plaque forms

containing several points of suppuraton This plaque is labeled as anthrax

Diabet

c and immunosuppressed pat

ents are at higher risk

Characteristics of Folliculitis

1 Hot tub or swimming pool folliculits caused by Pseudomonas aeru-

ginosa

2 HIV associated pruritc folliculits or eosinophilic folliculits

Treatment

In mild cases treatment of choice comprises antseptcs and topic an-

tbiotcs

In more severe cases treatment of choice requires oral antbiotcs

Large sized lesions must be drained and a microbiological culture must be

performed to rule out methicillin-resistant Staphylococcus aureus MRSA

Acne Vulgaris

Acne is an inflammatory disease of the pilosebaceous follicle as a con-

sequence of an alteraton in follicular keratnizaton It aff ects adoles-

cents and young adults

Etology is multfactorial alteraton of keratnizaton of follicular infun-

dibulum quanttatve and qualitatve alteraton of sebum producton in

the sebaceous gland and alteratons of bacterial microflora (increase in

quant

ty of P acnes)

Aggravatng factors are stress androgenic oral contraceptves and the

use of cosmetc products that are not oil-free

Clinical Presentation

A comedo is the inital lesion which can be closed (whitehead) or open

(blackhead) and it evolves into inflammatory lesions that listed in as-

cending order of severity are papules pustules nodules and cysts

Lesions progress and leave scars Scars can be increased if lesions are

manipulated

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Amer ican Manual of Examinat ion in Medicine (2CK)

2

Diff erent lesions habitually combine simultaneously so acne becomes

polymorphic It is located in sebaceous areas face back shoulders and

the center thoracic region

Diagnosis

Diagnosis is clinical

Treatment

bull Comedonal acne is treated with topic retnoids and benzoyl peroxide

bull Inflammatory acne treatment requires benzoyl peroxide combined

with topic antbiotcs (erythromycin and clindamycin) Systemic

antbiotc treatment with oral tetracyclines will be prescribed if re-

sponse to topic antbiotc treatment fails

bull Severe nodular cystc acne treatment involves the use of isotret-

noin (13-cis-retnoic acid) It is a derivatve of vitamin A Isotretnoin

produces atrophy in the sebaceous gland and regulates keratniza-

ton The most frequent side eff ect is cutaneous and mucosal xero-

sis Triglycerides cholesterol and transaminases should be moni-

tored as their values may increasebull It can be associated with depression

bull It is teratogenic so pregnancy should be avoided during treatment

and untl a month afer treatment

Pilonidal Cysts

Pilonidal cysts are abscesses in the sacrococcygeal region

This type of cysts has predominance in men between 20 and 40 years

of age It is believed that repeated trauma on the aff ected area favors

their appearance

Clinical Presentation

Pilonidal cysts present with an indurated lesion that is fluctuatng hot

painful but non-adherent to deep planes in the sacrococcygeal region

Pilonidal cysts may or may not be associated to cellulits and purulent drain-

age

Diagnosis

Diagnosis is clinical and anal or perirectal abscesses should be dismissed

Treatment

Treatment implies an incision and surgical drainage

On some occasions a general surgery is required

43 Fungal Infections

Pityriasis Versicolor

Versicolor pityriasis is caused by commensal yeast called Pityrosporum

ovale which transforms into its pathogen form (Malassezia furfur) It

especially aff ects young patents (15 - 45 years of age) but it is rare

in childhood and advanced age Versicolor pityriasis relates to heat

humidity and sebaceous hypersecreton It is characterized by the ap-

pearance of hyperchromic or hypochromic macules that desquamate

on scratching (nail sign) if infecton is actve Macules usually appear on

the center thoracic region and on the back that is to say on seborrheic

zones Relapses are habitual despite treatment

Diagnosis

Diagnosis is normally clinical To that purpose the following serve as

support

bull Woodrsquos lamp emits yellow-orange fluorescence

bull Potassium hydroxide (KOH) test filaments and round elements can

be observed (ldquospaghe and meatball appearancerdquo Figure 20)

Treatment

Treatment is performed with topical azoles Oral administraton applies

for extensive cases or immunosuppressed patents Diff erental diagno-

sis includes pink pityriasis and eczemas (Figure 21)

Figure 20 Versicolor pityriasis Histological cut

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Dermatology

Figure 21 Versicolor pityriasis

Candidiasis

The most common triggering agent is Candida albicans It is normally sapro-

phyt

c although under certain condit

ons candidiasis may become patho-genic (immunosuppression humidity pregnancy and contraceptves)

Clinical Forms

bull Intertrigo erythematous plaque in cutaneous folds Atrophy and

fissures are typically deep in the skin fold as well as satellite and

peripheral lesions (papules andor pustules)

bull Mucosa involvement may cause diverse symptomatology like vul-

vovaginits glossits and white papules in the anterior region of the

oral mucosa Candidal balanits is characterized by the presence of

punctform erosions and pustules on gland and balanopreputal

sulcus Candidal balanits ofen appears afer sexual intercourse or

afer oral antbiotc intake

Remember

Almost a 100 of HIV patients suffer from muguet throughout their diseasecourse

bull Candidiasis of nail fold is usually associated with periungual inflam-

maton (perionixis) and inital proximal aff ectaton which diff erent-

ates it from tnea unguium (Figure 22)

Figure 22 Candidiasis of nail fold

Treatment

Oral Candidiasis fluconazole or nystatn

Candidiasis of the skin (intertrigo) apply topical antfungal medicaton

and keep zone clean and dry

Dermatophytosis or TineasDermatophyte infectons aff ect the skin and keratnized structures like

hair and nails (there is no mucosa involvement) Clinical diagnosis is

achieved afer performing a culture Woodrsquos lamp test normally turns

out to be negatve In general Trichophyton dermatophyte rubrum is

the most frequent dermatophyte

Non Inflammatory Tineas

Non inflammatory tneas do not produce irreversible scarring alope-

cia while inflammatory forms do Tineas are treated with azoles de-

rivatves

The types of tnea are the following

bull Ringworm of the scalp ( t nea capi t s or t nea tonsurans) is charac-

teristc of childhood It presents with alopecic plaques broken hair

and desquamaton Infectons tend to resolve spontaneously with-

out leaving scars at the onset

of puberty

bull Ringworm of the body (herpes

circinatus or t nea corporis) are

erythematous desquamatve

plaques (with more actve bor-

ders) which are also circinate

and normally pruritc (Figure

23) Plaques grow eccentrically

with less actvity in the centerand more in the borders

bull Ringworm of the foot ( t nea

pedis) the most frequent is the

ldquoathlete footrdquo with desquama-

ton in interdigital spaces

bull Tinea incognito refers to tnea

wrongly treated with cort-

coids what makes diagnosis

diffi cult as the lesion has been modified Figure 24)

Figure 24 Tinea incognito secondary to treatment with topical steroids

Figure 23 Herpes circinatus

(tinea corpis)

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Amer ican Manual of Examinat ion in Medicine (2CK)

4

bull Ringworm of the groin (t nea cruris or eczema marginatum von

hebra) formed by erythematous desquamatve plaque with more

actve borders (Figure 25)

Figure 25 Ringworm of the groin (tinea cruris)

bull Tinea unguium subungualhyperkeratosis with onychol-

ysis but without perionixis

(Figure 26)

Diagnosis

Clinical diagnosis is reached afer

performing a culture

Treatment

Treatment involves topical an-

tfungal medicaton in localized

areas

Oral antfungal medicaton is used in extensive forms nail fold or scalp

involvement

44 Parasitic Infections

Pediculosis

Pediculosis is transmied by direct contact or by contact with fomites

which release toxins that produce intense pruritus

Clinical Presentation

Pediculosis capi t s intense pruritus predominant in retroauricular and

occipital regions occasionally with excoriatons and impetginizaton

secondary to excoriatons

Pediculosis corporis intense pruritus in patents with poor hygiene or

who live in overcrowded conditons

Pediculosis pubis genital and pubic pruritus Brownish-grey macules

called maculae ceruleae are typical on underwear and skin These pig-

mentatons appear as a result of a reducton in hemoglobin by a para-

site enzyme

Diagnosis

Diagnosis is clinical and by direct visualizaton

Treatment

Pediculosis is treated with malathion lindane or topical permethrin

Scabies

Scabies is originated by an acarus known as Sarcoptes scabiei It has an

incubaton period of 1 month

Clinical Presentation

Scabies produces generalized pruritus more intense at night The pa-

tent usually catches the infestaton which is passed to the patentrsquos

relat

ves It is common tofi

nd that a recent trip to a tropical country hasbeen made Lesions appear between the fingers (Figure 27) in wrists

feet genitalia mammary areola and axilla but back and face are usu-

ally spared The most specific lesion is the acarine burrow in whose less

scaly end the advancing zone the mite lies Nodules are frequent in

axilla and genitals (nodular scabies)

bull Norwegian scabies is typical of the immunosuppressed Patents

present with generalized hyperkeratosis and scabs Norwegian sca-

bies produce lile pruritus but it is very contagious because there

are many acari

bull Nodular scabies involves the persistence of pruritc nodules despite

treatment Lesions usually appear in axilla and genitalia Pruritus is

due to a hypersensitvity phenomenon because of the acarus al-

ready dead Nodular scabies is treated with cortcoids

Figure 27 Scabies Acarine burrow

Treatment

bull Permethrin cream at 5 is the treatment of choice It is lile toxic

so it can be used in children and pregnant women

bull Topical lindane at 1 irritates and is neurotoxic therefore it is con-

traindicated in pregnant women and children

bull Oral ivermectn is utlized in cases of resistance to prior treatments

There is stll lile experience as to its use but in a first instance a

Figure 26 Tinea unguium

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Dermatology

single dose would be enough to cure scabies (already used by vet-

erinarians)

45 Ischemia

Decubitus Ulcers

Decubitus ulcers are the result of ischemic necrosis by contnuous pres-

sure on an area which restricts microcirculaton in that zone

Clinical Presentation

Decubitus ulcers are present in patents in bed with scarce mobilizaton

It is favored by bone prominences and lack of fat tssue If sensitvity

decreases there is more risk of formaton of decubitus ulcers

Diagnosis

Diagnosis is achieved based on medical records and clinical presentaton

Treatment

Preventon is of the utmost importance as well as frequent mobiliza-

ton of the patent in bed

Once ulcers have been established hydrocolloid dressings are used for

healing but sometmes surgical debridement is necessary

Gangrene

Gangrene means tssue necrosis

There are three types dry gangrene wet gangrene and gas gangrene

Clinical Presentation

Dry gangrene is due to ischemia generally secondary to atherosclero-

sis Clinical presentaton involves pain cold and paleness of extremi-

tes Once tssue is established it turns bluish-black in color and dry

Wet gangrene is owing to bacterial flora Tissue presents with an edem-

atous appearance either with blisters or pus

Gas gangrene caused by C perfringens It is normally located on re-

cent surgery Bacteria precociously destroyt

ssue producing gas It is amedical emergency

Diagnosis

Clinical diagnosis is obtained by microbiological culture

Treatment

Treatment requires surgical debridement with amputaton if necessary

and associaton of broad spectrum antbiotherapy

Gas gangrene is treated with hyperbaric oxygen

46 Miscellaneous

Acanthosis Nigricans

Acanthosis nigricans are vel-

vet-like papillomatous brown

plaques in neck axilla and groin

folds (Figure 28)

It is associated with diabetes

mellitus Cushingrsquos disease poly-

cystc ovarian syndrome and

obesity

The malignant form of acantho-

sis nigricans is a paraneoplastc

syndrome that diff erentates

from the benign form because

the laer has mucosal and pal-

moplantar involvement

Lichen Planus

Lichen planus is an inflammatory idiopathic disease that equally aff ects

both genders with higher frequency in middle age

Lichen planus has been related to diverse drugs like gold salts

anti-malarial medication and thiazides It has been also linked to

hepatitis C virus infection however this association is currently

doubtful

Clinical Presentation

Lichen planus presents with red-violaceous polygonal flat papulesquite pruritc which localizes on the flexor side of wrists forearms an-

kles and lumbosacral and flank regions On its surface a whitsh retcu-

late can be observed (Wickhamrsquos striae) About 60 - 70 of the cases

present with lesions in oral and genital mucosa oral which appear as

whitsh retculated lesions (Figures 29 and 30)

Figure 29 Lichen planus of oral mucosa with typical whitish

reticulate

Figure 28 Acanthosis nigricans

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Amer ican Manual of Examinat ion in Medicine (2CK)

6

Violaceous papules

with white stretch marks

Lichenoid lymphocyte

in1047297ltrate (band formation)

Destruction

of basal layer

Figure 30 Lymphocytic interface reaction (lichen planus)

Treatment

Mild forms are treated with topical cortcoids

Severe cases require oral cortcoids psoralens plus ultraviolet light of

the A wavelength (PUVA) or cyclosporine

Rosacea

Rosacea is a chronic disease of unknown pathogenesis characterized

by erythema and acneiform lesions on the face It aff ects middle aged

women (between 30 and 50 years of age) more

Rosacea etopathogenesis is unknown although there is involvement of

vasomotor lability infecton by Demodex folliculorum photo exposureand genetc predispositon

Clinical Presentation

Rosacea symptomatology comprises facial flushing episodes that end

up by provoking a persistent erythema telangiectasias and papulopus-

tular lesions without comedos Over tme ocular lesions and hyperpla-

sia of sof tssue may develop

Treatment

Avoid vasodilator stmuli

Mild cases require topical metronidazole or azelaic acid

Moderate cases need doxycycline or oral minocyclines

Severe cases are treated with oral isotretnoin at low doses

Pink Pityriasis

Gilbertrsquos pink pityriasis is an acute self-limitng dermatosis which main-

ly aff ects young adults It is of unknown origin although a viral etology

is suspected (there is some speculaton as to links with human herpes-

virus type 7)

Clinical Presentation

Erupton starts with an erythematous plaque between 2 and 5 cm of

diameter with a desquamatve central collaree ofen localized on the

trunk (heraldic mother patch Figure 31)

Figure 31 Pink pityriasis

Around a week later oval papules appear on the trunk and extremi-

tes These papules share similar characteristcs with the mother patch

though the first ones are smaller and distributed according to skin ten-

sion lines Pink pityriasis may be asymptomatc however it is some-

tmes linked to pruritus Lesions may last between 4 and 8 weeks and

disappear without leaving scars

Diagnosis and Treatment

Diagnosis is clinical Treatment is seldom needed and recommended

therapies in the past (PUVA erythromycin or oral antvirals) have not

shown clearly favorable results

Vitiligo

Vitligo is characterized by achromic macules by melanocyte destruc-

ton

Clinical Presentation

Vitligo shows achromic macules of chronic course and variable progres-

sion

Lesions are predominant on acral and periorificial areas They also show

the Koebner phenomenon

Patents may have markers of autoimmune diseases (ie antthyroid

antbodies and diabetes) but these diseases seldom manifest them-

selves

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Dermatology

Treatment

Localized lesions require topical cortcoids

Extensive or generalized lesions are treated with ultraviolet light B

(UVB) or PUVA

Strict solar photoprotecton is indispensable (Figure 32)

Figure 32 Vitiligo

47 Neoplasias

Seborrheic Keratosis

Seborrheic keratosis is the most frequent benign tumor in human be-

ings since it is part of cutaneous aging

Clinical Presentation

Seborrheic keratosis presents with hyperkeratosic papules with an oily

or velvet-like texture crests fissures and horny plugs on their surface

These papules are normally pigmented showing a brownish-black color

Treatment

No treatment is required as lesions do not become malignant

Seborrheic keratosis can be addressed with cureage or cryotherapy

Actinic keratosis

Actnic keratosis is the most common precancerous lesion and aff ects

almost a 100 of the populaton in sunny areas

Clinical Presentation

Actnic keratosis is characterized by erythematous and desquamatve

papules which are hyperkeratosic and rough on touch developing a

chronic course

Diagnosis

Diagnosis is clinical

Treatment

Treatment entails applicaton of topical 5-fluorouracil topical imiqui-

mod cryotherapy or surgery

If underlying carcinoma is suspected a biopsy must be performed to

rule out suspicion

Epidermoid Carcinoma

Epidermoid carcinoma is the second most frequent cutaneous tumor

Solar photo exposure is the main etological factor which is why epider-

moid carcinoma appears in zones of prolonged solar exposure like the

face Most carcinomas appear over premalignant lesions (actnic kera-

tosis and leukoplakia among others)

Clinical Presentation

Clinical presentaton reveals erythematous or erythematosquamous

plaques Over tme these plaques form papules and tumors which of-

ten become ulceratve and bleed

Diagnosis

Diagnosis is based on clinical suspicion and histopathological confirmaton

Treatment

Surgery with safety margins is the treatment of choice In carcinomas

in situ cryotherapy can be used as well as topical imiquimod electro-

coagulaton or CO2 laser techniques in destructon of tumors Radio-therapy may also be used in some cases

Basal Cellular Carcinoma

Basal cellular carcinoma is the most frequent cutaneous tumor Chronic so-

lar photo exposure is the main etological factor hence most of these car-

cinomas aff ect the facial zone in patents who are 40 years of age or older

Gorlinrsquos syndrome should be considered if multple basal cellular carci-

nomas are found in non photo exposed areas

Clinical Presentation

Basal cell carcinoma shows a pearly pink papule and superficial telan-

giectasias

It is localized over healthy skin and never aff ects mucosae

Treatment

Surgery is the treatment of choice Mohs surgery is performed in zones

where surrounding healthy tssue needs to be preserved Other alter-

natves are cryotherapy imiquimod electrocoagulaton radiotherapy

photodynamic therapy and intralesional interferon Prognosis is excel-

lent as growth is slow and metastasis exceptonal

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8

Melanoma

Melanoma is the most aggressive cutaneous tumor given its ability to

metastasize

Risk factors comprise solar photo exposure clear phototype the pres-

ence of dysplastc nevus or a high number of melanocytc nevi Fam-

ily history is quite important as some genetc mutatons determine a

higher risk of developing the disease

Clinical Forms

See Figure 33

Diagnosis

Precocious diagnosis is essental to perform precocious surgical extrpaton

The ABCDE criteria can help patents to see if they need to seek medical

consultaton (asymmetry of lesion uneven borders color and diameter

greater than 6 mm or abnormal evolut

on)

The Breslow index is the thickness of the lesion measured in millimeters

and is the main prognosis factor

Treatment

The base of treatment is precocious surgical extrpaton If the Breslow

index is less than 1 mm margins of 1 cm will be performed If Breslow

index is greater than 1 mm margins will be of 2 cm

For melanomas with a Breslow index greater than 1 mm the sentnel

ganglion must be located This is the first draining lymph node of the

territory where the tumor is localized If the ganglion is positve re-

gional lymphadenectomy will be performed along with interferon ad-ministraton (Figure 34)

In situ Extirpation 05 cm Follow-up

Breslow lt 1 mm Extirpation 1 cm Follow-up

Lymphadenectomy

Breslow gt 4 mm Interferon

Breslow ge 1 mm Extirpation 2 cm Sentinel ganglion

+

Figure 34 Melanoma treatment

Kaposirsquos sarcoma

Kaposirsquos sarcoma is the most common cutaneous tumor in HIV patents

Clinical presentation

Kaposirsquos sarcoma has a course with violaceous fusiform macules whichovertme may evolve into indurated nodules with blackberry appearance

This type of sarcoma has been linked to herpesvirus type 8 both in HIV

and seronegatve patents (Table 3)

EPIDERMAL KAPOSIrsquoS 983080HIV983081 CLASSIC KAPOSIrsquoS

Homosexual youth (95) The elderly

Diffuse and bilateral

(frequently in palate and face)

Unilateral plaques

(lower extremities)

Frequent mucosal and visceral involvement Not so frequent

middot Precocious lymphatic invasion

middot Aggressive

Not so precocious

Table 3 Differences between epidermal and classic Kaposirsquos sarcoma

Nodular melanoma

15

Middle-aged men

middot On healthy skin

middot Any zone

middot Sudden onset

middot Uniform black nodulemiddot Rapidly invasive (vertical growth without radial)middot Frequent ulceration and bleeding

Worst histological prognosis

Lentigo malignant melanoma

10

Elderly women

90 on facephotoexposedzones of aging skins(chronic exposure)

Spot that growsduring many years (gt 10)then progresses (nodule)

Better prognosis

Acral lentinginous melanoma

5ndash10 ( 60 black and Asian race)

Elderly men

middot Sole (ankle) handsmucosa ungual bed

middot No relation to photo exposure

middot Macule with mosaic appearance (spot that grows)middot Some amelanisticmiddot Bad prognosis due to late diagnosis

Melanoma of super1047297cial extension

70

Young women

middot 30 previous nervusmiddot Intermittent exposuremiddot Men back middot Women legs

More frequent

middot Macula with mosaic appearance in colors that grows 4-5 years and then in1047297ltrates (nodule)middot Metastasis 35 to 70

Figure 33 Clinical forms of malignant melanoma

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Dermatology

Diagnosis

Diagnosis relies on clinical suspicion and histopathological confirma-

ton

Treatment

Treatment of localized forms can include surgical extrpaton radiother-

apy or intralesional vinblastne

If the sarcoma is disseminated optons involve interferon or chemo-

therapy

Mycosis Fungoides

Mycosis fungoides is a T-cell lymphoma of low-grade malignancy Its

clinical course may be very slow and surpass 50 years Three stages are

clinically diff erentated

1 Eczematous or macular phase predominantly truncular erythema-

tous macules with years of evoluton They resemble a chromic ec-

zema Histology is unspecifi

c at this stage2 Infiltratve plaque phase infiltrated erythematous plaques appear

Histology is diagnostc at this stage A dermal infiltrate of atypical

lymphocytes band forms can be observed composed of CD+4 T

lymphocytes with cerebriform nuclei There is a marked epidermo-

tropism with the presence of clusters of intraepidermal lympho-

cytes called Pautrierrsquos microabscesses (Figure 35)

Figure 35 Mycosis fungoides Infiltrative plaque phase

3 Tumoral phase erythematous exophytc plaques start to appear

(tumors) with a tendency to ulceraton They can have a large size

Histology may become unspecific again as epidermotropism disap-

pears

In more advanced stages of the disease there is aff ectaton of extra-

cutaneous organs such as lymph nodes liver spleen lungs and bone

marrow Besides there may be blastc transformaton Other possible

complicaton is sepsis by Staphylococcus aureus

These three stages usually develop consecutvely nevertheless there

may patents whose debut starts directly with the tumoral stage

Remember

Microabscesses of mycosis fungoides are due to lymphocytes and are calledPautrierrsquos abscesses Psoriasis microabscesses result from neutrophils andare labeled as Munro-Sabouraud

Seacutezary Syndrome

Seacutezary syndrome can be considered as the leukemic phase of T-cell cu-

taneous lymphoma It is defined by the triad erythroderma (Figure 36

lymphadenopathies and the existence of more than 1000 Seacutezary cellsper milliliter in peripheral blood Seacutezary cells are atypical T- lymphocyte

with cerebriform nuclei

Very intense pruritus is characteristc For many authors Seacutezary syn-

drome is an aggressive clinical form and a bad prognosis of a mycosis

fungoides

Figure 36 Erythroderma due to Seacutezary syndrome

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Dermatology

Chapter 01

Skin

LayersThere are three skin layers epidermis dermis and subcutaneous cel-

lular tssue (Figure 1)

Reticular layer

Sebaceous(Oil) gland

Hair

follicle

Deep

arteriovenousplexusSweat

glandDermal Papillae

Super1047297cial arteriovenousplexus

Subcutaneoustissue

Dermis

Epidermis

Figure 1 Microscopic structure of normal skin

Chapter 02

TerminologyElemental

Cutaneous Lesions

21 Clinical Lesions

Primary Clinical Lesions bull Fluid-filled

Vesicle raised formaton less than 05 cm

Blister lesion equal or greater than 05 cm

Phlyctena large blister

Pustule vesicle of purulent content

Cyst encapsulated lesion of semi-solid or liquid content

bull Of solid consistency

Macule a patch of skin that changed color which is neither

raised nor depressed (non palpable)

When a macule is red in color it is described as erythematous If

it does not disappear afer a diascopy it is regarded as purpuric

(it translates the existence of extravasated blood)

In diff erental diagnosis of purpuric lesions senile purpura must

be taken into account which consists in the presence of viola-

ceous macules in areas exposed to trauma as a consequence

of capillary fragility Other cause for purpura is leukocytoclastc

vasculits which typically gives palpable purpuric papules but

not nodules

Papule small solid circumscribed elevaton of the skin of less

than 1 cm which resolves without leaving a scar It is called

plaque if it is equal or greater than 1 cm Unlike macule both

are palpable

Wheal erythematous edematous plate of dermal origin and of

fleetng evoluton (it disappears in less than 24 hours) It is char-

acteristc of urtcaria

Nodule circumscribed hypodermal lesion identfied by palpa-

ton It may or may not be raised (ldquoit is palpable rather than vis-

iblerdquo) Nodules are typical lesions of panniculits like the ery-

thema nodosum

Tubercle circumscribed infi

ltrated and raised nodule that usu-ally leaves a scar once it has resolved

Gumma granulomatous inflammaton that sofens and opens

gradually

Secondary Clinical Lesions

bull Secondary clinical lesions expected to disappear on their own

Scales plates in the stratum corneum which come off by them-

selves

Scab secreton or exudate or dried blood over the skin

Slough black necrotc plate of tssue with demarcated bor-

ders

bull Solutons of contnuity Erosion loss of epidermal substance that heals without leaving

a scar

Ulcer loss of epidermal and dermal substance that leaves a scar

afer healing

Excoriaton erosion secondary to scratching

Fissure crack that reaches high dermis as a result of hyperkera-

tosis

bull Others

Sclerosis skin induraton with elastcity loss due to fibrosis and

dermal collagenizaton

Scar fibrous tssue that replaces normal skin

Lichenifi

cat

on thickening of the epidermis with accentuat

on ofskin folds secondary to chronic scratching

Intertrigo cutaneous lesion located in skin folds

Telangiectasia arboriform erythematous macule secondary to

permanent dilaton of cutaneous vessels

Poikiloderma hypopigmented and hyperpigmented areas

with atrophy and telangiectasias Poikiloderma is unspecific

and it translates into the presence of chronic cutaneous dam-

age

As a summary Figure 2 lists the main cutaneous elemental lesions com-

mented on this item

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2

bull Type II is mediated by IgM and IgG G Cytotoxic Hemolytc anemia

bull Type I is mediated by immune complexes Toxicodermas

bull Type IV is mediated by T lymphocytes (cellular) Contact derma-

tts

32 Atopic Dermatitis

Atopic dermatts is an inflammatory disorder of the skin with chronic

and recurring presentaton which aff ects 12 - 15 of children popula-

ton Atopic dermatts manifests itself by dry skin and pruritus

Patents have more risk of bacterial secondary infectons (S aureus) and

viral infectons (simple herpes virus SHV or mollusca)

There is a variety of triggering factors or factors that maintain eczema

outbreaks aeroallergens (dust mites) bacterial antgens (S aureus)

food (ovoalbumin) and psychological stress among others

Clinical Presentation

Clinical presentaton is usually in the form of greasy erythematous

and desquamatve papules or plaques on the scalp (cradle cap in the

cases of newborns) central area of the face sternal region axilla and

or groin In newborns this presentaton can be generalized causing

Leinerrsquos erythroderma desquamatvum in adults it is likely to be re-

lated to blepharits

Diff erental diagnosis includes atopic eczema in children but diff eren-

tal diagnosis in adults reveals subacute erythematous lupus or pink

pityriasis when the trunk is involved and inverted psoriasis when skin

folds are aff ected

Remember

Letterer-Siwe disease can cause lesions similar to infantile seborrheicdermatitis However unlike infantile seborrheic dermatitis Letterer-Siwedisease is associated with lymphadenopathies and hepatosplenomegaly

Remember

Impetigo key words (yellowish scabs) should not be mistaken for seborrheicdermatitis key words (yellowish scales)

Diagnosis

Atopic dermatts has a clinical diagnosis Patents may present with eo-

sinophilia and increase of IgE values

Treatment

It is essental for the patent to follow certain rules in his lifestyle This

means the patent must avoid wearing perfumed products (like cologne

and cream) being exposed to extreme temperatures the use of fabric

sofeners and carpets or fluff y toys (because of possible sensitzaton of

dust mites) Besides the patent needs to wear 100 coon clothing

Macule Vesicle

Wheal Fissure

Papule Ulcer

Nodule Cyst

Figure 2 Cutaneous elemental lesions

22 Histological Lesions

The following are histological lesions of the skin

bull Hyperkeratosis increase in the stratum corneum (warts and psoriasis)

bull Hypergranulosis granular layer thickening

bull Acanthosis thickening of the stratum spinosum

bull Acantholysis rupture of intercellular bridges of the stratum spino-

sum (typical of pemphigus)

bull Spongiosis intercellular intraepidermal edema (characteristc of eczema)

bull Ballooning intracellular edema (herpes)

bull Parakeratosis presence of nuclei in the stratum corneum (typical

of psoriasis)

bull Dyskeratosis abnormal keratnizaton of individual cells of the stra-

tum spinosum (typical of Darierrsquos disease)

bull Papillomatosis lengthening of dermal papillae (psoriasis)

Chapter 03

Allergic and

Immune-mediated

Diseases

31 Hypersensibility Reactions

bull Type I is mediated by IgE It is the most rapid Anaphylaxis asthma

and urtcaria

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Dermatology

Precocious treatment is of the utmost importance

Topic cortcoids are the first line treatment

It is worth to remember that prolonged use of topic cortcoids can have

local and systemic secondary side eff ects

The second line of treatment involves immunomodulators (tacrolimus

and pimecrolimus) These can be used in children older than 2 years of

age

For acute outbreaks oral cortcoids are used in short cycles and not as

maintenance To stop medicaton suddenly may cause a rebound eff ect

33 Contact Eczema

The appearance of contact eczema is immunologically mediated (type

IV hypersensit

vity) against foreign agents acquired by percutaneouspenetraton Contact eczema requires prior sensitzaton to allergen

It is more common in adults than in children

Diagnosis

Diagnosis is established with clinical records and epicutaneous tests of

contact These tests are performed once lesions have been resolved by

applying patches with allergens on healthy skin leaving them in contact

with the skin during 48 hours They are read afer 48 and 96 hours The

intensity of reacton is measured qualitatvely negatve weak positve

(erythema) strong positve (papules-vesicles) or extreme positve (blis-

ters)

Treatment

Avoid contact with the allergen

Treatment of acute eczema implies applicaton of topic poultce (zinc

sulphate sodium borate) and cortcoids if lesions are limited and sys-

tem poultce if lesions are generalized

34 Seborrheic Dermatitis

Seborrheic Dermatts is a quite frequent disease It aff ects 4 - 5 of the

populaton Etology of seborrheic dermatts is unknown although it

has been related to an abnormal immunological response to a fungus

called Pityrosporum ovale Seborrheic dermatts is more frequent and

intense when associated to neurological processes alcoholism and im-

munodeficiencies

Clinical Presentation

According to patentrsquos age

a Seborrheic dermatts in infants Yellowish scales on scalp known

as cradle cab

b Seborrheic dermatts in adult erythematous desquamatng papu-

les or plates in fat areas of the facial region and scalp

Diagnosis

Diagnosis of this conditon is clinical

TreatmentTreatment involves antfungals associated with topic cortcoids Sebor-

rheic dermatts on the scalp is usually linked to a keratolytc agent like

the salicylic acid

35 Psoriasis

Psoriasis is a chronic inflammatory disease of the skin that presents

with outbreaks Psoriasis aff ects 1-2 of the populaton and can ap-

pear at any age with a maximum of incidence between 20 and 30 yearsof age There is a family history in a third of the patents

Plates are the characteristc erythematous desquamatng lesions well

delimited with a superficial thick and white-pearl scale

The most frequent clinical form is vulgar psoriasis or psoriasis in plates

Lesions are localized at extensor surfaces (elbows and knees) and the

scalp The umbilical and the lumbosacral areas are ofen aff ected

Nail involvement is frequent and is most common with a pi ng ap-

pearance This form is lile specific The forms that combine hyperkera-

tosis and distal onycholysis are more specific Oil spot is the most char-

acteristc sign (Figure 3)

Figure 3 Generalized pustular psoriasis

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4

Diagnosis

Diagnosis of this conditon is generally clinical

If there is no certainty a biopsy must be done which will reveal hyper-

keratosis acanthosis and parakeratosis

There is an increase in polymorphonuclears (sterile abscesses) in the

stratum corneum which are called Munro abscesses

Treatment (Table 1)

For moderate severe forms of psoriasis that do not respond to clas-

sical systemic treatments (see table) They are monoclonal antbod-

ies against proinflammatory substances that are high in patents with

psoriasis [alpha tumor necrosis factor (TNF) interleukin IL 12 and

23] Some of them are infliximab adalimumab ustekinumab and

etanercept

36 Urticaria

Urtcaria is an immunologic and inflammatory reacton of the skin

against diverse etological factors Independently of the cause release

of histamine and other inflammatory mediators occurs which cause va-

sodilaton and increase in capillary permeability producing an edema in

superficial dermis Urtcarias are divided in acute and chronic urtcarias

depending on whether outbreaks persist more or less than six weeks

About 60 of acute urtcarias are idiopathic Chronic urtcarias show a

higher percentage

Urtcarias of known origin are usually due to infectons drugs or food

Clinical Presentation

Clinical presentaton is characterized by the appearance of pruritc wheals

that last less than 24 hours and can be accompanied with angioedema

TREATMENT USES SIDE EFFECTS AND CONTRAINDICATIONS

Topic Mild-moderatepsoriasis

(lt 25 body

surface)

Emollients (urea glycerin) Moisturizing

Keratolytics (salicylic acid) Eliminate excess of scales

Reductants (dithranol) Hyperkeratotic plaques middot Stain skin and clothing

middot Irritating

middot Acneiform eruptions

Corticoids middot Stable psoriasis

in plates

middot The most used

middot Tachyphylaxis

middot Percutaneous absorption

middot Possible new outbreak after stopping medication

middot Avoid prolonged treatment

Vitamin D analogues

(calcitriol calcipotriol and

tacalcitol)

Stable psoriasis in plates middot Irritating in face and skin folds

middot Hypercalcemia

Systemic Moderate-

severe psoriasis

(gt 25 body

surface)

Psoralens plus ultraviolet

light of the A wavelength(PUVA)

Combinable with topics

and retinoids (RePUVA)

middot Cutaneous aging and carcinogenesis

middot Erythroderma and xerosis middot Immunosuppression

middot Hepatitis by psoralens

middot Not in children pregnancy patients with hepatic or renal

insuffi ciency photosensitivity or cutaneous precancerosis

middot Cataracts

middot It accumulates in the crystalline during 24 h (sunglasses)

Retinoids (acitretin) middot Severe psoriasis

pustular

or erythrodermic

middot It is not usually used

in women in fertile age

(see side effects)

middot Cutaneous dryness (the most frequent)

middot Hypertriglyceridemia

middot Hypercholesterolemia

middot Increase in transaminases

middot Diffuse alopecia

middot Vertebral hyperostosis ligamentous calci1047297cations

middot Teratogenicity avoid pregnancy until 2 years after

1047297nishing treatment

middot Avoid in children and patients with hepatic or renal failure

Cyclosporine A middot In1047298ammatory severe

psoriasis resistant to

other treatments

middot Rapid action

middot Rebound effect

middot Nephrotoxicity

middot High blood pressure (HBP)

middot Epitheliomas and lymphomas

middot Hypertrichosis

middot Gingival hyperplasia

middot Hyperuricemia

Methotrexate middot Severe psoriasis

resistant to other

treatments

middot Psoriatic arthropathy

middot Hepatotoxicity

middot Myelosuppression

middot Teratogenicity until 3 months after ending treatment

middot Photosensitivity

Table 1 Psoriasis treatment

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Dermatology

Vasculits urtcaria should be ruled out when lesions last more than 24 hours

and are accompanied with systemic clinical symptoms (ie arthralgias)

Treatment

Oral anthistamine therapy is the treatment of choice

Systemic cortcoids for severe or refractory cases

Adrenalin for severe cases with anaphylaxis

37 Toxicodermas

Toxicodermas are quite variable cutaneous reactons that appear afer

drug administraton They are one of the most frequent side eff ects of

drugs The causatve agents for many toxicodermas stll remains un-

known either immunological or not and clinical presentaton does not

facilitate agent dist

nct

on

Morbilliform exanthem is the most frequent A morbilliform exanthem

is a generalized erupton formed by symmetric and confluent macules

and papules that usually start by the trunk

They can appear one or two weeks afer taking the drug

A morbilliform exanthem can be associated with fever pruritus and eo-

sinophilia

The most frequent are non steroid ant-inflammatories antbiotcs (sul-

phamides and penicillins) antepileptcs allopurinol and N acetyl-cystene

DiagnosisDiagnosis is according to clinical presentaton

Treatment

Treatment implies withdrawal of potentally responsible drug Topic or

systemic anthistamines and cortcoids are given according to the extent

of symptoms (Figure 4)

Figure 4 Morbilliform exanthem due to amoxicillin

38 Multiform Erythema

Stevens-Johnson Syndrome

and Toxic Epidermal Necrolysis

Multform erythemas (ME) are of undetermined etopathogenesis

regarded as a cutaneous reacton against a diversity of stmuli Their

histologies show similarites what leads to consideraton of a common

pathogenesis

Clinical Presentation

Three diff erent groups have been described although many a tme their

clinical symptoms overlap

bull Erythema multforme minor is the most frequent with around 80

of the cases It usually precedes a symptomatc infecton by simple

herpes virus (60) or subclinical infecton about 15 days before

Erythema multforme minor manifests itself on extensor surfaces

at hands elbows and feet as a symmetric erupton of erythema-

tous edematous lesions with target-shape (herpes iris of Batemanor rosee-paerned lesion) with a violaceous sometmes bullous

center (Figure 5)

Mucosal aff ectaton is rare with small erosions in oral mucosa Erythe-

ma multforme minor tends to recurrence with subsequent outbreaks

of herpetc lesions

Figure 5 Erythema multiforme minor Herpes iris of Bateman

bull Erythema mult

forme major or Stevens-Johnson syndrome is therarest It normally has a prodromal period of untl 14 days with fe-

ver cough cephalea arthralgias and other symptoms Subsequent

to the prodromal period erythematous edematous plates appear

which are more extensive with a tendency to form blisters and

greater mucosal erosions (mouth genitals pharynx larynx and

conjunctve Figure 6) Systemic symptoms are normal and do not

tend to recurrence

The most frequent etological factors are drugs [sulphamides non

steroid ant-inflammatory drugs (NSAIDs) antconvulsants and an-

tbiotcs in decreasing order) Infectous agents have been also in-

volved mainly mycoplasma pneumoniae

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6

Figure 6 Exudative erythema multiforme major

bull Toxic epidermal necrolysis (TEN) many authors consider it the

most severe form of erythema multforme major arguing the same

pharmacological agents A morbilliform rash appears which is rap-idly confluent comprising almost the entre skin surface with flaccid

blisters that leave wide areas of denuded skin Involvement of sev-

eral mucosae is constant

Complicatons ofen occur (pneumonia digestve hemorrhage re-

nal failure and hemodynamic shock) with mortality rates close to

25 In children it must be performed a diff erental diagnosis with

staphylococcal scalded skin syndrome which does not aff ect mu-

cosae

Remember

Diseases that have the Nikolsky sign are TEN staphylococcal scalded skinsyndrome (SSSS) and pemphigus In TEN the whole epidermis comes off(bad prognosis) while in SSSS epidermal detachment occurs at the granularlayer

Histopathology

It must be highlighted the eff acement of dermoepidermal juncton by a

lymphohistocytc infiltrate and vacuolar degeneraton of the baseline lay-

er with necrotc keratnocytes In TEN keratnocytes necrosis is massive

Treatment

In ME minor only symptomat

c treatment is prescribed with topiccortcoids and oral anthistamines Treatment for herpes simplex virus

(HSV) infecton is useful to prevent ME lesions if patent is in the inital

stage of the viral infecton

ME major requires treatment of the underlying infecton or withdrawal

of implied drug and support measures The use of oral steroids accord-

ing to the patentrsquos general state is under discussion

A patent with TEN requires to be admied at the burn treatment room

with monitoring of hematocrit hydroelectrolytc balance and antbiotc

prophylaxis and support measures It is controversial the use of system-

ic cortcoids immunoglobulins andor cyclosporine

39 Erythema Nodosum

Erythema nodosum is the most frequent panniculits Painful erythema-

tous nodules occur mainly in the anterior side of legs with a self-limit-

ing course and predominantly aff ectng young women (Figure 7)

Figure 7 Erythema nodosum

They heal without leaving a scar within a period of four to six weeks

Erythema nodosum may be accompanied with fever deterioraton of

the general state and arthralgias

Patents with erythema nodosum may have a false positve VDRL

Etiology

This conditon is thought to be an immunological response triggered by

multple and diff erent stmuli bacterial fungal and viral infectons sys-temic diseases (sarcoidosis inflammatory intestnal disease Behcetrsquos

syndrome) neoplasias (lymphomas and leukemias) and drugs (oral

contraceptves sulphamides bromides and iodines)

Diagnosis

Erythema nodosum requires a deep biopsy to reveal septal panniculits

without vasculits

Complementary tests can be performed to rule out systemic involvement

for example chest X-ray Mantoux and antstreptolysin O antbody (ASLO)

Treatment Treatment entails eliminatng underlying cause if found then rest and

ant-inflammatories

310 Bullous Pemphigoid

and Pemphigus Vulgaris

See Table 2 and Figures 8 9 10 and 11

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Dermatology

Intercellular

substance ac

middot Pemphigus

Lineal

storage

in lucid

layer

-

Anti-Collagen Ac

Lucid

layer

Thick

layer

Basal

sublayer

Granular

storage

in papillary

dermis

middot Pemphigoid bullousmiddot Herpes gestationis

middot Acquired blistering epidermolysis

middot Dermatitis herpetiformis

Figure 8 Key points for histological diagnosis

of autoimmune blistering diseases

Figure 9 Pemphigus vulgaris

Figure 10 Pemphigus vulgaris with oral mucosa involvement with

erosions

Figure 11 Pemphigoid bullous Tense blisters No sign of Nikolsky

PEMPHIGUS VULGARISGENERALLY

IDIOPATHICHERPES GESTATIONIS

DERMATITIS

HERPETIFORMIS

Clinical presentation middot 40-50 years of age

middot They usually affect mucosae

middot No pruritus

middot Flaccid blister

middot Nikolsky

middot Elderly

middot Sometimes mucosae

middot With pruritus

middot Tense blister

middot No Nikolsky

middot Pregnant women

middot No mucosae

middot With pruritus

middot Herpetiform

middot No Nikolsky

middot 15-35 years of age

middot No mucosae

middot With pruritus

middot Herpetiform

middot No NikolskyDirect immuno1047298uorescence (DIF) IgG IgG IgG IgA

Histology middot INTRAepidermal blister

middot There is acantholysis

middot SUBepidermal blister

middot There are eosinophils

middot SUBepidermal blister

middot There are eosinophils

middot SUBepidermal blister

middot Neutrophils in dermis

Treatment Corticoids at high doses

immunosuppressants rituximab

and immunoglobulins

Corticoids Corticoids Diet +- dapsone

Remember Mortality rate 10 The most frequent Relapse if new

pregnancy

Associated to enteropathy

by gluten 90

Table 2 Autoimmune blistering diseases

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Amer ican Manual of Examinat ion in Medicine (2CK)

8

Chapter 04

Infectious Diseases

41 Viral Infections

Simple Herpes

Infection by Simple Herpes Virus

There are two types of simple herpes (Figure 12)

bull Type I is responsible for most extragenital herpes and 20 of the

genital herpes

bull Type II causes genital herpes and a small percentage of extragenital

herpes

Figure 12 Herpes simplex

Contagion is produced by direct contact though the carrier may be as-

ymptomatc Afer primary infecton virus remains silent in the sensi-

tve porton of cranial or spinal ganglia Immunosuppressed patents

endure the greatest severity of this conditon

Clinical Presentation

bull Extragenital simple herpes recurring orofacial herpes simplex is

the most frequent Most primary infect

ons are asymptomat

c Only5 manifest themselves in the form of herpetc gingivostomatts a

profile characterized by oral ulcers with cervical adenopathy and af-

fectaton of the patentrsquos general state (Figure 13) During relapses

clinical symptoms are milder with cluster vesicles on an erythema-

tous base Some factors facilitate relapses trauma sunlight cold

stress fever and the menstrual cycle

bull Genital simple herpes is the most common cause of genital ulcers

afer trauma Primary infecton is usually symptomatc and occurs

between 3 to 14 days afer sexual contact It causes clustered ulcers

in the balanopreputal sulcus or in the prepuce with painful inguinal

adenopathy Relapses are less severe than primary infecton and oc-

cur more frequently when genital herpes is due to HSV type II

Figure 13 Herpetic gingivostomatitis

bull Eczema herpetcum or Kaposi varicelliform erupton dissemina-

ton of herpetc infecton on pre-existng dermatosis (above all

atopic dermatt

s) bull Neonatal herpes is due to intrapartum contagion of HSV-II with

neurological involvement general deterioraton and skin vesicles or

ulcers

bull Other clinical forms are herpes gladiatorum herpetc whitlow and

keratoconjunctvits

Diagnosis

Diagnosis of this conditon is mainly clinical Virological culture is the

most reliable method of confirmaton The extent of a smear of the le-

sions (Tzanck cytodiagnosis) allows visualizaton of multnucleated cells

and intranuclear inclusions which become evident through histological

study

Treatment

Mild forms do not need treatment Treatment is required in the follow-

ing cases

bull Primary infecton

bull Severe or frequent relapses if they aff ect life quality

bull Complicatons like erythema multforme and eczema herpetcum

Drug of choice is oral acyclovir and its derivatves (valacyclovir famci-

clovir) Topic antvirals have not proven useful favoring maceraton of

lesions and thus over infecton It is not infrequent that topic antvirals

cause allergic contact dermatts due to hypersensitvity

Varicella-Zoster Virus

A primary infecton gives way to varicella (see Pediatrics secton) Afer

varicella the virus remains latent in the sensitve porton of the neural

ganglia and when relapse occurs it leads to zoster herpes

bull Varicella the following symptoms appear afer 15 days of incubaton

fever cephalea pruritus and polymorphic lesions in diff erent stages

macules papules vesicles (Figure 14) ulcers and scabs (starry sky

appearance) Mucosal (ulcers) and scalp involvement is characteristc

Manipulaton can leave scars Bacterial over infecton of lesions is the

most usual complicaton About 20 of adults suff er from varicella

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Dermatology

pneumonia radiologically demonstrable but clinical symptomatology is

only present in around 4 of the cases

Figure 14 Typical vesicles in patients with varicella

bull Zoster herpes thoracic zoster herpes is the most usual It sel-

dom occurs more than once throughout a personrsquos lifetime

It is characterized by vesicles on pre-existing erythema with

metameric distribution and lateral extension The most com-

mon complication is post herpetic neuralgia more frequent in

advanced age Carbamazepine or tricyclic antidepressants (Fig-

ure 15)

Figure 15 Zoster herpes

Special Clinical Forms

Special clinical forms are as follow

bull Ramsay-Hunt syndrome aff ectaton of geniculate ganglion of the

facial nerve

It produces vesicles in the outer ear external auditory canal and

pharynx homolateral facial paralysis deafness and vertgo

bull Ophthalmic involvement can result in severe keratts and requires ur-

gent referral to an ophthalmologist Suspicion should exist on patents

that present herpetc lesions on the tp of the nose) (Hutchinsonrsquos sign)

bull Disseminated zoster herpes several dermatomes are aff ected bilat-

erally Ramsay-Hunt syndrome is characteristc in the immunosup-

pressed

Remember

Affectation of the nose tip makes it necessary for ophthalmologicalexamination because the nose tip is innervated by the same nerve thatinnervates the cornea (1047297rst branch of the trigeminal nerve)

Treatment

Varicella without complicatons is treated symptomatcally Antvirals

are reserved for severe or complicated forms There is a commercial-

ized vaccine of live virus whose indicatons are stll under discussion

Zoster herpes must be treated with antvirals when detected during the

first 48-72 hours and aff ectng patents with

bull Immunosuppression

bull Age above 55

Special clinical forms previously cited

Drugs to be used are oral acyclovir and its derivatves (valacyclovir and

famciclovir) They accelerate the cure of lesions and decrease the inten-

sity of post herpetc neuralgia Patents with renal failure need a dose

adjustment as acyclovir is nephrotoxic These patents are adminis-

tered brivudine in a single daily dose

Molluscum ContagiosumDome shaped pink papules with central umbilicaton (Figure 16) Mol-

luscum contagiosum is typical of children that go to swimming pools It

is also present in the genital zone afer sexual contact and in immuno-

suppressed patents It is caused by Poxvirus

Figure 16 Molluscum contagiosum

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Amer ican Manual of Examinat ion in Medicine (2CK)

0

Lesions are asymptomatc

Diagnosis

Diagnosis is clinical Histology reveals characteristc inclusion bodies

Treatment

Lesions can resolve spontaneously

Cureage cryotherapy or local trichloroacetc acid are eff ectve meth-

ods to destroy lesions

Warts

Human papillomavirus can cause verruca vulgaris palmoplantar and

flat warts and condyloma accuminata Human papillomavirus is the

most frequent sexual transmied disease

Some subtypes of this virus (16 18) are of high risk and can cause epi-

dermoid carcinomas

Direct contact is the mechanism of contagion

Diagnosis

Diagnosis of this conditon is clinical

Staining with acetc acid can help visualize mucosal lesions

Treatment

Genital warts are treated with cryotherapy podophyllotoxin trichloro-

acetc acid imiquimod and 5-fluorouracil

Cervical lesions should be monitored by cytology and biopsy whenever

necessary to rule out cervical cancer (Figures 17 and 18)

Figure 17 Warts in HIV patient

Figure 18 Condyloma accuminata

42 Bacterial Infections

Impetigo

Impetgo is a very contagious superficial infecton without systemic re-

percussion and normally mixed etology by Gram positve cocci (strep-

tococci and staphylococci) Classically the most frequent accepted

cause was Streptococcus pyogenes However at present Staphylococcus

aureus stands out as the predominant cause

The most typical form is impetgo contagiosa (Figure 19) character-

ized by honey-colored (meliceric) scabs which normally appear on

the face and other exposed areas It is typical of children Although

infrequent poststreptococcal glomerulonephrits is a dreadful com-

plicaton

Figure 19 Impetigo contagiosa

On the contrary rheumatc fever shows no relaton to cutaneous strep-

tococcal infectons but only with pharyngeal infectons

There are other less habitual forms called bullous impetgo exclusively

of staphylococcal origin Clinical presentaton involves the presence of

blisters and erosions on the aff ected skin as a consequence of the epi-

dermolytc toxins that these bacteria contain Impetgo is treated with

topical mupirocin penicillin or oral fusidic acid

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Dermatology

Cellulitis

Cellulits is an infecton that aff ects deep dermis and subcutaneous cel-

lular tssues normally caused by streptococci (Streptococcus pyogenes

or of group A)

Community methicillin-resistant S aureus (CMRSA) is a triggering agent

that is becoming more and more frequent

Most common risk factors are diabetes chronic venous insuffi ciency

and immunosuppression

Clinical Presentation

Cellulits presents with erythematous plaques that are ill-defined pain-

ful and hot It is usually accompanied with fever and chills

Diagnosis

Diagnosis is clinical If there is an open door a culture of this area may

help see the source germ and resistance to ant

biot

cs

It is important to rule out abscesses osteomyelits and necrotzing fas-

ciits

If bacteremia is suspected blood cultures need to be performed

Treatment

Treatment implies oral antbiotcs for 7-10 days to cover Gram positve

cocci They are intravenously administered in case of lack of response

to oral treatment involvement of hands or periorbital zone diabetes or

extremes of age

Necrotizing FasciitisNecrotzing fasciits is a deep infecton up to muscular fascia that pro-

duces very intense pain and subsequent anesthesia

In 10 of the cases cellulits is due to an infecton by S pyogenes In the

remaining cases it occurs by a polymicrobial infecton caused by aerobes

and anaerobes including S aureus E coli and Clostridium perfringens

There may be prior history of trauma or surgery

Clinical Presentation

Clinical presentat

on involves pain of sudden onset and edema on theaff ected zone Pain may progress to anesthesia There appears subse-

quent erythema that progresses rapidly into necrosis

Characteristc clinical signs are tssue necrosis blisters intense pain

and gas producton

Diagnosis

Diagnosis is clinical and requires image testng X-rays or a computed

tomography CT

A biopsy of the border of the lesion helps achieve diagnosis

Treatment

Treatment entails precocious surgical debridement It is a surgical emer-

gency In additon to surgery broad-spectrum antbiotherapy will be

needed

Folliculitis

Folliculits is an infecton and inflammaton of one or several follicles

caused mainly by staphylococci

Clinical Presentation

Folliculits shows pustules with follicular distributon

When the infecton is deeper it is called furuncle

If several furuncles are infected a fluctuatng erythematous plaque forms

containing several points of suppuraton This plaque is labeled as anthrax

Diabet

c and immunosuppressed pat

ents are at higher risk

Characteristics of Folliculitis

1 Hot tub or swimming pool folliculits caused by Pseudomonas aeru-

ginosa

2 HIV associated pruritc folliculits or eosinophilic folliculits

Treatment

In mild cases treatment of choice comprises antseptcs and topic an-

tbiotcs

In more severe cases treatment of choice requires oral antbiotcs

Large sized lesions must be drained and a microbiological culture must be

performed to rule out methicillin-resistant Staphylococcus aureus MRSA

Acne Vulgaris

Acne is an inflammatory disease of the pilosebaceous follicle as a con-

sequence of an alteraton in follicular keratnizaton It aff ects adoles-

cents and young adults

Etology is multfactorial alteraton of keratnizaton of follicular infun-

dibulum quanttatve and qualitatve alteraton of sebum producton in

the sebaceous gland and alteratons of bacterial microflora (increase in

quant

ty of P acnes)

Aggravatng factors are stress androgenic oral contraceptves and the

use of cosmetc products that are not oil-free

Clinical Presentation

A comedo is the inital lesion which can be closed (whitehead) or open

(blackhead) and it evolves into inflammatory lesions that listed in as-

cending order of severity are papules pustules nodules and cysts

Lesions progress and leave scars Scars can be increased if lesions are

manipulated

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Amer ican Manual of Examinat ion in Medicine (2CK)

2

Diff erent lesions habitually combine simultaneously so acne becomes

polymorphic It is located in sebaceous areas face back shoulders and

the center thoracic region

Diagnosis

Diagnosis is clinical

Treatment

bull Comedonal acne is treated with topic retnoids and benzoyl peroxide

bull Inflammatory acne treatment requires benzoyl peroxide combined

with topic antbiotcs (erythromycin and clindamycin) Systemic

antbiotc treatment with oral tetracyclines will be prescribed if re-

sponse to topic antbiotc treatment fails

bull Severe nodular cystc acne treatment involves the use of isotret-

noin (13-cis-retnoic acid) It is a derivatve of vitamin A Isotretnoin

produces atrophy in the sebaceous gland and regulates keratniza-

ton The most frequent side eff ect is cutaneous and mucosal xero-

sis Triglycerides cholesterol and transaminases should be moni-

tored as their values may increasebull It can be associated with depression

bull It is teratogenic so pregnancy should be avoided during treatment

and untl a month afer treatment

Pilonidal Cysts

Pilonidal cysts are abscesses in the sacrococcygeal region

This type of cysts has predominance in men between 20 and 40 years

of age It is believed that repeated trauma on the aff ected area favors

their appearance

Clinical Presentation

Pilonidal cysts present with an indurated lesion that is fluctuatng hot

painful but non-adherent to deep planes in the sacrococcygeal region

Pilonidal cysts may or may not be associated to cellulits and purulent drain-

age

Diagnosis

Diagnosis is clinical and anal or perirectal abscesses should be dismissed

Treatment

Treatment implies an incision and surgical drainage

On some occasions a general surgery is required

43 Fungal Infections

Pityriasis Versicolor

Versicolor pityriasis is caused by commensal yeast called Pityrosporum

ovale which transforms into its pathogen form (Malassezia furfur) It

especially aff ects young patents (15 - 45 years of age) but it is rare

in childhood and advanced age Versicolor pityriasis relates to heat

humidity and sebaceous hypersecreton It is characterized by the ap-

pearance of hyperchromic or hypochromic macules that desquamate

on scratching (nail sign) if infecton is actve Macules usually appear on

the center thoracic region and on the back that is to say on seborrheic

zones Relapses are habitual despite treatment

Diagnosis

Diagnosis is normally clinical To that purpose the following serve as

support

bull Woodrsquos lamp emits yellow-orange fluorescence

bull Potassium hydroxide (KOH) test filaments and round elements can

be observed (ldquospaghe and meatball appearancerdquo Figure 20)

Treatment

Treatment is performed with topical azoles Oral administraton applies

for extensive cases or immunosuppressed patents Diff erental diagno-

sis includes pink pityriasis and eczemas (Figure 21)

Figure 20 Versicolor pityriasis Histological cut

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Dermatology

Figure 21 Versicolor pityriasis

Candidiasis

The most common triggering agent is Candida albicans It is normally sapro-

phyt

c although under certain condit

ons candidiasis may become patho-genic (immunosuppression humidity pregnancy and contraceptves)

Clinical Forms

bull Intertrigo erythematous plaque in cutaneous folds Atrophy and

fissures are typically deep in the skin fold as well as satellite and

peripheral lesions (papules andor pustules)

bull Mucosa involvement may cause diverse symptomatology like vul-

vovaginits glossits and white papules in the anterior region of the

oral mucosa Candidal balanits is characterized by the presence of

punctform erosions and pustules on gland and balanopreputal

sulcus Candidal balanits ofen appears afer sexual intercourse or

afer oral antbiotc intake

Remember

Almost a 100 of HIV patients suffer from muguet throughout their diseasecourse

bull Candidiasis of nail fold is usually associated with periungual inflam-

maton (perionixis) and inital proximal aff ectaton which diff erent-

ates it from tnea unguium (Figure 22)

Figure 22 Candidiasis of nail fold

Treatment

Oral Candidiasis fluconazole or nystatn

Candidiasis of the skin (intertrigo) apply topical antfungal medicaton

and keep zone clean and dry

Dermatophytosis or TineasDermatophyte infectons aff ect the skin and keratnized structures like

hair and nails (there is no mucosa involvement) Clinical diagnosis is

achieved afer performing a culture Woodrsquos lamp test normally turns

out to be negatve In general Trichophyton dermatophyte rubrum is

the most frequent dermatophyte

Non Inflammatory Tineas

Non inflammatory tneas do not produce irreversible scarring alope-

cia while inflammatory forms do Tineas are treated with azoles de-

rivatves

The types of tnea are the following

bull Ringworm of the scalp ( t nea capi t s or t nea tonsurans) is charac-

teristc of childhood It presents with alopecic plaques broken hair

and desquamaton Infectons tend to resolve spontaneously with-

out leaving scars at the onset

of puberty

bull Ringworm of the body (herpes

circinatus or t nea corporis) are

erythematous desquamatve

plaques (with more actve bor-

ders) which are also circinate

and normally pruritc (Figure

23) Plaques grow eccentrically

with less actvity in the centerand more in the borders

bull Ringworm of the foot ( t nea

pedis) the most frequent is the

ldquoathlete footrdquo with desquama-

ton in interdigital spaces

bull Tinea incognito refers to tnea

wrongly treated with cort-

coids what makes diagnosis

diffi cult as the lesion has been modified Figure 24)

Figure 24 Tinea incognito secondary to treatment with topical steroids

Figure 23 Herpes circinatus

(tinea corpis)

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Amer ican Manual of Examinat ion in Medicine (2CK)

4

bull Ringworm of the groin (t nea cruris or eczema marginatum von

hebra) formed by erythematous desquamatve plaque with more

actve borders (Figure 25)

Figure 25 Ringworm of the groin (tinea cruris)

bull Tinea unguium subungualhyperkeratosis with onychol-

ysis but without perionixis

(Figure 26)

Diagnosis

Clinical diagnosis is reached afer

performing a culture

Treatment

Treatment involves topical an-

tfungal medicaton in localized

areas

Oral antfungal medicaton is used in extensive forms nail fold or scalp

involvement

44 Parasitic Infections

Pediculosis

Pediculosis is transmied by direct contact or by contact with fomites

which release toxins that produce intense pruritus

Clinical Presentation

Pediculosis capi t s intense pruritus predominant in retroauricular and

occipital regions occasionally with excoriatons and impetginizaton

secondary to excoriatons

Pediculosis corporis intense pruritus in patents with poor hygiene or

who live in overcrowded conditons

Pediculosis pubis genital and pubic pruritus Brownish-grey macules

called maculae ceruleae are typical on underwear and skin These pig-

mentatons appear as a result of a reducton in hemoglobin by a para-

site enzyme

Diagnosis

Diagnosis is clinical and by direct visualizaton

Treatment

Pediculosis is treated with malathion lindane or topical permethrin

Scabies

Scabies is originated by an acarus known as Sarcoptes scabiei It has an

incubaton period of 1 month

Clinical Presentation

Scabies produces generalized pruritus more intense at night The pa-

tent usually catches the infestaton which is passed to the patentrsquos

relat

ves It is common tofi

nd that a recent trip to a tropical country hasbeen made Lesions appear between the fingers (Figure 27) in wrists

feet genitalia mammary areola and axilla but back and face are usu-

ally spared The most specific lesion is the acarine burrow in whose less

scaly end the advancing zone the mite lies Nodules are frequent in

axilla and genitals (nodular scabies)

bull Norwegian scabies is typical of the immunosuppressed Patents

present with generalized hyperkeratosis and scabs Norwegian sca-

bies produce lile pruritus but it is very contagious because there

are many acari

bull Nodular scabies involves the persistence of pruritc nodules despite

treatment Lesions usually appear in axilla and genitalia Pruritus is

due to a hypersensitvity phenomenon because of the acarus al-

ready dead Nodular scabies is treated with cortcoids

Figure 27 Scabies Acarine burrow

Treatment

bull Permethrin cream at 5 is the treatment of choice It is lile toxic

so it can be used in children and pregnant women

bull Topical lindane at 1 irritates and is neurotoxic therefore it is con-

traindicated in pregnant women and children

bull Oral ivermectn is utlized in cases of resistance to prior treatments

There is stll lile experience as to its use but in a first instance a

Figure 26 Tinea unguium

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Dermatology

single dose would be enough to cure scabies (already used by vet-

erinarians)

45 Ischemia

Decubitus Ulcers

Decubitus ulcers are the result of ischemic necrosis by contnuous pres-

sure on an area which restricts microcirculaton in that zone

Clinical Presentation

Decubitus ulcers are present in patents in bed with scarce mobilizaton

It is favored by bone prominences and lack of fat tssue If sensitvity

decreases there is more risk of formaton of decubitus ulcers

Diagnosis

Diagnosis is achieved based on medical records and clinical presentaton

Treatment

Preventon is of the utmost importance as well as frequent mobiliza-

ton of the patent in bed

Once ulcers have been established hydrocolloid dressings are used for

healing but sometmes surgical debridement is necessary

Gangrene

Gangrene means tssue necrosis

There are three types dry gangrene wet gangrene and gas gangrene

Clinical Presentation

Dry gangrene is due to ischemia generally secondary to atherosclero-

sis Clinical presentaton involves pain cold and paleness of extremi-

tes Once tssue is established it turns bluish-black in color and dry

Wet gangrene is owing to bacterial flora Tissue presents with an edem-

atous appearance either with blisters or pus

Gas gangrene caused by C perfringens It is normally located on re-

cent surgery Bacteria precociously destroyt

ssue producing gas It is amedical emergency

Diagnosis

Clinical diagnosis is obtained by microbiological culture

Treatment

Treatment requires surgical debridement with amputaton if necessary

and associaton of broad spectrum antbiotherapy

Gas gangrene is treated with hyperbaric oxygen

46 Miscellaneous

Acanthosis Nigricans

Acanthosis nigricans are vel-

vet-like papillomatous brown

plaques in neck axilla and groin

folds (Figure 28)

It is associated with diabetes

mellitus Cushingrsquos disease poly-

cystc ovarian syndrome and

obesity

The malignant form of acantho-

sis nigricans is a paraneoplastc

syndrome that diff erentates

from the benign form because

the laer has mucosal and pal-

moplantar involvement

Lichen Planus

Lichen planus is an inflammatory idiopathic disease that equally aff ects

both genders with higher frequency in middle age

Lichen planus has been related to diverse drugs like gold salts

anti-malarial medication and thiazides It has been also linked to

hepatitis C virus infection however this association is currently

doubtful

Clinical Presentation

Lichen planus presents with red-violaceous polygonal flat papulesquite pruritc which localizes on the flexor side of wrists forearms an-

kles and lumbosacral and flank regions On its surface a whitsh retcu-

late can be observed (Wickhamrsquos striae) About 60 - 70 of the cases

present with lesions in oral and genital mucosa oral which appear as

whitsh retculated lesions (Figures 29 and 30)

Figure 29 Lichen planus of oral mucosa with typical whitish

reticulate

Figure 28 Acanthosis nigricans

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Amer ican Manual of Examinat ion in Medicine (2CK)

6

Violaceous papules

with white stretch marks

Lichenoid lymphocyte

in1047297ltrate (band formation)

Destruction

of basal layer

Figure 30 Lymphocytic interface reaction (lichen planus)

Treatment

Mild forms are treated with topical cortcoids

Severe cases require oral cortcoids psoralens plus ultraviolet light of

the A wavelength (PUVA) or cyclosporine

Rosacea

Rosacea is a chronic disease of unknown pathogenesis characterized

by erythema and acneiform lesions on the face It aff ects middle aged

women (between 30 and 50 years of age) more

Rosacea etopathogenesis is unknown although there is involvement of

vasomotor lability infecton by Demodex folliculorum photo exposureand genetc predispositon

Clinical Presentation

Rosacea symptomatology comprises facial flushing episodes that end

up by provoking a persistent erythema telangiectasias and papulopus-

tular lesions without comedos Over tme ocular lesions and hyperpla-

sia of sof tssue may develop

Treatment

Avoid vasodilator stmuli

Mild cases require topical metronidazole or azelaic acid

Moderate cases need doxycycline or oral minocyclines

Severe cases are treated with oral isotretnoin at low doses

Pink Pityriasis

Gilbertrsquos pink pityriasis is an acute self-limitng dermatosis which main-

ly aff ects young adults It is of unknown origin although a viral etology

is suspected (there is some speculaton as to links with human herpes-

virus type 7)

Clinical Presentation

Erupton starts with an erythematous plaque between 2 and 5 cm of

diameter with a desquamatve central collaree ofen localized on the

trunk (heraldic mother patch Figure 31)

Figure 31 Pink pityriasis

Around a week later oval papules appear on the trunk and extremi-

tes These papules share similar characteristcs with the mother patch

though the first ones are smaller and distributed according to skin ten-

sion lines Pink pityriasis may be asymptomatc however it is some-

tmes linked to pruritus Lesions may last between 4 and 8 weeks and

disappear without leaving scars

Diagnosis and Treatment

Diagnosis is clinical Treatment is seldom needed and recommended

therapies in the past (PUVA erythromycin or oral antvirals) have not

shown clearly favorable results

Vitiligo

Vitligo is characterized by achromic macules by melanocyte destruc-

ton

Clinical Presentation

Vitligo shows achromic macules of chronic course and variable progres-

sion

Lesions are predominant on acral and periorificial areas They also show

the Koebner phenomenon

Patents may have markers of autoimmune diseases (ie antthyroid

antbodies and diabetes) but these diseases seldom manifest them-

selves

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Dermatology

Treatment

Localized lesions require topical cortcoids

Extensive or generalized lesions are treated with ultraviolet light B

(UVB) or PUVA

Strict solar photoprotecton is indispensable (Figure 32)

Figure 32 Vitiligo

47 Neoplasias

Seborrheic Keratosis

Seborrheic keratosis is the most frequent benign tumor in human be-

ings since it is part of cutaneous aging

Clinical Presentation

Seborrheic keratosis presents with hyperkeratosic papules with an oily

or velvet-like texture crests fissures and horny plugs on their surface

These papules are normally pigmented showing a brownish-black color

Treatment

No treatment is required as lesions do not become malignant

Seborrheic keratosis can be addressed with cureage or cryotherapy

Actinic keratosis

Actnic keratosis is the most common precancerous lesion and aff ects

almost a 100 of the populaton in sunny areas

Clinical Presentation

Actnic keratosis is characterized by erythematous and desquamatve

papules which are hyperkeratosic and rough on touch developing a

chronic course

Diagnosis

Diagnosis is clinical

Treatment

Treatment entails applicaton of topical 5-fluorouracil topical imiqui-

mod cryotherapy or surgery

If underlying carcinoma is suspected a biopsy must be performed to

rule out suspicion

Epidermoid Carcinoma

Epidermoid carcinoma is the second most frequent cutaneous tumor

Solar photo exposure is the main etological factor which is why epider-

moid carcinoma appears in zones of prolonged solar exposure like the

face Most carcinomas appear over premalignant lesions (actnic kera-

tosis and leukoplakia among others)

Clinical Presentation

Clinical presentaton reveals erythematous or erythematosquamous

plaques Over tme these plaques form papules and tumors which of-

ten become ulceratve and bleed

Diagnosis

Diagnosis is based on clinical suspicion and histopathological confirmaton

Treatment

Surgery with safety margins is the treatment of choice In carcinomas

in situ cryotherapy can be used as well as topical imiquimod electro-

coagulaton or CO2 laser techniques in destructon of tumors Radio-therapy may also be used in some cases

Basal Cellular Carcinoma

Basal cellular carcinoma is the most frequent cutaneous tumor Chronic so-

lar photo exposure is the main etological factor hence most of these car-

cinomas aff ect the facial zone in patents who are 40 years of age or older

Gorlinrsquos syndrome should be considered if multple basal cellular carci-

nomas are found in non photo exposed areas

Clinical Presentation

Basal cell carcinoma shows a pearly pink papule and superficial telan-

giectasias

It is localized over healthy skin and never aff ects mucosae

Treatment

Surgery is the treatment of choice Mohs surgery is performed in zones

where surrounding healthy tssue needs to be preserved Other alter-

natves are cryotherapy imiquimod electrocoagulaton radiotherapy

photodynamic therapy and intralesional interferon Prognosis is excel-

lent as growth is slow and metastasis exceptonal

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Amer ican Manual of Examinat ion in Medicine (2CK)

8

Melanoma

Melanoma is the most aggressive cutaneous tumor given its ability to

metastasize

Risk factors comprise solar photo exposure clear phototype the pres-

ence of dysplastc nevus or a high number of melanocytc nevi Fam-

ily history is quite important as some genetc mutatons determine a

higher risk of developing the disease

Clinical Forms

See Figure 33

Diagnosis

Precocious diagnosis is essental to perform precocious surgical extrpaton

The ABCDE criteria can help patents to see if they need to seek medical

consultaton (asymmetry of lesion uneven borders color and diameter

greater than 6 mm or abnormal evolut

on)

The Breslow index is the thickness of the lesion measured in millimeters

and is the main prognosis factor

Treatment

The base of treatment is precocious surgical extrpaton If the Breslow

index is less than 1 mm margins of 1 cm will be performed If Breslow

index is greater than 1 mm margins will be of 2 cm

For melanomas with a Breslow index greater than 1 mm the sentnel

ganglion must be located This is the first draining lymph node of the

territory where the tumor is localized If the ganglion is positve re-

gional lymphadenectomy will be performed along with interferon ad-ministraton (Figure 34)

In situ Extirpation 05 cm Follow-up

Breslow lt 1 mm Extirpation 1 cm Follow-up

Lymphadenectomy

Breslow gt 4 mm Interferon

Breslow ge 1 mm Extirpation 2 cm Sentinel ganglion

+

Figure 34 Melanoma treatment

Kaposirsquos sarcoma

Kaposirsquos sarcoma is the most common cutaneous tumor in HIV patents

Clinical presentation

Kaposirsquos sarcoma has a course with violaceous fusiform macules whichovertme may evolve into indurated nodules with blackberry appearance

This type of sarcoma has been linked to herpesvirus type 8 both in HIV

and seronegatve patents (Table 3)

EPIDERMAL KAPOSIrsquoS 983080HIV983081 CLASSIC KAPOSIrsquoS

Homosexual youth (95) The elderly

Diffuse and bilateral

(frequently in palate and face)

Unilateral plaques

(lower extremities)

Frequent mucosal and visceral involvement Not so frequent

middot Precocious lymphatic invasion

middot Aggressive

Not so precocious

Table 3 Differences between epidermal and classic Kaposirsquos sarcoma

Nodular melanoma

15

Middle-aged men

middot On healthy skin

middot Any zone

middot Sudden onset

middot Uniform black nodulemiddot Rapidly invasive (vertical growth without radial)middot Frequent ulceration and bleeding

Worst histological prognosis

Lentigo malignant melanoma

10

Elderly women

90 on facephotoexposedzones of aging skins(chronic exposure)

Spot that growsduring many years (gt 10)then progresses (nodule)

Better prognosis

Acral lentinginous melanoma

5ndash10 ( 60 black and Asian race)

Elderly men

middot Sole (ankle) handsmucosa ungual bed

middot No relation to photo exposure

middot Macule with mosaic appearance (spot that grows)middot Some amelanisticmiddot Bad prognosis due to late diagnosis

Melanoma of super1047297cial extension

70

Young women

middot 30 previous nervusmiddot Intermittent exposuremiddot Men back middot Women legs

More frequent

middot Macula with mosaic appearance in colors that grows 4-5 years and then in1047297ltrates (nodule)middot Metastasis 35 to 70

Figure 33 Clinical forms of malignant melanoma

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Dermatology

Diagnosis

Diagnosis relies on clinical suspicion and histopathological confirma-

ton

Treatment

Treatment of localized forms can include surgical extrpaton radiother-

apy or intralesional vinblastne

If the sarcoma is disseminated optons involve interferon or chemo-

therapy

Mycosis Fungoides

Mycosis fungoides is a T-cell lymphoma of low-grade malignancy Its

clinical course may be very slow and surpass 50 years Three stages are

clinically diff erentated

1 Eczematous or macular phase predominantly truncular erythema-

tous macules with years of evoluton They resemble a chromic ec-

zema Histology is unspecifi

c at this stage2 Infiltratve plaque phase infiltrated erythematous plaques appear

Histology is diagnostc at this stage A dermal infiltrate of atypical

lymphocytes band forms can be observed composed of CD+4 T

lymphocytes with cerebriform nuclei There is a marked epidermo-

tropism with the presence of clusters of intraepidermal lympho-

cytes called Pautrierrsquos microabscesses (Figure 35)

Figure 35 Mycosis fungoides Infiltrative plaque phase

3 Tumoral phase erythematous exophytc plaques start to appear

(tumors) with a tendency to ulceraton They can have a large size

Histology may become unspecific again as epidermotropism disap-

pears

In more advanced stages of the disease there is aff ectaton of extra-

cutaneous organs such as lymph nodes liver spleen lungs and bone

marrow Besides there may be blastc transformaton Other possible

complicaton is sepsis by Staphylococcus aureus

These three stages usually develop consecutvely nevertheless there

may patents whose debut starts directly with the tumoral stage

Remember

Microabscesses of mycosis fungoides are due to lymphocytes and are calledPautrierrsquos abscesses Psoriasis microabscesses result from neutrophils andare labeled as Munro-Sabouraud

Seacutezary Syndrome

Seacutezary syndrome can be considered as the leukemic phase of T-cell cu-

taneous lymphoma It is defined by the triad erythroderma (Figure 36

lymphadenopathies and the existence of more than 1000 Seacutezary cellsper milliliter in peripheral blood Seacutezary cells are atypical T- lymphocyte

with cerebriform nuclei

Very intense pruritus is characteristc For many authors Seacutezary syn-

drome is an aggressive clinical form and a bad prognosis of a mycosis

fungoides

Figure 36 Erythroderma due to Seacutezary syndrome

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Amer ican Manual of Examinat ion in Medicine (2CK)

2

bull Type II is mediated by IgM and IgG G Cytotoxic Hemolytc anemia

bull Type I is mediated by immune complexes Toxicodermas

bull Type IV is mediated by T lymphocytes (cellular) Contact derma-

tts

32 Atopic Dermatitis

Atopic dermatts is an inflammatory disorder of the skin with chronic

and recurring presentaton which aff ects 12 - 15 of children popula-

ton Atopic dermatts manifests itself by dry skin and pruritus

Patents have more risk of bacterial secondary infectons (S aureus) and

viral infectons (simple herpes virus SHV or mollusca)

There is a variety of triggering factors or factors that maintain eczema

outbreaks aeroallergens (dust mites) bacterial antgens (S aureus)

food (ovoalbumin) and psychological stress among others

Clinical Presentation

Clinical presentaton is usually in the form of greasy erythematous

and desquamatve papules or plaques on the scalp (cradle cap in the

cases of newborns) central area of the face sternal region axilla and

or groin In newborns this presentaton can be generalized causing

Leinerrsquos erythroderma desquamatvum in adults it is likely to be re-

lated to blepharits

Diff erental diagnosis includes atopic eczema in children but diff eren-

tal diagnosis in adults reveals subacute erythematous lupus or pink

pityriasis when the trunk is involved and inverted psoriasis when skin

folds are aff ected

Remember

Letterer-Siwe disease can cause lesions similar to infantile seborrheicdermatitis However unlike infantile seborrheic dermatitis Letterer-Siwedisease is associated with lymphadenopathies and hepatosplenomegaly

Remember

Impetigo key words (yellowish scabs) should not be mistaken for seborrheicdermatitis key words (yellowish scales)

Diagnosis

Atopic dermatts has a clinical diagnosis Patents may present with eo-

sinophilia and increase of IgE values

Treatment

It is essental for the patent to follow certain rules in his lifestyle This

means the patent must avoid wearing perfumed products (like cologne

and cream) being exposed to extreme temperatures the use of fabric

sofeners and carpets or fluff y toys (because of possible sensitzaton of

dust mites) Besides the patent needs to wear 100 coon clothing

Macule Vesicle

Wheal Fissure

Papule Ulcer

Nodule Cyst

Figure 2 Cutaneous elemental lesions

22 Histological Lesions

The following are histological lesions of the skin

bull Hyperkeratosis increase in the stratum corneum (warts and psoriasis)

bull Hypergranulosis granular layer thickening

bull Acanthosis thickening of the stratum spinosum

bull Acantholysis rupture of intercellular bridges of the stratum spino-

sum (typical of pemphigus)

bull Spongiosis intercellular intraepidermal edema (characteristc of eczema)

bull Ballooning intracellular edema (herpes)

bull Parakeratosis presence of nuclei in the stratum corneum (typical

of psoriasis)

bull Dyskeratosis abnormal keratnizaton of individual cells of the stra-

tum spinosum (typical of Darierrsquos disease)

bull Papillomatosis lengthening of dermal papillae (psoriasis)

Chapter 03

Allergic and

Immune-mediated

Diseases

31 Hypersensibility Reactions

bull Type I is mediated by IgE It is the most rapid Anaphylaxis asthma

and urtcaria

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Dermatology

Precocious treatment is of the utmost importance

Topic cortcoids are the first line treatment

It is worth to remember that prolonged use of topic cortcoids can have

local and systemic secondary side eff ects

The second line of treatment involves immunomodulators (tacrolimus

and pimecrolimus) These can be used in children older than 2 years of

age

For acute outbreaks oral cortcoids are used in short cycles and not as

maintenance To stop medicaton suddenly may cause a rebound eff ect

33 Contact Eczema

The appearance of contact eczema is immunologically mediated (type

IV hypersensit

vity) against foreign agents acquired by percutaneouspenetraton Contact eczema requires prior sensitzaton to allergen

It is more common in adults than in children

Diagnosis

Diagnosis is established with clinical records and epicutaneous tests of

contact These tests are performed once lesions have been resolved by

applying patches with allergens on healthy skin leaving them in contact

with the skin during 48 hours They are read afer 48 and 96 hours The

intensity of reacton is measured qualitatvely negatve weak positve

(erythema) strong positve (papules-vesicles) or extreme positve (blis-

ters)

Treatment

Avoid contact with the allergen

Treatment of acute eczema implies applicaton of topic poultce (zinc

sulphate sodium borate) and cortcoids if lesions are limited and sys-

tem poultce if lesions are generalized

34 Seborrheic Dermatitis

Seborrheic Dermatts is a quite frequent disease It aff ects 4 - 5 of the

populaton Etology of seborrheic dermatts is unknown although it

has been related to an abnormal immunological response to a fungus

called Pityrosporum ovale Seborrheic dermatts is more frequent and

intense when associated to neurological processes alcoholism and im-

munodeficiencies

Clinical Presentation

According to patentrsquos age

a Seborrheic dermatts in infants Yellowish scales on scalp known

as cradle cab

b Seborrheic dermatts in adult erythematous desquamatng papu-

les or plates in fat areas of the facial region and scalp

Diagnosis

Diagnosis of this conditon is clinical

TreatmentTreatment involves antfungals associated with topic cortcoids Sebor-

rheic dermatts on the scalp is usually linked to a keratolytc agent like

the salicylic acid

35 Psoriasis

Psoriasis is a chronic inflammatory disease of the skin that presents

with outbreaks Psoriasis aff ects 1-2 of the populaton and can ap-

pear at any age with a maximum of incidence between 20 and 30 yearsof age There is a family history in a third of the patents

Plates are the characteristc erythematous desquamatng lesions well

delimited with a superficial thick and white-pearl scale

The most frequent clinical form is vulgar psoriasis or psoriasis in plates

Lesions are localized at extensor surfaces (elbows and knees) and the

scalp The umbilical and the lumbosacral areas are ofen aff ected

Nail involvement is frequent and is most common with a pi ng ap-

pearance This form is lile specific The forms that combine hyperkera-

tosis and distal onycholysis are more specific Oil spot is the most char-

acteristc sign (Figure 3)

Figure 3 Generalized pustular psoriasis

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Amer ican Manual of Examinat ion in Medicine (2CK)

4

Diagnosis

Diagnosis of this conditon is generally clinical

If there is no certainty a biopsy must be done which will reveal hyper-

keratosis acanthosis and parakeratosis

There is an increase in polymorphonuclears (sterile abscesses) in the

stratum corneum which are called Munro abscesses

Treatment (Table 1)

For moderate severe forms of psoriasis that do not respond to clas-

sical systemic treatments (see table) They are monoclonal antbod-

ies against proinflammatory substances that are high in patents with

psoriasis [alpha tumor necrosis factor (TNF) interleukin IL 12 and

23] Some of them are infliximab adalimumab ustekinumab and

etanercept

36 Urticaria

Urtcaria is an immunologic and inflammatory reacton of the skin

against diverse etological factors Independently of the cause release

of histamine and other inflammatory mediators occurs which cause va-

sodilaton and increase in capillary permeability producing an edema in

superficial dermis Urtcarias are divided in acute and chronic urtcarias

depending on whether outbreaks persist more or less than six weeks

About 60 of acute urtcarias are idiopathic Chronic urtcarias show a

higher percentage

Urtcarias of known origin are usually due to infectons drugs or food

Clinical Presentation

Clinical presentaton is characterized by the appearance of pruritc wheals

that last less than 24 hours and can be accompanied with angioedema

TREATMENT USES SIDE EFFECTS AND CONTRAINDICATIONS

Topic Mild-moderatepsoriasis

(lt 25 body

surface)

Emollients (urea glycerin) Moisturizing

Keratolytics (salicylic acid) Eliminate excess of scales

Reductants (dithranol) Hyperkeratotic plaques middot Stain skin and clothing

middot Irritating

middot Acneiform eruptions

Corticoids middot Stable psoriasis

in plates

middot The most used

middot Tachyphylaxis

middot Percutaneous absorption

middot Possible new outbreak after stopping medication

middot Avoid prolonged treatment

Vitamin D analogues

(calcitriol calcipotriol and

tacalcitol)

Stable psoriasis in plates middot Irritating in face and skin folds

middot Hypercalcemia

Systemic Moderate-

severe psoriasis

(gt 25 body

surface)

Psoralens plus ultraviolet

light of the A wavelength(PUVA)

Combinable with topics

and retinoids (RePUVA)

middot Cutaneous aging and carcinogenesis

middot Erythroderma and xerosis middot Immunosuppression

middot Hepatitis by psoralens

middot Not in children pregnancy patients with hepatic or renal

insuffi ciency photosensitivity or cutaneous precancerosis

middot Cataracts

middot It accumulates in the crystalline during 24 h (sunglasses)

Retinoids (acitretin) middot Severe psoriasis

pustular

or erythrodermic

middot It is not usually used

in women in fertile age

(see side effects)

middot Cutaneous dryness (the most frequent)

middot Hypertriglyceridemia

middot Hypercholesterolemia

middot Increase in transaminases

middot Diffuse alopecia

middot Vertebral hyperostosis ligamentous calci1047297cations

middot Teratogenicity avoid pregnancy until 2 years after

1047297nishing treatment

middot Avoid in children and patients with hepatic or renal failure

Cyclosporine A middot In1047298ammatory severe

psoriasis resistant to

other treatments

middot Rapid action

middot Rebound effect

middot Nephrotoxicity

middot High blood pressure (HBP)

middot Epitheliomas and lymphomas

middot Hypertrichosis

middot Gingival hyperplasia

middot Hyperuricemia

Methotrexate middot Severe psoriasis

resistant to other

treatments

middot Psoriatic arthropathy

middot Hepatotoxicity

middot Myelosuppression

middot Teratogenicity until 3 months after ending treatment

middot Photosensitivity

Table 1 Psoriasis treatment

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Dermatology

Vasculits urtcaria should be ruled out when lesions last more than 24 hours

and are accompanied with systemic clinical symptoms (ie arthralgias)

Treatment

Oral anthistamine therapy is the treatment of choice

Systemic cortcoids for severe or refractory cases

Adrenalin for severe cases with anaphylaxis

37 Toxicodermas

Toxicodermas are quite variable cutaneous reactons that appear afer

drug administraton They are one of the most frequent side eff ects of

drugs The causatve agents for many toxicodermas stll remains un-

known either immunological or not and clinical presentaton does not

facilitate agent dist

nct

on

Morbilliform exanthem is the most frequent A morbilliform exanthem

is a generalized erupton formed by symmetric and confluent macules

and papules that usually start by the trunk

They can appear one or two weeks afer taking the drug

A morbilliform exanthem can be associated with fever pruritus and eo-

sinophilia

The most frequent are non steroid ant-inflammatories antbiotcs (sul-

phamides and penicillins) antepileptcs allopurinol and N acetyl-cystene

DiagnosisDiagnosis is according to clinical presentaton

Treatment

Treatment implies withdrawal of potentally responsible drug Topic or

systemic anthistamines and cortcoids are given according to the extent

of symptoms (Figure 4)

Figure 4 Morbilliform exanthem due to amoxicillin

38 Multiform Erythema

Stevens-Johnson Syndrome

and Toxic Epidermal Necrolysis

Multform erythemas (ME) are of undetermined etopathogenesis

regarded as a cutaneous reacton against a diversity of stmuli Their

histologies show similarites what leads to consideraton of a common

pathogenesis

Clinical Presentation

Three diff erent groups have been described although many a tme their

clinical symptoms overlap

bull Erythema multforme minor is the most frequent with around 80

of the cases It usually precedes a symptomatc infecton by simple

herpes virus (60) or subclinical infecton about 15 days before

Erythema multforme minor manifests itself on extensor surfaces

at hands elbows and feet as a symmetric erupton of erythema-

tous edematous lesions with target-shape (herpes iris of Batemanor rosee-paerned lesion) with a violaceous sometmes bullous

center (Figure 5)

Mucosal aff ectaton is rare with small erosions in oral mucosa Erythe-

ma multforme minor tends to recurrence with subsequent outbreaks

of herpetc lesions

Figure 5 Erythema multiforme minor Herpes iris of Bateman

bull Erythema mult

forme major or Stevens-Johnson syndrome is therarest It normally has a prodromal period of untl 14 days with fe-

ver cough cephalea arthralgias and other symptoms Subsequent

to the prodromal period erythematous edematous plates appear

which are more extensive with a tendency to form blisters and

greater mucosal erosions (mouth genitals pharynx larynx and

conjunctve Figure 6) Systemic symptoms are normal and do not

tend to recurrence

The most frequent etological factors are drugs [sulphamides non

steroid ant-inflammatory drugs (NSAIDs) antconvulsants and an-

tbiotcs in decreasing order) Infectous agents have been also in-

volved mainly mycoplasma pneumoniae

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6

Figure 6 Exudative erythema multiforme major

bull Toxic epidermal necrolysis (TEN) many authors consider it the

most severe form of erythema multforme major arguing the same

pharmacological agents A morbilliform rash appears which is rap-idly confluent comprising almost the entre skin surface with flaccid

blisters that leave wide areas of denuded skin Involvement of sev-

eral mucosae is constant

Complicatons ofen occur (pneumonia digestve hemorrhage re-

nal failure and hemodynamic shock) with mortality rates close to

25 In children it must be performed a diff erental diagnosis with

staphylococcal scalded skin syndrome which does not aff ect mu-

cosae

Remember

Diseases that have the Nikolsky sign are TEN staphylococcal scalded skinsyndrome (SSSS) and pemphigus In TEN the whole epidermis comes off(bad prognosis) while in SSSS epidermal detachment occurs at the granularlayer

Histopathology

It must be highlighted the eff acement of dermoepidermal juncton by a

lymphohistocytc infiltrate and vacuolar degeneraton of the baseline lay-

er with necrotc keratnocytes In TEN keratnocytes necrosis is massive

Treatment

In ME minor only symptomat

c treatment is prescribed with topiccortcoids and oral anthistamines Treatment for herpes simplex virus

(HSV) infecton is useful to prevent ME lesions if patent is in the inital

stage of the viral infecton

ME major requires treatment of the underlying infecton or withdrawal

of implied drug and support measures The use of oral steroids accord-

ing to the patentrsquos general state is under discussion

A patent with TEN requires to be admied at the burn treatment room

with monitoring of hematocrit hydroelectrolytc balance and antbiotc

prophylaxis and support measures It is controversial the use of system-

ic cortcoids immunoglobulins andor cyclosporine

39 Erythema Nodosum

Erythema nodosum is the most frequent panniculits Painful erythema-

tous nodules occur mainly in the anterior side of legs with a self-limit-

ing course and predominantly aff ectng young women (Figure 7)

Figure 7 Erythema nodosum

They heal without leaving a scar within a period of four to six weeks

Erythema nodosum may be accompanied with fever deterioraton of

the general state and arthralgias

Patents with erythema nodosum may have a false positve VDRL

Etiology

This conditon is thought to be an immunological response triggered by

multple and diff erent stmuli bacterial fungal and viral infectons sys-temic diseases (sarcoidosis inflammatory intestnal disease Behcetrsquos

syndrome) neoplasias (lymphomas and leukemias) and drugs (oral

contraceptves sulphamides bromides and iodines)

Diagnosis

Erythema nodosum requires a deep biopsy to reveal septal panniculits

without vasculits

Complementary tests can be performed to rule out systemic involvement

for example chest X-ray Mantoux and antstreptolysin O antbody (ASLO)

Treatment Treatment entails eliminatng underlying cause if found then rest and

ant-inflammatories

310 Bullous Pemphigoid

and Pemphigus Vulgaris

See Table 2 and Figures 8 9 10 and 11

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Dermatology

Intercellular

substance ac

middot Pemphigus

Lineal

storage

in lucid

layer

-

Anti-Collagen Ac

Lucid

layer

Thick

layer

Basal

sublayer

Granular

storage

in papillary

dermis

middot Pemphigoid bullousmiddot Herpes gestationis

middot Acquired blistering epidermolysis

middot Dermatitis herpetiformis

Figure 8 Key points for histological diagnosis

of autoimmune blistering diseases

Figure 9 Pemphigus vulgaris

Figure 10 Pemphigus vulgaris with oral mucosa involvement with

erosions

Figure 11 Pemphigoid bullous Tense blisters No sign of Nikolsky

PEMPHIGUS VULGARISGENERALLY

IDIOPATHICHERPES GESTATIONIS

DERMATITIS

HERPETIFORMIS

Clinical presentation middot 40-50 years of age

middot They usually affect mucosae

middot No pruritus

middot Flaccid blister

middot Nikolsky

middot Elderly

middot Sometimes mucosae

middot With pruritus

middot Tense blister

middot No Nikolsky

middot Pregnant women

middot No mucosae

middot With pruritus

middot Herpetiform

middot No Nikolsky

middot 15-35 years of age

middot No mucosae

middot With pruritus

middot Herpetiform

middot No NikolskyDirect immuno1047298uorescence (DIF) IgG IgG IgG IgA

Histology middot INTRAepidermal blister

middot There is acantholysis

middot SUBepidermal blister

middot There are eosinophils

middot SUBepidermal blister

middot There are eosinophils

middot SUBepidermal blister

middot Neutrophils in dermis

Treatment Corticoids at high doses

immunosuppressants rituximab

and immunoglobulins

Corticoids Corticoids Diet +- dapsone

Remember Mortality rate 10 The most frequent Relapse if new

pregnancy

Associated to enteropathy

by gluten 90

Table 2 Autoimmune blistering diseases

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8

Chapter 04

Infectious Diseases

41 Viral Infections

Simple Herpes

Infection by Simple Herpes Virus

There are two types of simple herpes (Figure 12)

bull Type I is responsible for most extragenital herpes and 20 of the

genital herpes

bull Type II causes genital herpes and a small percentage of extragenital

herpes

Figure 12 Herpes simplex

Contagion is produced by direct contact though the carrier may be as-

ymptomatc Afer primary infecton virus remains silent in the sensi-

tve porton of cranial or spinal ganglia Immunosuppressed patents

endure the greatest severity of this conditon

Clinical Presentation

bull Extragenital simple herpes recurring orofacial herpes simplex is

the most frequent Most primary infect

ons are asymptomat

c Only5 manifest themselves in the form of herpetc gingivostomatts a

profile characterized by oral ulcers with cervical adenopathy and af-

fectaton of the patentrsquos general state (Figure 13) During relapses

clinical symptoms are milder with cluster vesicles on an erythema-

tous base Some factors facilitate relapses trauma sunlight cold

stress fever and the menstrual cycle

bull Genital simple herpes is the most common cause of genital ulcers

afer trauma Primary infecton is usually symptomatc and occurs

between 3 to 14 days afer sexual contact It causes clustered ulcers

in the balanopreputal sulcus or in the prepuce with painful inguinal

adenopathy Relapses are less severe than primary infecton and oc-

cur more frequently when genital herpes is due to HSV type II

Figure 13 Herpetic gingivostomatitis

bull Eczema herpetcum or Kaposi varicelliform erupton dissemina-

ton of herpetc infecton on pre-existng dermatosis (above all

atopic dermatt

s) bull Neonatal herpes is due to intrapartum contagion of HSV-II with

neurological involvement general deterioraton and skin vesicles or

ulcers

bull Other clinical forms are herpes gladiatorum herpetc whitlow and

keratoconjunctvits

Diagnosis

Diagnosis of this conditon is mainly clinical Virological culture is the

most reliable method of confirmaton The extent of a smear of the le-

sions (Tzanck cytodiagnosis) allows visualizaton of multnucleated cells

and intranuclear inclusions which become evident through histological

study

Treatment

Mild forms do not need treatment Treatment is required in the follow-

ing cases

bull Primary infecton

bull Severe or frequent relapses if they aff ect life quality

bull Complicatons like erythema multforme and eczema herpetcum

Drug of choice is oral acyclovir and its derivatves (valacyclovir famci-

clovir) Topic antvirals have not proven useful favoring maceraton of

lesions and thus over infecton It is not infrequent that topic antvirals

cause allergic contact dermatts due to hypersensitvity

Varicella-Zoster Virus

A primary infecton gives way to varicella (see Pediatrics secton) Afer

varicella the virus remains latent in the sensitve porton of the neural

ganglia and when relapse occurs it leads to zoster herpes

bull Varicella the following symptoms appear afer 15 days of incubaton

fever cephalea pruritus and polymorphic lesions in diff erent stages

macules papules vesicles (Figure 14) ulcers and scabs (starry sky

appearance) Mucosal (ulcers) and scalp involvement is characteristc

Manipulaton can leave scars Bacterial over infecton of lesions is the

most usual complicaton About 20 of adults suff er from varicella

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Dermatology

pneumonia radiologically demonstrable but clinical symptomatology is

only present in around 4 of the cases

Figure 14 Typical vesicles in patients with varicella

bull Zoster herpes thoracic zoster herpes is the most usual It sel-

dom occurs more than once throughout a personrsquos lifetime

It is characterized by vesicles on pre-existing erythema with

metameric distribution and lateral extension The most com-

mon complication is post herpetic neuralgia more frequent in

advanced age Carbamazepine or tricyclic antidepressants (Fig-

ure 15)

Figure 15 Zoster herpes

Special Clinical Forms

Special clinical forms are as follow

bull Ramsay-Hunt syndrome aff ectaton of geniculate ganglion of the

facial nerve

It produces vesicles in the outer ear external auditory canal and

pharynx homolateral facial paralysis deafness and vertgo

bull Ophthalmic involvement can result in severe keratts and requires ur-

gent referral to an ophthalmologist Suspicion should exist on patents

that present herpetc lesions on the tp of the nose) (Hutchinsonrsquos sign)

bull Disseminated zoster herpes several dermatomes are aff ected bilat-

erally Ramsay-Hunt syndrome is characteristc in the immunosup-

pressed

Remember

Affectation of the nose tip makes it necessary for ophthalmologicalexamination because the nose tip is innervated by the same nerve thatinnervates the cornea (1047297rst branch of the trigeminal nerve)

Treatment

Varicella without complicatons is treated symptomatcally Antvirals

are reserved for severe or complicated forms There is a commercial-

ized vaccine of live virus whose indicatons are stll under discussion

Zoster herpes must be treated with antvirals when detected during the

first 48-72 hours and aff ectng patents with

bull Immunosuppression

bull Age above 55

Special clinical forms previously cited

Drugs to be used are oral acyclovir and its derivatves (valacyclovir and

famciclovir) They accelerate the cure of lesions and decrease the inten-

sity of post herpetc neuralgia Patents with renal failure need a dose

adjustment as acyclovir is nephrotoxic These patents are adminis-

tered brivudine in a single daily dose

Molluscum ContagiosumDome shaped pink papules with central umbilicaton (Figure 16) Mol-

luscum contagiosum is typical of children that go to swimming pools It

is also present in the genital zone afer sexual contact and in immuno-

suppressed patents It is caused by Poxvirus

Figure 16 Molluscum contagiosum

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Amer ican Manual of Examinat ion in Medicine (2CK)

0

Lesions are asymptomatc

Diagnosis

Diagnosis is clinical Histology reveals characteristc inclusion bodies

Treatment

Lesions can resolve spontaneously

Cureage cryotherapy or local trichloroacetc acid are eff ectve meth-

ods to destroy lesions

Warts

Human papillomavirus can cause verruca vulgaris palmoplantar and

flat warts and condyloma accuminata Human papillomavirus is the

most frequent sexual transmied disease

Some subtypes of this virus (16 18) are of high risk and can cause epi-

dermoid carcinomas

Direct contact is the mechanism of contagion

Diagnosis

Diagnosis of this conditon is clinical

Staining with acetc acid can help visualize mucosal lesions

Treatment

Genital warts are treated with cryotherapy podophyllotoxin trichloro-

acetc acid imiquimod and 5-fluorouracil

Cervical lesions should be monitored by cytology and biopsy whenever

necessary to rule out cervical cancer (Figures 17 and 18)

Figure 17 Warts in HIV patient

Figure 18 Condyloma accuminata

42 Bacterial Infections

Impetigo

Impetgo is a very contagious superficial infecton without systemic re-

percussion and normally mixed etology by Gram positve cocci (strep-

tococci and staphylococci) Classically the most frequent accepted

cause was Streptococcus pyogenes However at present Staphylococcus

aureus stands out as the predominant cause

The most typical form is impetgo contagiosa (Figure 19) character-

ized by honey-colored (meliceric) scabs which normally appear on

the face and other exposed areas It is typical of children Although

infrequent poststreptococcal glomerulonephrits is a dreadful com-

plicaton

Figure 19 Impetigo contagiosa

On the contrary rheumatc fever shows no relaton to cutaneous strep-

tococcal infectons but only with pharyngeal infectons

There are other less habitual forms called bullous impetgo exclusively

of staphylococcal origin Clinical presentaton involves the presence of

blisters and erosions on the aff ected skin as a consequence of the epi-

dermolytc toxins that these bacteria contain Impetgo is treated with

topical mupirocin penicillin or oral fusidic acid

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Dermatology

Cellulitis

Cellulits is an infecton that aff ects deep dermis and subcutaneous cel-

lular tssues normally caused by streptococci (Streptococcus pyogenes

or of group A)

Community methicillin-resistant S aureus (CMRSA) is a triggering agent

that is becoming more and more frequent

Most common risk factors are diabetes chronic venous insuffi ciency

and immunosuppression

Clinical Presentation

Cellulits presents with erythematous plaques that are ill-defined pain-

ful and hot It is usually accompanied with fever and chills

Diagnosis

Diagnosis is clinical If there is an open door a culture of this area may

help see the source germ and resistance to ant

biot

cs

It is important to rule out abscesses osteomyelits and necrotzing fas-

ciits

If bacteremia is suspected blood cultures need to be performed

Treatment

Treatment implies oral antbiotcs for 7-10 days to cover Gram positve

cocci They are intravenously administered in case of lack of response

to oral treatment involvement of hands or periorbital zone diabetes or

extremes of age

Necrotizing FasciitisNecrotzing fasciits is a deep infecton up to muscular fascia that pro-

duces very intense pain and subsequent anesthesia

In 10 of the cases cellulits is due to an infecton by S pyogenes In the

remaining cases it occurs by a polymicrobial infecton caused by aerobes

and anaerobes including S aureus E coli and Clostridium perfringens

There may be prior history of trauma or surgery

Clinical Presentation

Clinical presentat

on involves pain of sudden onset and edema on theaff ected zone Pain may progress to anesthesia There appears subse-

quent erythema that progresses rapidly into necrosis

Characteristc clinical signs are tssue necrosis blisters intense pain

and gas producton

Diagnosis

Diagnosis is clinical and requires image testng X-rays or a computed

tomography CT

A biopsy of the border of the lesion helps achieve diagnosis

Treatment

Treatment entails precocious surgical debridement It is a surgical emer-

gency In additon to surgery broad-spectrum antbiotherapy will be

needed

Folliculitis

Folliculits is an infecton and inflammaton of one or several follicles

caused mainly by staphylococci

Clinical Presentation

Folliculits shows pustules with follicular distributon

When the infecton is deeper it is called furuncle

If several furuncles are infected a fluctuatng erythematous plaque forms

containing several points of suppuraton This plaque is labeled as anthrax

Diabet

c and immunosuppressed pat

ents are at higher risk

Characteristics of Folliculitis

1 Hot tub or swimming pool folliculits caused by Pseudomonas aeru-

ginosa

2 HIV associated pruritc folliculits or eosinophilic folliculits

Treatment

In mild cases treatment of choice comprises antseptcs and topic an-

tbiotcs

In more severe cases treatment of choice requires oral antbiotcs

Large sized lesions must be drained and a microbiological culture must be

performed to rule out methicillin-resistant Staphylococcus aureus MRSA

Acne Vulgaris

Acne is an inflammatory disease of the pilosebaceous follicle as a con-

sequence of an alteraton in follicular keratnizaton It aff ects adoles-

cents and young adults

Etology is multfactorial alteraton of keratnizaton of follicular infun-

dibulum quanttatve and qualitatve alteraton of sebum producton in

the sebaceous gland and alteratons of bacterial microflora (increase in

quant

ty of P acnes)

Aggravatng factors are stress androgenic oral contraceptves and the

use of cosmetc products that are not oil-free

Clinical Presentation

A comedo is the inital lesion which can be closed (whitehead) or open

(blackhead) and it evolves into inflammatory lesions that listed in as-

cending order of severity are papules pustules nodules and cysts

Lesions progress and leave scars Scars can be increased if lesions are

manipulated

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Amer ican Manual of Examinat ion in Medicine (2CK)

2

Diff erent lesions habitually combine simultaneously so acne becomes

polymorphic It is located in sebaceous areas face back shoulders and

the center thoracic region

Diagnosis

Diagnosis is clinical

Treatment

bull Comedonal acne is treated with topic retnoids and benzoyl peroxide

bull Inflammatory acne treatment requires benzoyl peroxide combined

with topic antbiotcs (erythromycin and clindamycin) Systemic

antbiotc treatment with oral tetracyclines will be prescribed if re-

sponse to topic antbiotc treatment fails

bull Severe nodular cystc acne treatment involves the use of isotret-

noin (13-cis-retnoic acid) It is a derivatve of vitamin A Isotretnoin

produces atrophy in the sebaceous gland and regulates keratniza-

ton The most frequent side eff ect is cutaneous and mucosal xero-

sis Triglycerides cholesterol and transaminases should be moni-

tored as their values may increasebull It can be associated with depression

bull It is teratogenic so pregnancy should be avoided during treatment

and untl a month afer treatment

Pilonidal Cysts

Pilonidal cysts are abscesses in the sacrococcygeal region

This type of cysts has predominance in men between 20 and 40 years

of age It is believed that repeated trauma on the aff ected area favors

their appearance

Clinical Presentation

Pilonidal cysts present with an indurated lesion that is fluctuatng hot

painful but non-adherent to deep planes in the sacrococcygeal region

Pilonidal cysts may or may not be associated to cellulits and purulent drain-

age

Diagnosis

Diagnosis is clinical and anal or perirectal abscesses should be dismissed

Treatment

Treatment implies an incision and surgical drainage

On some occasions a general surgery is required

43 Fungal Infections

Pityriasis Versicolor

Versicolor pityriasis is caused by commensal yeast called Pityrosporum

ovale which transforms into its pathogen form (Malassezia furfur) It

especially aff ects young patents (15 - 45 years of age) but it is rare

in childhood and advanced age Versicolor pityriasis relates to heat

humidity and sebaceous hypersecreton It is characterized by the ap-

pearance of hyperchromic or hypochromic macules that desquamate

on scratching (nail sign) if infecton is actve Macules usually appear on

the center thoracic region and on the back that is to say on seborrheic

zones Relapses are habitual despite treatment

Diagnosis

Diagnosis is normally clinical To that purpose the following serve as

support

bull Woodrsquos lamp emits yellow-orange fluorescence

bull Potassium hydroxide (KOH) test filaments and round elements can

be observed (ldquospaghe and meatball appearancerdquo Figure 20)

Treatment

Treatment is performed with topical azoles Oral administraton applies

for extensive cases or immunosuppressed patents Diff erental diagno-

sis includes pink pityriasis and eczemas (Figure 21)

Figure 20 Versicolor pityriasis Histological cut

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Dermatology

Figure 21 Versicolor pityriasis

Candidiasis

The most common triggering agent is Candida albicans It is normally sapro-

phyt

c although under certain condit

ons candidiasis may become patho-genic (immunosuppression humidity pregnancy and contraceptves)

Clinical Forms

bull Intertrigo erythematous plaque in cutaneous folds Atrophy and

fissures are typically deep in the skin fold as well as satellite and

peripheral lesions (papules andor pustules)

bull Mucosa involvement may cause diverse symptomatology like vul-

vovaginits glossits and white papules in the anterior region of the

oral mucosa Candidal balanits is characterized by the presence of

punctform erosions and pustules on gland and balanopreputal

sulcus Candidal balanits ofen appears afer sexual intercourse or

afer oral antbiotc intake

Remember

Almost a 100 of HIV patients suffer from muguet throughout their diseasecourse

bull Candidiasis of nail fold is usually associated with periungual inflam-

maton (perionixis) and inital proximal aff ectaton which diff erent-

ates it from tnea unguium (Figure 22)

Figure 22 Candidiasis of nail fold

Treatment

Oral Candidiasis fluconazole or nystatn

Candidiasis of the skin (intertrigo) apply topical antfungal medicaton

and keep zone clean and dry

Dermatophytosis or TineasDermatophyte infectons aff ect the skin and keratnized structures like

hair and nails (there is no mucosa involvement) Clinical diagnosis is

achieved afer performing a culture Woodrsquos lamp test normally turns

out to be negatve In general Trichophyton dermatophyte rubrum is

the most frequent dermatophyte

Non Inflammatory Tineas

Non inflammatory tneas do not produce irreversible scarring alope-

cia while inflammatory forms do Tineas are treated with azoles de-

rivatves

The types of tnea are the following

bull Ringworm of the scalp ( t nea capi t s or t nea tonsurans) is charac-

teristc of childhood It presents with alopecic plaques broken hair

and desquamaton Infectons tend to resolve spontaneously with-

out leaving scars at the onset

of puberty

bull Ringworm of the body (herpes

circinatus or t nea corporis) are

erythematous desquamatve

plaques (with more actve bor-

ders) which are also circinate

and normally pruritc (Figure

23) Plaques grow eccentrically

with less actvity in the centerand more in the borders

bull Ringworm of the foot ( t nea

pedis) the most frequent is the

ldquoathlete footrdquo with desquama-

ton in interdigital spaces

bull Tinea incognito refers to tnea

wrongly treated with cort-

coids what makes diagnosis

diffi cult as the lesion has been modified Figure 24)

Figure 24 Tinea incognito secondary to treatment with topical steroids

Figure 23 Herpes circinatus

(tinea corpis)

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Amer ican Manual of Examinat ion in Medicine (2CK)

4

bull Ringworm of the groin (t nea cruris or eczema marginatum von

hebra) formed by erythematous desquamatve plaque with more

actve borders (Figure 25)

Figure 25 Ringworm of the groin (tinea cruris)

bull Tinea unguium subungualhyperkeratosis with onychol-

ysis but without perionixis

(Figure 26)

Diagnosis

Clinical diagnosis is reached afer

performing a culture

Treatment

Treatment involves topical an-

tfungal medicaton in localized

areas

Oral antfungal medicaton is used in extensive forms nail fold or scalp

involvement

44 Parasitic Infections

Pediculosis

Pediculosis is transmied by direct contact or by contact with fomites

which release toxins that produce intense pruritus

Clinical Presentation

Pediculosis capi t s intense pruritus predominant in retroauricular and

occipital regions occasionally with excoriatons and impetginizaton

secondary to excoriatons

Pediculosis corporis intense pruritus in patents with poor hygiene or

who live in overcrowded conditons

Pediculosis pubis genital and pubic pruritus Brownish-grey macules

called maculae ceruleae are typical on underwear and skin These pig-

mentatons appear as a result of a reducton in hemoglobin by a para-

site enzyme

Diagnosis

Diagnosis is clinical and by direct visualizaton

Treatment

Pediculosis is treated with malathion lindane or topical permethrin

Scabies

Scabies is originated by an acarus known as Sarcoptes scabiei It has an

incubaton period of 1 month

Clinical Presentation

Scabies produces generalized pruritus more intense at night The pa-

tent usually catches the infestaton which is passed to the patentrsquos

relat

ves It is common tofi

nd that a recent trip to a tropical country hasbeen made Lesions appear between the fingers (Figure 27) in wrists

feet genitalia mammary areola and axilla but back and face are usu-

ally spared The most specific lesion is the acarine burrow in whose less

scaly end the advancing zone the mite lies Nodules are frequent in

axilla and genitals (nodular scabies)

bull Norwegian scabies is typical of the immunosuppressed Patents

present with generalized hyperkeratosis and scabs Norwegian sca-

bies produce lile pruritus but it is very contagious because there

are many acari

bull Nodular scabies involves the persistence of pruritc nodules despite

treatment Lesions usually appear in axilla and genitalia Pruritus is

due to a hypersensitvity phenomenon because of the acarus al-

ready dead Nodular scabies is treated with cortcoids

Figure 27 Scabies Acarine burrow

Treatment

bull Permethrin cream at 5 is the treatment of choice It is lile toxic

so it can be used in children and pregnant women

bull Topical lindane at 1 irritates and is neurotoxic therefore it is con-

traindicated in pregnant women and children

bull Oral ivermectn is utlized in cases of resistance to prior treatments

There is stll lile experience as to its use but in a first instance a

Figure 26 Tinea unguium

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Dermatology

single dose would be enough to cure scabies (already used by vet-

erinarians)

45 Ischemia

Decubitus Ulcers

Decubitus ulcers are the result of ischemic necrosis by contnuous pres-

sure on an area which restricts microcirculaton in that zone

Clinical Presentation

Decubitus ulcers are present in patents in bed with scarce mobilizaton

It is favored by bone prominences and lack of fat tssue If sensitvity

decreases there is more risk of formaton of decubitus ulcers

Diagnosis

Diagnosis is achieved based on medical records and clinical presentaton

Treatment

Preventon is of the utmost importance as well as frequent mobiliza-

ton of the patent in bed

Once ulcers have been established hydrocolloid dressings are used for

healing but sometmes surgical debridement is necessary

Gangrene

Gangrene means tssue necrosis

There are three types dry gangrene wet gangrene and gas gangrene

Clinical Presentation

Dry gangrene is due to ischemia generally secondary to atherosclero-

sis Clinical presentaton involves pain cold and paleness of extremi-

tes Once tssue is established it turns bluish-black in color and dry

Wet gangrene is owing to bacterial flora Tissue presents with an edem-

atous appearance either with blisters or pus

Gas gangrene caused by C perfringens It is normally located on re-

cent surgery Bacteria precociously destroyt

ssue producing gas It is amedical emergency

Diagnosis

Clinical diagnosis is obtained by microbiological culture

Treatment

Treatment requires surgical debridement with amputaton if necessary

and associaton of broad spectrum antbiotherapy

Gas gangrene is treated with hyperbaric oxygen

46 Miscellaneous

Acanthosis Nigricans

Acanthosis nigricans are vel-

vet-like papillomatous brown

plaques in neck axilla and groin

folds (Figure 28)

It is associated with diabetes

mellitus Cushingrsquos disease poly-

cystc ovarian syndrome and

obesity

The malignant form of acantho-

sis nigricans is a paraneoplastc

syndrome that diff erentates

from the benign form because

the laer has mucosal and pal-

moplantar involvement

Lichen Planus

Lichen planus is an inflammatory idiopathic disease that equally aff ects

both genders with higher frequency in middle age

Lichen planus has been related to diverse drugs like gold salts

anti-malarial medication and thiazides It has been also linked to

hepatitis C virus infection however this association is currently

doubtful

Clinical Presentation

Lichen planus presents with red-violaceous polygonal flat papulesquite pruritc which localizes on the flexor side of wrists forearms an-

kles and lumbosacral and flank regions On its surface a whitsh retcu-

late can be observed (Wickhamrsquos striae) About 60 - 70 of the cases

present with lesions in oral and genital mucosa oral which appear as

whitsh retculated lesions (Figures 29 and 30)

Figure 29 Lichen planus of oral mucosa with typical whitish

reticulate

Figure 28 Acanthosis nigricans

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Amer ican Manual of Examinat ion in Medicine (2CK)

6

Violaceous papules

with white stretch marks

Lichenoid lymphocyte

in1047297ltrate (band formation)

Destruction

of basal layer

Figure 30 Lymphocytic interface reaction (lichen planus)

Treatment

Mild forms are treated with topical cortcoids

Severe cases require oral cortcoids psoralens plus ultraviolet light of

the A wavelength (PUVA) or cyclosporine

Rosacea

Rosacea is a chronic disease of unknown pathogenesis characterized

by erythema and acneiform lesions on the face It aff ects middle aged

women (between 30 and 50 years of age) more

Rosacea etopathogenesis is unknown although there is involvement of

vasomotor lability infecton by Demodex folliculorum photo exposureand genetc predispositon

Clinical Presentation

Rosacea symptomatology comprises facial flushing episodes that end

up by provoking a persistent erythema telangiectasias and papulopus-

tular lesions without comedos Over tme ocular lesions and hyperpla-

sia of sof tssue may develop

Treatment

Avoid vasodilator stmuli

Mild cases require topical metronidazole or azelaic acid

Moderate cases need doxycycline or oral minocyclines

Severe cases are treated with oral isotretnoin at low doses

Pink Pityriasis

Gilbertrsquos pink pityriasis is an acute self-limitng dermatosis which main-

ly aff ects young adults It is of unknown origin although a viral etology

is suspected (there is some speculaton as to links with human herpes-

virus type 7)

Clinical Presentation

Erupton starts with an erythematous plaque between 2 and 5 cm of

diameter with a desquamatve central collaree ofen localized on the

trunk (heraldic mother patch Figure 31)

Figure 31 Pink pityriasis

Around a week later oval papules appear on the trunk and extremi-

tes These papules share similar characteristcs with the mother patch

though the first ones are smaller and distributed according to skin ten-

sion lines Pink pityriasis may be asymptomatc however it is some-

tmes linked to pruritus Lesions may last between 4 and 8 weeks and

disappear without leaving scars

Diagnosis and Treatment

Diagnosis is clinical Treatment is seldom needed and recommended

therapies in the past (PUVA erythromycin or oral antvirals) have not

shown clearly favorable results

Vitiligo

Vitligo is characterized by achromic macules by melanocyte destruc-

ton

Clinical Presentation

Vitligo shows achromic macules of chronic course and variable progres-

sion

Lesions are predominant on acral and periorificial areas They also show

the Koebner phenomenon

Patents may have markers of autoimmune diseases (ie antthyroid

antbodies and diabetes) but these diseases seldom manifest them-

selves

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Dermatology

Treatment

Localized lesions require topical cortcoids

Extensive or generalized lesions are treated with ultraviolet light B

(UVB) or PUVA

Strict solar photoprotecton is indispensable (Figure 32)

Figure 32 Vitiligo

47 Neoplasias

Seborrheic Keratosis

Seborrheic keratosis is the most frequent benign tumor in human be-

ings since it is part of cutaneous aging

Clinical Presentation

Seborrheic keratosis presents with hyperkeratosic papules with an oily

or velvet-like texture crests fissures and horny plugs on their surface

These papules are normally pigmented showing a brownish-black color

Treatment

No treatment is required as lesions do not become malignant

Seborrheic keratosis can be addressed with cureage or cryotherapy

Actinic keratosis

Actnic keratosis is the most common precancerous lesion and aff ects

almost a 100 of the populaton in sunny areas

Clinical Presentation

Actnic keratosis is characterized by erythematous and desquamatve

papules which are hyperkeratosic and rough on touch developing a

chronic course

Diagnosis

Diagnosis is clinical

Treatment

Treatment entails applicaton of topical 5-fluorouracil topical imiqui-

mod cryotherapy or surgery

If underlying carcinoma is suspected a biopsy must be performed to

rule out suspicion

Epidermoid Carcinoma

Epidermoid carcinoma is the second most frequent cutaneous tumor

Solar photo exposure is the main etological factor which is why epider-

moid carcinoma appears in zones of prolonged solar exposure like the

face Most carcinomas appear over premalignant lesions (actnic kera-

tosis and leukoplakia among others)

Clinical Presentation

Clinical presentaton reveals erythematous or erythematosquamous

plaques Over tme these plaques form papules and tumors which of-

ten become ulceratve and bleed

Diagnosis

Diagnosis is based on clinical suspicion and histopathological confirmaton

Treatment

Surgery with safety margins is the treatment of choice In carcinomas

in situ cryotherapy can be used as well as topical imiquimod electro-

coagulaton or CO2 laser techniques in destructon of tumors Radio-therapy may also be used in some cases

Basal Cellular Carcinoma

Basal cellular carcinoma is the most frequent cutaneous tumor Chronic so-

lar photo exposure is the main etological factor hence most of these car-

cinomas aff ect the facial zone in patents who are 40 years of age or older

Gorlinrsquos syndrome should be considered if multple basal cellular carci-

nomas are found in non photo exposed areas

Clinical Presentation

Basal cell carcinoma shows a pearly pink papule and superficial telan-

giectasias

It is localized over healthy skin and never aff ects mucosae

Treatment

Surgery is the treatment of choice Mohs surgery is performed in zones

where surrounding healthy tssue needs to be preserved Other alter-

natves are cryotherapy imiquimod electrocoagulaton radiotherapy

photodynamic therapy and intralesional interferon Prognosis is excel-

lent as growth is slow and metastasis exceptonal

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Amer ican Manual of Examinat ion in Medicine (2CK)

8

Melanoma

Melanoma is the most aggressive cutaneous tumor given its ability to

metastasize

Risk factors comprise solar photo exposure clear phototype the pres-

ence of dysplastc nevus or a high number of melanocytc nevi Fam-

ily history is quite important as some genetc mutatons determine a

higher risk of developing the disease

Clinical Forms

See Figure 33

Diagnosis

Precocious diagnosis is essental to perform precocious surgical extrpaton

The ABCDE criteria can help patents to see if they need to seek medical

consultaton (asymmetry of lesion uneven borders color and diameter

greater than 6 mm or abnormal evolut

on)

The Breslow index is the thickness of the lesion measured in millimeters

and is the main prognosis factor

Treatment

The base of treatment is precocious surgical extrpaton If the Breslow

index is less than 1 mm margins of 1 cm will be performed If Breslow

index is greater than 1 mm margins will be of 2 cm

For melanomas with a Breslow index greater than 1 mm the sentnel

ganglion must be located This is the first draining lymph node of the

territory where the tumor is localized If the ganglion is positve re-

gional lymphadenectomy will be performed along with interferon ad-ministraton (Figure 34)

In situ Extirpation 05 cm Follow-up

Breslow lt 1 mm Extirpation 1 cm Follow-up

Lymphadenectomy

Breslow gt 4 mm Interferon

Breslow ge 1 mm Extirpation 2 cm Sentinel ganglion

+

Figure 34 Melanoma treatment

Kaposirsquos sarcoma

Kaposirsquos sarcoma is the most common cutaneous tumor in HIV patents

Clinical presentation

Kaposirsquos sarcoma has a course with violaceous fusiform macules whichovertme may evolve into indurated nodules with blackberry appearance

This type of sarcoma has been linked to herpesvirus type 8 both in HIV

and seronegatve patents (Table 3)

EPIDERMAL KAPOSIrsquoS 983080HIV983081 CLASSIC KAPOSIrsquoS

Homosexual youth (95) The elderly

Diffuse and bilateral

(frequently in palate and face)

Unilateral plaques

(lower extremities)

Frequent mucosal and visceral involvement Not so frequent

middot Precocious lymphatic invasion

middot Aggressive

Not so precocious

Table 3 Differences between epidermal and classic Kaposirsquos sarcoma

Nodular melanoma

15

Middle-aged men

middot On healthy skin

middot Any zone

middot Sudden onset

middot Uniform black nodulemiddot Rapidly invasive (vertical growth without radial)middot Frequent ulceration and bleeding

Worst histological prognosis

Lentigo malignant melanoma

10

Elderly women

90 on facephotoexposedzones of aging skins(chronic exposure)

Spot that growsduring many years (gt 10)then progresses (nodule)

Better prognosis

Acral lentinginous melanoma

5ndash10 ( 60 black and Asian race)

Elderly men

middot Sole (ankle) handsmucosa ungual bed

middot No relation to photo exposure

middot Macule with mosaic appearance (spot that grows)middot Some amelanisticmiddot Bad prognosis due to late diagnosis

Melanoma of super1047297cial extension

70

Young women

middot 30 previous nervusmiddot Intermittent exposuremiddot Men back middot Women legs

More frequent

middot Macula with mosaic appearance in colors that grows 4-5 years and then in1047297ltrates (nodule)middot Metastasis 35 to 70

Figure 33 Clinical forms of malignant melanoma

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Dermatology

Diagnosis

Diagnosis relies on clinical suspicion and histopathological confirma-

ton

Treatment

Treatment of localized forms can include surgical extrpaton radiother-

apy or intralesional vinblastne

If the sarcoma is disseminated optons involve interferon or chemo-

therapy

Mycosis Fungoides

Mycosis fungoides is a T-cell lymphoma of low-grade malignancy Its

clinical course may be very slow and surpass 50 years Three stages are

clinically diff erentated

1 Eczematous or macular phase predominantly truncular erythema-

tous macules with years of evoluton They resemble a chromic ec-

zema Histology is unspecifi

c at this stage2 Infiltratve plaque phase infiltrated erythematous plaques appear

Histology is diagnostc at this stage A dermal infiltrate of atypical

lymphocytes band forms can be observed composed of CD+4 T

lymphocytes with cerebriform nuclei There is a marked epidermo-

tropism with the presence of clusters of intraepidermal lympho-

cytes called Pautrierrsquos microabscesses (Figure 35)

Figure 35 Mycosis fungoides Infiltrative plaque phase

3 Tumoral phase erythematous exophytc plaques start to appear

(tumors) with a tendency to ulceraton They can have a large size

Histology may become unspecific again as epidermotropism disap-

pears

In more advanced stages of the disease there is aff ectaton of extra-

cutaneous organs such as lymph nodes liver spleen lungs and bone

marrow Besides there may be blastc transformaton Other possible

complicaton is sepsis by Staphylococcus aureus

These three stages usually develop consecutvely nevertheless there

may patents whose debut starts directly with the tumoral stage

Remember

Microabscesses of mycosis fungoides are due to lymphocytes and are calledPautrierrsquos abscesses Psoriasis microabscesses result from neutrophils andare labeled as Munro-Sabouraud

Seacutezary Syndrome

Seacutezary syndrome can be considered as the leukemic phase of T-cell cu-

taneous lymphoma It is defined by the triad erythroderma (Figure 36

lymphadenopathies and the existence of more than 1000 Seacutezary cellsper milliliter in peripheral blood Seacutezary cells are atypical T- lymphocyte

with cerebriform nuclei

Very intense pruritus is characteristc For many authors Seacutezary syn-

drome is an aggressive clinical form and a bad prognosis of a mycosis

fungoides

Figure 36 Erythroderma due to Seacutezary syndrome

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Dermatology

Precocious treatment is of the utmost importance

Topic cortcoids are the first line treatment

It is worth to remember that prolonged use of topic cortcoids can have

local and systemic secondary side eff ects

The second line of treatment involves immunomodulators (tacrolimus

and pimecrolimus) These can be used in children older than 2 years of

age

For acute outbreaks oral cortcoids are used in short cycles and not as

maintenance To stop medicaton suddenly may cause a rebound eff ect

33 Contact Eczema

The appearance of contact eczema is immunologically mediated (type

IV hypersensit

vity) against foreign agents acquired by percutaneouspenetraton Contact eczema requires prior sensitzaton to allergen

It is more common in adults than in children

Diagnosis

Diagnosis is established with clinical records and epicutaneous tests of

contact These tests are performed once lesions have been resolved by

applying patches with allergens on healthy skin leaving them in contact

with the skin during 48 hours They are read afer 48 and 96 hours The

intensity of reacton is measured qualitatvely negatve weak positve

(erythema) strong positve (papules-vesicles) or extreme positve (blis-

ters)

Treatment

Avoid contact with the allergen

Treatment of acute eczema implies applicaton of topic poultce (zinc

sulphate sodium borate) and cortcoids if lesions are limited and sys-

tem poultce if lesions are generalized

34 Seborrheic Dermatitis

Seborrheic Dermatts is a quite frequent disease It aff ects 4 - 5 of the

populaton Etology of seborrheic dermatts is unknown although it

has been related to an abnormal immunological response to a fungus

called Pityrosporum ovale Seborrheic dermatts is more frequent and

intense when associated to neurological processes alcoholism and im-

munodeficiencies

Clinical Presentation

According to patentrsquos age

a Seborrheic dermatts in infants Yellowish scales on scalp known

as cradle cab

b Seborrheic dermatts in adult erythematous desquamatng papu-

les or plates in fat areas of the facial region and scalp

Diagnosis

Diagnosis of this conditon is clinical

TreatmentTreatment involves antfungals associated with topic cortcoids Sebor-

rheic dermatts on the scalp is usually linked to a keratolytc agent like

the salicylic acid

35 Psoriasis

Psoriasis is a chronic inflammatory disease of the skin that presents

with outbreaks Psoriasis aff ects 1-2 of the populaton and can ap-

pear at any age with a maximum of incidence between 20 and 30 yearsof age There is a family history in a third of the patents

Plates are the characteristc erythematous desquamatng lesions well

delimited with a superficial thick and white-pearl scale

The most frequent clinical form is vulgar psoriasis or psoriasis in plates

Lesions are localized at extensor surfaces (elbows and knees) and the

scalp The umbilical and the lumbosacral areas are ofen aff ected

Nail involvement is frequent and is most common with a pi ng ap-

pearance This form is lile specific The forms that combine hyperkera-

tosis and distal onycholysis are more specific Oil spot is the most char-

acteristc sign (Figure 3)

Figure 3 Generalized pustular psoriasis

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4

Diagnosis

Diagnosis of this conditon is generally clinical

If there is no certainty a biopsy must be done which will reveal hyper-

keratosis acanthosis and parakeratosis

There is an increase in polymorphonuclears (sterile abscesses) in the

stratum corneum which are called Munro abscesses

Treatment (Table 1)

For moderate severe forms of psoriasis that do not respond to clas-

sical systemic treatments (see table) They are monoclonal antbod-

ies against proinflammatory substances that are high in patents with

psoriasis [alpha tumor necrosis factor (TNF) interleukin IL 12 and

23] Some of them are infliximab adalimumab ustekinumab and

etanercept

36 Urticaria

Urtcaria is an immunologic and inflammatory reacton of the skin

against diverse etological factors Independently of the cause release

of histamine and other inflammatory mediators occurs which cause va-

sodilaton and increase in capillary permeability producing an edema in

superficial dermis Urtcarias are divided in acute and chronic urtcarias

depending on whether outbreaks persist more or less than six weeks

About 60 of acute urtcarias are idiopathic Chronic urtcarias show a

higher percentage

Urtcarias of known origin are usually due to infectons drugs or food

Clinical Presentation

Clinical presentaton is characterized by the appearance of pruritc wheals

that last less than 24 hours and can be accompanied with angioedema

TREATMENT USES SIDE EFFECTS AND CONTRAINDICATIONS

Topic Mild-moderatepsoriasis

(lt 25 body

surface)

Emollients (urea glycerin) Moisturizing

Keratolytics (salicylic acid) Eliminate excess of scales

Reductants (dithranol) Hyperkeratotic plaques middot Stain skin and clothing

middot Irritating

middot Acneiform eruptions

Corticoids middot Stable psoriasis

in plates

middot The most used

middot Tachyphylaxis

middot Percutaneous absorption

middot Possible new outbreak after stopping medication

middot Avoid prolonged treatment

Vitamin D analogues

(calcitriol calcipotriol and

tacalcitol)

Stable psoriasis in plates middot Irritating in face and skin folds

middot Hypercalcemia

Systemic Moderate-

severe psoriasis

(gt 25 body

surface)

Psoralens plus ultraviolet

light of the A wavelength(PUVA)

Combinable with topics

and retinoids (RePUVA)

middot Cutaneous aging and carcinogenesis

middot Erythroderma and xerosis middot Immunosuppression

middot Hepatitis by psoralens

middot Not in children pregnancy patients with hepatic or renal

insuffi ciency photosensitivity or cutaneous precancerosis

middot Cataracts

middot It accumulates in the crystalline during 24 h (sunglasses)

Retinoids (acitretin) middot Severe psoriasis

pustular

or erythrodermic

middot It is not usually used

in women in fertile age

(see side effects)

middot Cutaneous dryness (the most frequent)

middot Hypertriglyceridemia

middot Hypercholesterolemia

middot Increase in transaminases

middot Diffuse alopecia

middot Vertebral hyperostosis ligamentous calci1047297cations

middot Teratogenicity avoid pregnancy until 2 years after

1047297nishing treatment

middot Avoid in children and patients with hepatic or renal failure

Cyclosporine A middot In1047298ammatory severe

psoriasis resistant to

other treatments

middot Rapid action

middot Rebound effect

middot Nephrotoxicity

middot High blood pressure (HBP)

middot Epitheliomas and lymphomas

middot Hypertrichosis

middot Gingival hyperplasia

middot Hyperuricemia

Methotrexate middot Severe psoriasis

resistant to other

treatments

middot Psoriatic arthropathy

middot Hepatotoxicity

middot Myelosuppression

middot Teratogenicity until 3 months after ending treatment

middot Photosensitivity

Table 1 Psoriasis treatment

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Dermatology

Vasculits urtcaria should be ruled out when lesions last more than 24 hours

and are accompanied with systemic clinical symptoms (ie arthralgias)

Treatment

Oral anthistamine therapy is the treatment of choice

Systemic cortcoids for severe or refractory cases

Adrenalin for severe cases with anaphylaxis

37 Toxicodermas

Toxicodermas are quite variable cutaneous reactons that appear afer

drug administraton They are one of the most frequent side eff ects of

drugs The causatve agents for many toxicodermas stll remains un-

known either immunological or not and clinical presentaton does not

facilitate agent dist

nct

on

Morbilliform exanthem is the most frequent A morbilliform exanthem

is a generalized erupton formed by symmetric and confluent macules

and papules that usually start by the trunk

They can appear one or two weeks afer taking the drug

A morbilliform exanthem can be associated with fever pruritus and eo-

sinophilia

The most frequent are non steroid ant-inflammatories antbiotcs (sul-

phamides and penicillins) antepileptcs allopurinol and N acetyl-cystene

DiagnosisDiagnosis is according to clinical presentaton

Treatment

Treatment implies withdrawal of potentally responsible drug Topic or

systemic anthistamines and cortcoids are given according to the extent

of symptoms (Figure 4)

Figure 4 Morbilliform exanthem due to amoxicillin

38 Multiform Erythema

Stevens-Johnson Syndrome

and Toxic Epidermal Necrolysis

Multform erythemas (ME) are of undetermined etopathogenesis

regarded as a cutaneous reacton against a diversity of stmuli Their

histologies show similarites what leads to consideraton of a common

pathogenesis

Clinical Presentation

Three diff erent groups have been described although many a tme their

clinical symptoms overlap

bull Erythema multforme minor is the most frequent with around 80

of the cases It usually precedes a symptomatc infecton by simple

herpes virus (60) or subclinical infecton about 15 days before

Erythema multforme minor manifests itself on extensor surfaces

at hands elbows and feet as a symmetric erupton of erythema-

tous edematous lesions with target-shape (herpes iris of Batemanor rosee-paerned lesion) with a violaceous sometmes bullous

center (Figure 5)

Mucosal aff ectaton is rare with small erosions in oral mucosa Erythe-

ma multforme minor tends to recurrence with subsequent outbreaks

of herpetc lesions

Figure 5 Erythema multiforme minor Herpes iris of Bateman

bull Erythema mult

forme major or Stevens-Johnson syndrome is therarest It normally has a prodromal period of untl 14 days with fe-

ver cough cephalea arthralgias and other symptoms Subsequent

to the prodromal period erythematous edematous plates appear

which are more extensive with a tendency to form blisters and

greater mucosal erosions (mouth genitals pharynx larynx and

conjunctve Figure 6) Systemic symptoms are normal and do not

tend to recurrence

The most frequent etological factors are drugs [sulphamides non

steroid ant-inflammatory drugs (NSAIDs) antconvulsants and an-

tbiotcs in decreasing order) Infectous agents have been also in-

volved mainly mycoplasma pneumoniae

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6

Figure 6 Exudative erythema multiforme major

bull Toxic epidermal necrolysis (TEN) many authors consider it the

most severe form of erythema multforme major arguing the same

pharmacological agents A morbilliform rash appears which is rap-idly confluent comprising almost the entre skin surface with flaccid

blisters that leave wide areas of denuded skin Involvement of sev-

eral mucosae is constant

Complicatons ofen occur (pneumonia digestve hemorrhage re-

nal failure and hemodynamic shock) with mortality rates close to

25 In children it must be performed a diff erental diagnosis with

staphylococcal scalded skin syndrome which does not aff ect mu-

cosae

Remember

Diseases that have the Nikolsky sign are TEN staphylococcal scalded skinsyndrome (SSSS) and pemphigus In TEN the whole epidermis comes off(bad prognosis) while in SSSS epidermal detachment occurs at the granularlayer

Histopathology

It must be highlighted the eff acement of dermoepidermal juncton by a

lymphohistocytc infiltrate and vacuolar degeneraton of the baseline lay-

er with necrotc keratnocytes In TEN keratnocytes necrosis is massive

Treatment

In ME minor only symptomat

c treatment is prescribed with topiccortcoids and oral anthistamines Treatment for herpes simplex virus

(HSV) infecton is useful to prevent ME lesions if patent is in the inital

stage of the viral infecton

ME major requires treatment of the underlying infecton or withdrawal

of implied drug and support measures The use of oral steroids accord-

ing to the patentrsquos general state is under discussion

A patent with TEN requires to be admied at the burn treatment room

with monitoring of hematocrit hydroelectrolytc balance and antbiotc

prophylaxis and support measures It is controversial the use of system-

ic cortcoids immunoglobulins andor cyclosporine

39 Erythema Nodosum

Erythema nodosum is the most frequent panniculits Painful erythema-

tous nodules occur mainly in the anterior side of legs with a self-limit-

ing course and predominantly aff ectng young women (Figure 7)

Figure 7 Erythema nodosum

They heal without leaving a scar within a period of four to six weeks

Erythema nodosum may be accompanied with fever deterioraton of

the general state and arthralgias

Patents with erythema nodosum may have a false positve VDRL

Etiology

This conditon is thought to be an immunological response triggered by

multple and diff erent stmuli bacterial fungal and viral infectons sys-temic diseases (sarcoidosis inflammatory intestnal disease Behcetrsquos

syndrome) neoplasias (lymphomas and leukemias) and drugs (oral

contraceptves sulphamides bromides and iodines)

Diagnosis

Erythema nodosum requires a deep biopsy to reveal septal panniculits

without vasculits

Complementary tests can be performed to rule out systemic involvement

for example chest X-ray Mantoux and antstreptolysin O antbody (ASLO)

Treatment Treatment entails eliminatng underlying cause if found then rest and

ant-inflammatories

310 Bullous Pemphigoid

and Pemphigus Vulgaris

See Table 2 and Figures 8 9 10 and 11

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Dermatology

Intercellular

substance ac

middot Pemphigus

Lineal

storage

in lucid

layer

-

Anti-Collagen Ac

Lucid

layer

Thick

layer

Basal

sublayer

Granular

storage

in papillary

dermis

middot Pemphigoid bullousmiddot Herpes gestationis

middot Acquired blistering epidermolysis

middot Dermatitis herpetiformis

Figure 8 Key points for histological diagnosis

of autoimmune blistering diseases

Figure 9 Pemphigus vulgaris

Figure 10 Pemphigus vulgaris with oral mucosa involvement with

erosions

Figure 11 Pemphigoid bullous Tense blisters No sign of Nikolsky

PEMPHIGUS VULGARISGENERALLY

IDIOPATHICHERPES GESTATIONIS

DERMATITIS

HERPETIFORMIS

Clinical presentation middot 40-50 years of age

middot They usually affect mucosae

middot No pruritus

middot Flaccid blister

middot Nikolsky

middot Elderly

middot Sometimes mucosae

middot With pruritus

middot Tense blister

middot No Nikolsky

middot Pregnant women

middot No mucosae

middot With pruritus

middot Herpetiform

middot No Nikolsky

middot 15-35 years of age

middot No mucosae

middot With pruritus

middot Herpetiform

middot No NikolskyDirect immuno1047298uorescence (DIF) IgG IgG IgG IgA

Histology middot INTRAepidermal blister

middot There is acantholysis

middot SUBepidermal blister

middot There are eosinophils

middot SUBepidermal blister

middot There are eosinophils

middot SUBepidermal blister

middot Neutrophils in dermis

Treatment Corticoids at high doses

immunosuppressants rituximab

and immunoglobulins

Corticoids Corticoids Diet +- dapsone

Remember Mortality rate 10 The most frequent Relapse if new

pregnancy

Associated to enteropathy

by gluten 90

Table 2 Autoimmune blistering diseases

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8

Chapter 04

Infectious Diseases

41 Viral Infections

Simple Herpes

Infection by Simple Herpes Virus

There are two types of simple herpes (Figure 12)

bull Type I is responsible for most extragenital herpes and 20 of the

genital herpes

bull Type II causes genital herpes and a small percentage of extragenital

herpes

Figure 12 Herpes simplex

Contagion is produced by direct contact though the carrier may be as-

ymptomatc Afer primary infecton virus remains silent in the sensi-

tve porton of cranial or spinal ganglia Immunosuppressed patents

endure the greatest severity of this conditon

Clinical Presentation

bull Extragenital simple herpes recurring orofacial herpes simplex is

the most frequent Most primary infect

ons are asymptomat

c Only5 manifest themselves in the form of herpetc gingivostomatts a

profile characterized by oral ulcers with cervical adenopathy and af-

fectaton of the patentrsquos general state (Figure 13) During relapses

clinical symptoms are milder with cluster vesicles on an erythema-

tous base Some factors facilitate relapses trauma sunlight cold

stress fever and the menstrual cycle

bull Genital simple herpes is the most common cause of genital ulcers

afer trauma Primary infecton is usually symptomatc and occurs

between 3 to 14 days afer sexual contact It causes clustered ulcers

in the balanopreputal sulcus or in the prepuce with painful inguinal

adenopathy Relapses are less severe than primary infecton and oc-

cur more frequently when genital herpes is due to HSV type II

Figure 13 Herpetic gingivostomatitis

bull Eczema herpetcum or Kaposi varicelliform erupton dissemina-

ton of herpetc infecton on pre-existng dermatosis (above all

atopic dermatt

s) bull Neonatal herpes is due to intrapartum contagion of HSV-II with

neurological involvement general deterioraton and skin vesicles or

ulcers

bull Other clinical forms are herpes gladiatorum herpetc whitlow and

keratoconjunctvits

Diagnosis

Diagnosis of this conditon is mainly clinical Virological culture is the

most reliable method of confirmaton The extent of a smear of the le-

sions (Tzanck cytodiagnosis) allows visualizaton of multnucleated cells

and intranuclear inclusions which become evident through histological

study

Treatment

Mild forms do not need treatment Treatment is required in the follow-

ing cases

bull Primary infecton

bull Severe or frequent relapses if they aff ect life quality

bull Complicatons like erythema multforme and eczema herpetcum

Drug of choice is oral acyclovir and its derivatves (valacyclovir famci-

clovir) Topic antvirals have not proven useful favoring maceraton of

lesions and thus over infecton It is not infrequent that topic antvirals

cause allergic contact dermatts due to hypersensitvity

Varicella-Zoster Virus

A primary infecton gives way to varicella (see Pediatrics secton) Afer

varicella the virus remains latent in the sensitve porton of the neural

ganglia and when relapse occurs it leads to zoster herpes

bull Varicella the following symptoms appear afer 15 days of incubaton

fever cephalea pruritus and polymorphic lesions in diff erent stages

macules papules vesicles (Figure 14) ulcers and scabs (starry sky

appearance) Mucosal (ulcers) and scalp involvement is characteristc

Manipulaton can leave scars Bacterial over infecton of lesions is the

most usual complicaton About 20 of adults suff er from varicella

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Dermatology

pneumonia radiologically demonstrable but clinical symptomatology is

only present in around 4 of the cases

Figure 14 Typical vesicles in patients with varicella

bull Zoster herpes thoracic zoster herpes is the most usual It sel-

dom occurs more than once throughout a personrsquos lifetime

It is characterized by vesicles on pre-existing erythema with

metameric distribution and lateral extension The most com-

mon complication is post herpetic neuralgia more frequent in

advanced age Carbamazepine or tricyclic antidepressants (Fig-

ure 15)

Figure 15 Zoster herpes

Special Clinical Forms

Special clinical forms are as follow

bull Ramsay-Hunt syndrome aff ectaton of geniculate ganglion of the

facial nerve

It produces vesicles in the outer ear external auditory canal and

pharynx homolateral facial paralysis deafness and vertgo

bull Ophthalmic involvement can result in severe keratts and requires ur-

gent referral to an ophthalmologist Suspicion should exist on patents

that present herpetc lesions on the tp of the nose) (Hutchinsonrsquos sign)

bull Disseminated zoster herpes several dermatomes are aff ected bilat-

erally Ramsay-Hunt syndrome is characteristc in the immunosup-

pressed

Remember

Affectation of the nose tip makes it necessary for ophthalmologicalexamination because the nose tip is innervated by the same nerve thatinnervates the cornea (1047297rst branch of the trigeminal nerve)

Treatment

Varicella without complicatons is treated symptomatcally Antvirals

are reserved for severe or complicated forms There is a commercial-

ized vaccine of live virus whose indicatons are stll under discussion

Zoster herpes must be treated with antvirals when detected during the

first 48-72 hours and aff ectng patents with

bull Immunosuppression

bull Age above 55

Special clinical forms previously cited

Drugs to be used are oral acyclovir and its derivatves (valacyclovir and

famciclovir) They accelerate the cure of lesions and decrease the inten-

sity of post herpetc neuralgia Patents with renal failure need a dose

adjustment as acyclovir is nephrotoxic These patents are adminis-

tered brivudine in a single daily dose

Molluscum ContagiosumDome shaped pink papules with central umbilicaton (Figure 16) Mol-

luscum contagiosum is typical of children that go to swimming pools It

is also present in the genital zone afer sexual contact and in immuno-

suppressed patents It is caused by Poxvirus

Figure 16 Molluscum contagiosum

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0

Lesions are asymptomatc

Diagnosis

Diagnosis is clinical Histology reveals characteristc inclusion bodies

Treatment

Lesions can resolve spontaneously

Cureage cryotherapy or local trichloroacetc acid are eff ectve meth-

ods to destroy lesions

Warts

Human papillomavirus can cause verruca vulgaris palmoplantar and

flat warts and condyloma accuminata Human papillomavirus is the

most frequent sexual transmied disease

Some subtypes of this virus (16 18) are of high risk and can cause epi-

dermoid carcinomas

Direct contact is the mechanism of contagion

Diagnosis

Diagnosis of this conditon is clinical

Staining with acetc acid can help visualize mucosal lesions

Treatment

Genital warts are treated with cryotherapy podophyllotoxin trichloro-

acetc acid imiquimod and 5-fluorouracil

Cervical lesions should be monitored by cytology and biopsy whenever

necessary to rule out cervical cancer (Figures 17 and 18)

Figure 17 Warts in HIV patient

Figure 18 Condyloma accuminata

42 Bacterial Infections

Impetigo

Impetgo is a very contagious superficial infecton without systemic re-

percussion and normally mixed etology by Gram positve cocci (strep-

tococci and staphylococci) Classically the most frequent accepted

cause was Streptococcus pyogenes However at present Staphylococcus

aureus stands out as the predominant cause

The most typical form is impetgo contagiosa (Figure 19) character-

ized by honey-colored (meliceric) scabs which normally appear on

the face and other exposed areas It is typical of children Although

infrequent poststreptococcal glomerulonephrits is a dreadful com-

plicaton

Figure 19 Impetigo contagiosa

On the contrary rheumatc fever shows no relaton to cutaneous strep-

tococcal infectons but only with pharyngeal infectons

There are other less habitual forms called bullous impetgo exclusively

of staphylococcal origin Clinical presentaton involves the presence of

blisters and erosions on the aff ected skin as a consequence of the epi-

dermolytc toxins that these bacteria contain Impetgo is treated with

topical mupirocin penicillin or oral fusidic acid

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Dermatology

Cellulitis

Cellulits is an infecton that aff ects deep dermis and subcutaneous cel-

lular tssues normally caused by streptococci (Streptococcus pyogenes

or of group A)

Community methicillin-resistant S aureus (CMRSA) is a triggering agent

that is becoming more and more frequent

Most common risk factors are diabetes chronic venous insuffi ciency

and immunosuppression

Clinical Presentation

Cellulits presents with erythematous plaques that are ill-defined pain-

ful and hot It is usually accompanied with fever and chills

Diagnosis

Diagnosis is clinical If there is an open door a culture of this area may

help see the source germ and resistance to ant

biot

cs

It is important to rule out abscesses osteomyelits and necrotzing fas-

ciits

If bacteremia is suspected blood cultures need to be performed

Treatment

Treatment implies oral antbiotcs for 7-10 days to cover Gram positve

cocci They are intravenously administered in case of lack of response

to oral treatment involvement of hands or periorbital zone diabetes or

extremes of age

Necrotizing FasciitisNecrotzing fasciits is a deep infecton up to muscular fascia that pro-

duces very intense pain and subsequent anesthesia

In 10 of the cases cellulits is due to an infecton by S pyogenes In the

remaining cases it occurs by a polymicrobial infecton caused by aerobes

and anaerobes including S aureus E coli and Clostridium perfringens

There may be prior history of trauma or surgery

Clinical Presentation

Clinical presentat

on involves pain of sudden onset and edema on theaff ected zone Pain may progress to anesthesia There appears subse-

quent erythema that progresses rapidly into necrosis

Characteristc clinical signs are tssue necrosis blisters intense pain

and gas producton

Diagnosis

Diagnosis is clinical and requires image testng X-rays or a computed

tomography CT

A biopsy of the border of the lesion helps achieve diagnosis

Treatment

Treatment entails precocious surgical debridement It is a surgical emer-

gency In additon to surgery broad-spectrum antbiotherapy will be

needed

Folliculitis

Folliculits is an infecton and inflammaton of one or several follicles

caused mainly by staphylococci

Clinical Presentation

Folliculits shows pustules with follicular distributon

When the infecton is deeper it is called furuncle

If several furuncles are infected a fluctuatng erythematous plaque forms

containing several points of suppuraton This plaque is labeled as anthrax

Diabet

c and immunosuppressed pat

ents are at higher risk

Characteristics of Folliculitis

1 Hot tub or swimming pool folliculits caused by Pseudomonas aeru-

ginosa

2 HIV associated pruritc folliculits or eosinophilic folliculits

Treatment

In mild cases treatment of choice comprises antseptcs and topic an-

tbiotcs

In more severe cases treatment of choice requires oral antbiotcs

Large sized lesions must be drained and a microbiological culture must be

performed to rule out methicillin-resistant Staphylococcus aureus MRSA

Acne Vulgaris

Acne is an inflammatory disease of the pilosebaceous follicle as a con-

sequence of an alteraton in follicular keratnizaton It aff ects adoles-

cents and young adults

Etology is multfactorial alteraton of keratnizaton of follicular infun-

dibulum quanttatve and qualitatve alteraton of sebum producton in

the sebaceous gland and alteratons of bacterial microflora (increase in

quant

ty of P acnes)

Aggravatng factors are stress androgenic oral contraceptves and the

use of cosmetc products that are not oil-free

Clinical Presentation

A comedo is the inital lesion which can be closed (whitehead) or open

(blackhead) and it evolves into inflammatory lesions that listed in as-

cending order of severity are papules pustules nodules and cysts

Lesions progress and leave scars Scars can be increased if lesions are

manipulated

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Amer ican Manual of Examinat ion in Medicine (2CK)

2

Diff erent lesions habitually combine simultaneously so acne becomes

polymorphic It is located in sebaceous areas face back shoulders and

the center thoracic region

Diagnosis

Diagnosis is clinical

Treatment

bull Comedonal acne is treated with topic retnoids and benzoyl peroxide

bull Inflammatory acne treatment requires benzoyl peroxide combined

with topic antbiotcs (erythromycin and clindamycin) Systemic

antbiotc treatment with oral tetracyclines will be prescribed if re-

sponse to topic antbiotc treatment fails

bull Severe nodular cystc acne treatment involves the use of isotret-

noin (13-cis-retnoic acid) It is a derivatve of vitamin A Isotretnoin

produces atrophy in the sebaceous gland and regulates keratniza-

ton The most frequent side eff ect is cutaneous and mucosal xero-

sis Triglycerides cholesterol and transaminases should be moni-

tored as their values may increasebull It can be associated with depression

bull It is teratogenic so pregnancy should be avoided during treatment

and untl a month afer treatment

Pilonidal Cysts

Pilonidal cysts are abscesses in the sacrococcygeal region

This type of cysts has predominance in men between 20 and 40 years

of age It is believed that repeated trauma on the aff ected area favors

their appearance

Clinical Presentation

Pilonidal cysts present with an indurated lesion that is fluctuatng hot

painful but non-adherent to deep planes in the sacrococcygeal region

Pilonidal cysts may or may not be associated to cellulits and purulent drain-

age

Diagnosis

Diagnosis is clinical and anal or perirectal abscesses should be dismissed

Treatment

Treatment implies an incision and surgical drainage

On some occasions a general surgery is required

43 Fungal Infections

Pityriasis Versicolor

Versicolor pityriasis is caused by commensal yeast called Pityrosporum

ovale which transforms into its pathogen form (Malassezia furfur) It

especially aff ects young patents (15 - 45 years of age) but it is rare

in childhood and advanced age Versicolor pityriasis relates to heat

humidity and sebaceous hypersecreton It is characterized by the ap-

pearance of hyperchromic or hypochromic macules that desquamate

on scratching (nail sign) if infecton is actve Macules usually appear on

the center thoracic region and on the back that is to say on seborrheic

zones Relapses are habitual despite treatment

Diagnosis

Diagnosis is normally clinical To that purpose the following serve as

support

bull Woodrsquos lamp emits yellow-orange fluorescence

bull Potassium hydroxide (KOH) test filaments and round elements can

be observed (ldquospaghe and meatball appearancerdquo Figure 20)

Treatment

Treatment is performed with topical azoles Oral administraton applies

for extensive cases or immunosuppressed patents Diff erental diagno-

sis includes pink pityriasis and eczemas (Figure 21)

Figure 20 Versicolor pityriasis Histological cut

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Dermatology

Figure 21 Versicolor pityriasis

Candidiasis

The most common triggering agent is Candida albicans It is normally sapro-

phyt

c although under certain condit

ons candidiasis may become patho-genic (immunosuppression humidity pregnancy and contraceptves)

Clinical Forms

bull Intertrigo erythematous plaque in cutaneous folds Atrophy and

fissures are typically deep in the skin fold as well as satellite and

peripheral lesions (papules andor pustules)

bull Mucosa involvement may cause diverse symptomatology like vul-

vovaginits glossits and white papules in the anterior region of the

oral mucosa Candidal balanits is characterized by the presence of

punctform erosions and pustules on gland and balanopreputal

sulcus Candidal balanits ofen appears afer sexual intercourse or

afer oral antbiotc intake

Remember

Almost a 100 of HIV patients suffer from muguet throughout their diseasecourse

bull Candidiasis of nail fold is usually associated with periungual inflam-

maton (perionixis) and inital proximal aff ectaton which diff erent-

ates it from tnea unguium (Figure 22)

Figure 22 Candidiasis of nail fold

Treatment

Oral Candidiasis fluconazole or nystatn

Candidiasis of the skin (intertrigo) apply topical antfungal medicaton

and keep zone clean and dry

Dermatophytosis or TineasDermatophyte infectons aff ect the skin and keratnized structures like

hair and nails (there is no mucosa involvement) Clinical diagnosis is

achieved afer performing a culture Woodrsquos lamp test normally turns

out to be negatve In general Trichophyton dermatophyte rubrum is

the most frequent dermatophyte

Non Inflammatory Tineas

Non inflammatory tneas do not produce irreversible scarring alope-

cia while inflammatory forms do Tineas are treated with azoles de-

rivatves

The types of tnea are the following

bull Ringworm of the scalp ( t nea capi t s or t nea tonsurans) is charac-

teristc of childhood It presents with alopecic plaques broken hair

and desquamaton Infectons tend to resolve spontaneously with-

out leaving scars at the onset

of puberty

bull Ringworm of the body (herpes

circinatus or t nea corporis) are

erythematous desquamatve

plaques (with more actve bor-

ders) which are also circinate

and normally pruritc (Figure

23) Plaques grow eccentrically

with less actvity in the centerand more in the borders

bull Ringworm of the foot ( t nea

pedis) the most frequent is the

ldquoathlete footrdquo with desquama-

ton in interdigital spaces

bull Tinea incognito refers to tnea

wrongly treated with cort-

coids what makes diagnosis

diffi cult as the lesion has been modified Figure 24)

Figure 24 Tinea incognito secondary to treatment with topical steroids

Figure 23 Herpes circinatus

(tinea corpis)

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Amer ican Manual of Examinat ion in Medicine (2CK)

4

bull Ringworm of the groin (t nea cruris or eczema marginatum von

hebra) formed by erythematous desquamatve plaque with more

actve borders (Figure 25)

Figure 25 Ringworm of the groin (tinea cruris)

bull Tinea unguium subungualhyperkeratosis with onychol-

ysis but without perionixis

(Figure 26)

Diagnosis

Clinical diagnosis is reached afer

performing a culture

Treatment

Treatment involves topical an-

tfungal medicaton in localized

areas

Oral antfungal medicaton is used in extensive forms nail fold or scalp

involvement

44 Parasitic Infections

Pediculosis

Pediculosis is transmied by direct contact or by contact with fomites

which release toxins that produce intense pruritus

Clinical Presentation

Pediculosis capi t s intense pruritus predominant in retroauricular and

occipital regions occasionally with excoriatons and impetginizaton

secondary to excoriatons

Pediculosis corporis intense pruritus in patents with poor hygiene or

who live in overcrowded conditons

Pediculosis pubis genital and pubic pruritus Brownish-grey macules

called maculae ceruleae are typical on underwear and skin These pig-

mentatons appear as a result of a reducton in hemoglobin by a para-

site enzyme

Diagnosis

Diagnosis is clinical and by direct visualizaton

Treatment

Pediculosis is treated with malathion lindane or topical permethrin

Scabies

Scabies is originated by an acarus known as Sarcoptes scabiei It has an

incubaton period of 1 month

Clinical Presentation

Scabies produces generalized pruritus more intense at night The pa-

tent usually catches the infestaton which is passed to the patentrsquos

relat

ves It is common tofi

nd that a recent trip to a tropical country hasbeen made Lesions appear between the fingers (Figure 27) in wrists

feet genitalia mammary areola and axilla but back and face are usu-

ally spared The most specific lesion is the acarine burrow in whose less

scaly end the advancing zone the mite lies Nodules are frequent in

axilla and genitals (nodular scabies)

bull Norwegian scabies is typical of the immunosuppressed Patents

present with generalized hyperkeratosis and scabs Norwegian sca-

bies produce lile pruritus but it is very contagious because there

are many acari

bull Nodular scabies involves the persistence of pruritc nodules despite

treatment Lesions usually appear in axilla and genitalia Pruritus is

due to a hypersensitvity phenomenon because of the acarus al-

ready dead Nodular scabies is treated with cortcoids

Figure 27 Scabies Acarine burrow

Treatment

bull Permethrin cream at 5 is the treatment of choice It is lile toxic

so it can be used in children and pregnant women

bull Topical lindane at 1 irritates and is neurotoxic therefore it is con-

traindicated in pregnant women and children

bull Oral ivermectn is utlized in cases of resistance to prior treatments

There is stll lile experience as to its use but in a first instance a

Figure 26 Tinea unguium

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Dermatology

single dose would be enough to cure scabies (already used by vet-

erinarians)

45 Ischemia

Decubitus Ulcers

Decubitus ulcers are the result of ischemic necrosis by contnuous pres-

sure on an area which restricts microcirculaton in that zone

Clinical Presentation

Decubitus ulcers are present in patents in bed with scarce mobilizaton

It is favored by bone prominences and lack of fat tssue If sensitvity

decreases there is more risk of formaton of decubitus ulcers

Diagnosis

Diagnosis is achieved based on medical records and clinical presentaton

Treatment

Preventon is of the utmost importance as well as frequent mobiliza-

ton of the patent in bed

Once ulcers have been established hydrocolloid dressings are used for

healing but sometmes surgical debridement is necessary

Gangrene

Gangrene means tssue necrosis

There are three types dry gangrene wet gangrene and gas gangrene

Clinical Presentation

Dry gangrene is due to ischemia generally secondary to atherosclero-

sis Clinical presentaton involves pain cold and paleness of extremi-

tes Once tssue is established it turns bluish-black in color and dry

Wet gangrene is owing to bacterial flora Tissue presents with an edem-

atous appearance either with blisters or pus

Gas gangrene caused by C perfringens It is normally located on re-

cent surgery Bacteria precociously destroyt

ssue producing gas It is amedical emergency

Diagnosis

Clinical diagnosis is obtained by microbiological culture

Treatment

Treatment requires surgical debridement with amputaton if necessary

and associaton of broad spectrum antbiotherapy

Gas gangrene is treated with hyperbaric oxygen

46 Miscellaneous

Acanthosis Nigricans

Acanthosis nigricans are vel-

vet-like papillomatous brown

plaques in neck axilla and groin

folds (Figure 28)

It is associated with diabetes

mellitus Cushingrsquos disease poly-

cystc ovarian syndrome and

obesity

The malignant form of acantho-

sis nigricans is a paraneoplastc

syndrome that diff erentates

from the benign form because

the laer has mucosal and pal-

moplantar involvement

Lichen Planus

Lichen planus is an inflammatory idiopathic disease that equally aff ects

both genders with higher frequency in middle age

Lichen planus has been related to diverse drugs like gold salts

anti-malarial medication and thiazides It has been also linked to

hepatitis C virus infection however this association is currently

doubtful

Clinical Presentation

Lichen planus presents with red-violaceous polygonal flat papulesquite pruritc which localizes on the flexor side of wrists forearms an-

kles and lumbosacral and flank regions On its surface a whitsh retcu-

late can be observed (Wickhamrsquos striae) About 60 - 70 of the cases

present with lesions in oral and genital mucosa oral which appear as

whitsh retculated lesions (Figures 29 and 30)

Figure 29 Lichen planus of oral mucosa with typical whitish

reticulate

Figure 28 Acanthosis nigricans

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Amer ican Manual of Examinat ion in Medicine (2CK)

6

Violaceous papules

with white stretch marks

Lichenoid lymphocyte

in1047297ltrate (band formation)

Destruction

of basal layer

Figure 30 Lymphocytic interface reaction (lichen planus)

Treatment

Mild forms are treated with topical cortcoids

Severe cases require oral cortcoids psoralens plus ultraviolet light of

the A wavelength (PUVA) or cyclosporine

Rosacea

Rosacea is a chronic disease of unknown pathogenesis characterized

by erythema and acneiform lesions on the face It aff ects middle aged

women (between 30 and 50 years of age) more

Rosacea etopathogenesis is unknown although there is involvement of

vasomotor lability infecton by Demodex folliculorum photo exposureand genetc predispositon

Clinical Presentation

Rosacea symptomatology comprises facial flushing episodes that end

up by provoking a persistent erythema telangiectasias and papulopus-

tular lesions without comedos Over tme ocular lesions and hyperpla-

sia of sof tssue may develop

Treatment

Avoid vasodilator stmuli

Mild cases require topical metronidazole or azelaic acid

Moderate cases need doxycycline or oral minocyclines

Severe cases are treated with oral isotretnoin at low doses

Pink Pityriasis

Gilbertrsquos pink pityriasis is an acute self-limitng dermatosis which main-

ly aff ects young adults It is of unknown origin although a viral etology

is suspected (there is some speculaton as to links with human herpes-

virus type 7)

Clinical Presentation

Erupton starts with an erythematous plaque between 2 and 5 cm of

diameter with a desquamatve central collaree ofen localized on the

trunk (heraldic mother patch Figure 31)

Figure 31 Pink pityriasis

Around a week later oval papules appear on the trunk and extremi-

tes These papules share similar characteristcs with the mother patch

though the first ones are smaller and distributed according to skin ten-

sion lines Pink pityriasis may be asymptomatc however it is some-

tmes linked to pruritus Lesions may last between 4 and 8 weeks and

disappear without leaving scars

Diagnosis and Treatment

Diagnosis is clinical Treatment is seldom needed and recommended

therapies in the past (PUVA erythromycin or oral antvirals) have not

shown clearly favorable results

Vitiligo

Vitligo is characterized by achromic macules by melanocyte destruc-

ton

Clinical Presentation

Vitligo shows achromic macules of chronic course and variable progres-

sion

Lesions are predominant on acral and periorificial areas They also show

the Koebner phenomenon

Patents may have markers of autoimmune diseases (ie antthyroid

antbodies and diabetes) but these diseases seldom manifest them-

selves

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Dermatology

Treatment

Localized lesions require topical cortcoids

Extensive or generalized lesions are treated with ultraviolet light B

(UVB) or PUVA

Strict solar photoprotecton is indispensable (Figure 32)

Figure 32 Vitiligo

47 Neoplasias

Seborrheic Keratosis

Seborrheic keratosis is the most frequent benign tumor in human be-

ings since it is part of cutaneous aging

Clinical Presentation

Seborrheic keratosis presents with hyperkeratosic papules with an oily

or velvet-like texture crests fissures and horny plugs on their surface

These papules are normally pigmented showing a brownish-black color

Treatment

No treatment is required as lesions do not become malignant

Seborrheic keratosis can be addressed with cureage or cryotherapy

Actinic keratosis

Actnic keratosis is the most common precancerous lesion and aff ects

almost a 100 of the populaton in sunny areas

Clinical Presentation

Actnic keratosis is characterized by erythematous and desquamatve

papules which are hyperkeratosic and rough on touch developing a

chronic course

Diagnosis

Diagnosis is clinical

Treatment

Treatment entails applicaton of topical 5-fluorouracil topical imiqui-

mod cryotherapy or surgery

If underlying carcinoma is suspected a biopsy must be performed to

rule out suspicion

Epidermoid Carcinoma

Epidermoid carcinoma is the second most frequent cutaneous tumor

Solar photo exposure is the main etological factor which is why epider-

moid carcinoma appears in zones of prolonged solar exposure like the

face Most carcinomas appear over premalignant lesions (actnic kera-

tosis and leukoplakia among others)

Clinical Presentation

Clinical presentaton reveals erythematous or erythematosquamous

plaques Over tme these plaques form papules and tumors which of-

ten become ulceratve and bleed

Diagnosis

Diagnosis is based on clinical suspicion and histopathological confirmaton

Treatment

Surgery with safety margins is the treatment of choice In carcinomas

in situ cryotherapy can be used as well as topical imiquimod electro-

coagulaton or CO2 laser techniques in destructon of tumors Radio-therapy may also be used in some cases

Basal Cellular Carcinoma

Basal cellular carcinoma is the most frequent cutaneous tumor Chronic so-

lar photo exposure is the main etological factor hence most of these car-

cinomas aff ect the facial zone in patents who are 40 years of age or older

Gorlinrsquos syndrome should be considered if multple basal cellular carci-

nomas are found in non photo exposed areas

Clinical Presentation

Basal cell carcinoma shows a pearly pink papule and superficial telan-

giectasias

It is localized over healthy skin and never aff ects mucosae

Treatment

Surgery is the treatment of choice Mohs surgery is performed in zones

where surrounding healthy tssue needs to be preserved Other alter-

natves are cryotherapy imiquimod electrocoagulaton radiotherapy

photodynamic therapy and intralesional interferon Prognosis is excel-

lent as growth is slow and metastasis exceptonal

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Amer ican Manual of Examinat ion in Medicine (2CK)

8

Melanoma

Melanoma is the most aggressive cutaneous tumor given its ability to

metastasize

Risk factors comprise solar photo exposure clear phototype the pres-

ence of dysplastc nevus or a high number of melanocytc nevi Fam-

ily history is quite important as some genetc mutatons determine a

higher risk of developing the disease

Clinical Forms

See Figure 33

Diagnosis

Precocious diagnosis is essental to perform precocious surgical extrpaton

The ABCDE criteria can help patents to see if they need to seek medical

consultaton (asymmetry of lesion uneven borders color and diameter

greater than 6 mm or abnormal evolut

on)

The Breslow index is the thickness of the lesion measured in millimeters

and is the main prognosis factor

Treatment

The base of treatment is precocious surgical extrpaton If the Breslow

index is less than 1 mm margins of 1 cm will be performed If Breslow

index is greater than 1 mm margins will be of 2 cm

For melanomas with a Breslow index greater than 1 mm the sentnel

ganglion must be located This is the first draining lymph node of the

territory where the tumor is localized If the ganglion is positve re-

gional lymphadenectomy will be performed along with interferon ad-ministraton (Figure 34)

In situ Extirpation 05 cm Follow-up

Breslow lt 1 mm Extirpation 1 cm Follow-up

Lymphadenectomy

Breslow gt 4 mm Interferon

Breslow ge 1 mm Extirpation 2 cm Sentinel ganglion

+

Figure 34 Melanoma treatment

Kaposirsquos sarcoma

Kaposirsquos sarcoma is the most common cutaneous tumor in HIV patents

Clinical presentation

Kaposirsquos sarcoma has a course with violaceous fusiform macules whichovertme may evolve into indurated nodules with blackberry appearance

This type of sarcoma has been linked to herpesvirus type 8 both in HIV

and seronegatve patents (Table 3)

EPIDERMAL KAPOSIrsquoS 983080HIV983081 CLASSIC KAPOSIrsquoS

Homosexual youth (95) The elderly

Diffuse and bilateral

(frequently in palate and face)

Unilateral plaques

(lower extremities)

Frequent mucosal and visceral involvement Not so frequent

middot Precocious lymphatic invasion

middot Aggressive

Not so precocious

Table 3 Differences between epidermal and classic Kaposirsquos sarcoma

Nodular melanoma

15

Middle-aged men

middot On healthy skin

middot Any zone

middot Sudden onset

middot Uniform black nodulemiddot Rapidly invasive (vertical growth without radial)middot Frequent ulceration and bleeding

Worst histological prognosis

Lentigo malignant melanoma

10

Elderly women

90 on facephotoexposedzones of aging skins(chronic exposure)

Spot that growsduring many years (gt 10)then progresses (nodule)

Better prognosis

Acral lentinginous melanoma

5ndash10 ( 60 black and Asian race)

Elderly men

middot Sole (ankle) handsmucosa ungual bed

middot No relation to photo exposure

middot Macule with mosaic appearance (spot that grows)middot Some amelanisticmiddot Bad prognosis due to late diagnosis

Melanoma of super1047297cial extension

70

Young women

middot 30 previous nervusmiddot Intermittent exposuremiddot Men back middot Women legs

More frequent

middot Macula with mosaic appearance in colors that grows 4-5 years and then in1047297ltrates (nodule)middot Metastasis 35 to 70

Figure 33 Clinical forms of malignant melanoma

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Dermatology

Diagnosis

Diagnosis relies on clinical suspicion and histopathological confirma-

ton

Treatment

Treatment of localized forms can include surgical extrpaton radiother-

apy or intralesional vinblastne

If the sarcoma is disseminated optons involve interferon or chemo-

therapy

Mycosis Fungoides

Mycosis fungoides is a T-cell lymphoma of low-grade malignancy Its

clinical course may be very slow and surpass 50 years Three stages are

clinically diff erentated

1 Eczematous or macular phase predominantly truncular erythema-

tous macules with years of evoluton They resemble a chromic ec-

zema Histology is unspecifi

c at this stage2 Infiltratve plaque phase infiltrated erythematous plaques appear

Histology is diagnostc at this stage A dermal infiltrate of atypical

lymphocytes band forms can be observed composed of CD+4 T

lymphocytes with cerebriform nuclei There is a marked epidermo-

tropism with the presence of clusters of intraepidermal lympho-

cytes called Pautrierrsquos microabscesses (Figure 35)

Figure 35 Mycosis fungoides Infiltrative plaque phase

3 Tumoral phase erythematous exophytc plaques start to appear

(tumors) with a tendency to ulceraton They can have a large size

Histology may become unspecific again as epidermotropism disap-

pears

In more advanced stages of the disease there is aff ectaton of extra-

cutaneous organs such as lymph nodes liver spleen lungs and bone

marrow Besides there may be blastc transformaton Other possible

complicaton is sepsis by Staphylococcus aureus

These three stages usually develop consecutvely nevertheless there

may patents whose debut starts directly with the tumoral stage

Remember

Microabscesses of mycosis fungoides are due to lymphocytes and are calledPautrierrsquos abscesses Psoriasis microabscesses result from neutrophils andare labeled as Munro-Sabouraud

Seacutezary Syndrome

Seacutezary syndrome can be considered as the leukemic phase of T-cell cu-

taneous lymphoma It is defined by the triad erythroderma (Figure 36

lymphadenopathies and the existence of more than 1000 Seacutezary cellsper milliliter in peripheral blood Seacutezary cells are atypical T- lymphocyte

with cerebriform nuclei

Very intense pruritus is characteristc For many authors Seacutezary syn-

drome is an aggressive clinical form and a bad prognosis of a mycosis

fungoides

Figure 36 Erythroderma due to Seacutezary syndrome

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Amer ican Manual of Examinat ion in Medicine (2CK)

4

Diagnosis

Diagnosis of this conditon is generally clinical

If there is no certainty a biopsy must be done which will reveal hyper-

keratosis acanthosis and parakeratosis

There is an increase in polymorphonuclears (sterile abscesses) in the

stratum corneum which are called Munro abscesses

Treatment (Table 1)

For moderate severe forms of psoriasis that do not respond to clas-

sical systemic treatments (see table) They are monoclonal antbod-

ies against proinflammatory substances that are high in patents with

psoriasis [alpha tumor necrosis factor (TNF) interleukin IL 12 and

23] Some of them are infliximab adalimumab ustekinumab and

etanercept

36 Urticaria

Urtcaria is an immunologic and inflammatory reacton of the skin

against diverse etological factors Independently of the cause release

of histamine and other inflammatory mediators occurs which cause va-

sodilaton and increase in capillary permeability producing an edema in

superficial dermis Urtcarias are divided in acute and chronic urtcarias

depending on whether outbreaks persist more or less than six weeks

About 60 of acute urtcarias are idiopathic Chronic urtcarias show a

higher percentage

Urtcarias of known origin are usually due to infectons drugs or food

Clinical Presentation

Clinical presentaton is characterized by the appearance of pruritc wheals

that last less than 24 hours and can be accompanied with angioedema

TREATMENT USES SIDE EFFECTS AND CONTRAINDICATIONS

Topic Mild-moderatepsoriasis

(lt 25 body

surface)

Emollients (urea glycerin) Moisturizing

Keratolytics (salicylic acid) Eliminate excess of scales

Reductants (dithranol) Hyperkeratotic plaques middot Stain skin and clothing

middot Irritating

middot Acneiform eruptions

Corticoids middot Stable psoriasis

in plates

middot The most used

middot Tachyphylaxis

middot Percutaneous absorption

middot Possible new outbreak after stopping medication

middot Avoid prolonged treatment

Vitamin D analogues

(calcitriol calcipotriol and

tacalcitol)

Stable psoriasis in plates middot Irritating in face and skin folds

middot Hypercalcemia

Systemic Moderate-

severe psoriasis

(gt 25 body

surface)

Psoralens plus ultraviolet

light of the A wavelength(PUVA)

Combinable with topics

and retinoids (RePUVA)

middot Cutaneous aging and carcinogenesis

middot Erythroderma and xerosis middot Immunosuppression

middot Hepatitis by psoralens

middot Not in children pregnancy patients with hepatic or renal

insuffi ciency photosensitivity or cutaneous precancerosis

middot Cataracts

middot It accumulates in the crystalline during 24 h (sunglasses)

Retinoids (acitretin) middot Severe psoriasis

pustular

or erythrodermic

middot It is not usually used

in women in fertile age

(see side effects)

middot Cutaneous dryness (the most frequent)

middot Hypertriglyceridemia

middot Hypercholesterolemia

middot Increase in transaminases

middot Diffuse alopecia

middot Vertebral hyperostosis ligamentous calci1047297cations

middot Teratogenicity avoid pregnancy until 2 years after

1047297nishing treatment

middot Avoid in children and patients with hepatic or renal failure

Cyclosporine A middot In1047298ammatory severe

psoriasis resistant to

other treatments

middot Rapid action

middot Rebound effect

middot Nephrotoxicity

middot High blood pressure (HBP)

middot Epitheliomas and lymphomas

middot Hypertrichosis

middot Gingival hyperplasia

middot Hyperuricemia

Methotrexate middot Severe psoriasis

resistant to other

treatments

middot Psoriatic arthropathy

middot Hepatotoxicity

middot Myelosuppression

middot Teratogenicity until 3 months after ending treatment

middot Photosensitivity

Table 1 Psoriasis treatment

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Dermatology

Vasculits urtcaria should be ruled out when lesions last more than 24 hours

and are accompanied with systemic clinical symptoms (ie arthralgias)

Treatment

Oral anthistamine therapy is the treatment of choice

Systemic cortcoids for severe or refractory cases

Adrenalin for severe cases with anaphylaxis

37 Toxicodermas

Toxicodermas are quite variable cutaneous reactons that appear afer

drug administraton They are one of the most frequent side eff ects of

drugs The causatve agents for many toxicodermas stll remains un-

known either immunological or not and clinical presentaton does not

facilitate agent dist

nct

on

Morbilliform exanthem is the most frequent A morbilliform exanthem

is a generalized erupton formed by symmetric and confluent macules

and papules that usually start by the trunk

They can appear one or two weeks afer taking the drug

A morbilliform exanthem can be associated with fever pruritus and eo-

sinophilia

The most frequent are non steroid ant-inflammatories antbiotcs (sul-

phamides and penicillins) antepileptcs allopurinol and N acetyl-cystene

DiagnosisDiagnosis is according to clinical presentaton

Treatment

Treatment implies withdrawal of potentally responsible drug Topic or

systemic anthistamines and cortcoids are given according to the extent

of symptoms (Figure 4)

Figure 4 Morbilliform exanthem due to amoxicillin

38 Multiform Erythema

Stevens-Johnson Syndrome

and Toxic Epidermal Necrolysis

Multform erythemas (ME) are of undetermined etopathogenesis

regarded as a cutaneous reacton against a diversity of stmuli Their

histologies show similarites what leads to consideraton of a common

pathogenesis

Clinical Presentation

Three diff erent groups have been described although many a tme their

clinical symptoms overlap

bull Erythema multforme minor is the most frequent with around 80

of the cases It usually precedes a symptomatc infecton by simple

herpes virus (60) or subclinical infecton about 15 days before

Erythema multforme minor manifests itself on extensor surfaces

at hands elbows and feet as a symmetric erupton of erythema-

tous edematous lesions with target-shape (herpes iris of Batemanor rosee-paerned lesion) with a violaceous sometmes bullous

center (Figure 5)

Mucosal aff ectaton is rare with small erosions in oral mucosa Erythe-

ma multforme minor tends to recurrence with subsequent outbreaks

of herpetc lesions

Figure 5 Erythema multiforme minor Herpes iris of Bateman

bull Erythema mult

forme major or Stevens-Johnson syndrome is therarest It normally has a prodromal period of untl 14 days with fe-

ver cough cephalea arthralgias and other symptoms Subsequent

to the prodromal period erythematous edematous plates appear

which are more extensive with a tendency to form blisters and

greater mucosal erosions (mouth genitals pharynx larynx and

conjunctve Figure 6) Systemic symptoms are normal and do not

tend to recurrence

The most frequent etological factors are drugs [sulphamides non

steroid ant-inflammatory drugs (NSAIDs) antconvulsants and an-

tbiotcs in decreasing order) Infectous agents have been also in-

volved mainly mycoplasma pneumoniae

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Amer ican Manual of Examinat ion in Medicine (2CK)

6

Figure 6 Exudative erythema multiforme major

bull Toxic epidermal necrolysis (TEN) many authors consider it the

most severe form of erythema multforme major arguing the same

pharmacological agents A morbilliform rash appears which is rap-idly confluent comprising almost the entre skin surface with flaccid

blisters that leave wide areas of denuded skin Involvement of sev-

eral mucosae is constant

Complicatons ofen occur (pneumonia digestve hemorrhage re-

nal failure and hemodynamic shock) with mortality rates close to

25 In children it must be performed a diff erental diagnosis with

staphylococcal scalded skin syndrome which does not aff ect mu-

cosae

Remember

Diseases that have the Nikolsky sign are TEN staphylococcal scalded skinsyndrome (SSSS) and pemphigus In TEN the whole epidermis comes off(bad prognosis) while in SSSS epidermal detachment occurs at the granularlayer

Histopathology

It must be highlighted the eff acement of dermoepidermal juncton by a

lymphohistocytc infiltrate and vacuolar degeneraton of the baseline lay-

er with necrotc keratnocytes In TEN keratnocytes necrosis is massive

Treatment

In ME minor only symptomat

c treatment is prescribed with topiccortcoids and oral anthistamines Treatment for herpes simplex virus

(HSV) infecton is useful to prevent ME lesions if patent is in the inital

stage of the viral infecton

ME major requires treatment of the underlying infecton or withdrawal

of implied drug and support measures The use of oral steroids accord-

ing to the patentrsquos general state is under discussion

A patent with TEN requires to be admied at the burn treatment room

with monitoring of hematocrit hydroelectrolytc balance and antbiotc

prophylaxis and support measures It is controversial the use of system-

ic cortcoids immunoglobulins andor cyclosporine

39 Erythema Nodosum

Erythema nodosum is the most frequent panniculits Painful erythema-

tous nodules occur mainly in the anterior side of legs with a self-limit-

ing course and predominantly aff ectng young women (Figure 7)

Figure 7 Erythema nodosum

They heal without leaving a scar within a period of four to six weeks

Erythema nodosum may be accompanied with fever deterioraton of

the general state and arthralgias

Patents with erythema nodosum may have a false positve VDRL

Etiology

This conditon is thought to be an immunological response triggered by

multple and diff erent stmuli bacterial fungal and viral infectons sys-temic diseases (sarcoidosis inflammatory intestnal disease Behcetrsquos

syndrome) neoplasias (lymphomas and leukemias) and drugs (oral

contraceptves sulphamides bromides and iodines)

Diagnosis

Erythema nodosum requires a deep biopsy to reveal septal panniculits

without vasculits

Complementary tests can be performed to rule out systemic involvement

for example chest X-ray Mantoux and antstreptolysin O antbody (ASLO)

Treatment Treatment entails eliminatng underlying cause if found then rest and

ant-inflammatories

310 Bullous Pemphigoid

and Pemphigus Vulgaris

See Table 2 and Figures 8 9 10 and 11

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Dermatology

Intercellular

substance ac

middot Pemphigus

Lineal

storage

in lucid

layer

-

Anti-Collagen Ac

Lucid

layer

Thick

layer

Basal

sublayer

Granular

storage

in papillary

dermis

middot Pemphigoid bullousmiddot Herpes gestationis

middot Acquired blistering epidermolysis

middot Dermatitis herpetiformis

Figure 8 Key points for histological diagnosis

of autoimmune blistering diseases

Figure 9 Pemphigus vulgaris

Figure 10 Pemphigus vulgaris with oral mucosa involvement with

erosions

Figure 11 Pemphigoid bullous Tense blisters No sign of Nikolsky

PEMPHIGUS VULGARISGENERALLY

IDIOPATHICHERPES GESTATIONIS

DERMATITIS

HERPETIFORMIS

Clinical presentation middot 40-50 years of age

middot They usually affect mucosae

middot No pruritus

middot Flaccid blister

middot Nikolsky

middot Elderly

middot Sometimes mucosae

middot With pruritus

middot Tense blister

middot No Nikolsky

middot Pregnant women

middot No mucosae

middot With pruritus

middot Herpetiform

middot No Nikolsky

middot 15-35 years of age

middot No mucosae

middot With pruritus

middot Herpetiform

middot No NikolskyDirect immuno1047298uorescence (DIF) IgG IgG IgG IgA

Histology middot INTRAepidermal blister

middot There is acantholysis

middot SUBepidermal blister

middot There are eosinophils

middot SUBepidermal blister

middot There are eosinophils

middot SUBepidermal blister

middot Neutrophils in dermis

Treatment Corticoids at high doses

immunosuppressants rituximab

and immunoglobulins

Corticoids Corticoids Diet +- dapsone

Remember Mortality rate 10 The most frequent Relapse if new

pregnancy

Associated to enteropathy

by gluten 90

Table 2 Autoimmune blistering diseases

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Amer ican Manual of Examinat ion in Medicine (2CK)

8

Chapter 04

Infectious Diseases

41 Viral Infections

Simple Herpes

Infection by Simple Herpes Virus

There are two types of simple herpes (Figure 12)

bull Type I is responsible for most extragenital herpes and 20 of the

genital herpes

bull Type II causes genital herpes and a small percentage of extragenital

herpes

Figure 12 Herpes simplex

Contagion is produced by direct contact though the carrier may be as-

ymptomatc Afer primary infecton virus remains silent in the sensi-

tve porton of cranial or spinal ganglia Immunosuppressed patents

endure the greatest severity of this conditon

Clinical Presentation

bull Extragenital simple herpes recurring orofacial herpes simplex is

the most frequent Most primary infect

ons are asymptomat

c Only5 manifest themselves in the form of herpetc gingivostomatts a

profile characterized by oral ulcers with cervical adenopathy and af-

fectaton of the patentrsquos general state (Figure 13) During relapses

clinical symptoms are milder with cluster vesicles on an erythema-

tous base Some factors facilitate relapses trauma sunlight cold

stress fever and the menstrual cycle

bull Genital simple herpes is the most common cause of genital ulcers

afer trauma Primary infecton is usually symptomatc and occurs

between 3 to 14 days afer sexual contact It causes clustered ulcers

in the balanopreputal sulcus or in the prepuce with painful inguinal

adenopathy Relapses are less severe than primary infecton and oc-

cur more frequently when genital herpes is due to HSV type II

Figure 13 Herpetic gingivostomatitis

bull Eczema herpetcum or Kaposi varicelliform erupton dissemina-

ton of herpetc infecton on pre-existng dermatosis (above all

atopic dermatt

s) bull Neonatal herpes is due to intrapartum contagion of HSV-II with

neurological involvement general deterioraton and skin vesicles or

ulcers

bull Other clinical forms are herpes gladiatorum herpetc whitlow and

keratoconjunctvits

Diagnosis

Diagnosis of this conditon is mainly clinical Virological culture is the

most reliable method of confirmaton The extent of a smear of the le-

sions (Tzanck cytodiagnosis) allows visualizaton of multnucleated cells

and intranuclear inclusions which become evident through histological

study

Treatment

Mild forms do not need treatment Treatment is required in the follow-

ing cases

bull Primary infecton

bull Severe or frequent relapses if they aff ect life quality

bull Complicatons like erythema multforme and eczema herpetcum

Drug of choice is oral acyclovir and its derivatves (valacyclovir famci-

clovir) Topic antvirals have not proven useful favoring maceraton of

lesions and thus over infecton It is not infrequent that topic antvirals

cause allergic contact dermatts due to hypersensitvity

Varicella-Zoster Virus

A primary infecton gives way to varicella (see Pediatrics secton) Afer

varicella the virus remains latent in the sensitve porton of the neural

ganglia and when relapse occurs it leads to zoster herpes

bull Varicella the following symptoms appear afer 15 days of incubaton

fever cephalea pruritus and polymorphic lesions in diff erent stages

macules papules vesicles (Figure 14) ulcers and scabs (starry sky

appearance) Mucosal (ulcers) and scalp involvement is characteristc

Manipulaton can leave scars Bacterial over infecton of lesions is the

most usual complicaton About 20 of adults suff er from varicella

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Dermatology

pneumonia radiologically demonstrable but clinical symptomatology is

only present in around 4 of the cases

Figure 14 Typical vesicles in patients with varicella

bull Zoster herpes thoracic zoster herpes is the most usual It sel-

dom occurs more than once throughout a personrsquos lifetime

It is characterized by vesicles on pre-existing erythema with

metameric distribution and lateral extension The most com-

mon complication is post herpetic neuralgia more frequent in

advanced age Carbamazepine or tricyclic antidepressants (Fig-

ure 15)

Figure 15 Zoster herpes

Special Clinical Forms

Special clinical forms are as follow

bull Ramsay-Hunt syndrome aff ectaton of geniculate ganglion of the

facial nerve

It produces vesicles in the outer ear external auditory canal and

pharynx homolateral facial paralysis deafness and vertgo

bull Ophthalmic involvement can result in severe keratts and requires ur-

gent referral to an ophthalmologist Suspicion should exist on patents

that present herpetc lesions on the tp of the nose) (Hutchinsonrsquos sign)

bull Disseminated zoster herpes several dermatomes are aff ected bilat-

erally Ramsay-Hunt syndrome is characteristc in the immunosup-

pressed

Remember

Affectation of the nose tip makes it necessary for ophthalmologicalexamination because the nose tip is innervated by the same nerve thatinnervates the cornea (1047297rst branch of the trigeminal nerve)

Treatment

Varicella without complicatons is treated symptomatcally Antvirals

are reserved for severe or complicated forms There is a commercial-

ized vaccine of live virus whose indicatons are stll under discussion

Zoster herpes must be treated with antvirals when detected during the

first 48-72 hours and aff ectng patents with

bull Immunosuppression

bull Age above 55

Special clinical forms previously cited

Drugs to be used are oral acyclovir and its derivatves (valacyclovir and

famciclovir) They accelerate the cure of lesions and decrease the inten-

sity of post herpetc neuralgia Patents with renal failure need a dose

adjustment as acyclovir is nephrotoxic These patents are adminis-

tered brivudine in a single daily dose

Molluscum ContagiosumDome shaped pink papules with central umbilicaton (Figure 16) Mol-

luscum contagiosum is typical of children that go to swimming pools It

is also present in the genital zone afer sexual contact and in immuno-

suppressed patents It is caused by Poxvirus

Figure 16 Molluscum contagiosum

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Amer ican Manual of Examinat ion in Medicine (2CK)

0

Lesions are asymptomatc

Diagnosis

Diagnosis is clinical Histology reveals characteristc inclusion bodies

Treatment

Lesions can resolve spontaneously

Cureage cryotherapy or local trichloroacetc acid are eff ectve meth-

ods to destroy lesions

Warts

Human papillomavirus can cause verruca vulgaris palmoplantar and

flat warts and condyloma accuminata Human papillomavirus is the

most frequent sexual transmied disease

Some subtypes of this virus (16 18) are of high risk and can cause epi-

dermoid carcinomas

Direct contact is the mechanism of contagion

Diagnosis

Diagnosis of this conditon is clinical

Staining with acetc acid can help visualize mucosal lesions

Treatment

Genital warts are treated with cryotherapy podophyllotoxin trichloro-

acetc acid imiquimod and 5-fluorouracil

Cervical lesions should be monitored by cytology and biopsy whenever

necessary to rule out cervical cancer (Figures 17 and 18)

Figure 17 Warts in HIV patient

Figure 18 Condyloma accuminata

42 Bacterial Infections

Impetigo

Impetgo is a very contagious superficial infecton without systemic re-

percussion and normally mixed etology by Gram positve cocci (strep-

tococci and staphylococci) Classically the most frequent accepted

cause was Streptococcus pyogenes However at present Staphylococcus

aureus stands out as the predominant cause

The most typical form is impetgo contagiosa (Figure 19) character-

ized by honey-colored (meliceric) scabs which normally appear on

the face and other exposed areas It is typical of children Although

infrequent poststreptococcal glomerulonephrits is a dreadful com-

plicaton

Figure 19 Impetigo contagiosa

On the contrary rheumatc fever shows no relaton to cutaneous strep-

tococcal infectons but only with pharyngeal infectons

There are other less habitual forms called bullous impetgo exclusively

of staphylococcal origin Clinical presentaton involves the presence of

blisters and erosions on the aff ected skin as a consequence of the epi-

dermolytc toxins that these bacteria contain Impetgo is treated with

topical mupirocin penicillin or oral fusidic acid

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Dermatology

Cellulitis

Cellulits is an infecton that aff ects deep dermis and subcutaneous cel-

lular tssues normally caused by streptococci (Streptococcus pyogenes

or of group A)

Community methicillin-resistant S aureus (CMRSA) is a triggering agent

that is becoming more and more frequent

Most common risk factors are diabetes chronic venous insuffi ciency

and immunosuppression

Clinical Presentation

Cellulits presents with erythematous plaques that are ill-defined pain-

ful and hot It is usually accompanied with fever and chills

Diagnosis

Diagnosis is clinical If there is an open door a culture of this area may

help see the source germ and resistance to ant

biot

cs

It is important to rule out abscesses osteomyelits and necrotzing fas-

ciits

If bacteremia is suspected blood cultures need to be performed

Treatment

Treatment implies oral antbiotcs for 7-10 days to cover Gram positve

cocci They are intravenously administered in case of lack of response

to oral treatment involvement of hands or periorbital zone diabetes or

extremes of age

Necrotizing FasciitisNecrotzing fasciits is a deep infecton up to muscular fascia that pro-

duces very intense pain and subsequent anesthesia

In 10 of the cases cellulits is due to an infecton by S pyogenes In the

remaining cases it occurs by a polymicrobial infecton caused by aerobes

and anaerobes including S aureus E coli and Clostridium perfringens

There may be prior history of trauma or surgery

Clinical Presentation

Clinical presentat

on involves pain of sudden onset and edema on theaff ected zone Pain may progress to anesthesia There appears subse-

quent erythema that progresses rapidly into necrosis

Characteristc clinical signs are tssue necrosis blisters intense pain

and gas producton

Diagnosis

Diagnosis is clinical and requires image testng X-rays or a computed

tomography CT

A biopsy of the border of the lesion helps achieve diagnosis

Treatment

Treatment entails precocious surgical debridement It is a surgical emer-

gency In additon to surgery broad-spectrum antbiotherapy will be

needed

Folliculitis

Folliculits is an infecton and inflammaton of one or several follicles

caused mainly by staphylococci

Clinical Presentation

Folliculits shows pustules with follicular distributon

When the infecton is deeper it is called furuncle

If several furuncles are infected a fluctuatng erythematous plaque forms

containing several points of suppuraton This plaque is labeled as anthrax

Diabet

c and immunosuppressed pat

ents are at higher risk

Characteristics of Folliculitis

1 Hot tub or swimming pool folliculits caused by Pseudomonas aeru-

ginosa

2 HIV associated pruritc folliculits or eosinophilic folliculits

Treatment

In mild cases treatment of choice comprises antseptcs and topic an-

tbiotcs

In more severe cases treatment of choice requires oral antbiotcs

Large sized lesions must be drained and a microbiological culture must be

performed to rule out methicillin-resistant Staphylococcus aureus MRSA

Acne Vulgaris

Acne is an inflammatory disease of the pilosebaceous follicle as a con-

sequence of an alteraton in follicular keratnizaton It aff ects adoles-

cents and young adults

Etology is multfactorial alteraton of keratnizaton of follicular infun-

dibulum quanttatve and qualitatve alteraton of sebum producton in

the sebaceous gland and alteratons of bacterial microflora (increase in

quant

ty of P acnes)

Aggravatng factors are stress androgenic oral contraceptves and the

use of cosmetc products that are not oil-free

Clinical Presentation

A comedo is the inital lesion which can be closed (whitehead) or open

(blackhead) and it evolves into inflammatory lesions that listed in as-

cending order of severity are papules pustules nodules and cysts

Lesions progress and leave scars Scars can be increased if lesions are

manipulated

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Amer ican Manual of Examinat ion in Medicine (2CK)

2

Diff erent lesions habitually combine simultaneously so acne becomes

polymorphic It is located in sebaceous areas face back shoulders and

the center thoracic region

Diagnosis

Diagnosis is clinical

Treatment

bull Comedonal acne is treated with topic retnoids and benzoyl peroxide

bull Inflammatory acne treatment requires benzoyl peroxide combined

with topic antbiotcs (erythromycin and clindamycin) Systemic

antbiotc treatment with oral tetracyclines will be prescribed if re-

sponse to topic antbiotc treatment fails

bull Severe nodular cystc acne treatment involves the use of isotret-

noin (13-cis-retnoic acid) It is a derivatve of vitamin A Isotretnoin

produces atrophy in the sebaceous gland and regulates keratniza-

ton The most frequent side eff ect is cutaneous and mucosal xero-

sis Triglycerides cholesterol and transaminases should be moni-

tored as their values may increasebull It can be associated with depression

bull It is teratogenic so pregnancy should be avoided during treatment

and untl a month afer treatment

Pilonidal Cysts

Pilonidal cysts are abscesses in the sacrococcygeal region

This type of cysts has predominance in men between 20 and 40 years

of age It is believed that repeated trauma on the aff ected area favors

their appearance

Clinical Presentation

Pilonidal cysts present with an indurated lesion that is fluctuatng hot

painful but non-adherent to deep planes in the sacrococcygeal region

Pilonidal cysts may or may not be associated to cellulits and purulent drain-

age

Diagnosis

Diagnosis is clinical and anal or perirectal abscesses should be dismissed

Treatment

Treatment implies an incision and surgical drainage

On some occasions a general surgery is required

43 Fungal Infections

Pityriasis Versicolor

Versicolor pityriasis is caused by commensal yeast called Pityrosporum

ovale which transforms into its pathogen form (Malassezia furfur) It

especially aff ects young patents (15 - 45 years of age) but it is rare

in childhood and advanced age Versicolor pityriasis relates to heat

humidity and sebaceous hypersecreton It is characterized by the ap-

pearance of hyperchromic or hypochromic macules that desquamate

on scratching (nail sign) if infecton is actve Macules usually appear on

the center thoracic region and on the back that is to say on seborrheic

zones Relapses are habitual despite treatment

Diagnosis

Diagnosis is normally clinical To that purpose the following serve as

support

bull Woodrsquos lamp emits yellow-orange fluorescence

bull Potassium hydroxide (KOH) test filaments and round elements can

be observed (ldquospaghe and meatball appearancerdquo Figure 20)

Treatment

Treatment is performed with topical azoles Oral administraton applies

for extensive cases or immunosuppressed patents Diff erental diagno-

sis includes pink pityriasis and eczemas (Figure 21)

Figure 20 Versicolor pityriasis Histological cut

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Dermatology

Figure 21 Versicolor pityriasis

Candidiasis

The most common triggering agent is Candida albicans It is normally sapro-

phyt

c although under certain condit

ons candidiasis may become patho-genic (immunosuppression humidity pregnancy and contraceptves)

Clinical Forms

bull Intertrigo erythematous plaque in cutaneous folds Atrophy and

fissures are typically deep in the skin fold as well as satellite and

peripheral lesions (papules andor pustules)

bull Mucosa involvement may cause diverse symptomatology like vul-

vovaginits glossits and white papules in the anterior region of the

oral mucosa Candidal balanits is characterized by the presence of

punctform erosions and pustules on gland and balanopreputal

sulcus Candidal balanits ofen appears afer sexual intercourse or

afer oral antbiotc intake

Remember

Almost a 100 of HIV patients suffer from muguet throughout their diseasecourse

bull Candidiasis of nail fold is usually associated with periungual inflam-

maton (perionixis) and inital proximal aff ectaton which diff erent-

ates it from tnea unguium (Figure 22)

Figure 22 Candidiasis of nail fold

Treatment

Oral Candidiasis fluconazole or nystatn

Candidiasis of the skin (intertrigo) apply topical antfungal medicaton

and keep zone clean and dry

Dermatophytosis or TineasDermatophyte infectons aff ect the skin and keratnized structures like

hair and nails (there is no mucosa involvement) Clinical diagnosis is

achieved afer performing a culture Woodrsquos lamp test normally turns

out to be negatve In general Trichophyton dermatophyte rubrum is

the most frequent dermatophyte

Non Inflammatory Tineas

Non inflammatory tneas do not produce irreversible scarring alope-

cia while inflammatory forms do Tineas are treated with azoles de-

rivatves

The types of tnea are the following

bull Ringworm of the scalp ( t nea capi t s or t nea tonsurans) is charac-

teristc of childhood It presents with alopecic plaques broken hair

and desquamaton Infectons tend to resolve spontaneously with-

out leaving scars at the onset

of puberty

bull Ringworm of the body (herpes

circinatus or t nea corporis) are

erythematous desquamatve

plaques (with more actve bor-

ders) which are also circinate

and normally pruritc (Figure

23) Plaques grow eccentrically

with less actvity in the centerand more in the borders

bull Ringworm of the foot ( t nea

pedis) the most frequent is the

ldquoathlete footrdquo with desquama-

ton in interdigital spaces

bull Tinea incognito refers to tnea

wrongly treated with cort-

coids what makes diagnosis

diffi cult as the lesion has been modified Figure 24)

Figure 24 Tinea incognito secondary to treatment with topical steroids

Figure 23 Herpes circinatus

(tinea corpis)

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Amer ican Manual of Examinat ion in Medicine (2CK)

4

bull Ringworm of the groin (t nea cruris or eczema marginatum von

hebra) formed by erythematous desquamatve plaque with more

actve borders (Figure 25)

Figure 25 Ringworm of the groin (tinea cruris)

bull Tinea unguium subungualhyperkeratosis with onychol-

ysis but without perionixis

(Figure 26)

Diagnosis

Clinical diagnosis is reached afer

performing a culture

Treatment

Treatment involves topical an-

tfungal medicaton in localized

areas

Oral antfungal medicaton is used in extensive forms nail fold or scalp

involvement

44 Parasitic Infections

Pediculosis

Pediculosis is transmied by direct contact or by contact with fomites

which release toxins that produce intense pruritus

Clinical Presentation

Pediculosis capi t s intense pruritus predominant in retroauricular and

occipital regions occasionally with excoriatons and impetginizaton

secondary to excoriatons

Pediculosis corporis intense pruritus in patents with poor hygiene or

who live in overcrowded conditons

Pediculosis pubis genital and pubic pruritus Brownish-grey macules

called maculae ceruleae are typical on underwear and skin These pig-

mentatons appear as a result of a reducton in hemoglobin by a para-

site enzyme

Diagnosis

Diagnosis is clinical and by direct visualizaton

Treatment

Pediculosis is treated with malathion lindane or topical permethrin

Scabies

Scabies is originated by an acarus known as Sarcoptes scabiei It has an

incubaton period of 1 month

Clinical Presentation

Scabies produces generalized pruritus more intense at night The pa-

tent usually catches the infestaton which is passed to the patentrsquos

relat

ves It is common tofi

nd that a recent trip to a tropical country hasbeen made Lesions appear between the fingers (Figure 27) in wrists

feet genitalia mammary areola and axilla but back and face are usu-

ally spared The most specific lesion is the acarine burrow in whose less

scaly end the advancing zone the mite lies Nodules are frequent in

axilla and genitals (nodular scabies)

bull Norwegian scabies is typical of the immunosuppressed Patents

present with generalized hyperkeratosis and scabs Norwegian sca-

bies produce lile pruritus but it is very contagious because there

are many acari

bull Nodular scabies involves the persistence of pruritc nodules despite

treatment Lesions usually appear in axilla and genitalia Pruritus is

due to a hypersensitvity phenomenon because of the acarus al-

ready dead Nodular scabies is treated with cortcoids

Figure 27 Scabies Acarine burrow

Treatment

bull Permethrin cream at 5 is the treatment of choice It is lile toxic

so it can be used in children and pregnant women

bull Topical lindane at 1 irritates and is neurotoxic therefore it is con-

traindicated in pregnant women and children

bull Oral ivermectn is utlized in cases of resistance to prior treatments

There is stll lile experience as to its use but in a first instance a

Figure 26 Tinea unguium

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Dermatology

single dose would be enough to cure scabies (already used by vet-

erinarians)

45 Ischemia

Decubitus Ulcers

Decubitus ulcers are the result of ischemic necrosis by contnuous pres-

sure on an area which restricts microcirculaton in that zone

Clinical Presentation

Decubitus ulcers are present in patents in bed with scarce mobilizaton

It is favored by bone prominences and lack of fat tssue If sensitvity

decreases there is more risk of formaton of decubitus ulcers

Diagnosis

Diagnosis is achieved based on medical records and clinical presentaton

Treatment

Preventon is of the utmost importance as well as frequent mobiliza-

ton of the patent in bed

Once ulcers have been established hydrocolloid dressings are used for

healing but sometmes surgical debridement is necessary

Gangrene

Gangrene means tssue necrosis

There are three types dry gangrene wet gangrene and gas gangrene

Clinical Presentation

Dry gangrene is due to ischemia generally secondary to atherosclero-

sis Clinical presentaton involves pain cold and paleness of extremi-

tes Once tssue is established it turns bluish-black in color and dry

Wet gangrene is owing to bacterial flora Tissue presents with an edem-

atous appearance either with blisters or pus

Gas gangrene caused by C perfringens It is normally located on re-

cent surgery Bacteria precociously destroyt

ssue producing gas It is amedical emergency

Diagnosis

Clinical diagnosis is obtained by microbiological culture

Treatment

Treatment requires surgical debridement with amputaton if necessary

and associaton of broad spectrum antbiotherapy

Gas gangrene is treated with hyperbaric oxygen

46 Miscellaneous

Acanthosis Nigricans

Acanthosis nigricans are vel-

vet-like papillomatous brown

plaques in neck axilla and groin

folds (Figure 28)

It is associated with diabetes

mellitus Cushingrsquos disease poly-

cystc ovarian syndrome and

obesity

The malignant form of acantho-

sis nigricans is a paraneoplastc

syndrome that diff erentates

from the benign form because

the laer has mucosal and pal-

moplantar involvement

Lichen Planus

Lichen planus is an inflammatory idiopathic disease that equally aff ects

both genders with higher frequency in middle age

Lichen planus has been related to diverse drugs like gold salts

anti-malarial medication and thiazides It has been also linked to

hepatitis C virus infection however this association is currently

doubtful

Clinical Presentation

Lichen planus presents with red-violaceous polygonal flat papulesquite pruritc which localizes on the flexor side of wrists forearms an-

kles and lumbosacral and flank regions On its surface a whitsh retcu-

late can be observed (Wickhamrsquos striae) About 60 - 70 of the cases

present with lesions in oral and genital mucosa oral which appear as

whitsh retculated lesions (Figures 29 and 30)

Figure 29 Lichen planus of oral mucosa with typical whitish

reticulate

Figure 28 Acanthosis nigricans

8182019 USMLE_01_1415_MANUAL_DMpdf

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Amer ican Manual of Examinat ion in Medicine (2CK)

6

Violaceous papules

with white stretch marks

Lichenoid lymphocyte

in1047297ltrate (band formation)

Destruction

of basal layer

Figure 30 Lymphocytic interface reaction (lichen planus)

Treatment

Mild forms are treated with topical cortcoids

Severe cases require oral cortcoids psoralens plus ultraviolet light of

the A wavelength (PUVA) or cyclosporine

Rosacea

Rosacea is a chronic disease of unknown pathogenesis characterized

by erythema and acneiform lesions on the face It aff ects middle aged

women (between 30 and 50 years of age) more

Rosacea etopathogenesis is unknown although there is involvement of

vasomotor lability infecton by Demodex folliculorum photo exposureand genetc predispositon

Clinical Presentation

Rosacea symptomatology comprises facial flushing episodes that end

up by provoking a persistent erythema telangiectasias and papulopus-

tular lesions without comedos Over tme ocular lesions and hyperpla-

sia of sof tssue may develop

Treatment

Avoid vasodilator stmuli

Mild cases require topical metronidazole or azelaic acid

Moderate cases need doxycycline or oral minocyclines

Severe cases are treated with oral isotretnoin at low doses

Pink Pityriasis

Gilbertrsquos pink pityriasis is an acute self-limitng dermatosis which main-

ly aff ects young adults It is of unknown origin although a viral etology

is suspected (there is some speculaton as to links with human herpes-

virus type 7)

Clinical Presentation

Erupton starts with an erythematous plaque between 2 and 5 cm of

diameter with a desquamatve central collaree ofen localized on the

trunk (heraldic mother patch Figure 31)

Figure 31 Pink pityriasis

Around a week later oval papules appear on the trunk and extremi-

tes These papules share similar characteristcs with the mother patch

though the first ones are smaller and distributed according to skin ten-

sion lines Pink pityriasis may be asymptomatc however it is some-

tmes linked to pruritus Lesions may last between 4 and 8 weeks and

disappear without leaving scars

Diagnosis and Treatment

Diagnosis is clinical Treatment is seldom needed and recommended

therapies in the past (PUVA erythromycin or oral antvirals) have not

shown clearly favorable results

Vitiligo

Vitligo is characterized by achromic macules by melanocyte destruc-

ton

Clinical Presentation

Vitligo shows achromic macules of chronic course and variable progres-

sion

Lesions are predominant on acral and periorificial areas They also show

the Koebner phenomenon

Patents may have markers of autoimmune diseases (ie antthyroid

antbodies and diabetes) but these diseases seldom manifest them-

selves

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Dermatology

Treatment

Localized lesions require topical cortcoids

Extensive or generalized lesions are treated with ultraviolet light B

(UVB) or PUVA

Strict solar photoprotecton is indispensable (Figure 32)

Figure 32 Vitiligo

47 Neoplasias

Seborrheic Keratosis

Seborrheic keratosis is the most frequent benign tumor in human be-

ings since it is part of cutaneous aging

Clinical Presentation

Seborrheic keratosis presents with hyperkeratosic papules with an oily

or velvet-like texture crests fissures and horny plugs on their surface

These papules are normally pigmented showing a brownish-black color

Treatment

No treatment is required as lesions do not become malignant

Seborrheic keratosis can be addressed with cureage or cryotherapy

Actinic keratosis

Actnic keratosis is the most common precancerous lesion and aff ects

almost a 100 of the populaton in sunny areas

Clinical Presentation

Actnic keratosis is characterized by erythematous and desquamatve

papules which are hyperkeratosic and rough on touch developing a

chronic course

Diagnosis

Diagnosis is clinical

Treatment

Treatment entails applicaton of topical 5-fluorouracil topical imiqui-

mod cryotherapy or surgery

If underlying carcinoma is suspected a biopsy must be performed to

rule out suspicion

Epidermoid Carcinoma

Epidermoid carcinoma is the second most frequent cutaneous tumor

Solar photo exposure is the main etological factor which is why epider-

moid carcinoma appears in zones of prolonged solar exposure like the

face Most carcinomas appear over premalignant lesions (actnic kera-

tosis and leukoplakia among others)

Clinical Presentation

Clinical presentaton reveals erythematous or erythematosquamous

plaques Over tme these plaques form papules and tumors which of-

ten become ulceratve and bleed

Diagnosis

Diagnosis is based on clinical suspicion and histopathological confirmaton

Treatment

Surgery with safety margins is the treatment of choice In carcinomas

in situ cryotherapy can be used as well as topical imiquimod electro-

coagulaton or CO2 laser techniques in destructon of tumors Radio-therapy may also be used in some cases

Basal Cellular Carcinoma

Basal cellular carcinoma is the most frequent cutaneous tumor Chronic so-

lar photo exposure is the main etological factor hence most of these car-

cinomas aff ect the facial zone in patents who are 40 years of age or older

Gorlinrsquos syndrome should be considered if multple basal cellular carci-

nomas are found in non photo exposed areas

Clinical Presentation

Basal cell carcinoma shows a pearly pink papule and superficial telan-

giectasias

It is localized over healthy skin and never aff ects mucosae

Treatment

Surgery is the treatment of choice Mohs surgery is performed in zones

where surrounding healthy tssue needs to be preserved Other alter-

natves are cryotherapy imiquimod electrocoagulaton radiotherapy

photodynamic therapy and intralesional interferon Prognosis is excel-

lent as growth is slow and metastasis exceptonal

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8

Melanoma

Melanoma is the most aggressive cutaneous tumor given its ability to

metastasize

Risk factors comprise solar photo exposure clear phototype the pres-

ence of dysplastc nevus or a high number of melanocytc nevi Fam-

ily history is quite important as some genetc mutatons determine a

higher risk of developing the disease

Clinical Forms

See Figure 33

Diagnosis

Precocious diagnosis is essental to perform precocious surgical extrpaton

The ABCDE criteria can help patents to see if they need to seek medical

consultaton (asymmetry of lesion uneven borders color and diameter

greater than 6 mm or abnormal evolut

on)

The Breslow index is the thickness of the lesion measured in millimeters

and is the main prognosis factor

Treatment

The base of treatment is precocious surgical extrpaton If the Breslow

index is less than 1 mm margins of 1 cm will be performed If Breslow

index is greater than 1 mm margins will be of 2 cm

For melanomas with a Breslow index greater than 1 mm the sentnel

ganglion must be located This is the first draining lymph node of the

territory where the tumor is localized If the ganglion is positve re-

gional lymphadenectomy will be performed along with interferon ad-ministraton (Figure 34)

In situ Extirpation 05 cm Follow-up

Breslow lt 1 mm Extirpation 1 cm Follow-up

Lymphadenectomy

Breslow gt 4 mm Interferon

Breslow ge 1 mm Extirpation 2 cm Sentinel ganglion

+

Figure 34 Melanoma treatment

Kaposirsquos sarcoma

Kaposirsquos sarcoma is the most common cutaneous tumor in HIV patents

Clinical presentation

Kaposirsquos sarcoma has a course with violaceous fusiform macules whichovertme may evolve into indurated nodules with blackberry appearance

This type of sarcoma has been linked to herpesvirus type 8 both in HIV

and seronegatve patents (Table 3)

EPIDERMAL KAPOSIrsquoS 983080HIV983081 CLASSIC KAPOSIrsquoS

Homosexual youth (95) The elderly

Diffuse and bilateral

(frequently in palate and face)

Unilateral plaques

(lower extremities)

Frequent mucosal and visceral involvement Not so frequent

middot Precocious lymphatic invasion

middot Aggressive

Not so precocious

Table 3 Differences between epidermal and classic Kaposirsquos sarcoma

Nodular melanoma

15

Middle-aged men

middot On healthy skin

middot Any zone

middot Sudden onset

middot Uniform black nodulemiddot Rapidly invasive (vertical growth without radial)middot Frequent ulceration and bleeding

Worst histological prognosis

Lentigo malignant melanoma

10

Elderly women

90 on facephotoexposedzones of aging skins(chronic exposure)

Spot that growsduring many years (gt 10)then progresses (nodule)

Better prognosis

Acral lentinginous melanoma

5ndash10 ( 60 black and Asian race)

Elderly men

middot Sole (ankle) handsmucosa ungual bed

middot No relation to photo exposure

middot Macule with mosaic appearance (spot that grows)middot Some amelanisticmiddot Bad prognosis due to late diagnosis

Melanoma of super1047297cial extension

70

Young women

middot 30 previous nervusmiddot Intermittent exposuremiddot Men back middot Women legs

More frequent

middot Macula with mosaic appearance in colors that grows 4-5 years and then in1047297ltrates (nodule)middot Metastasis 35 to 70

Figure 33 Clinical forms of malignant melanoma

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Dermatology

Diagnosis

Diagnosis relies on clinical suspicion and histopathological confirma-

ton

Treatment

Treatment of localized forms can include surgical extrpaton radiother-

apy or intralesional vinblastne

If the sarcoma is disseminated optons involve interferon or chemo-

therapy

Mycosis Fungoides

Mycosis fungoides is a T-cell lymphoma of low-grade malignancy Its

clinical course may be very slow and surpass 50 years Three stages are

clinically diff erentated

1 Eczematous or macular phase predominantly truncular erythema-

tous macules with years of evoluton They resemble a chromic ec-

zema Histology is unspecifi

c at this stage2 Infiltratve plaque phase infiltrated erythematous plaques appear

Histology is diagnostc at this stage A dermal infiltrate of atypical

lymphocytes band forms can be observed composed of CD+4 T

lymphocytes with cerebriform nuclei There is a marked epidermo-

tropism with the presence of clusters of intraepidermal lympho-

cytes called Pautrierrsquos microabscesses (Figure 35)

Figure 35 Mycosis fungoides Infiltrative plaque phase

3 Tumoral phase erythematous exophytc plaques start to appear

(tumors) with a tendency to ulceraton They can have a large size

Histology may become unspecific again as epidermotropism disap-

pears

In more advanced stages of the disease there is aff ectaton of extra-

cutaneous organs such as lymph nodes liver spleen lungs and bone

marrow Besides there may be blastc transformaton Other possible

complicaton is sepsis by Staphylococcus aureus

These three stages usually develop consecutvely nevertheless there

may patents whose debut starts directly with the tumoral stage

Remember

Microabscesses of mycosis fungoides are due to lymphocytes and are calledPautrierrsquos abscesses Psoriasis microabscesses result from neutrophils andare labeled as Munro-Sabouraud

Seacutezary Syndrome

Seacutezary syndrome can be considered as the leukemic phase of T-cell cu-

taneous lymphoma It is defined by the triad erythroderma (Figure 36

lymphadenopathies and the existence of more than 1000 Seacutezary cellsper milliliter in peripheral blood Seacutezary cells are atypical T- lymphocyte

with cerebriform nuclei

Very intense pruritus is characteristc For many authors Seacutezary syn-

drome is an aggressive clinical form and a bad prognosis of a mycosis

fungoides

Figure 36 Erythroderma due to Seacutezary syndrome

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Dermatology

Vasculits urtcaria should be ruled out when lesions last more than 24 hours

and are accompanied with systemic clinical symptoms (ie arthralgias)

Treatment

Oral anthistamine therapy is the treatment of choice

Systemic cortcoids for severe or refractory cases

Adrenalin for severe cases with anaphylaxis

37 Toxicodermas

Toxicodermas are quite variable cutaneous reactons that appear afer

drug administraton They are one of the most frequent side eff ects of

drugs The causatve agents for many toxicodermas stll remains un-

known either immunological or not and clinical presentaton does not

facilitate agent dist

nct

on

Morbilliform exanthem is the most frequent A morbilliform exanthem

is a generalized erupton formed by symmetric and confluent macules

and papules that usually start by the trunk

They can appear one or two weeks afer taking the drug

A morbilliform exanthem can be associated with fever pruritus and eo-

sinophilia

The most frequent are non steroid ant-inflammatories antbiotcs (sul-

phamides and penicillins) antepileptcs allopurinol and N acetyl-cystene

DiagnosisDiagnosis is according to clinical presentaton

Treatment

Treatment implies withdrawal of potentally responsible drug Topic or

systemic anthistamines and cortcoids are given according to the extent

of symptoms (Figure 4)

Figure 4 Morbilliform exanthem due to amoxicillin

38 Multiform Erythema

Stevens-Johnson Syndrome

and Toxic Epidermal Necrolysis

Multform erythemas (ME) are of undetermined etopathogenesis

regarded as a cutaneous reacton against a diversity of stmuli Their

histologies show similarites what leads to consideraton of a common

pathogenesis

Clinical Presentation

Three diff erent groups have been described although many a tme their

clinical symptoms overlap

bull Erythema multforme minor is the most frequent with around 80

of the cases It usually precedes a symptomatc infecton by simple

herpes virus (60) or subclinical infecton about 15 days before

Erythema multforme minor manifests itself on extensor surfaces

at hands elbows and feet as a symmetric erupton of erythema-

tous edematous lesions with target-shape (herpes iris of Batemanor rosee-paerned lesion) with a violaceous sometmes bullous

center (Figure 5)

Mucosal aff ectaton is rare with small erosions in oral mucosa Erythe-

ma multforme minor tends to recurrence with subsequent outbreaks

of herpetc lesions

Figure 5 Erythema multiforme minor Herpes iris of Bateman

bull Erythema mult

forme major or Stevens-Johnson syndrome is therarest It normally has a prodromal period of untl 14 days with fe-

ver cough cephalea arthralgias and other symptoms Subsequent

to the prodromal period erythematous edematous plates appear

which are more extensive with a tendency to form blisters and

greater mucosal erosions (mouth genitals pharynx larynx and

conjunctve Figure 6) Systemic symptoms are normal and do not

tend to recurrence

The most frequent etological factors are drugs [sulphamides non

steroid ant-inflammatory drugs (NSAIDs) antconvulsants and an-

tbiotcs in decreasing order) Infectous agents have been also in-

volved mainly mycoplasma pneumoniae

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Amer ican Manual of Examinat ion in Medicine (2CK)

6

Figure 6 Exudative erythema multiforme major

bull Toxic epidermal necrolysis (TEN) many authors consider it the

most severe form of erythema multforme major arguing the same

pharmacological agents A morbilliform rash appears which is rap-idly confluent comprising almost the entre skin surface with flaccid

blisters that leave wide areas of denuded skin Involvement of sev-

eral mucosae is constant

Complicatons ofen occur (pneumonia digestve hemorrhage re-

nal failure and hemodynamic shock) with mortality rates close to

25 In children it must be performed a diff erental diagnosis with

staphylococcal scalded skin syndrome which does not aff ect mu-

cosae

Remember

Diseases that have the Nikolsky sign are TEN staphylococcal scalded skinsyndrome (SSSS) and pemphigus In TEN the whole epidermis comes off(bad prognosis) while in SSSS epidermal detachment occurs at the granularlayer

Histopathology

It must be highlighted the eff acement of dermoepidermal juncton by a

lymphohistocytc infiltrate and vacuolar degeneraton of the baseline lay-

er with necrotc keratnocytes In TEN keratnocytes necrosis is massive

Treatment

In ME minor only symptomat

c treatment is prescribed with topiccortcoids and oral anthistamines Treatment for herpes simplex virus

(HSV) infecton is useful to prevent ME lesions if patent is in the inital

stage of the viral infecton

ME major requires treatment of the underlying infecton or withdrawal

of implied drug and support measures The use of oral steroids accord-

ing to the patentrsquos general state is under discussion

A patent with TEN requires to be admied at the burn treatment room

with monitoring of hematocrit hydroelectrolytc balance and antbiotc

prophylaxis and support measures It is controversial the use of system-

ic cortcoids immunoglobulins andor cyclosporine

39 Erythema Nodosum

Erythema nodosum is the most frequent panniculits Painful erythema-

tous nodules occur mainly in the anterior side of legs with a self-limit-

ing course and predominantly aff ectng young women (Figure 7)

Figure 7 Erythema nodosum

They heal without leaving a scar within a period of four to six weeks

Erythema nodosum may be accompanied with fever deterioraton of

the general state and arthralgias

Patents with erythema nodosum may have a false positve VDRL

Etiology

This conditon is thought to be an immunological response triggered by

multple and diff erent stmuli bacterial fungal and viral infectons sys-temic diseases (sarcoidosis inflammatory intestnal disease Behcetrsquos

syndrome) neoplasias (lymphomas and leukemias) and drugs (oral

contraceptves sulphamides bromides and iodines)

Diagnosis

Erythema nodosum requires a deep biopsy to reveal septal panniculits

without vasculits

Complementary tests can be performed to rule out systemic involvement

for example chest X-ray Mantoux and antstreptolysin O antbody (ASLO)

Treatment Treatment entails eliminatng underlying cause if found then rest and

ant-inflammatories

310 Bullous Pemphigoid

and Pemphigus Vulgaris

See Table 2 and Figures 8 9 10 and 11

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Dermatology

Intercellular

substance ac

middot Pemphigus

Lineal

storage

in lucid

layer

-

Anti-Collagen Ac

Lucid

layer

Thick

layer

Basal

sublayer

Granular

storage

in papillary

dermis

middot Pemphigoid bullousmiddot Herpes gestationis

middot Acquired blistering epidermolysis

middot Dermatitis herpetiformis

Figure 8 Key points for histological diagnosis

of autoimmune blistering diseases

Figure 9 Pemphigus vulgaris

Figure 10 Pemphigus vulgaris with oral mucosa involvement with

erosions

Figure 11 Pemphigoid bullous Tense blisters No sign of Nikolsky

PEMPHIGUS VULGARISGENERALLY

IDIOPATHICHERPES GESTATIONIS

DERMATITIS

HERPETIFORMIS

Clinical presentation middot 40-50 years of age

middot They usually affect mucosae

middot No pruritus

middot Flaccid blister

middot Nikolsky

middot Elderly

middot Sometimes mucosae

middot With pruritus

middot Tense blister

middot No Nikolsky

middot Pregnant women

middot No mucosae

middot With pruritus

middot Herpetiform

middot No Nikolsky

middot 15-35 years of age

middot No mucosae

middot With pruritus

middot Herpetiform

middot No NikolskyDirect immuno1047298uorescence (DIF) IgG IgG IgG IgA

Histology middot INTRAepidermal blister

middot There is acantholysis

middot SUBepidermal blister

middot There are eosinophils

middot SUBepidermal blister

middot There are eosinophils

middot SUBepidermal blister

middot Neutrophils in dermis

Treatment Corticoids at high doses

immunosuppressants rituximab

and immunoglobulins

Corticoids Corticoids Diet +- dapsone

Remember Mortality rate 10 The most frequent Relapse if new

pregnancy

Associated to enteropathy

by gluten 90

Table 2 Autoimmune blistering diseases

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8

Chapter 04

Infectious Diseases

41 Viral Infections

Simple Herpes

Infection by Simple Herpes Virus

There are two types of simple herpes (Figure 12)

bull Type I is responsible for most extragenital herpes and 20 of the

genital herpes

bull Type II causes genital herpes and a small percentage of extragenital

herpes

Figure 12 Herpes simplex

Contagion is produced by direct contact though the carrier may be as-

ymptomatc Afer primary infecton virus remains silent in the sensi-

tve porton of cranial or spinal ganglia Immunosuppressed patents

endure the greatest severity of this conditon

Clinical Presentation

bull Extragenital simple herpes recurring orofacial herpes simplex is

the most frequent Most primary infect

ons are asymptomat

c Only5 manifest themselves in the form of herpetc gingivostomatts a

profile characterized by oral ulcers with cervical adenopathy and af-

fectaton of the patentrsquos general state (Figure 13) During relapses

clinical symptoms are milder with cluster vesicles on an erythema-

tous base Some factors facilitate relapses trauma sunlight cold

stress fever and the menstrual cycle

bull Genital simple herpes is the most common cause of genital ulcers

afer trauma Primary infecton is usually symptomatc and occurs

between 3 to 14 days afer sexual contact It causes clustered ulcers

in the balanopreputal sulcus or in the prepuce with painful inguinal

adenopathy Relapses are less severe than primary infecton and oc-

cur more frequently when genital herpes is due to HSV type II

Figure 13 Herpetic gingivostomatitis

bull Eczema herpetcum or Kaposi varicelliform erupton dissemina-

ton of herpetc infecton on pre-existng dermatosis (above all

atopic dermatt

s) bull Neonatal herpes is due to intrapartum contagion of HSV-II with

neurological involvement general deterioraton and skin vesicles or

ulcers

bull Other clinical forms are herpes gladiatorum herpetc whitlow and

keratoconjunctvits

Diagnosis

Diagnosis of this conditon is mainly clinical Virological culture is the

most reliable method of confirmaton The extent of a smear of the le-

sions (Tzanck cytodiagnosis) allows visualizaton of multnucleated cells

and intranuclear inclusions which become evident through histological

study

Treatment

Mild forms do not need treatment Treatment is required in the follow-

ing cases

bull Primary infecton

bull Severe or frequent relapses if they aff ect life quality

bull Complicatons like erythema multforme and eczema herpetcum

Drug of choice is oral acyclovir and its derivatves (valacyclovir famci-

clovir) Topic antvirals have not proven useful favoring maceraton of

lesions and thus over infecton It is not infrequent that topic antvirals

cause allergic contact dermatts due to hypersensitvity

Varicella-Zoster Virus

A primary infecton gives way to varicella (see Pediatrics secton) Afer

varicella the virus remains latent in the sensitve porton of the neural

ganglia and when relapse occurs it leads to zoster herpes

bull Varicella the following symptoms appear afer 15 days of incubaton

fever cephalea pruritus and polymorphic lesions in diff erent stages

macules papules vesicles (Figure 14) ulcers and scabs (starry sky

appearance) Mucosal (ulcers) and scalp involvement is characteristc

Manipulaton can leave scars Bacterial over infecton of lesions is the

most usual complicaton About 20 of adults suff er from varicella

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Dermatology

pneumonia radiologically demonstrable but clinical symptomatology is

only present in around 4 of the cases

Figure 14 Typical vesicles in patients with varicella

bull Zoster herpes thoracic zoster herpes is the most usual It sel-

dom occurs more than once throughout a personrsquos lifetime

It is characterized by vesicles on pre-existing erythema with

metameric distribution and lateral extension The most com-

mon complication is post herpetic neuralgia more frequent in

advanced age Carbamazepine or tricyclic antidepressants (Fig-

ure 15)

Figure 15 Zoster herpes

Special Clinical Forms

Special clinical forms are as follow

bull Ramsay-Hunt syndrome aff ectaton of geniculate ganglion of the

facial nerve

It produces vesicles in the outer ear external auditory canal and

pharynx homolateral facial paralysis deafness and vertgo

bull Ophthalmic involvement can result in severe keratts and requires ur-

gent referral to an ophthalmologist Suspicion should exist on patents

that present herpetc lesions on the tp of the nose) (Hutchinsonrsquos sign)

bull Disseminated zoster herpes several dermatomes are aff ected bilat-

erally Ramsay-Hunt syndrome is characteristc in the immunosup-

pressed

Remember

Affectation of the nose tip makes it necessary for ophthalmologicalexamination because the nose tip is innervated by the same nerve thatinnervates the cornea (1047297rst branch of the trigeminal nerve)

Treatment

Varicella without complicatons is treated symptomatcally Antvirals

are reserved for severe or complicated forms There is a commercial-

ized vaccine of live virus whose indicatons are stll under discussion

Zoster herpes must be treated with antvirals when detected during the

first 48-72 hours and aff ectng patents with

bull Immunosuppression

bull Age above 55

Special clinical forms previously cited

Drugs to be used are oral acyclovir and its derivatves (valacyclovir and

famciclovir) They accelerate the cure of lesions and decrease the inten-

sity of post herpetc neuralgia Patents with renal failure need a dose

adjustment as acyclovir is nephrotoxic These patents are adminis-

tered brivudine in a single daily dose

Molluscum ContagiosumDome shaped pink papules with central umbilicaton (Figure 16) Mol-

luscum contagiosum is typical of children that go to swimming pools It

is also present in the genital zone afer sexual contact and in immuno-

suppressed patents It is caused by Poxvirus

Figure 16 Molluscum contagiosum

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Amer ican Manual of Examinat ion in Medicine (2CK)

0

Lesions are asymptomatc

Diagnosis

Diagnosis is clinical Histology reveals characteristc inclusion bodies

Treatment

Lesions can resolve spontaneously

Cureage cryotherapy or local trichloroacetc acid are eff ectve meth-

ods to destroy lesions

Warts

Human papillomavirus can cause verruca vulgaris palmoplantar and

flat warts and condyloma accuminata Human papillomavirus is the

most frequent sexual transmied disease

Some subtypes of this virus (16 18) are of high risk and can cause epi-

dermoid carcinomas

Direct contact is the mechanism of contagion

Diagnosis

Diagnosis of this conditon is clinical

Staining with acetc acid can help visualize mucosal lesions

Treatment

Genital warts are treated with cryotherapy podophyllotoxin trichloro-

acetc acid imiquimod and 5-fluorouracil

Cervical lesions should be monitored by cytology and biopsy whenever

necessary to rule out cervical cancer (Figures 17 and 18)

Figure 17 Warts in HIV patient

Figure 18 Condyloma accuminata

42 Bacterial Infections

Impetigo

Impetgo is a very contagious superficial infecton without systemic re-

percussion and normally mixed etology by Gram positve cocci (strep-

tococci and staphylococci) Classically the most frequent accepted

cause was Streptococcus pyogenes However at present Staphylococcus

aureus stands out as the predominant cause

The most typical form is impetgo contagiosa (Figure 19) character-

ized by honey-colored (meliceric) scabs which normally appear on

the face and other exposed areas It is typical of children Although

infrequent poststreptococcal glomerulonephrits is a dreadful com-

plicaton

Figure 19 Impetigo contagiosa

On the contrary rheumatc fever shows no relaton to cutaneous strep-

tococcal infectons but only with pharyngeal infectons

There are other less habitual forms called bullous impetgo exclusively

of staphylococcal origin Clinical presentaton involves the presence of

blisters and erosions on the aff ected skin as a consequence of the epi-

dermolytc toxins that these bacteria contain Impetgo is treated with

topical mupirocin penicillin or oral fusidic acid

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Dermatology

Cellulitis

Cellulits is an infecton that aff ects deep dermis and subcutaneous cel-

lular tssues normally caused by streptococci (Streptococcus pyogenes

or of group A)

Community methicillin-resistant S aureus (CMRSA) is a triggering agent

that is becoming more and more frequent

Most common risk factors are diabetes chronic venous insuffi ciency

and immunosuppression

Clinical Presentation

Cellulits presents with erythematous plaques that are ill-defined pain-

ful and hot It is usually accompanied with fever and chills

Diagnosis

Diagnosis is clinical If there is an open door a culture of this area may

help see the source germ and resistance to ant

biot

cs

It is important to rule out abscesses osteomyelits and necrotzing fas-

ciits

If bacteremia is suspected blood cultures need to be performed

Treatment

Treatment implies oral antbiotcs for 7-10 days to cover Gram positve

cocci They are intravenously administered in case of lack of response

to oral treatment involvement of hands or periorbital zone diabetes or

extremes of age

Necrotizing FasciitisNecrotzing fasciits is a deep infecton up to muscular fascia that pro-

duces very intense pain and subsequent anesthesia

In 10 of the cases cellulits is due to an infecton by S pyogenes In the

remaining cases it occurs by a polymicrobial infecton caused by aerobes

and anaerobes including S aureus E coli and Clostridium perfringens

There may be prior history of trauma or surgery

Clinical Presentation

Clinical presentat

on involves pain of sudden onset and edema on theaff ected zone Pain may progress to anesthesia There appears subse-

quent erythema that progresses rapidly into necrosis

Characteristc clinical signs are tssue necrosis blisters intense pain

and gas producton

Diagnosis

Diagnosis is clinical and requires image testng X-rays or a computed

tomography CT

A biopsy of the border of the lesion helps achieve diagnosis

Treatment

Treatment entails precocious surgical debridement It is a surgical emer-

gency In additon to surgery broad-spectrum antbiotherapy will be

needed

Folliculitis

Folliculits is an infecton and inflammaton of one or several follicles

caused mainly by staphylococci

Clinical Presentation

Folliculits shows pustules with follicular distributon

When the infecton is deeper it is called furuncle

If several furuncles are infected a fluctuatng erythematous plaque forms

containing several points of suppuraton This plaque is labeled as anthrax

Diabet

c and immunosuppressed pat

ents are at higher risk

Characteristics of Folliculitis

1 Hot tub or swimming pool folliculits caused by Pseudomonas aeru-

ginosa

2 HIV associated pruritc folliculits or eosinophilic folliculits

Treatment

In mild cases treatment of choice comprises antseptcs and topic an-

tbiotcs

In more severe cases treatment of choice requires oral antbiotcs

Large sized lesions must be drained and a microbiological culture must be

performed to rule out methicillin-resistant Staphylococcus aureus MRSA

Acne Vulgaris

Acne is an inflammatory disease of the pilosebaceous follicle as a con-

sequence of an alteraton in follicular keratnizaton It aff ects adoles-

cents and young adults

Etology is multfactorial alteraton of keratnizaton of follicular infun-

dibulum quanttatve and qualitatve alteraton of sebum producton in

the sebaceous gland and alteratons of bacterial microflora (increase in

quant

ty of P acnes)

Aggravatng factors are stress androgenic oral contraceptves and the

use of cosmetc products that are not oil-free

Clinical Presentation

A comedo is the inital lesion which can be closed (whitehead) or open

(blackhead) and it evolves into inflammatory lesions that listed in as-

cending order of severity are papules pustules nodules and cysts

Lesions progress and leave scars Scars can be increased if lesions are

manipulated

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Amer ican Manual of Examinat ion in Medicine (2CK)

2

Diff erent lesions habitually combine simultaneously so acne becomes

polymorphic It is located in sebaceous areas face back shoulders and

the center thoracic region

Diagnosis

Diagnosis is clinical

Treatment

bull Comedonal acne is treated with topic retnoids and benzoyl peroxide

bull Inflammatory acne treatment requires benzoyl peroxide combined

with topic antbiotcs (erythromycin and clindamycin) Systemic

antbiotc treatment with oral tetracyclines will be prescribed if re-

sponse to topic antbiotc treatment fails

bull Severe nodular cystc acne treatment involves the use of isotret-

noin (13-cis-retnoic acid) It is a derivatve of vitamin A Isotretnoin

produces atrophy in the sebaceous gland and regulates keratniza-

ton The most frequent side eff ect is cutaneous and mucosal xero-

sis Triglycerides cholesterol and transaminases should be moni-

tored as their values may increasebull It can be associated with depression

bull It is teratogenic so pregnancy should be avoided during treatment

and untl a month afer treatment

Pilonidal Cysts

Pilonidal cysts are abscesses in the sacrococcygeal region

This type of cysts has predominance in men between 20 and 40 years

of age It is believed that repeated trauma on the aff ected area favors

their appearance

Clinical Presentation

Pilonidal cysts present with an indurated lesion that is fluctuatng hot

painful but non-adherent to deep planes in the sacrococcygeal region

Pilonidal cysts may or may not be associated to cellulits and purulent drain-

age

Diagnosis

Diagnosis is clinical and anal or perirectal abscesses should be dismissed

Treatment

Treatment implies an incision and surgical drainage

On some occasions a general surgery is required

43 Fungal Infections

Pityriasis Versicolor

Versicolor pityriasis is caused by commensal yeast called Pityrosporum

ovale which transforms into its pathogen form (Malassezia furfur) It

especially aff ects young patents (15 - 45 years of age) but it is rare

in childhood and advanced age Versicolor pityriasis relates to heat

humidity and sebaceous hypersecreton It is characterized by the ap-

pearance of hyperchromic or hypochromic macules that desquamate

on scratching (nail sign) if infecton is actve Macules usually appear on

the center thoracic region and on the back that is to say on seborrheic

zones Relapses are habitual despite treatment

Diagnosis

Diagnosis is normally clinical To that purpose the following serve as

support

bull Woodrsquos lamp emits yellow-orange fluorescence

bull Potassium hydroxide (KOH) test filaments and round elements can

be observed (ldquospaghe and meatball appearancerdquo Figure 20)

Treatment

Treatment is performed with topical azoles Oral administraton applies

for extensive cases or immunosuppressed patents Diff erental diagno-

sis includes pink pityriasis and eczemas (Figure 21)

Figure 20 Versicolor pityriasis Histological cut

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Dermatology

Figure 21 Versicolor pityriasis

Candidiasis

The most common triggering agent is Candida albicans It is normally sapro-

phyt

c although under certain condit

ons candidiasis may become patho-genic (immunosuppression humidity pregnancy and contraceptves)

Clinical Forms

bull Intertrigo erythematous plaque in cutaneous folds Atrophy and

fissures are typically deep in the skin fold as well as satellite and

peripheral lesions (papules andor pustules)

bull Mucosa involvement may cause diverse symptomatology like vul-

vovaginits glossits and white papules in the anterior region of the

oral mucosa Candidal balanits is characterized by the presence of

punctform erosions and pustules on gland and balanopreputal

sulcus Candidal balanits ofen appears afer sexual intercourse or

afer oral antbiotc intake

Remember

Almost a 100 of HIV patients suffer from muguet throughout their diseasecourse

bull Candidiasis of nail fold is usually associated with periungual inflam-

maton (perionixis) and inital proximal aff ectaton which diff erent-

ates it from tnea unguium (Figure 22)

Figure 22 Candidiasis of nail fold

Treatment

Oral Candidiasis fluconazole or nystatn

Candidiasis of the skin (intertrigo) apply topical antfungal medicaton

and keep zone clean and dry

Dermatophytosis or TineasDermatophyte infectons aff ect the skin and keratnized structures like

hair and nails (there is no mucosa involvement) Clinical diagnosis is

achieved afer performing a culture Woodrsquos lamp test normally turns

out to be negatve In general Trichophyton dermatophyte rubrum is

the most frequent dermatophyte

Non Inflammatory Tineas

Non inflammatory tneas do not produce irreversible scarring alope-

cia while inflammatory forms do Tineas are treated with azoles de-

rivatves

The types of tnea are the following

bull Ringworm of the scalp ( t nea capi t s or t nea tonsurans) is charac-

teristc of childhood It presents with alopecic plaques broken hair

and desquamaton Infectons tend to resolve spontaneously with-

out leaving scars at the onset

of puberty

bull Ringworm of the body (herpes

circinatus or t nea corporis) are

erythematous desquamatve

plaques (with more actve bor-

ders) which are also circinate

and normally pruritc (Figure

23) Plaques grow eccentrically

with less actvity in the centerand more in the borders

bull Ringworm of the foot ( t nea

pedis) the most frequent is the

ldquoathlete footrdquo with desquama-

ton in interdigital spaces

bull Tinea incognito refers to tnea

wrongly treated with cort-

coids what makes diagnosis

diffi cult as the lesion has been modified Figure 24)

Figure 24 Tinea incognito secondary to treatment with topical steroids

Figure 23 Herpes circinatus

(tinea corpis)

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Amer ican Manual of Examinat ion in Medicine (2CK)

4

bull Ringworm of the groin (t nea cruris or eczema marginatum von

hebra) formed by erythematous desquamatve plaque with more

actve borders (Figure 25)

Figure 25 Ringworm of the groin (tinea cruris)

bull Tinea unguium subungualhyperkeratosis with onychol-

ysis but without perionixis

(Figure 26)

Diagnosis

Clinical diagnosis is reached afer

performing a culture

Treatment

Treatment involves topical an-

tfungal medicaton in localized

areas

Oral antfungal medicaton is used in extensive forms nail fold or scalp

involvement

44 Parasitic Infections

Pediculosis

Pediculosis is transmied by direct contact or by contact with fomites

which release toxins that produce intense pruritus

Clinical Presentation

Pediculosis capi t s intense pruritus predominant in retroauricular and

occipital regions occasionally with excoriatons and impetginizaton

secondary to excoriatons

Pediculosis corporis intense pruritus in patents with poor hygiene or

who live in overcrowded conditons

Pediculosis pubis genital and pubic pruritus Brownish-grey macules

called maculae ceruleae are typical on underwear and skin These pig-

mentatons appear as a result of a reducton in hemoglobin by a para-

site enzyme

Diagnosis

Diagnosis is clinical and by direct visualizaton

Treatment

Pediculosis is treated with malathion lindane or topical permethrin

Scabies

Scabies is originated by an acarus known as Sarcoptes scabiei It has an

incubaton period of 1 month

Clinical Presentation

Scabies produces generalized pruritus more intense at night The pa-

tent usually catches the infestaton which is passed to the patentrsquos

relat

ves It is common tofi

nd that a recent trip to a tropical country hasbeen made Lesions appear between the fingers (Figure 27) in wrists

feet genitalia mammary areola and axilla but back and face are usu-

ally spared The most specific lesion is the acarine burrow in whose less

scaly end the advancing zone the mite lies Nodules are frequent in

axilla and genitals (nodular scabies)

bull Norwegian scabies is typical of the immunosuppressed Patents

present with generalized hyperkeratosis and scabs Norwegian sca-

bies produce lile pruritus but it is very contagious because there

are many acari

bull Nodular scabies involves the persistence of pruritc nodules despite

treatment Lesions usually appear in axilla and genitalia Pruritus is

due to a hypersensitvity phenomenon because of the acarus al-

ready dead Nodular scabies is treated with cortcoids

Figure 27 Scabies Acarine burrow

Treatment

bull Permethrin cream at 5 is the treatment of choice It is lile toxic

so it can be used in children and pregnant women

bull Topical lindane at 1 irritates and is neurotoxic therefore it is con-

traindicated in pregnant women and children

bull Oral ivermectn is utlized in cases of resistance to prior treatments

There is stll lile experience as to its use but in a first instance a

Figure 26 Tinea unguium

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Dermatology

single dose would be enough to cure scabies (already used by vet-

erinarians)

45 Ischemia

Decubitus Ulcers

Decubitus ulcers are the result of ischemic necrosis by contnuous pres-

sure on an area which restricts microcirculaton in that zone

Clinical Presentation

Decubitus ulcers are present in patents in bed with scarce mobilizaton

It is favored by bone prominences and lack of fat tssue If sensitvity

decreases there is more risk of formaton of decubitus ulcers

Diagnosis

Diagnosis is achieved based on medical records and clinical presentaton

Treatment

Preventon is of the utmost importance as well as frequent mobiliza-

ton of the patent in bed

Once ulcers have been established hydrocolloid dressings are used for

healing but sometmes surgical debridement is necessary

Gangrene

Gangrene means tssue necrosis

There are three types dry gangrene wet gangrene and gas gangrene

Clinical Presentation

Dry gangrene is due to ischemia generally secondary to atherosclero-

sis Clinical presentaton involves pain cold and paleness of extremi-

tes Once tssue is established it turns bluish-black in color and dry

Wet gangrene is owing to bacterial flora Tissue presents with an edem-

atous appearance either with blisters or pus

Gas gangrene caused by C perfringens It is normally located on re-

cent surgery Bacteria precociously destroyt

ssue producing gas It is amedical emergency

Diagnosis

Clinical diagnosis is obtained by microbiological culture

Treatment

Treatment requires surgical debridement with amputaton if necessary

and associaton of broad spectrum antbiotherapy

Gas gangrene is treated with hyperbaric oxygen

46 Miscellaneous

Acanthosis Nigricans

Acanthosis nigricans are vel-

vet-like papillomatous brown

plaques in neck axilla and groin

folds (Figure 28)

It is associated with diabetes

mellitus Cushingrsquos disease poly-

cystc ovarian syndrome and

obesity

The malignant form of acantho-

sis nigricans is a paraneoplastc

syndrome that diff erentates

from the benign form because

the laer has mucosal and pal-

moplantar involvement

Lichen Planus

Lichen planus is an inflammatory idiopathic disease that equally aff ects

both genders with higher frequency in middle age

Lichen planus has been related to diverse drugs like gold salts

anti-malarial medication and thiazides It has been also linked to

hepatitis C virus infection however this association is currently

doubtful

Clinical Presentation

Lichen planus presents with red-violaceous polygonal flat papulesquite pruritc which localizes on the flexor side of wrists forearms an-

kles and lumbosacral and flank regions On its surface a whitsh retcu-

late can be observed (Wickhamrsquos striae) About 60 - 70 of the cases

present with lesions in oral and genital mucosa oral which appear as

whitsh retculated lesions (Figures 29 and 30)

Figure 29 Lichen planus of oral mucosa with typical whitish

reticulate

Figure 28 Acanthosis nigricans

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Amer ican Manual of Examinat ion in Medicine (2CK)

6

Violaceous papules

with white stretch marks

Lichenoid lymphocyte

in1047297ltrate (band formation)

Destruction

of basal layer

Figure 30 Lymphocytic interface reaction (lichen planus)

Treatment

Mild forms are treated with topical cortcoids

Severe cases require oral cortcoids psoralens plus ultraviolet light of

the A wavelength (PUVA) or cyclosporine

Rosacea

Rosacea is a chronic disease of unknown pathogenesis characterized

by erythema and acneiform lesions on the face It aff ects middle aged

women (between 30 and 50 years of age) more

Rosacea etopathogenesis is unknown although there is involvement of

vasomotor lability infecton by Demodex folliculorum photo exposureand genetc predispositon

Clinical Presentation

Rosacea symptomatology comprises facial flushing episodes that end

up by provoking a persistent erythema telangiectasias and papulopus-

tular lesions without comedos Over tme ocular lesions and hyperpla-

sia of sof tssue may develop

Treatment

Avoid vasodilator stmuli

Mild cases require topical metronidazole or azelaic acid

Moderate cases need doxycycline or oral minocyclines

Severe cases are treated with oral isotretnoin at low doses

Pink Pityriasis

Gilbertrsquos pink pityriasis is an acute self-limitng dermatosis which main-

ly aff ects young adults It is of unknown origin although a viral etology

is suspected (there is some speculaton as to links with human herpes-

virus type 7)

Clinical Presentation

Erupton starts with an erythematous plaque between 2 and 5 cm of

diameter with a desquamatve central collaree ofen localized on the

trunk (heraldic mother patch Figure 31)

Figure 31 Pink pityriasis

Around a week later oval papules appear on the trunk and extremi-

tes These papules share similar characteristcs with the mother patch

though the first ones are smaller and distributed according to skin ten-

sion lines Pink pityriasis may be asymptomatc however it is some-

tmes linked to pruritus Lesions may last between 4 and 8 weeks and

disappear without leaving scars

Diagnosis and Treatment

Diagnosis is clinical Treatment is seldom needed and recommended

therapies in the past (PUVA erythromycin or oral antvirals) have not

shown clearly favorable results

Vitiligo

Vitligo is characterized by achromic macules by melanocyte destruc-

ton

Clinical Presentation

Vitligo shows achromic macules of chronic course and variable progres-

sion

Lesions are predominant on acral and periorificial areas They also show

the Koebner phenomenon

Patents may have markers of autoimmune diseases (ie antthyroid

antbodies and diabetes) but these diseases seldom manifest them-

selves

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Dermatology

Treatment

Localized lesions require topical cortcoids

Extensive or generalized lesions are treated with ultraviolet light B

(UVB) or PUVA

Strict solar photoprotecton is indispensable (Figure 32)

Figure 32 Vitiligo

47 Neoplasias

Seborrheic Keratosis

Seborrheic keratosis is the most frequent benign tumor in human be-

ings since it is part of cutaneous aging

Clinical Presentation

Seborrheic keratosis presents with hyperkeratosic papules with an oily

or velvet-like texture crests fissures and horny plugs on their surface

These papules are normally pigmented showing a brownish-black color

Treatment

No treatment is required as lesions do not become malignant

Seborrheic keratosis can be addressed with cureage or cryotherapy

Actinic keratosis

Actnic keratosis is the most common precancerous lesion and aff ects

almost a 100 of the populaton in sunny areas

Clinical Presentation

Actnic keratosis is characterized by erythematous and desquamatve

papules which are hyperkeratosic and rough on touch developing a

chronic course

Diagnosis

Diagnosis is clinical

Treatment

Treatment entails applicaton of topical 5-fluorouracil topical imiqui-

mod cryotherapy or surgery

If underlying carcinoma is suspected a biopsy must be performed to

rule out suspicion

Epidermoid Carcinoma

Epidermoid carcinoma is the second most frequent cutaneous tumor

Solar photo exposure is the main etological factor which is why epider-

moid carcinoma appears in zones of prolonged solar exposure like the

face Most carcinomas appear over premalignant lesions (actnic kera-

tosis and leukoplakia among others)

Clinical Presentation

Clinical presentaton reveals erythematous or erythematosquamous

plaques Over tme these plaques form papules and tumors which of-

ten become ulceratve and bleed

Diagnosis

Diagnosis is based on clinical suspicion and histopathological confirmaton

Treatment

Surgery with safety margins is the treatment of choice In carcinomas

in situ cryotherapy can be used as well as topical imiquimod electro-

coagulaton or CO2 laser techniques in destructon of tumors Radio-therapy may also be used in some cases

Basal Cellular Carcinoma

Basal cellular carcinoma is the most frequent cutaneous tumor Chronic so-

lar photo exposure is the main etological factor hence most of these car-

cinomas aff ect the facial zone in patents who are 40 years of age or older

Gorlinrsquos syndrome should be considered if multple basal cellular carci-

nomas are found in non photo exposed areas

Clinical Presentation

Basal cell carcinoma shows a pearly pink papule and superficial telan-

giectasias

It is localized over healthy skin and never aff ects mucosae

Treatment

Surgery is the treatment of choice Mohs surgery is performed in zones

where surrounding healthy tssue needs to be preserved Other alter-

natves are cryotherapy imiquimod electrocoagulaton radiotherapy

photodynamic therapy and intralesional interferon Prognosis is excel-

lent as growth is slow and metastasis exceptonal

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Amer ican Manual of Examinat ion in Medicine (2CK)

8

Melanoma

Melanoma is the most aggressive cutaneous tumor given its ability to

metastasize

Risk factors comprise solar photo exposure clear phototype the pres-

ence of dysplastc nevus or a high number of melanocytc nevi Fam-

ily history is quite important as some genetc mutatons determine a

higher risk of developing the disease

Clinical Forms

See Figure 33

Diagnosis

Precocious diagnosis is essental to perform precocious surgical extrpaton

The ABCDE criteria can help patents to see if they need to seek medical

consultaton (asymmetry of lesion uneven borders color and diameter

greater than 6 mm or abnormal evolut

on)

The Breslow index is the thickness of the lesion measured in millimeters

and is the main prognosis factor

Treatment

The base of treatment is precocious surgical extrpaton If the Breslow

index is less than 1 mm margins of 1 cm will be performed If Breslow

index is greater than 1 mm margins will be of 2 cm

For melanomas with a Breslow index greater than 1 mm the sentnel

ganglion must be located This is the first draining lymph node of the

territory where the tumor is localized If the ganglion is positve re-

gional lymphadenectomy will be performed along with interferon ad-ministraton (Figure 34)

In situ Extirpation 05 cm Follow-up

Breslow lt 1 mm Extirpation 1 cm Follow-up

Lymphadenectomy

Breslow gt 4 mm Interferon

Breslow ge 1 mm Extirpation 2 cm Sentinel ganglion

+

Figure 34 Melanoma treatment

Kaposirsquos sarcoma

Kaposirsquos sarcoma is the most common cutaneous tumor in HIV patents

Clinical presentation

Kaposirsquos sarcoma has a course with violaceous fusiform macules whichovertme may evolve into indurated nodules with blackberry appearance

This type of sarcoma has been linked to herpesvirus type 8 both in HIV

and seronegatve patents (Table 3)

EPIDERMAL KAPOSIrsquoS 983080HIV983081 CLASSIC KAPOSIrsquoS

Homosexual youth (95) The elderly

Diffuse and bilateral

(frequently in palate and face)

Unilateral plaques

(lower extremities)

Frequent mucosal and visceral involvement Not so frequent

middot Precocious lymphatic invasion

middot Aggressive

Not so precocious

Table 3 Differences between epidermal and classic Kaposirsquos sarcoma

Nodular melanoma

15

Middle-aged men

middot On healthy skin

middot Any zone

middot Sudden onset

middot Uniform black nodulemiddot Rapidly invasive (vertical growth without radial)middot Frequent ulceration and bleeding

Worst histological prognosis

Lentigo malignant melanoma

10

Elderly women

90 on facephotoexposedzones of aging skins(chronic exposure)

Spot that growsduring many years (gt 10)then progresses (nodule)

Better prognosis

Acral lentinginous melanoma

5ndash10 ( 60 black and Asian race)

Elderly men

middot Sole (ankle) handsmucosa ungual bed

middot No relation to photo exposure

middot Macule with mosaic appearance (spot that grows)middot Some amelanisticmiddot Bad prognosis due to late diagnosis

Melanoma of super1047297cial extension

70

Young women

middot 30 previous nervusmiddot Intermittent exposuremiddot Men back middot Women legs

More frequent

middot Macula with mosaic appearance in colors that grows 4-5 years and then in1047297ltrates (nodule)middot Metastasis 35 to 70

Figure 33 Clinical forms of malignant melanoma

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Dermatology

Diagnosis

Diagnosis relies on clinical suspicion and histopathological confirma-

ton

Treatment

Treatment of localized forms can include surgical extrpaton radiother-

apy or intralesional vinblastne

If the sarcoma is disseminated optons involve interferon or chemo-

therapy

Mycosis Fungoides

Mycosis fungoides is a T-cell lymphoma of low-grade malignancy Its

clinical course may be very slow and surpass 50 years Three stages are

clinically diff erentated

1 Eczematous or macular phase predominantly truncular erythema-

tous macules with years of evoluton They resemble a chromic ec-

zema Histology is unspecifi

c at this stage2 Infiltratve plaque phase infiltrated erythematous plaques appear

Histology is diagnostc at this stage A dermal infiltrate of atypical

lymphocytes band forms can be observed composed of CD+4 T

lymphocytes with cerebriform nuclei There is a marked epidermo-

tropism with the presence of clusters of intraepidermal lympho-

cytes called Pautrierrsquos microabscesses (Figure 35)

Figure 35 Mycosis fungoides Infiltrative plaque phase

3 Tumoral phase erythematous exophytc plaques start to appear

(tumors) with a tendency to ulceraton They can have a large size

Histology may become unspecific again as epidermotropism disap-

pears

In more advanced stages of the disease there is aff ectaton of extra-

cutaneous organs such as lymph nodes liver spleen lungs and bone

marrow Besides there may be blastc transformaton Other possible

complicaton is sepsis by Staphylococcus aureus

These three stages usually develop consecutvely nevertheless there

may patents whose debut starts directly with the tumoral stage

Remember

Microabscesses of mycosis fungoides are due to lymphocytes and are calledPautrierrsquos abscesses Psoriasis microabscesses result from neutrophils andare labeled as Munro-Sabouraud

Seacutezary Syndrome

Seacutezary syndrome can be considered as the leukemic phase of T-cell cu-

taneous lymphoma It is defined by the triad erythroderma (Figure 36

lymphadenopathies and the existence of more than 1000 Seacutezary cellsper milliliter in peripheral blood Seacutezary cells are atypical T- lymphocyte

with cerebriform nuclei

Very intense pruritus is characteristc For many authors Seacutezary syn-

drome is an aggressive clinical form and a bad prognosis of a mycosis

fungoides

Figure 36 Erythroderma due to Seacutezary syndrome

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Amer ican Manual of Examinat ion in Medicine (2CK)

6

Figure 6 Exudative erythema multiforme major

bull Toxic epidermal necrolysis (TEN) many authors consider it the

most severe form of erythema multforme major arguing the same

pharmacological agents A morbilliform rash appears which is rap-idly confluent comprising almost the entre skin surface with flaccid

blisters that leave wide areas of denuded skin Involvement of sev-

eral mucosae is constant

Complicatons ofen occur (pneumonia digestve hemorrhage re-

nal failure and hemodynamic shock) with mortality rates close to

25 In children it must be performed a diff erental diagnosis with

staphylococcal scalded skin syndrome which does not aff ect mu-

cosae

Remember

Diseases that have the Nikolsky sign are TEN staphylococcal scalded skinsyndrome (SSSS) and pemphigus In TEN the whole epidermis comes off(bad prognosis) while in SSSS epidermal detachment occurs at the granularlayer

Histopathology

It must be highlighted the eff acement of dermoepidermal juncton by a

lymphohistocytc infiltrate and vacuolar degeneraton of the baseline lay-

er with necrotc keratnocytes In TEN keratnocytes necrosis is massive

Treatment

In ME minor only symptomat

c treatment is prescribed with topiccortcoids and oral anthistamines Treatment for herpes simplex virus

(HSV) infecton is useful to prevent ME lesions if patent is in the inital

stage of the viral infecton

ME major requires treatment of the underlying infecton or withdrawal

of implied drug and support measures The use of oral steroids accord-

ing to the patentrsquos general state is under discussion

A patent with TEN requires to be admied at the burn treatment room

with monitoring of hematocrit hydroelectrolytc balance and antbiotc

prophylaxis and support measures It is controversial the use of system-

ic cortcoids immunoglobulins andor cyclosporine

39 Erythema Nodosum

Erythema nodosum is the most frequent panniculits Painful erythema-

tous nodules occur mainly in the anterior side of legs with a self-limit-

ing course and predominantly aff ectng young women (Figure 7)

Figure 7 Erythema nodosum

They heal without leaving a scar within a period of four to six weeks

Erythema nodosum may be accompanied with fever deterioraton of

the general state and arthralgias

Patents with erythema nodosum may have a false positve VDRL

Etiology

This conditon is thought to be an immunological response triggered by

multple and diff erent stmuli bacterial fungal and viral infectons sys-temic diseases (sarcoidosis inflammatory intestnal disease Behcetrsquos

syndrome) neoplasias (lymphomas and leukemias) and drugs (oral

contraceptves sulphamides bromides and iodines)

Diagnosis

Erythema nodosum requires a deep biopsy to reveal septal panniculits

without vasculits

Complementary tests can be performed to rule out systemic involvement

for example chest X-ray Mantoux and antstreptolysin O antbody (ASLO)

Treatment Treatment entails eliminatng underlying cause if found then rest and

ant-inflammatories

310 Bullous Pemphigoid

and Pemphigus Vulgaris

See Table 2 and Figures 8 9 10 and 11

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Dermatology

Intercellular

substance ac

middot Pemphigus

Lineal

storage

in lucid

layer

-

Anti-Collagen Ac

Lucid

layer

Thick

layer

Basal

sublayer

Granular

storage

in papillary

dermis

middot Pemphigoid bullousmiddot Herpes gestationis

middot Acquired blistering epidermolysis

middot Dermatitis herpetiformis

Figure 8 Key points for histological diagnosis

of autoimmune blistering diseases

Figure 9 Pemphigus vulgaris

Figure 10 Pemphigus vulgaris with oral mucosa involvement with

erosions

Figure 11 Pemphigoid bullous Tense blisters No sign of Nikolsky

PEMPHIGUS VULGARISGENERALLY

IDIOPATHICHERPES GESTATIONIS

DERMATITIS

HERPETIFORMIS

Clinical presentation middot 40-50 years of age

middot They usually affect mucosae

middot No pruritus

middot Flaccid blister

middot Nikolsky

middot Elderly

middot Sometimes mucosae

middot With pruritus

middot Tense blister

middot No Nikolsky

middot Pregnant women

middot No mucosae

middot With pruritus

middot Herpetiform

middot No Nikolsky

middot 15-35 years of age

middot No mucosae

middot With pruritus

middot Herpetiform

middot No NikolskyDirect immuno1047298uorescence (DIF) IgG IgG IgG IgA

Histology middot INTRAepidermal blister

middot There is acantholysis

middot SUBepidermal blister

middot There are eosinophils

middot SUBepidermal blister

middot There are eosinophils

middot SUBepidermal blister

middot Neutrophils in dermis

Treatment Corticoids at high doses

immunosuppressants rituximab

and immunoglobulins

Corticoids Corticoids Diet +- dapsone

Remember Mortality rate 10 The most frequent Relapse if new

pregnancy

Associated to enteropathy

by gluten 90

Table 2 Autoimmune blistering diseases

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Amer ican Manual of Examinat ion in Medicine (2CK)

8

Chapter 04

Infectious Diseases

41 Viral Infections

Simple Herpes

Infection by Simple Herpes Virus

There are two types of simple herpes (Figure 12)

bull Type I is responsible for most extragenital herpes and 20 of the

genital herpes

bull Type II causes genital herpes and a small percentage of extragenital

herpes

Figure 12 Herpes simplex

Contagion is produced by direct contact though the carrier may be as-

ymptomatc Afer primary infecton virus remains silent in the sensi-

tve porton of cranial or spinal ganglia Immunosuppressed patents

endure the greatest severity of this conditon

Clinical Presentation

bull Extragenital simple herpes recurring orofacial herpes simplex is

the most frequent Most primary infect

ons are asymptomat

c Only5 manifest themselves in the form of herpetc gingivostomatts a

profile characterized by oral ulcers with cervical adenopathy and af-

fectaton of the patentrsquos general state (Figure 13) During relapses

clinical symptoms are milder with cluster vesicles on an erythema-

tous base Some factors facilitate relapses trauma sunlight cold

stress fever and the menstrual cycle

bull Genital simple herpes is the most common cause of genital ulcers

afer trauma Primary infecton is usually symptomatc and occurs

between 3 to 14 days afer sexual contact It causes clustered ulcers

in the balanopreputal sulcus or in the prepuce with painful inguinal

adenopathy Relapses are less severe than primary infecton and oc-

cur more frequently when genital herpes is due to HSV type II

Figure 13 Herpetic gingivostomatitis

bull Eczema herpetcum or Kaposi varicelliform erupton dissemina-

ton of herpetc infecton on pre-existng dermatosis (above all

atopic dermatt

s) bull Neonatal herpes is due to intrapartum contagion of HSV-II with

neurological involvement general deterioraton and skin vesicles or

ulcers

bull Other clinical forms are herpes gladiatorum herpetc whitlow and

keratoconjunctvits

Diagnosis

Diagnosis of this conditon is mainly clinical Virological culture is the

most reliable method of confirmaton The extent of a smear of the le-

sions (Tzanck cytodiagnosis) allows visualizaton of multnucleated cells

and intranuclear inclusions which become evident through histological

study

Treatment

Mild forms do not need treatment Treatment is required in the follow-

ing cases

bull Primary infecton

bull Severe or frequent relapses if they aff ect life quality

bull Complicatons like erythema multforme and eczema herpetcum

Drug of choice is oral acyclovir and its derivatves (valacyclovir famci-

clovir) Topic antvirals have not proven useful favoring maceraton of

lesions and thus over infecton It is not infrequent that topic antvirals

cause allergic contact dermatts due to hypersensitvity

Varicella-Zoster Virus

A primary infecton gives way to varicella (see Pediatrics secton) Afer

varicella the virus remains latent in the sensitve porton of the neural

ganglia and when relapse occurs it leads to zoster herpes

bull Varicella the following symptoms appear afer 15 days of incubaton

fever cephalea pruritus and polymorphic lesions in diff erent stages

macules papules vesicles (Figure 14) ulcers and scabs (starry sky

appearance) Mucosal (ulcers) and scalp involvement is characteristc

Manipulaton can leave scars Bacterial over infecton of lesions is the

most usual complicaton About 20 of adults suff er from varicella

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Dermatology

pneumonia radiologically demonstrable but clinical symptomatology is

only present in around 4 of the cases

Figure 14 Typical vesicles in patients with varicella

bull Zoster herpes thoracic zoster herpes is the most usual It sel-

dom occurs more than once throughout a personrsquos lifetime

It is characterized by vesicles on pre-existing erythema with

metameric distribution and lateral extension The most com-

mon complication is post herpetic neuralgia more frequent in

advanced age Carbamazepine or tricyclic antidepressants (Fig-

ure 15)

Figure 15 Zoster herpes

Special Clinical Forms

Special clinical forms are as follow

bull Ramsay-Hunt syndrome aff ectaton of geniculate ganglion of the

facial nerve

It produces vesicles in the outer ear external auditory canal and

pharynx homolateral facial paralysis deafness and vertgo

bull Ophthalmic involvement can result in severe keratts and requires ur-

gent referral to an ophthalmologist Suspicion should exist on patents

that present herpetc lesions on the tp of the nose) (Hutchinsonrsquos sign)

bull Disseminated zoster herpes several dermatomes are aff ected bilat-

erally Ramsay-Hunt syndrome is characteristc in the immunosup-

pressed

Remember

Affectation of the nose tip makes it necessary for ophthalmologicalexamination because the nose tip is innervated by the same nerve thatinnervates the cornea (1047297rst branch of the trigeminal nerve)

Treatment

Varicella without complicatons is treated symptomatcally Antvirals

are reserved for severe or complicated forms There is a commercial-

ized vaccine of live virus whose indicatons are stll under discussion

Zoster herpes must be treated with antvirals when detected during the

first 48-72 hours and aff ectng patents with

bull Immunosuppression

bull Age above 55

Special clinical forms previously cited

Drugs to be used are oral acyclovir and its derivatves (valacyclovir and

famciclovir) They accelerate the cure of lesions and decrease the inten-

sity of post herpetc neuralgia Patents with renal failure need a dose

adjustment as acyclovir is nephrotoxic These patents are adminis-

tered brivudine in a single daily dose

Molluscum ContagiosumDome shaped pink papules with central umbilicaton (Figure 16) Mol-

luscum contagiosum is typical of children that go to swimming pools It

is also present in the genital zone afer sexual contact and in immuno-

suppressed patents It is caused by Poxvirus

Figure 16 Molluscum contagiosum

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Amer ican Manual of Examinat ion in Medicine (2CK)

0

Lesions are asymptomatc

Diagnosis

Diagnosis is clinical Histology reveals characteristc inclusion bodies

Treatment

Lesions can resolve spontaneously

Cureage cryotherapy or local trichloroacetc acid are eff ectve meth-

ods to destroy lesions

Warts

Human papillomavirus can cause verruca vulgaris palmoplantar and

flat warts and condyloma accuminata Human papillomavirus is the

most frequent sexual transmied disease

Some subtypes of this virus (16 18) are of high risk and can cause epi-

dermoid carcinomas

Direct contact is the mechanism of contagion

Diagnosis

Diagnosis of this conditon is clinical

Staining with acetc acid can help visualize mucosal lesions

Treatment

Genital warts are treated with cryotherapy podophyllotoxin trichloro-

acetc acid imiquimod and 5-fluorouracil

Cervical lesions should be monitored by cytology and biopsy whenever

necessary to rule out cervical cancer (Figures 17 and 18)

Figure 17 Warts in HIV patient

Figure 18 Condyloma accuminata

42 Bacterial Infections

Impetigo

Impetgo is a very contagious superficial infecton without systemic re-

percussion and normally mixed etology by Gram positve cocci (strep-

tococci and staphylococci) Classically the most frequent accepted

cause was Streptococcus pyogenes However at present Staphylococcus

aureus stands out as the predominant cause

The most typical form is impetgo contagiosa (Figure 19) character-

ized by honey-colored (meliceric) scabs which normally appear on

the face and other exposed areas It is typical of children Although

infrequent poststreptococcal glomerulonephrits is a dreadful com-

plicaton

Figure 19 Impetigo contagiosa

On the contrary rheumatc fever shows no relaton to cutaneous strep-

tococcal infectons but only with pharyngeal infectons

There are other less habitual forms called bullous impetgo exclusively

of staphylococcal origin Clinical presentaton involves the presence of

blisters and erosions on the aff ected skin as a consequence of the epi-

dermolytc toxins that these bacteria contain Impetgo is treated with

topical mupirocin penicillin or oral fusidic acid

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Dermatology

Cellulitis

Cellulits is an infecton that aff ects deep dermis and subcutaneous cel-

lular tssues normally caused by streptococci (Streptococcus pyogenes

or of group A)

Community methicillin-resistant S aureus (CMRSA) is a triggering agent

that is becoming more and more frequent

Most common risk factors are diabetes chronic venous insuffi ciency

and immunosuppression

Clinical Presentation

Cellulits presents with erythematous plaques that are ill-defined pain-

ful and hot It is usually accompanied with fever and chills

Diagnosis

Diagnosis is clinical If there is an open door a culture of this area may

help see the source germ and resistance to ant

biot

cs

It is important to rule out abscesses osteomyelits and necrotzing fas-

ciits

If bacteremia is suspected blood cultures need to be performed

Treatment

Treatment implies oral antbiotcs for 7-10 days to cover Gram positve

cocci They are intravenously administered in case of lack of response

to oral treatment involvement of hands or periorbital zone diabetes or

extremes of age

Necrotizing FasciitisNecrotzing fasciits is a deep infecton up to muscular fascia that pro-

duces very intense pain and subsequent anesthesia

In 10 of the cases cellulits is due to an infecton by S pyogenes In the

remaining cases it occurs by a polymicrobial infecton caused by aerobes

and anaerobes including S aureus E coli and Clostridium perfringens

There may be prior history of trauma or surgery

Clinical Presentation

Clinical presentat

on involves pain of sudden onset and edema on theaff ected zone Pain may progress to anesthesia There appears subse-

quent erythema that progresses rapidly into necrosis

Characteristc clinical signs are tssue necrosis blisters intense pain

and gas producton

Diagnosis

Diagnosis is clinical and requires image testng X-rays or a computed

tomography CT

A biopsy of the border of the lesion helps achieve diagnosis

Treatment

Treatment entails precocious surgical debridement It is a surgical emer-

gency In additon to surgery broad-spectrum antbiotherapy will be

needed

Folliculitis

Folliculits is an infecton and inflammaton of one or several follicles

caused mainly by staphylococci

Clinical Presentation

Folliculits shows pustules with follicular distributon

When the infecton is deeper it is called furuncle

If several furuncles are infected a fluctuatng erythematous plaque forms

containing several points of suppuraton This plaque is labeled as anthrax

Diabet

c and immunosuppressed pat

ents are at higher risk

Characteristics of Folliculitis

1 Hot tub or swimming pool folliculits caused by Pseudomonas aeru-

ginosa

2 HIV associated pruritc folliculits or eosinophilic folliculits

Treatment

In mild cases treatment of choice comprises antseptcs and topic an-

tbiotcs

In more severe cases treatment of choice requires oral antbiotcs

Large sized lesions must be drained and a microbiological culture must be

performed to rule out methicillin-resistant Staphylococcus aureus MRSA

Acne Vulgaris

Acne is an inflammatory disease of the pilosebaceous follicle as a con-

sequence of an alteraton in follicular keratnizaton It aff ects adoles-

cents and young adults

Etology is multfactorial alteraton of keratnizaton of follicular infun-

dibulum quanttatve and qualitatve alteraton of sebum producton in

the sebaceous gland and alteratons of bacterial microflora (increase in

quant

ty of P acnes)

Aggravatng factors are stress androgenic oral contraceptves and the

use of cosmetc products that are not oil-free

Clinical Presentation

A comedo is the inital lesion which can be closed (whitehead) or open

(blackhead) and it evolves into inflammatory lesions that listed in as-

cending order of severity are papules pustules nodules and cysts

Lesions progress and leave scars Scars can be increased if lesions are

manipulated

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Amer ican Manual of Examinat ion in Medicine (2CK)

2

Diff erent lesions habitually combine simultaneously so acne becomes

polymorphic It is located in sebaceous areas face back shoulders and

the center thoracic region

Diagnosis

Diagnosis is clinical

Treatment

bull Comedonal acne is treated with topic retnoids and benzoyl peroxide

bull Inflammatory acne treatment requires benzoyl peroxide combined

with topic antbiotcs (erythromycin and clindamycin) Systemic

antbiotc treatment with oral tetracyclines will be prescribed if re-

sponse to topic antbiotc treatment fails

bull Severe nodular cystc acne treatment involves the use of isotret-

noin (13-cis-retnoic acid) It is a derivatve of vitamin A Isotretnoin

produces atrophy in the sebaceous gland and regulates keratniza-

ton The most frequent side eff ect is cutaneous and mucosal xero-

sis Triglycerides cholesterol and transaminases should be moni-

tored as their values may increasebull It can be associated with depression

bull It is teratogenic so pregnancy should be avoided during treatment

and untl a month afer treatment

Pilonidal Cysts

Pilonidal cysts are abscesses in the sacrococcygeal region

This type of cysts has predominance in men between 20 and 40 years

of age It is believed that repeated trauma on the aff ected area favors

their appearance

Clinical Presentation

Pilonidal cysts present with an indurated lesion that is fluctuatng hot

painful but non-adherent to deep planes in the sacrococcygeal region

Pilonidal cysts may or may not be associated to cellulits and purulent drain-

age

Diagnosis

Diagnosis is clinical and anal or perirectal abscesses should be dismissed

Treatment

Treatment implies an incision and surgical drainage

On some occasions a general surgery is required

43 Fungal Infections

Pityriasis Versicolor

Versicolor pityriasis is caused by commensal yeast called Pityrosporum

ovale which transforms into its pathogen form (Malassezia furfur) It

especially aff ects young patents (15 - 45 years of age) but it is rare

in childhood and advanced age Versicolor pityriasis relates to heat

humidity and sebaceous hypersecreton It is characterized by the ap-

pearance of hyperchromic or hypochromic macules that desquamate

on scratching (nail sign) if infecton is actve Macules usually appear on

the center thoracic region and on the back that is to say on seborrheic

zones Relapses are habitual despite treatment

Diagnosis

Diagnosis is normally clinical To that purpose the following serve as

support

bull Woodrsquos lamp emits yellow-orange fluorescence

bull Potassium hydroxide (KOH) test filaments and round elements can

be observed (ldquospaghe and meatball appearancerdquo Figure 20)

Treatment

Treatment is performed with topical azoles Oral administraton applies

for extensive cases or immunosuppressed patents Diff erental diagno-

sis includes pink pityriasis and eczemas (Figure 21)

Figure 20 Versicolor pityriasis Histological cut

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Dermatology

Figure 21 Versicolor pityriasis

Candidiasis

The most common triggering agent is Candida albicans It is normally sapro-

phyt

c although under certain condit

ons candidiasis may become patho-genic (immunosuppression humidity pregnancy and contraceptves)

Clinical Forms

bull Intertrigo erythematous plaque in cutaneous folds Atrophy and

fissures are typically deep in the skin fold as well as satellite and

peripheral lesions (papules andor pustules)

bull Mucosa involvement may cause diverse symptomatology like vul-

vovaginits glossits and white papules in the anterior region of the

oral mucosa Candidal balanits is characterized by the presence of

punctform erosions and pustules on gland and balanopreputal

sulcus Candidal balanits ofen appears afer sexual intercourse or

afer oral antbiotc intake

Remember

Almost a 100 of HIV patients suffer from muguet throughout their diseasecourse

bull Candidiasis of nail fold is usually associated with periungual inflam-

maton (perionixis) and inital proximal aff ectaton which diff erent-

ates it from tnea unguium (Figure 22)

Figure 22 Candidiasis of nail fold

Treatment

Oral Candidiasis fluconazole or nystatn

Candidiasis of the skin (intertrigo) apply topical antfungal medicaton

and keep zone clean and dry

Dermatophytosis or TineasDermatophyte infectons aff ect the skin and keratnized structures like

hair and nails (there is no mucosa involvement) Clinical diagnosis is

achieved afer performing a culture Woodrsquos lamp test normally turns

out to be negatve In general Trichophyton dermatophyte rubrum is

the most frequent dermatophyte

Non Inflammatory Tineas

Non inflammatory tneas do not produce irreversible scarring alope-

cia while inflammatory forms do Tineas are treated with azoles de-

rivatves

The types of tnea are the following

bull Ringworm of the scalp ( t nea capi t s or t nea tonsurans) is charac-

teristc of childhood It presents with alopecic plaques broken hair

and desquamaton Infectons tend to resolve spontaneously with-

out leaving scars at the onset

of puberty

bull Ringworm of the body (herpes

circinatus or t nea corporis) are

erythematous desquamatve

plaques (with more actve bor-

ders) which are also circinate

and normally pruritc (Figure

23) Plaques grow eccentrically

with less actvity in the centerand more in the borders

bull Ringworm of the foot ( t nea

pedis) the most frequent is the

ldquoathlete footrdquo with desquama-

ton in interdigital spaces

bull Tinea incognito refers to tnea

wrongly treated with cort-

coids what makes diagnosis

diffi cult as the lesion has been modified Figure 24)

Figure 24 Tinea incognito secondary to treatment with topical steroids

Figure 23 Herpes circinatus

(tinea corpis)

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Amer ican Manual of Examinat ion in Medicine (2CK)

4

bull Ringworm of the groin (t nea cruris or eczema marginatum von

hebra) formed by erythematous desquamatve plaque with more

actve borders (Figure 25)

Figure 25 Ringworm of the groin (tinea cruris)

bull Tinea unguium subungualhyperkeratosis with onychol-

ysis but without perionixis

(Figure 26)

Diagnosis

Clinical diagnosis is reached afer

performing a culture

Treatment

Treatment involves topical an-

tfungal medicaton in localized

areas

Oral antfungal medicaton is used in extensive forms nail fold or scalp

involvement

44 Parasitic Infections

Pediculosis

Pediculosis is transmied by direct contact or by contact with fomites

which release toxins that produce intense pruritus

Clinical Presentation

Pediculosis capi t s intense pruritus predominant in retroauricular and

occipital regions occasionally with excoriatons and impetginizaton

secondary to excoriatons

Pediculosis corporis intense pruritus in patents with poor hygiene or

who live in overcrowded conditons

Pediculosis pubis genital and pubic pruritus Brownish-grey macules

called maculae ceruleae are typical on underwear and skin These pig-

mentatons appear as a result of a reducton in hemoglobin by a para-

site enzyme

Diagnosis

Diagnosis is clinical and by direct visualizaton

Treatment

Pediculosis is treated with malathion lindane or topical permethrin

Scabies

Scabies is originated by an acarus known as Sarcoptes scabiei It has an

incubaton period of 1 month

Clinical Presentation

Scabies produces generalized pruritus more intense at night The pa-

tent usually catches the infestaton which is passed to the patentrsquos

relat

ves It is common tofi

nd that a recent trip to a tropical country hasbeen made Lesions appear between the fingers (Figure 27) in wrists

feet genitalia mammary areola and axilla but back and face are usu-

ally spared The most specific lesion is the acarine burrow in whose less

scaly end the advancing zone the mite lies Nodules are frequent in

axilla and genitals (nodular scabies)

bull Norwegian scabies is typical of the immunosuppressed Patents

present with generalized hyperkeratosis and scabs Norwegian sca-

bies produce lile pruritus but it is very contagious because there

are many acari

bull Nodular scabies involves the persistence of pruritc nodules despite

treatment Lesions usually appear in axilla and genitalia Pruritus is

due to a hypersensitvity phenomenon because of the acarus al-

ready dead Nodular scabies is treated with cortcoids

Figure 27 Scabies Acarine burrow

Treatment

bull Permethrin cream at 5 is the treatment of choice It is lile toxic

so it can be used in children and pregnant women

bull Topical lindane at 1 irritates and is neurotoxic therefore it is con-

traindicated in pregnant women and children

bull Oral ivermectn is utlized in cases of resistance to prior treatments

There is stll lile experience as to its use but in a first instance a

Figure 26 Tinea unguium

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Dermatology

single dose would be enough to cure scabies (already used by vet-

erinarians)

45 Ischemia

Decubitus Ulcers

Decubitus ulcers are the result of ischemic necrosis by contnuous pres-

sure on an area which restricts microcirculaton in that zone

Clinical Presentation

Decubitus ulcers are present in patents in bed with scarce mobilizaton

It is favored by bone prominences and lack of fat tssue If sensitvity

decreases there is more risk of formaton of decubitus ulcers

Diagnosis

Diagnosis is achieved based on medical records and clinical presentaton

Treatment

Preventon is of the utmost importance as well as frequent mobiliza-

ton of the patent in bed

Once ulcers have been established hydrocolloid dressings are used for

healing but sometmes surgical debridement is necessary

Gangrene

Gangrene means tssue necrosis

There are three types dry gangrene wet gangrene and gas gangrene

Clinical Presentation

Dry gangrene is due to ischemia generally secondary to atherosclero-

sis Clinical presentaton involves pain cold and paleness of extremi-

tes Once tssue is established it turns bluish-black in color and dry

Wet gangrene is owing to bacterial flora Tissue presents with an edem-

atous appearance either with blisters or pus

Gas gangrene caused by C perfringens It is normally located on re-

cent surgery Bacteria precociously destroyt

ssue producing gas It is amedical emergency

Diagnosis

Clinical diagnosis is obtained by microbiological culture

Treatment

Treatment requires surgical debridement with amputaton if necessary

and associaton of broad spectrum antbiotherapy

Gas gangrene is treated with hyperbaric oxygen

46 Miscellaneous

Acanthosis Nigricans

Acanthosis nigricans are vel-

vet-like papillomatous brown

plaques in neck axilla and groin

folds (Figure 28)

It is associated with diabetes

mellitus Cushingrsquos disease poly-

cystc ovarian syndrome and

obesity

The malignant form of acantho-

sis nigricans is a paraneoplastc

syndrome that diff erentates

from the benign form because

the laer has mucosal and pal-

moplantar involvement

Lichen Planus

Lichen planus is an inflammatory idiopathic disease that equally aff ects

both genders with higher frequency in middle age

Lichen planus has been related to diverse drugs like gold salts

anti-malarial medication and thiazides It has been also linked to

hepatitis C virus infection however this association is currently

doubtful

Clinical Presentation

Lichen planus presents with red-violaceous polygonal flat papulesquite pruritc which localizes on the flexor side of wrists forearms an-

kles and lumbosacral and flank regions On its surface a whitsh retcu-

late can be observed (Wickhamrsquos striae) About 60 - 70 of the cases

present with lesions in oral and genital mucosa oral which appear as

whitsh retculated lesions (Figures 29 and 30)

Figure 29 Lichen planus of oral mucosa with typical whitish

reticulate

Figure 28 Acanthosis nigricans

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Amer ican Manual of Examinat ion in Medicine (2CK)

6

Violaceous papules

with white stretch marks

Lichenoid lymphocyte

in1047297ltrate (band formation)

Destruction

of basal layer

Figure 30 Lymphocytic interface reaction (lichen planus)

Treatment

Mild forms are treated with topical cortcoids

Severe cases require oral cortcoids psoralens plus ultraviolet light of

the A wavelength (PUVA) or cyclosporine

Rosacea

Rosacea is a chronic disease of unknown pathogenesis characterized

by erythema and acneiform lesions on the face It aff ects middle aged

women (between 30 and 50 years of age) more

Rosacea etopathogenesis is unknown although there is involvement of

vasomotor lability infecton by Demodex folliculorum photo exposureand genetc predispositon

Clinical Presentation

Rosacea symptomatology comprises facial flushing episodes that end

up by provoking a persistent erythema telangiectasias and papulopus-

tular lesions without comedos Over tme ocular lesions and hyperpla-

sia of sof tssue may develop

Treatment

Avoid vasodilator stmuli

Mild cases require topical metronidazole or azelaic acid

Moderate cases need doxycycline or oral minocyclines

Severe cases are treated with oral isotretnoin at low doses

Pink Pityriasis

Gilbertrsquos pink pityriasis is an acute self-limitng dermatosis which main-

ly aff ects young adults It is of unknown origin although a viral etology

is suspected (there is some speculaton as to links with human herpes-

virus type 7)

Clinical Presentation

Erupton starts with an erythematous plaque between 2 and 5 cm of

diameter with a desquamatve central collaree ofen localized on the

trunk (heraldic mother patch Figure 31)

Figure 31 Pink pityriasis

Around a week later oval papules appear on the trunk and extremi-

tes These papules share similar characteristcs with the mother patch

though the first ones are smaller and distributed according to skin ten-

sion lines Pink pityriasis may be asymptomatc however it is some-

tmes linked to pruritus Lesions may last between 4 and 8 weeks and

disappear without leaving scars

Diagnosis and Treatment

Diagnosis is clinical Treatment is seldom needed and recommended

therapies in the past (PUVA erythromycin or oral antvirals) have not

shown clearly favorable results

Vitiligo

Vitligo is characterized by achromic macules by melanocyte destruc-

ton

Clinical Presentation

Vitligo shows achromic macules of chronic course and variable progres-

sion

Lesions are predominant on acral and periorificial areas They also show

the Koebner phenomenon

Patents may have markers of autoimmune diseases (ie antthyroid

antbodies and diabetes) but these diseases seldom manifest them-

selves

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Dermatology

Treatment

Localized lesions require topical cortcoids

Extensive or generalized lesions are treated with ultraviolet light B

(UVB) or PUVA

Strict solar photoprotecton is indispensable (Figure 32)

Figure 32 Vitiligo

47 Neoplasias

Seborrheic Keratosis

Seborrheic keratosis is the most frequent benign tumor in human be-

ings since it is part of cutaneous aging

Clinical Presentation

Seborrheic keratosis presents with hyperkeratosic papules with an oily

or velvet-like texture crests fissures and horny plugs on their surface

These papules are normally pigmented showing a brownish-black color

Treatment

No treatment is required as lesions do not become malignant

Seborrheic keratosis can be addressed with cureage or cryotherapy

Actinic keratosis

Actnic keratosis is the most common precancerous lesion and aff ects

almost a 100 of the populaton in sunny areas

Clinical Presentation

Actnic keratosis is characterized by erythematous and desquamatve

papules which are hyperkeratosic and rough on touch developing a

chronic course

Diagnosis

Diagnosis is clinical

Treatment

Treatment entails applicaton of topical 5-fluorouracil topical imiqui-

mod cryotherapy or surgery

If underlying carcinoma is suspected a biopsy must be performed to

rule out suspicion

Epidermoid Carcinoma

Epidermoid carcinoma is the second most frequent cutaneous tumor

Solar photo exposure is the main etological factor which is why epider-

moid carcinoma appears in zones of prolonged solar exposure like the

face Most carcinomas appear over premalignant lesions (actnic kera-

tosis and leukoplakia among others)

Clinical Presentation

Clinical presentaton reveals erythematous or erythematosquamous

plaques Over tme these plaques form papules and tumors which of-

ten become ulceratve and bleed

Diagnosis

Diagnosis is based on clinical suspicion and histopathological confirmaton

Treatment

Surgery with safety margins is the treatment of choice In carcinomas

in situ cryotherapy can be used as well as topical imiquimod electro-

coagulaton or CO2 laser techniques in destructon of tumors Radio-therapy may also be used in some cases

Basal Cellular Carcinoma

Basal cellular carcinoma is the most frequent cutaneous tumor Chronic so-

lar photo exposure is the main etological factor hence most of these car-

cinomas aff ect the facial zone in patents who are 40 years of age or older

Gorlinrsquos syndrome should be considered if multple basal cellular carci-

nomas are found in non photo exposed areas

Clinical Presentation

Basal cell carcinoma shows a pearly pink papule and superficial telan-

giectasias

It is localized over healthy skin and never aff ects mucosae

Treatment

Surgery is the treatment of choice Mohs surgery is performed in zones

where surrounding healthy tssue needs to be preserved Other alter-

natves are cryotherapy imiquimod electrocoagulaton radiotherapy

photodynamic therapy and intralesional interferon Prognosis is excel-

lent as growth is slow and metastasis exceptonal

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Amer ican Manual of Examinat ion in Medicine (2CK)

8

Melanoma

Melanoma is the most aggressive cutaneous tumor given its ability to

metastasize

Risk factors comprise solar photo exposure clear phototype the pres-

ence of dysplastc nevus or a high number of melanocytc nevi Fam-

ily history is quite important as some genetc mutatons determine a

higher risk of developing the disease

Clinical Forms

See Figure 33

Diagnosis

Precocious diagnosis is essental to perform precocious surgical extrpaton

The ABCDE criteria can help patents to see if they need to seek medical

consultaton (asymmetry of lesion uneven borders color and diameter

greater than 6 mm or abnormal evolut

on)

The Breslow index is the thickness of the lesion measured in millimeters

and is the main prognosis factor

Treatment

The base of treatment is precocious surgical extrpaton If the Breslow

index is less than 1 mm margins of 1 cm will be performed If Breslow

index is greater than 1 mm margins will be of 2 cm

For melanomas with a Breslow index greater than 1 mm the sentnel

ganglion must be located This is the first draining lymph node of the

territory where the tumor is localized If the ganglion is positve re-

gional lymphadenectomy will be performed along with interferon ad-ministraton (Figure 34)

In situ Extirpation 05 cm Follow-up

Breslow lt 1 mm Extirpation 1 cm Follow-up

Lymphadenectomy

Breslow gt 4 mm Interferon

Breslow ge 1 mm Extirpation 2 cm Sentinel ganglion

+

Figure 34 Melanoma treatment

Kaposirsquos sarcoma

Kaposirsquos sarcoma is the most common cutaneous tumor in HIV patents

Clinical presentation

Kaposirsquos sarcoma has a course with violaceous fusiform macules whichovertme may evolve into indurated nodules with blackberry appearance

This type of sarcoma has been linked to herpesvirus type 8 both in HIV

and seronegatve patents (Table 3)

EPIDERMAL KAPOSIrsquoS 983080HIV983081 CLASSIC KAPOSIrsquoS

Homosexual youth (95) The elderly

Diffuse and bilateral

(frequently in palate and face)

Unilateral plaques

(lower extremities)

Frequent mucosal and visceral involvement Not so frequent

middot Precocious lymphatic invasion

middot Aggressive

Not so precocious

Table 3 Differences between epidermal and classic Kaposirsquos sarcoma

Nodular melanoma

15

Middle-aged men

middot On healthy skin

middot Any zone

middot Sudden onset

middot Uniform black nodulemiddot Rapidly invasive (vertical growth without radial)middot Frequent ulceration and bleeding

Worst histological prognosis

Lentigo malignant melanoma

10

Elderly women

90 on facephotoexposedzones of aging skins(chronic exposure)

Spot that growsduring many years (gt 10)then progresses (nodule)

Better prognosis

Acral lentinginous melanoma

5ndash10 ( 60 black and Asian race)

Elderly men

middot Sole (ankle) handsmucosa ungual bed

middot No relation to photo exposure

middot Macule with mosaic appearance (spot that grows)middot Some amelanisticmiddot Bad prognosis due to late diagnosis

Melanoma of super1047297cial extension

70

Young women

middot 30 previous nervusmiddot Intermittent exposuremiddot Men back middot Women legs

More frequent

middot Macula with mosaic appearance in colors that grows 4-5 years and then in1047297ltrates (nodule)middot Metastasis 35 to 70

Figure 33 Clinical forms of malignant melanoma

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Dermatology

Diagnosis

Diagnosis relies on clinical suspicion and histopathological confirma-

ton

Treatment

Treatment of localized forms can include surgical extrpaton radiother-

apy or intralesional vinblastne

If the sarcoma is disseminated optons involve interferon or chemo-

therapy

Mycosis Fungoides

Mycosis fungoides is a T-cell lymphoma of low-grade malignancy Its

clinical course may be very slow and surpass 50 years Three stages are

clinically diff erentated

1 Eczematous or macular phase predominantly truncular erythema-

tous macules with years of evoluton They resemble a chromic ec-

zema Histology is unspecifi

c at this stage2 Infiltratve plaque phase infiltrated erythematous plaques appear

Histology is diagnostc at this stage A dermal infiltrate of atypical

lymphocytes band forms can be observed composed of CD+4 T

lymphocytes with cerebriform nuclei There is a marked epidermo-

tropism with the presence of clusters of intraepidermal lympho-

cytes called Pautrierrsquos microabscesses (Figure 35)

Figure 35 Mycosis fungoides Infiltrative plaque phase

3 Tumoral phase erythematous exophytc plaques start to appear

(tumors) with a tendency to ulceraton They can have a large size

Histology may become unspecific again as epidermotropism disap-

pears

In more advanced stages of the disease there is aff ectaton of extra-

cutaneous organs such as lymph nodes liver spleen lungs and bone

marrow Besides there may be blastc transformaton Other possible

complicaton is sepsis by Staphylococcus aureus

These three stages usually develop consecutvely nevertheless there

may patents whose debut starts directly with the tumoral stage

Remember

Microabscesses of mycosis fungoides are due to lymphocytes and are calledPautrierrsquos abscesses Psoriasis microabscesses result from neutrophils andare labeled as Munro-Sabouraud

Seacutezary Syndrome

Seacutezary syndrome can be considered as the leukemic phase of T-cell cu-

taneous lymphoma It is defined by the triad erythroderma (Figure 36

lymphadenopathies and the existence of more than 1000 Seacutezary cellsper milliliter in peripheral blood Seacutezary cells are atypical T- lymphocyte

with cerebriform nuclei

Very intense pruritus is characteristc For many authors Seacutezary syn-

drome is an aggressive clinical form and a bad prognosis of a mycosis

fungoides

Figure 36 Erythroderma due to Seacutezary syndrome

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Dermatology

Intercellular

substance ac

middot Pemphigus

Lineal

storage

in lucid

layer

-

Anti-Collagen Ac

Lucid

layer

Thick

layer

Basal

sublayer

Granular

storage

in papillary

dermis

middot Pemphigoid bullousmiddot Herpes gestationis

middot Acquired blistering epidermolysis

middot Dermatitis herpetiformis

Figure 8 Key points for histological diagnosis

of autoimmune blistering diseases

Figure 9 Pemphigus vulgaris

Figure 10 Pemphigus vulgaris with oral mucosa involvement with

erosions

Figure 11 Pemphigoid bullous Tense blisters No sign of Nikolsky

PEMPHIGUS VULGARISGENERALLY

IDIOPATHICHERPES GESTATIONIS

DERMATITIS

HERPETIFORMIS

Clinical presentation middot 40-50 years of age

middot They usually affect mucosae

middot No pruritus

middot Flaccid blister

middot Nikolsky

middot Elderly

middot Sometimes mucosae

middot With pruritus

middot Tense blister

middot No Nikolsky

middot Pregnant women

middot No mucosae

middot With pruritus

middot Herpetiform

middot No Nikolsky

middot 15-35 years of age

middot No mucosae

middot With pruritus

middot Herpetiform

middot No NikolskyDirect immuno1047298uorescence (DIF) IgG IgG IgG IgA

Histology middot INTRAepidermal blister

middot There is acantholysis

middot SUBepidermal blister

middot There are eosinophils

middot SUBepidermal blister

middot There are eosinophils

middot SUBepidermal blister

middot Neutrophils in dermis

Treatment Corticoids at high doses

immunosuppressants rituximab

and immunoglobulins

Corticoids Corticoids Diet +- dapsone

Remember Mortality rate 10 The most frequent Relapse if new

pregnancy

Associated to enteropathy

by gluten 90

Table 2 Autoimmune blistering diseases

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Amer ican Manual of Examinat ion in Medicine (2CK)

8

Chapter 04

Infectious Diseases

41 Viral Infections

Simple Herpes

Infection by Simple Herpes Virus

There are two types of simple herpes (Figure 12)

bull Type I is responsible for most extragenital herpes and 20 of the

genital herpes

bull Type II causes genital herpes and a small percentage of extragenital

herpes

Figure 12 Herpes simplex

Contagion is produced by direct contact though the carrier may be as-

ymptomatc Afer primary infecton virus remains silent in the sensi-

tve porton of cranial or spinal ganglia Immunosuppressed patents

endure the greatest severity of this conditon

Clinical Presentation

bull Extragenital simple herpes recurring orofacial herpes simplex is

the most frequent Most primary infect

ons are asymptomat

c Only5 manifest themselves in the form of herpetc gingivostomatts a

profile characterized by oral ulcers with cervical adenopathy and af-

fectaton of the patentrsquos general state (Figure 13) During relapses

clinical symptoms are milder with cluster vesicles on an erythema-

tous base Some factors facilitate relapses trauma sunlight cold

stress fever and the menstrual cycle

bull Genital simple herpes is the most common cause of genital ulcers

afer trauma Primary infecton is usually symptomatc and occurs

between 3 to 14 days afer sexual contact It causes clustered ulcers

in the balanopreputal sulcus or in the prepuce with painful inguinal

adenopathy Relapses are less severe than primary infecton and oc-

cur more frequently when genital herpes is due to HSV type II

Figure 13 Herpetic gingivostomatitis

bull Eczema herpetcum or Kaposi varicelliform erupton dissemina-

ton of herpetc infecton on pre-existng dermatosis (above all

atopic dermatt

s) bull Neonatal herpes is due to intrapartum contagion of HSV-II with

neurological involvement general deterioraton and skin vesicles or

ulcers

bull Other clinical forms are herpes gladiatorum herpetc whitlow and

keratoconjunctvits

Diagnosis

Diagnosis of this conditon is mainly clinical Virological culture is the

most reliable method of confirmaton The extent of a smear of the le-

sions (Tzanck cytodiagnosis) allows visualizaton of multnucleated cells

and intranuclear inclusions which become evident through histological

study

Treatment

Mild forms do not need treatment Treatment is required in the follow-

ing cases

bull Primary infecton

bull Severe or frequent relapses if they aff ect life quality

bull Complicatons like erythema multforme and eczema herpetcum

Drug of choice is oral acyclovir and its derivatves (valacyclovir famci-

clovir) Topic antvirals have not proven useful favoring maceraton of

lesions and thus over infecton It is not infrequent that topic antvirals

cause allergic contact dermatts due to hypersensitvity

Varicella-Zoster Virus

A primary infecton gives way to varicella (see Pediatrics secton) Afer

varicella the virus remains latent in the sensitve porton of the neural

ganglia and when relapse occurs it leads to zoster herpes

bull Varicella the following symptoms appear afer 15 days of incubaton

fever cephalea pruritus and polymorphic lesions in diff erent stages

macules papules vesicles (Figure 14) ulcers and scabs (starry sky

appearance) Mucosal (ulcers) and scalp involvement is characteristc

Manipulaton can leave scars Bacterial over infecton of lesions is the

most usual complicaton About 20 of adults suff er from varicella

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Dermatology

pneumonia radiologically demonstrable but clinical symptomatology is

only present in around 4 of the cases

Figure 14 Typical vesicles in patients with varicella

bull Zoster herpes thoracic zoster herpes is the most usual It sel-

dom occurs more than once throughout a personrsquos lifetime

It is characterized by vesicles on pre-existing erythema with

metameric distribution and lateral extension The most com-

mon complication is post herpetic neuralgia more frequent in

advanced age Carbamazepine or tricyclic antidepressants (Fig-

ure 15)

Figure 15 Zoster herpes

Special Clinical Forms

Special clinical forms are as follow

bull Ramsay-Hunt syndrome aff ectaton of geniculate ganglion of the

facial nerve

It produces vesicles in the outer ear external auditory canal and

pharynx homolateral facial paralysis deafness and vertgo

bull Ophthalmic involvement can result in severe keratts and requires ur-

gent referral to an ophthalmologist Suspicion should exist on patents

that present herpetc lesions on the tp of the nose) (Hutchinsonrsquos sign)

bull Disseminated zoster herpes several dermatomes are aff ected bilat-

erally Ramsay-Hunt syndrome is characteristc in the immunosup-

pressed

Remember

Affectation of the nose tip makes it necessary for ophthalmologicalexamination because the nose tip is innervated by the same nerve thatinnervates the cornea (1047297rst branch of the trigeminal nerve)

Treatment

Varicella without complicatons is treated symptomatcally Antvirals

are reserved for severe or complicated forms There is a commercial-

ized vaccine of live virus whose indicatons are stll under discussion

Zoster herpes must be treated with antvirals when detected during the

first 48-72 hours and aff ectng patents with

bull Immunosuppression

bull Age above 55

Special clinical forms previously cited

Drugs to be used are oral acyclovir and its derivatves (valacyclovir and

famciclovir) They accelerate the cure of lesions and decrease the inten-

sity of post herpetc neuralgia Patents with renal failure need a dose

adjustment as acyclovir is nephrotoxic These patents are adminis-

tered brivudine in a single daily dose

Molluscum ContagiosumDome shaped pink papules with central umbilicaton (Figure 16) Mol-

luscum contagiosum is typical of children that go to swimming pools It

is also present in the genital zone afer sexual contact and in immuno-

suppressed patents It is caused by Poxvirus

Figure 16 Molluscum contagiosum

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Amer ican Manual of Examinat ion in Medicine (2CK)

0

Lesions are asymptomatc

Diagnosis

Diagnosis is clinical Histology reveals characteristc inclusion bodies

Treatment

Lesions can resolve spontaneously

Cureage cryotherapy or local trichloroacetc acid are eff ectve meth-

ods to destroy lesions

Warts

Human papillomavirus can cause verruca vulgaris palmoplantar and

flat warts and condyloma accuminata Human papillomavirus is the

most frequent sexual transmied disease

Some subtypes of this virus (16 18) are of high risk and can cause epi-

dermoid carcinomas

Direct contact is the mechanism of contagion

Diagnosis

Diagnosis of this conditon is clinical

Staining with acetc acid can help visualize mucosal lesions

Treatment

Genital warts are treated with cryotherapy podophyllotoxin trichloro-

acetc acid imiquimod and 5-fluorouracil

Cervical lesions should be monitored by cytology and biopsy whenever

necessary to rule out cervical cancer (Figures 17 and 18)

Figure 17 Warts in HIV patient

Figure 18 Condyloma accuminata

42 Bacterial Infections

Impetigo

Impetgo is a very contagious superficial infecton without systemic re-

percussion and normally mixed etology by Gram positve cocci (strep-

tococci and staphylococci) Classically the most frequent accepted

cause was Streptococcus pyogenes However at present Staphylococcus

aureus stands out as the predominant cause

The most typical form is impetgo contagiosa (Figure 19) character-

ized by honey-colored (meliceric) scabs which normally appear on

the face and other exposed areas It is typical of children Although

infrequent poststreptococcal glomerulonephrits is a dreadful com-

plicaton

Figure 19 Impetigo contagiosa

On the contrary rheumatc fever shows no relaton to cutaneous strep-

tococcal infectons but only with pharyngeal infectons

There are other less habitual forms called bullous impetgo exclusively

of staphylococcal origin Clinical presentaton involves the presence of

blisters and erosions on the aff ected skin as a consequence of the epi-

dermolytc toxins that these bacteria contain Impetgo is treated with

topical mupirocin penicillin or oral fusidic acid

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Dermatology

Cellulitis

Cellulits is an infecton that aff ects deep dermis and subcutaneous cel-

lular tssues normally caused by streptococci (Streptococcus pyogenes

or of group A)

Community methicillin-resistant S aureus (CMRSA) is a triggering agent

that is becoming more and more frequent

Most common risk factors are diabetes chronic venous insuffi ciency

and immunosuppression

Clinical Presentation

Cellulits presents with erythematous plaques that are ill-defined pain-

ful and hot It is usually accompanied with fever and chills

Diagnosis

Diagnosis is clinical If there is an open door a culture of this area may

help see the source germ and resistance to ant

biot

cs

It is important to rule out abscesses osteomyelits and necrotzing fas-

ciits

If bacteremia is suspected blood cultures need to be performed

Treatment

Treatment implies oral antbiotcs for 7-10 days to cover Gram positve

cocci They are intravenously administered in case of lack of response

to oral treatment involvement of hands or periorbital zone diabetes or

extremes of age

Necrotizing FasciitisNecrotzing fasciits is a deep infecton up to muscular fascia that pro-

duces very intense pain and subsequent anesthesia

In 10 of the cases cellulits is due to an infecton by S pyogenes In the

remaining cases it occurs by a polymicrobial infecton caused by aerobes

and anaerobes including S aureus E coli and Clostridium perfringens

There may be prior history of trauma or surgery

Clinical Presentation

Clinical presentat

on involves pain of sudden onset and edema on theaff ected zone Pain may progress to anesthesia There appears subse-

quent erythema that progresses rapidly into necrosis

Characteristc clinical signs are tssue necrosis blisters intense pain

and gas producton

Diagnosis

Diagnosis is clinical and requires image testng X-rays or a computed

tomography CT

A biopsy of the border of the lesion helps achieve diagnosis

Treatment

Treatment entails precocious surgical debridement It is a surgical emer-

gency In additon to surgery broad-spectrum antbiotherapy will be

needed

Folliculitis

Folliculits is an infecton and inflammaton of one or several follicles

caused mainly by staphylococci

Clinical Presentation

Folliculits shows pustules with follicular distributon

When the infecton is deeper it is called furuncle

If several furuncles are infected a fluctuatng erythematous plaque forms

containing several points of suppuraton This plaque is labeled as anthrax

Diabet

c and immunosuppressed pat

ents are at higher risk

Characteristics of Folliculitis

1 Hot tub or swimming pool folliculits caused by Pseudomonas aeru-

ginosa

2 HIV associated pruritc folliculits or eosinophilic folliculits

Treatment

In mild cases treatment of choice comprises antseptcs and topic an-

tbiotcs

In more severe cases treatment of choice requires oral antbiotcs

Large sized lesions must be drained and a microbiological culture must be

performed to rule out methicillin-resistant Staphylococcus aureus MRSA

Acne Vulgaris

Acne is an inflammatory disease of the pilosebaceous follicle as a con-

sequence of an alteraton in follicular keratnizaton It aff ects adoles-

cents and young adults

Etology is multfactorial alteraton of keratnizaton of follicular infun-

dibulum quanttatve and qualitatve alteraton of sebum producton in

the sebaceous gland and alteratons of bacterial microflora (increase in

quant

ty of P acnes)

Aggravatng factors are stress androgenic oral contraceptves and the

use of cosmetc products that are not oil-free

Clinical Presentation

A comedo is the inital lesion which can be closed (whitehead) or open

(blackhead) and it evolves into inflammatory lesions that listed in as-

cending order of severity are papules pustules nodules and cysts

Lesions progress and leave scars Scars can be increased if lesions are

manipulated

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Amer ican Manual of Examinat ion in Medicine (2CK)

2

Diff erent lesions habitually combine simultaneously so acne becomes

polymorphic It is located in sebaceous areas face back shoulders and

the center thoracic region

Diagnosis

Diagnosis is clinical

Treatment

bull Comedonal acne is treated with topic retnoids and benzoyl peroxide

bull Inflammatory acne treatment requires benzoyl peroxide combined

with topic antbiotcs (erythromycin and clindamycin) Systemic

antbiotc treatment with oral tetracyclines will be prescribed if re-

sponse to topic antbiotc treatment fails

bull Severe nodular cystc acne treatment involves the use of isotret-

noin (13-cis-retnoic acid) It is a derivatve of vitamin A Isotretnoin

produces atrophy in the sebaceous gland and regulates keratniza-

ton The most frequent side eff ect is cutaneous and mucosal xero-

sis Triglycerides cholesterol and transaminases should be moni-

tored as their values may increasebull It can be associated with depression

bull It is teratogenic so pregnancy should be avoided during treatment

and untl a month afer treatment

Pilonidal Cysts

Pilonidal cysts are abscesses in the sacrococcygeal region

This type of cysts has predominance in men between 20 and 40 years

of age It is believed that repeated trauma on the aff ected area favors

their appearance

Clinical Presentation

Pilonidal cysts present with an indurated lesion that is fluctuatng hot

painful but non-adherent to deep planes in the sacrococcygeal region

Pilonidal cysts may or may not be associated to cellulits and purulent drain-

age

Diagnosis

Diagnosis is clinical and anal or perirectal abscesses should be dismissed

Treatment

Treatment implies an incision and surgical drainage

On some occasions a general surgery is required

43 Fungal Infections

Pityriasis Versicolor

Versicolor pityriasis is caused by commensal yeast called Pityrosporum

ovale which transforms into its pathogen form (Malassezia furfur) It

especially aff ects young patents (15 - 45 years of age) but it is rare

in childhood and advanced age Versicolor pityriasis relates to heat

humidity and sebaceous hypersecreton It is characterized by the ap-

pearance of hyperchromic or hypochromic macules that desquamate

on scratching (nail sign) if infecton is actve Macules usually appear on

the center thoracic region and on the back that is to say on seborrheic

zones Relapses are habitual despite treatment

Diagnosis

Diagnosis is normally clinical To that purpose the following serve as

support

bull Woodrsquos lamp emits yellow-orange fluorescence

bull Potassium hydroxide (KOH) test filaments and round elements can

be observed (ldquospaghe and meatball appearancerdquo Figure 20)

Treatment

Treatment is performed with topical azoles Oral administraton applies

for extensive cases or immunosuppressed patents Diff erental diagno-

sis includes pink pityriasis and eczemas (Figure 21)

Figure 20 Versicolor pityriasis Histological cut

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Dermatology

Figure 21 Versicolor pityriasis

Candidiasis

The most common triggering agent is Candida albicans It is normally sapro-

phyt

c although under certain condit

ons candidiasis may become patho-genic (immunosuppression humidity pregnancy and contraceptves)

Clinical Forms

bull Intertrigo erythematous plaque in cutaneous folds Atrophy and

fissures are typically deep in the skin fold as well as satellite and

peripheral lesions (papules andor pustules)

bull Mucosa involvement may cause diverse symptomatology like vul-

vovaginits glossits and white papules in the anterior region of the

oral mucosa Candidal balanits is characterized by the presence of

punctform erosions and pustules on gland and balanopreputal

sulcus Candidal balanits ofen appears afer sexual intercourse or

afer oral antbiotc intake

Remember

Almost a 100 of HIV patients suffer from muguet throughout their diseasecourse

bull Candidiasis of nail fold is usually associated with periungual inflam-

maton (perionixis) and inital proximal aff ectaton which diff erent-

ates it from tnea unguium (Figure 22)

Figure 22 Candidiasis of nail fold

Treatment

Oral Candidiasis fluconazole or nystatn

Candidiasis of the skin (intertrigo) apply topical antfungal medicaton

and keep zone clean and dry

Dermatophytosis or TineasDermatophyte infectons aff ect the skin and keratnized structures like

hair and nails (there is no mucosa involvement) Clinical diagnosis is

achieved afer performing a culture Woodrsquos lamp test normally turns

out to be negatve In general Trichophyton dermatophyte rubrum is

the most frequent dermatophyte

Non Inflammatory Tineas

Non inflammatory tneas do not produce irreversible scarring alope-

cia while inflammatory forms do Tineas are treated with azoles de-

rivatves

The types of tnea are the following

bull Ringworm of the scalp ( t nea capi t s or t nea tonsurans) is charac-

teristc of childhood It presents with alopecic plaques broken hair

and desquamaton Infectons tend to resolve spontaneously with-

out leaving scars at the onset

of puberty

bull Ringworm of the body (herpes

circinatus or t nea corporis) are

erythematous desquamatve

plaques (with more actve bor-

ders) which are also circinate

and normally pruritc (Figure

23) Plaques grow eccentrically

with less actvity in the centerand more in the borders

bull Ringworm of the foot ( t nea

pedis) the most frequent is the

ldquoathlete footrdquo with desquama-

ton in interdigital spaces

bull Tinea incognito refers to tnea

wrongly treated with cort-

coids what makes diagnosis

diffi cult as the lesion has been modified Figure 24)

Figure 24 Tinea incognito secondary to treatment with topical steroids

Figure 23 Herpes circinatus

(tinea corpis)

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Amer ican Manual of Examinat ion in Medicine (2CK)

4

bull Ringworm of the groin (t nea cruris or eczema marginatum von

hebra) formed by erythematous desquamatve plaque with more

actve borders (Figure 25)

Figure 25 Ringworm of the groin (tinea cruris)

bull Tinea unguium subungualhyperkeratosis with onychol-

ysis but without perionixis

(Figure 26)

Diagnosis

Clinical diagnosis is reached afer

performing a culture

Treatment

Treatment involves topical an-

tfungal medicaton in localized

areas

Oral antfungal medicaton is used in extensive forms nail fold or scalp

involvement

44 Parasitic Infections

Pediculosis

Pediculosis is transmied by direct contact or by contact with fomites

which release toxins that produce intense pruritus

Clinical Presentation

Pediculosis capi t s intense pruritus predominant in retroauricular and

occipital regions occasionally with excoriatons and impetginizaton

secondary to excoriatons

Pediculosis corporis intense pruritus in patents with poor hygiene or

who live in overcrowded conditons

Pediculosis pubis genital and pubic pruritus Brownish-grey macules

called maculae ceruleae are typical on underwear and skin These pig-

mentatons appear as a result of a reducton in hemoglobin by a para-

site enzyme

Diagnosis

Diagnosis is clinical and by direct visualizaton

Treatment

Pediculosis is treated with malathion lindane or topical permethrin

Scabies

Scabies is originated by an acarus known as Sarcoptes scabiei It has an

incubaton period of 1 month

Clinical Presentation

Scabies produces generalized pruritus more intense at night The pa-

tent usually catches the infestaton which is passed to the patentrsquos

relat

ves It is common tofi

nd that a recent trip to a tropical country hasbeen made Lesions appear between the fingers (Figure 27) in wrists

feet genitalia mammary areola and axilla but back and face are usu-

ally spared The most specific lesion is the acarine burrow in whose less

scaly end the advancing zone the mite lies Nodules are frequent in

axilla and genitals (nodular scabies)

bull Norwegian scabies is typical of the immunosuppressed Patents

present with generalized hyperkeratosis and scabs Norwegian sca-

bies produce lile pruritus but it is very contagious because there

are many acari

bull Nodular scabies involves the persistence of pruritc nodules despite

treatment Lesions usually appear in axilla and genitalia Pruritus is

due to a hypersensitvity phenomenon because of the acarus al-

ready dead Nodular scabies is treated with cortcoids

Figure 27 Scabies Acarine burrow

Treatment

bull Permethrin cream at 5 is the treatment of choice It is lile toxic

so it can be used in children and pregnant women

bull Topical lindane at 1 irritates and is neurotoxic therefore it is con-

traindicated in pregnant women and children

bull Oral ivermectn is utlized in cases of resistance to prior treatments

There is stll lile experience as to its use but in a first instance a

Figure 26 Tinea unguium

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Dermatology

single dose would be enough to cure scabies (already used by vet-

erinarians)

45 Ischemia

Decubitus Ulcers

Decubitus ulcers are the result of ischemic necrosis by contnuous pres-

sure on an area which restricts microcirculaton in that zone

Clinical Presentation

Decubitus ulcers are present in patents in bed with scarce mobilizaton

It is favored by bone prominences and lack of fat tssue If sensitvity

decreases there is more risk of formaton of decubitus ulcers

Diagnosis

Diagnosis is achieved based on medical records and clinical presentaton

Treatment

Preventon is of the utmost importance as well as frequent mobiliza-

ton of the patent in bed

Once ulcers have been established hydrocolloid dressings are used for

healing but sometmes surgical debridement is necessary

Gangrene

Gangrene means tssue necrosis

There are three types dry gangrene wet gangrene and gas gangrene

Clinical Presentation

Dry gangrene is due to ischemia generally secondary to atherosclero-

sis Clinical presentaton involves pain cold and paleness of extremi-

tes Once tssue is established it turns bluish-black in color and dry

Wet gangrene is owing to bacterial flora Tissue presents with an edem-

atous appearance either with blisters or pus

Gas gangrene caused by C perfringens It is normally located on re-

cent surgery Bacteria precociously destroyt

ssue producing gas It is amedical emergency

Diagnosis

Clinical diagnosis is obtained by microbiological culture

Treatment

Treatment requires surgical debridement with amputaton if necessary

and associaton of broad spectrum antbiotherapy

Gas gangrene is treated with hyperbaric oxygen

46 Miscellaneous

Acanthosis Nigricans

Acanthosis nigricans are vel-

vet-like papillomatous brown

plaques in neck axilla and groin

folds (Figure 28)

It is associated with diabetes

mellitus Cushingrsquos disease poly-

cystc ovarian syndrome and

obesity

The malignant form of acantho-

sis nigricans is a paraneoplastc

syndrome that diff erentates

from the benign form because

the laer has mucosal and pal-

moplantar involvement

Lichen Planus

Lichen planus is an inflammatory idiopathic disease that equally aff ects

both genders with higher frequency in middle age

Lichen planus has been related to diverse drugs like gold salts

anti-malarial medication and thiazides It has been also linked to

hepatitis C virus infection however this association is currently

doubtful

Clinical Presentation

Lichen planus presents with red-violaceous polygonal flat papulesquite pruritc which localizes on the flexor side of wrists forearms an-

kles and lumbosacral and flank regions On its surface a whitsh retcu-

late can be observed (Wickhamrsquos striae) About 60 - 70 of the cases

present with lesions in oral and genital mucosa oral which appear as

whitsh retculated lesions (Figures 29 and 30)

Figure 29 Lichen planus of oral mucosa with typical whitish

reticulate

Figure 28 Acanthosis nigricans

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Amer ican Manual of Examinat ion in Medicine (2CK)

6

Violaceous papules

with white stretch marks

Lichenoid lymphocyte

in1047297ltrate (band formation)

Destruction

of basal layer

Figure 30 Lymphocytic interface reaction (lichen planus)

Treatment

Mild forms are treated with topical cortcoids

Severe cases require oral cortcoids psoralens plus ultraviolet light of

the A wavelength (PUVA) or cyclosporine

Rosacea

Rosacea is a chronic disease of unknown pathogenesis characterized

by erythema and acneiform lesions on the face It aff ects middle aged

women (between 30 and 50 years of age) more

Rosacea etopathogenesis is unknown although there is involvement of

vasomotor lability infecton by Demodex folliculorum photo exposureand genetc predispositon

Clinical Presentation

Rosacea symptomatology comprises facial flushing episodes that end

up by provoking a persistent erythema telangiectasias and papulopus-

tular lesions without comedos Over tme ocular lesions and hyperpla-

sia of sof tssue may develop

Treatment

Avoid vasodilator stmuli

Mild cases require topical metronidazole or azelaic acid

Moderate cases need doxycycline or oral minocyclines

Severe cases are treated with oral isotretnoin at low doses

Pink Pityriasis

Gilbertrsquos pink pityriasis is an acute self-limitng dermatosis which main-

ly aff ects young adults It is of unknown origin although a viral etology

is suspected (there is some speculaton as to links with human herpes-

virus type 7)

Clinical Presentation

Erupton starts with an erythematous plaque between 2 and 5 cm of

diameter with a desquamatve central collaree ofen localized on the

trunk (heraldic mother patch Figure 31)

Figure 31 Pink pityriasis

Around a week later oval papules appear on the trunk and extremi-

tes These papules share similar characteristcs with the mother patch

though the first ones are smaller and distributed according to skin ten-

sion lines Pink pityriasis may be asymptomatc however it is some-

tmes linked to pruritus Lesions may last between 4 and 8 weeks and

disappear without leaving scars

Diagnosis and Treatment

Diagnosis is clinical Treatment is seldom needed and recommended

therapies in the past (PUVA erythromycin or oral antvirals) have not

shown clearly favorable results

Vitiligo

Vitligo is characterized by achromic macules by melanocyte destruc-

ton

Clinical Presentation

Vitligo shows achromic macules of chronic course and variable progres-

sion

Lesions are predominant on acral and periorificial areas They also show

the Koebner phenomenon

Patents may have markers of autoimmune diseases (ie antthyroid

antbodies and diabetes) but these diseases seldom manifest them-

selves

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Dermatology

Treatment

Localized lesions require topical cortcoids

Extensive or generalized lesions are treated with ultraviolet light B

(UVB) or PUVA

Strict solar photoprotecton is indispensable (Figure 32)

Figure 32 Vitiligo

47 Neoplasias

Seborrheic Keratosis

Seborrheic keratosis is the most frequent benign tumor in human be-

ings since it is part of cutaneous aging

Clinical Presentation

Seborrheic keratosis presents with hyperkeratosic papules with an oily

or velvet-like texture crests fissures and horny plugs on their surface

These papules are normally pigmented showing a brownish-black color

Treatment

No treatment is required as lesions do not become malignant

Seborrheic keratosis can be addressed with cureage or cryotherapy

Actinic keratosis

Actnic keratosis is the most common precancerous lesion and aff ects

almost a 100 of the populaton in sunny areas

Clinical Presentation

Actnic keratosis is characterized by erythematous and desquamatve

papules which are hyperkeratosic and rough on touch developing a

chronic course

Diagnosis

Diagnosis is clinical

Treatment

Treatment entails applicaton of topical 5-fluorouracil topical imiqui-

mod cryotherapy or surgery

If underlying carcinoma is suspected a biopsy must be performed to

rule out suspicion

Epidermoid Carcinoma

Epidermoid carcinoma is the second most frequent cutaneous tumor

Solar photo exposure is the main etological factor which is why epider-

moid carcinoma appears in zones of prolonged solar exposure like the

face Most carcinomas appear over premalignant lesions (actnic kera-

tosis and leukoplakia among others)

Clinical Presentation

Clinical presentaton reveals erythematous or erythematosquamous

plaques Over tme these plaques form papules and tumors which of-

ten become ulceratve and bleed

Diagnosis

Diagnosis is based on clinical suspicion and histopathological confirmaton

Treatment

Surgery with safety margins is the treatment of choice In carcinomas

in situ cryotherapy can be used as well as topical imiquimod electro-

coagulaton or CO2 laser techniques in destructon of tumors Radio-therapy may also be used in some cases

Basal Cellular Carcinoma

Basal cellular carcinoma is the most frequent cutaneous tumor Chronic so-

lar photo exposure is the main etological factor hence most of these car-

cinomas aff ect the facial zone in patents who are 40 years of age or older

Gorlinrsquos syndrome should be considered if multple basal cellular carci-

nomas are found in non photo exposed areas

Clinical Presentation

Basal cell carcinoma shows a pearly pink papule and superficial telan-

giectasias

It is localized over healthy skin and never aff ects mucosae

Treatment

Surgery is the treatment of choice Mohs surgery is performed in zones

where surrounding healthy tssue needs to be preserved Other alter-

natves are cryotherapy imiquimod electrocoagulaton radiotherapy

photodynamic therapy and intralesional interferon Prognosis is excel-

lent as growth is slow and metastasis exceptonal

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Amer ican Manual of Examinat ion in Medicine (2CK)

8

Melanoma

Melanoma is the most aggressive cutaneous tumor given its ability to

metastasize

Risk factors comprise solar photo exposure clear phototype the pres-

ence of dysplastc nevus or a high number of melanocytc nevi Fam-

ily history is quite important as some genetc mutatons determine a

higher risk of developing the disease

Clinical Forms

See Figure 33

Diagnosis

Precocious diagnosis is essental to perform precocious surgical extrpaton

The ABCDE criteria can help patents to see if they need to seek medical

consultaton (asymmetry of lesion uneven borders color and diameter

greater than 6 mm or abnormal evolut

on)

The Breslow index is the thickness of the lesion measured in millimeters

and is the main prognosis factor

Treatment

The base of treatment is precocious surgical extrpaton If the Breslow

index is less than 1 mm margins of 1 cm will be performed If Breslow

index is greater than 1 mm margins will be of 2 cm

For melanomas with a Breslow index greater than 1 mm the sentnel

ganglion must be located This is the first draining lymph node of the

territory where the tumor is localized If the ganglion is positve re-

gional lymphadenectomy will be performed along with interferon ad-ministraton (Figure 34)

In situ Extirpation 05 cm Follow-up

Breslow lt 1 mm Extirpation 1 cm Follow-up

Lymphadenectomy

Breslow gt 4 mm Interferon

Breslow ge 1 mm Extirpation 2 cm Sentinel ganglion

+

Figure 34 Melanoma treatment

Kaposirsquos sarcoma

Kaposirsquos sarcoma is the most common cutaneous tumor in HIV patents

Clinical presentation

Kaposirsquos sarcoma has a course with violaceous fusiform macules whichovertme may evolve into indurated nodules with blackberry appearance

This type of sarcoma has been linked to herpesvirus type 8 both in HIV

and seronegatve patents (Table 3)

EPIDERMAL KAPOSIrsquoS 983080HIV983081 CLASSIC KAPOSIrsquoS

Homosexual youth (95) The elderly

Diffuse and bilateral

(frequently in palate and face)

Unilateral plaques

(lower extremities)

Frequent mucosal and visceral involvement Not so frequent

middot Precocious lymphatic invasion

middot Aggressive

Not so precocious

Table 3 Differences between epidermal and classic Kaposirsquos sarcoma

Nodular melanoma

15

Middle-aged men

middot On healthy skin

middot Any zone

middot Sudden onset

middot Uniform black nodulemiddot Rapidly invasive (vertical growth without radial)middot Frequent ulceration and bleeding

Worst histological prognosis

Lentigo malignant melanoma

10

Elderly women

90 on facephotoexposedzones of aging skins(chronic exposure)

Spot that growsduring many years (gt 10)then progresses (nodule)

Better prognosis

Acral lentinginous melanoma

5ndash10 ( 60 black and Asian race)

Elderly men

middot Sole (ankle) handsmucosa ungual bed

middot No relation to photo exposure

middot Macule with mosaic appearance (spot that grows)middot Some amelanisticmiddot Bad prognosis due to late diagnosis

Melanoma of super1047297cial extension

70

Young women

middot 30 previous nervusmiddot Intermittent exposuremiddot Men back middot Women legs

More frequent

middot Macula with mosaic appearance in colors that grows 4-5 years and then in1047297ltrates (nodule)middot Metastasis 35 to 70

Figure 33 Clinical forms of malignant melanoma

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Dermatology

Diagnosis

Diagnosis relies on clinical suspicion and histopathological confirma-

ton

Treatment

Treatment of localized forms can include surgical extrpaton radiother-

apy or intralesional vinblastne

If the sarcoma is disseminated optons involve interferon or chemo-

therapy

Mycosis Fungoides

Mycosis fungoides is a T-cell lymphoma of low-grade malignancy Its

clinical course may be very slow and surpass 50 years Three stages are

clinically diff erentated

1 Eczematous or macular phase predominantly truncular erythema-

tous macules with years of evoluton They resemble a chromic ec-

zema Histology is unspecifi

c at this stage2 Infiltratve plaque phase infiltrated erythematous plaques appear

Histology is diagnostc at this stage A dermal infiltrate of atypical

lymphocytes band forms can be observed composed of CD+4 T

lymphocytes with cerebriform nuclei There is a marked epidermo-

tropism with the presence of clusters of intraepidermal lympho-

cytes called Pautrierrsquos microabscesses (Figure 35)

Figure 35 Mycosis fungoides Infiltrative plaque phase

3 Tumoral phase erythematous exophytc plaques start to appear

(tumors) with a tendency to ulceraton They can have a large size

Histology may become unspecific again as epidermotropism disap-

pears

In more advanced stages of the disease there is aff ectaton of extra-

cutaneous organs such as lymph nodes liver spleen lungs and bone

marrow Besides there may be blastc transformaton Other possible

complicaton is sepsis by Staphylococcus aureus

These three stages usually develop consecutvely nevertheless there

may patents whose debut starts directly with the tumoral stage

Remember

Microabscesses of mycosis fungoides are due to lymphocytes and are calledPautrierrsquos abscesses Psoriasis microabscesses result from neutrophils andare labeled as Munro-Sabouraud

Seacutezary Syndrome

Seacutezary syndrome can be considered as the leukemic phase of T-cell cu-

taneous lymphoma It is defined by the triad erythroderma (Figure 36

lymphadenopathies and the existence of more than 1000 Seacutezary cellsper milliliter in peripheral blood Seacutezary cells are atypical T- lymphocyte

with cerebriform nuclei

Very intense pruritus is characteristc For many authors Seacutezary syn-

drome is an aggressive clinical form and a bad prognosis of a mycosis

fungoides

Figure 36 Erythroderma due to Seacutezary syndrome

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Amer ican Manual of Examinat ion in Medicine (2CK)

8

Chapter 04

Infectious Diseases

41 Viral Infections

Simple Herpes

Infection by Simple Herpes Virus

There are two types of simple herpes (Figure 12)

bull Type I is responsible for most extragenital herpes and 20 of the

genital herpes

bull Type II causes genital herpes and a small percentage of extragenital

herpes

Figure 12 Herpes simplex

Contagion is produced by direct contact though the carrier may be as-

ymptomatc Afer primary infecton virus remains silent in the sensi-

tve porton of cranial or spinal ganglia Immunosuppressed patents

endure the greatest severity of this conditon

Clinical Presentation

bull Extragenital simple herpes recurring orofacial herpes simplex is

the most frequent Most primary infect

ons are asymptomat

c Only5 manifest themselves in the form of herpetc gingivostomatts a

profile characterized by oral ulcers with cervical adenopathy and af-

fectaton of the patentrsquos general state (Figure 13) During relapses

clinical symptoms are milder with cluster vesicles on an erythema-

tous base Some factors facilitate relapses trauma sunlight cold

stress fever and the menstrual cycle

bull Genital simple herpes is the most common cause of genital ulcers

afer trauma Primary infecton is usually symptomatc and occurs

between 3 to 14 days afer sexual contact It causes clustered ulcers

in the balanopreputal sulcus or in the prepuce with painful inguinal

adenopathy Relapses are less severe than primary infecton and oc-

cur more frequently when genital herpes is due to HSV type II

Figure 13 Herpetic gingivostomatitis

bull Eczema herpetcum or Kaposi varicelliform erupton dissemina-

ton of herpetc infecton on pre-existng dermatosis (above all

atopic dermatt

s) bull Neonatal herpes is due to intrapartum contagion of HSV-II with

neurological involvement general deterioraton and skin vesicles or

ulcers

bull Other clinical forms are herpes gladiatorum herpetc whitlow and

keratoconjunctvits

Diagnosis

Diagnosis of this conditon is mainly clinical Virological culture is the

most reliable method of confirmaton The extent of a smear of the le-

sions (Tzanck cytodiagnosis) allows visualizaton of multnucleated cells

and intranuclear inclusions which become evident through histological

study

Treatment

Mild forms do not need treatment Treatment is required in the follow-

ing cases

bull Primary infecton

bull Severe or frequent relapses if they aff ect life quality

bull Complicatons like erythema multforme and eczema herpetcum

Drug of choice is oral acyclovir and its derivatves (valacyclovir famci-

clovir) Topic antvirals have not proven useful favoring maceraton of

lesions and thus over infecton It is not infrequent that topic antvirals

cause allergic contact dermatts due to hypersensitvity

Varicella-Zoster Virus

A primary infecton gives way to varicella (see Pediatrics secton) Afer

varicella the virus remains latent in the sensitve porton of the neural

ganglia and when relapse occurs it leads to zoster herpes

bull Varicella the following symptoms appear afer 15 days of incubaton

fever cephalea pruritus and polymorphic lesions in diff erent stages

macules papules vesicles (Figure 14) ulcers and scabs (starry sky

appearance) Mucosal (ulcers) and scalp involvement is characteristc

Manipulaton can leave scars Bacterial over infecton of lesions is the

most usual complicaton About 20 of adults suff er from varicella

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Dermatology

pneumonia radiologically demonstrable but clinical symptomatology is

only present in around 4 of the cases

Figure 14 Typical vesicles in patients with varicella

bull Zoster herpes thoracic zoster herpes is the most usual It sel-

dom occurs more than once throughout a personrsquos lifetime

It is characterized by vesicles on pre-existing erythema with

metameric distribution and lateral extension The most com-

mon complication is post herpetic neuralgia more frequent in

advanced age Carbamazepine or tricyclic antidepressants (Fig-

ure 15)

Figure 15 Zoster herpes

Special Clinical Forms

Special clinical forms are as follow

bull Ramsay-Hunt syndrome aff ectaton of geniculate ganglion of the

facial nerve

It produces vesicles in the outer ear external auditory canal and

pharynx homolateral facial paralysis deafness and vertgo

bull Ophthalmic involvement can result in severe keratts and requires ur-

gent referral to an ophthalmologist Suspicion should exist on patents

that present herpetc lesions on the tp of the nose) (Hutchinsonrsquos sign)

bull Disseminated zoster herpes several dermatomes are aff ected bilat-

erally Ramsay-Hunt syndrome is characteristc in the immunosup-

pressed

Remember

Affectation of the nose tip makes it necessary for ophthalmologicalexamination because the nose tip is innervated by the same nerve thatinnervates the cornea (1047297rst branch of the trigeminal nerve)

Treatment

Varicella without complicatons is treated symptomatcally Antvirals

are reserved for severe or complicated forms There is a commercial-

ized vaccine of live virus whose indicatons are stll under discussion

Zoster herpes must be treated with antvirals when detected during the

first 48-72 hours and aff ectng patents with

bull Immunosuppression

bull Age above 55

Special clinical forms previously cited

Drugs to be used are oral acyclovir and its derivatves (valacyclovir and

famciclovir) They accelerate the cure of lesions and decrease the inten-

sity of post herpetc neuralgia Patents with renal failure need a dose

adjustment as acyclovir is nephrotoxic These patents are adminis-

tered brivudine in a single daily dose

Molluscum ContagiosumDome shaped pink papules with central umbilicaton (Figure 16) Mol-

luscum contagiosum is typical of children that go to swimming pools It

is also present in the genital zone afer sexual contact and in immuno-

suppressed patents It is caused by Poxvirus

Figure 16 Molluscum contagiosum

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Amer ican Manual of Examinat ion in Medicine (2CK)

0

Lesions are asymptomatc

Diagnosis

Diagnosis is clinical Histology reveals characteristc inclusion bodies

Treatment

Lesions can resolve spontaneously

Cureage cryotherapy or local trichloroacetc acid are eff ectve meth-

ods to destroy lesions

Warts

Human papillomavirus can cause verruca vulgaris palmoplantar and

flat warts and condyloma accuminata Human papillomavirus is the

most frequent sexual transmied disease

Some subtypes of this virus (16 18) are of high risk and can cause epi-

dermoid carcinomas

Direct contact is the mechanism of contagion

Diagnosis

Diagnosis of this conditon is clinical

Staining with acetc acid can help visualize mucosal lesions

Treatment

Genital warts are treated with cryotherapy podophyllotoxin trichloro-

acetc acid imiquimod and 5-fluorouracil

Cervical lesions should be monitored by cytology and biopsy whenever

necessary to rule out cervical cancer (Figures 17 and 18)

Figure 17 Warts in HIV patient

Figure 18 Condyloma accuminata

42 Bacterial Infections

Impetigo

Impetgo is a very contagious superficial infecton without systemic re-

percussion and normally mixed etology by Gram positve cocci (strep-

tococci and staphylococci) Classically the most frequent accepted

cause was Streptococcus pyogenes However at present Staphylococcus

aureus stands out as the predominant cause

The most typical form is impetgo contagiosa (Figure 19) character-

ized by honey-colored (meliceric) scabs which normally appear on

the face and other exposed areas It is typical of children Although

infrequent poststreptococcal glomerulonephrits is a dreadful com-

plicaton

Figure 19 Impetigo contagiosa

On the contrary rheumatc fever shows no relaton to cutaneous strep-

tococcal infectons but only with pharyngeal infectons

There are other less habitual forms called bullous impetgo exclusively

of staphylococcal origin Clinical presentaton involves the presence of

blisters and erosions on the aff ected skin as a consequence of the epi-

dermolytc toxins that these bacteria contain Impetgo is treated with

topical mupirocin penicillin or oral fusidic acid

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Dermatology

Cellulitis

Cellulits is an infecton that aff ects deep dermis and subcutaneous cel-

lular tssues normally caused by streptococci (Streptococcus pyogenes

or of group A)

Community methicillin-resistant S aureus (CMRSA) is a triggering agent

that is becoming more and more frequent

Most common risk factors are diabetes chronic venous insuffi ciency

and immunosuppression

Clinical Presentation

Cellulits presents with erythematous plaques that are ill-defined pain-

ful and hot It is usually accompanied with fever and chills

Diagnosis

Diagnosis is clinical If there is an open door a culture of this area may

help see the source germ and resistance to ant

biot

cs

It is important to rule out abscesses osteomyelits and necrotzing fas-

ciits

If bacteremia is suspected blood cultures need to be performed

Treatment

Treatment implies oral antbiotcs for 7-10 days to cover Gram positve

cocci They are intravenously administered in case of lack of response

to oral treatment involvement of hands or periorbital zone diabetes or

extremes of age

Necrotizing FasciitisNecrotzing fasciits is a deep infecton up to muscular fascia that pro-

duces very intense pain and subsequent anesthesia

In 10 of the cases cellulits is due to an infecton by S pyogenes In the

remaining cases it occurs by a polymicrobial infecton caused by aerobes

and anaerobes including S aureus E coli and Clostridium perfringens

There may be prior history of trauma or surgery

Clinical Presentation

Clinical presentat

on involves pain of sudden onset and edema on theaff ected zone Pain may progress to anesthesia There appears subse-

quent erythema that progresses rapidly into necrosis

Characteristc clinical signs are tssue necrosis blisters intense pain

and gas producton

Diagnosis

Diagnosis is clinical and requires image testng X-rays or a computed

tomography CT

A biopsy of the border of the lesion helps achieve diagnosis

Treatment

Treatment entails precocious surgical debridement It is a surgical emer-

gency In additon to surgery broad-spectrum antbiotherapy will be

needed

Folliculitis

Folliculits is an infecton and inflammaton of one or several follicles

caused mainly by staphylococci

Clinical Presentation

Folliculits shows pustules with follicular distributon

When the infecton is deeper it is called furuncle

If several furuncles are infected a fluctuatng erythematous plaque forms

containing several points of suppuraton This plaque is labeled as anthrax

Diabet

c and immunosuppressed pat

ents are at higher risk

Characteristics of Folliculitis

1 Hot tub or swimming pool folliculits caused by Pseudomonas aeru-

ginosa

2 HIV associated pruritc folliculits or eosinophilic folliculits

Treatment

In mild cases treatment of choice comprises antseptcs and topic an-

tbiotcs

In more severe cases treatment of choice requires oral antbiotcs

Large sized lesions must be drained and a microbiological culture must be

performed to rule out methicillin-resistant Staphylococcus aureus MRSA

Acne Vulgaris

Acne is an inflammatory disease of the pilosebaceous follicle as a con-

sequence of an alteraton in follicular keratnizaton It aff ects adoles-

cents and young adults

Etology is multfactorial alteraton of keratnizaton of follicular infun-

dibulum quanttatve and qualitatve alteraton of sebum producton in

the sebaceous gland and alteratons of bacterial microflora (increase in

quant

ty of P acnes)

Aggravatng factors are stress androgenic oral contraceptves and the

use of cosmetc products that are not oil-free

Clinical Presentation

A comedo is the inital lesion which can be closed (whitehead) or open

(blackhead) and it evolves into inflammatory lesions that listed in as-

cending order of severity are papules pustules nodules and cysts

Lesions progress and leave scars Scars can be increased if lesions are

manipulated

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Amer ican Manual of Examinat ion in Medicine (2CK)

2

Diff erent lesions habitually combine simultaneously so acne becomes

polymorphic It is located in sebaceous areas face back shoulders and

the center thoracic region

Diagnosis

Diagnosis is clinical

Treatment

bull Comedonal acne is treated with topic retnoids and benzoyl peroxide

bull Inflammatory acne treatment requires benzoyl peroxide combined

with topic antbiotcs (erythromycin and clindamycin) Systemic

antbiotc treatment with oral tetracyclines will be prescribed if re-

sponse to topic antbiotc treatment fails

bull Severe nodular cystc acne treatment involves the use of isotret-

noin (13-cis-retnoic acid) It is a derivatve of vitamin A Isotretnoin

produces atrophy in the sebaceous gland and regulates keratniza-

ton The most frequent side eff ect is cutaneous and mucosal xero-

sis Triglycerides cholesterol and transaminases should be moni-

tored as their values may increasebull It can be associated with depression

bull It is teratogenic so pregnancy should be avoided during treatment

and untl a month afer treatment

Pilonidal Cysts

Pilonidal cysts are abscesses in the sacrococcygeal region

This type of cysts has predominance in men between 20 and 40 years

of age It is believed that repeated trauma on the aff ected area favors

their appearance

Clinical Presentation

Pilonidal cysts present with an indurated lesion that is fluctuatng hot

painful but non-adherent to deep planes in the sacrococcygeal region

Pilonidal cysts may or may not be associated to cellulits and purulent drain-

age

Diagnosis

Diagnosis is clinical and anal or perirectal abscesses should be dismissed

Treatment

Treatment implies an incision and surgical drainage

On some occasions a general surgery is required

43 Fungal Infections

Pityriasis Versicolor

Versicolor pityriasis is caused by commensal yeast called Pityrosporum

ovale which transforms into its pathogen form (Malassezia furfur) It

especially aff ects young patents (15 - 45 years of age) but it is rare

in childhood and advanced age Versicolor pityriasis relates to heat

humidity and sebaceous hypersecreton It is characterized by the ap-

pearance of hyperchromic or hypochromic macules that desquamate

on scratching (nail sign) if infecton is actve Macules usually appear on

the center thoracic region and on the back that is to say on seborrheic

zones Relapses are habitual despite treatment

Diagnosis

Diagnosis is normally clinical To that purpose the following serve as

support

bull Woodrsquos lamp emits yellow-orange fluorescence

bull Potassium hydroxide (KOH) test filaments and round elements can

be observed (ldquospaghe and meatball appearancerdquo Figure 20)

Treatment

Treatment is performed with topical azoles Oral administraton applies

for extensive cases or immunosuppressed patents Diff erental diagno-

sis includes pink pityriasis and eczemas (Figure 21)

Figure 20 Versicolor pityriasis Histological cut

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Dermatology

Figure 21 Versicolor pityriasis

Candidiasis

The most common triggering agent is Candida albicans It is normally sapro-

phyt

c although under certain condit

ons candidiasis may become patho-genic (immunosuppression humidity pregnancy and contraceptves)

Clinical Forms

bull Intertrigo erythematous plaque in cutaneous folds Atrophy and

fissures are typically deep in the skin fold as well as satellite and

peripheral lesions (papules andor pustules)

bull Mucosa involvement may cause diverse symptomatology like vul-

vovaginits glossits and white papules in the anterior region of the

oral mucosa Candidal balanits is characterized by the presence of

punctform erosions and pustules on gland and balanopreputal

sulcus Candidal balanits ofen appears afer sexual intercourse or

afer oral antbiotc intake

Remember

Almost a 100 of HIV patients suffer from muguet throughout their diseasecourse

bull Candidiasis of nail fold is usually associated with periungual inflam-

maton (perionixis) and inital proximal aff ectaton which diff erent-

ates it from tnea unguium (Figure 22)

Figure 22 Candidiasis of nail fold

Treatment

Oral Candidiasis fluconazole or nystatn

Candidiasis of the skin (intertrigo) apply topical antfungal medicaton

and keep zone clean and dry

Dermatophytosis or TineasDermatophyte infectons aff ect the skin and keratnized structures like

hair and nails (there is no mucosa involvement) Clinical diagnosis is

achieved afer performing a culture Woodrsquos lamp test normally turns

out to be negatve In general Trichophyton dermatophyte rubrum is

the most frequent dermatophyte

Non Inflammatory Tineas

Non inflammatory tneas do not produce irreversible scarring alope-

cia while inflammatory forms do Tineas are treated with azoles de-

rivatves

The types of tnea are the following

bull Ringworm of the scalp ( t nea capi t s or t nea tonsurans) is charac-

teristc of childhood It presents with alopecic plaques broken hair

and desquamaton Infectons tend to resolve spontaneously with-

out leaving scars at the onset

of puberty

bull Ringworm of the body (herpes

circinatus or t nea corporis) are

erythematous desquamatve

plaques (with more actve bor-

ders) which are also circinate

and normally pruritc (Figure

23) Plaques grow eccentrically

with less actvity in the centerand more in the borders

bull Ringworm of the foot ( t nea

pedis) the most frequent is the

ldquoathlete footrdquo with desquama-

ton in interdigital spaces

bull Tinea incognito refers to tnea

wrongly treated with cort-

coids what makes diagnosis

diffi cult as the lesion has been modified Figure 24)

Figure 24 Tinea incognito secondary to treatment with topical steroids

Figure 23 Herpes circinatus

(tinea corpis)

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Amer ican Manual of Examinat ion in Medicine (2CK)

4

bull Ringworm of the groin (t nea cruris or eczema marginatum von

hebra) formed by erythematous desquamatve plaque with more

actve borders (Figure 25)

Figure 25 Ringworm of the groin (tinea cruris)

bull Tinea unguium subungualhyperkeratosis with onychol-

ysis but without perionixis

(Figure 26)

Diagnosis

Clinical diagnosis is reached afer

performing a culture

Treatment

Treatment involves topical an-

tfungal medicaton in localized

areas

Oral antfungal medicaton is used in extensive forms nail fold or scalp

involvement

44 Parasitic Infections

Pediculosis

Pediculosis is transmied by direct contact or by contact with fomites

which release toxins that produce intense pruritus

Clinical Presentation

Pediculosis capi t s intense pruritus predominant in retroauricular and

occipital regions occasionally with excoriatons and impetginizaton

secondary to excoriatons

Pediculosis corporis intense pruritus in patents with poor hygiene or

who live in overcrowded conditons

Pediculosis pubis genital and pubic pruritus Brownish-grey macules

called maculae ceruleae are typical on underwear and skin These pig-

mentatons appear as a result of a reducton in hemoglobin by a para-

site enzyme

Diagnosis

Diagnosis is clinical and by direct visualizaton

Treatment

Pediculosis is treated with malathion lindane or topical permethrin

Scabies

Scabies is originated by an acarus known as Sarcoptes scabiei It has an

incubaton period of 1 month

Clinical Presentation

Scabies produces generalized pruritus more intense at night The pa-

tent usually catches the infestaton which is passed to the patentrsquos

relat

ves It is common tofi

nd that a recent trip to a tropical country hasbeen made Lesions appear between the fingers (Figure 27) in wrists

feet genitalia mammary areola and axilla but back and face are usu-

ally spared The most specific lesion is the acarine burrow in whose less

scaly end the advancing zone the mite lies Nodules are frequent in

axilla and genitals (nodular scabies)

bull Norwegian scabies is typical of the immunosuppressed Patents

present with generalized hyperkeratosis and scabs Norwegian sca-

bies produce lile pruritus but it is very contagious because there

are many acari

bull Nodular scabies involves the persistence of pruritc nodules despite

treatment Lesions usually appear in axilla and genitalia Pruritus is

due to a hypersensitvity phenomenon because of the acarus al-

ready dead Nodular scabies is treated with cortcoids

Figure 27 Scabies Acarine burrow

Treatment

bull Permethrin cream at 5 is the treatment of choice It is lile toxic

so it can be used in children and pregnant women

bull Topical lindane at 1 irritates and is neurotoxic therefore it is con-

traindicated in pregnant women and children

bull Oral ivermectn is utlized in cases of resistance to prior treatments

There is stll lile experience as to its use but in a first instance a

Figure 26 Tinea unguium

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Dermatology

single dose would be enough to cure scabies (already used by vet-

erinarians)

45 Ischemia

Decubitus Ulcers

Decubitus ulcers are the result of ischemic necrosis by contnuous pres-

sure on an area which restricts microcirculaton in that zone

Clinical Presentation

Decubitus ulcers are present in patents in bed with scarce mobilizaton

It is favored by bone prominences and lack of fat tssue If sensitvity

decreases there is more risk of formaton of decubitus ulcers

Diagnosis

Diagnosis is achieved based on medical records and clinical presentaton

Treatment

Preventon is of the utmost importance as well as frequent mobiliza-

ton of the patent in bed

Once ulcers have been established hydrocolloid dressings are used for

healing but sometmes surgical debridement is necessary

Gangrene

Gangrene means tssue necrosis

There are three types dry gangrene wet gangrene and gas gangrene

Clinical Presentation

Dry gangrene is due to ischemia generally secondary to atherosclero-

sis Clinical presentaton involves pain cold and paleness of extremi-

tes Once tssue is established it turns bluish-black in color and dry

Wet gangrene is owing to bacterial flora Tissue presents with an edem-

atous appearance either with blisters or pus

Gas gangrene caused by C perfringens It is normally located on re-

cent surgery Bacteria precociously destroyt

ssue producing gas It is amedical emergency

Diagnosis

Clinical diagnosis is obtained by microbiological culture

Treatment

Treatment requires surgical debridement with amputaton if necessary

and associaton of broad spectrum antbiotherapy

Gas gangrene is treated with hyperbaric oxygen

46 Miscellaneous

Acanthosis Nigricans

Acanthosis nigricans are vel-

vet-like papillomatous brown

plaques in neck axilla and groin

folds (Figure 28)

It is associated with diabetes

mellitus Cushingrsquos disease poly-

cystc ovarian syndrome and

obesity

The malignant form of acantho-

sis nigricans is a paraneoplastc

syndrome that diff erentates

from the benign form because

the laer has mucosal and pal-

moplantar involvement

Lichen Planus

Lichen planus is an inflammatory idiopathic disease that equally aff ects

both genders with higher frequency in middle age

Lichen planus has been related to diverse drugs like gold salts

anti-malarial medication and thiazides It has been also linked to

hepatitis C virus infection however this association is currently

doubtful

Clinical Presentation

Lichen planus presents with red-violaceous polygonal flat papulesquite pruritc which localizes on the flexor side of wrists forearms an-

kles and lumbosacral and flank regions On its surface a whitsh retcu-

late can be observed (Wickhamrsquos striae) About 60 - 70 of the cases

present with lesions in oral and genital mucosa oral which appear as

whitsh retculated lesions (Figures 29 and 30)

Figure 29 Lichen planus of oral mucosa with typical whitish

reticulate

Figure 28 Acanthosis nigricans

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Amer ican Manual of Examinat ion in Medicine (2CK)

6

Violaceous papules

with white stretch marks

Lichenoid lymphocyte

in1047297ltrate (band formation)

Destruction

of basal layer

Figure 30 Lymphocytic interface reaction (lichen planus)

Treatment

Mild forms are treated with topical cortcoids

Severe cases require oral cortcoids psoralens plus ultraviolet light of

the A wavelength (PUVA) or cyclosporine

Rosacea

Rosacea is a chronic disease of unknown pathogenesis characterized

by erythema and acneiform lesions on the face It aff ects middle aged

women (between 30 and 50 years of age) more

Rosacea etopathogenesis is unknown although there is involvement of

vasomotor lability infecton by Demodex folliculorum photo exposureand genetc predispositon

Clinical Presentation

Rosacea symptomatology comprises facial flushing episodes that end

up by provoking a persistent erythema telangiectasias and papulopus-

tular lesions without comedos Over tme ocular lesions and hyperpla-

sia of sof tssue may develop

Treatment

Avoid vasodilator stmuli

Mild cases require topical metronidazole or azelaic acid

Moderate cases need doxycycline or oral minocyclines

Severe cases are treated with oral isotretnoin at low doses

Pink Pityriasis

Gilbertrsquos pink pityriasis is an acute self-limitng dermatosis which main-

ly aff ects young adults It is of unknown origin although a viral etology

is suspected (there is some speculaton as to links with human herpes-

virus type 7)

Clinical Presentation

Erupton starts with an erythematous plaque between 2 and 5 cm of

diameter with a desquamatve central collaree ofen localized on the

trunk (heraldic mother patch Figure 31)

Figure 31 Pink pityriasis

Around a week later oval papules appear on the trunk and extremi-

tes These papules share similar characteristcs with the mother patch

though the first ones are smaller and distributed according to skin ten-

sion lines Pink pityriasis may be asymptomatc however it is some-

tmes linked to pruritus Lesions may last between 4 and 8 weeks and

disappear without leaving scars

Diagnosis and Treatment

Diagnosis is clinical Treatment is seldom needed and recommended

therapies in the past (PUVA erythromycin or oral antvirals) have not

shown clearly favorable results

Vitiligo

Vitligo is characterized by achromic macules by melanocyte destruc-

ton

Clinical Presentation

Vitligo shows achromic macules of chronic course and variable progres-

sion

Lesions are predominant on acral and periorificial areas They also show

the Koebner phenomenon

Patents may have markers of autoimmune diseases (ie antthyroid

antbodies and diabetes) but these diseases seldom manifest them-

selves

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Dermatology

Treatment

Localized lesions require topical cortcoids

Extensive or generalized lesions are treated with ultraviolet light B

(UVB) or PUVA

Strict solar photoprotecton is indispensable (Figure 32)

Figure 32 Vitiligo

47 Neoplasias

Seborrheic Keratosis

Seborrheic keratosis is the most frequent benign tumor in human be-

ings since it is part of cutaneous aging

Clinical Presentation

Seborrheic keratosis presents with hyperkeratosic papules with an oily

or velvet-like texture crests fissures and horny plugs on their surface

These papules are normally pigmented showing a brownish-black color

Treatment

No treatment is required as lesions do not become malignant

Seborrheic keratosis can be addressed with cureage or cryotherapy

Actinic keratosis

Actnic keratosis is the most common precancerous lesion and aff ects

almost a 100 of the populaton in sunny areas

Clinical Presentation

Actnic keratosis is characterized by erythematous and desquamatve

papules which are hyperkeratosic and rough on touch developing a

chronic course

Diagnosis

Diagnosis is clinical

Treatment

Treatment entails applicaton of topical 5-fluorouracil topical imiqui-

mod cryotherapy or surgery

If underlying carcinoma is suspected a biopsy must be performed to

rule out suspicion

Epidermoid Carcinoma

Epidermoid carcinoma is the second most frequent cutaneous tumor

Solar photo exposure is the main etological factor which is why epider-

moid carcinoma appears in zones of prolonged solar exposure like the

face Most carcinomas appear over premalignant lesions (actnic kera-

tosis and leukoplakia among others)

Clinical Presentation

Clinical presentaton reveals erythematous or erythematosquamous

plaques Over tme these plaques form papules and tumors which of-

ten become ulceratve and bleed

Diagnosis

Diagnosis is based on clinical suspicion and histopathological confirmaton

Treatment

Surgery with safety margins is the treatment of choice In carcinomas

in situ cryotherapy can be used as well as topical imiquimod electro-

coagulaton or CO2 laser techniques in destructon of tumors Radio-therapy may also be used in some cases

Basal Cellular Carcinoma

Basal cellular carcinoma is the most frequent cutaneous tumor Chronic so-

lar photo exposure is the main etological factor hence most of these car-

cinomas aff ect the facial zone in patents who are 40 years of age or older

Gorlinrsquos syndrome should be considered if multple basal cellular carci-

nomas are found in non photo exposed areas

Clinical Presentation

Basal cell carcinoma shows a pearly pink papule and superficial telan-

giectasias

It is localized over healthy skin and never aff ects mucosae

Treatment

Surgery is the treatment of choice Mohs surgery is performed in zones

where surrounding healthy tssue needs to be preserved Other alter-

natves are cryotherapy imiquimod electrocoagulaton radiotherapy

photodynamic therapy and intralesional interferon Prognosis is excel-

lent as growth is slow and metastasis exceptonal

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Amer ican Manual of Examinat ion in Medicine (2CK)

8

Melanoma

Melanoma is the most aggressive cutaneous tumor given its ability to

metastasize

Risk factors comprise solar photo exposure clear phototype the pres-

ence of dysplastc nevus or a high number of melanocytc nevi Fam-

ily history is quite important as some genetc mutatons determine a

higher risk of developing the disease

Clinical Forms

See Figure 33

Diagnosis

Precocious diagnosis is essental to perform precocious surgical extrpaton

The ABCDE criteria can help patents to see if they need to seek medical

consultaton (asymmetry of lesion uneven borders color and diameter

greater than 6 mm or abnormal evolut

on)

The Breslow index is the thickness of the lesion measured in millimeters

and is the main prognosis factor

Treatment

The base of treatment is precocious surgical extrpaton If the Breslow

index is less than 1 mm margins of 1 cm will be performed If Breslow

index is greater than 1 mm margins will be of 2 cm

For melanomas with a Breslow index greater than 1 mm the sentnel

ganglion must be located This is the first draining lymph node of the

territory where the tumor is localized If the ganglion is positve re-

gional lymphadenectomy will be performed along with interferon ad-ministraton (Figure 34)

In situ Extirpation 05 cm Follow-up

Breslow lt 1 mm Extirpation 1 cm Follow-up

Lymphadenectomy

Breslow gt 4 mm Interferon

Breslow ge 1 mm Extirpation 2 cm Sentinel ganglion

+

Figure 34 Melanoma treatment

Kaposirsquos sarcoma

Kaposirsquos sarcoma is the most common cutaneous tumor in HIV patents

Clinical presentation

Kaposirsquos sarcoma has a course with violaceous fusiform macules whichovertme may evolve into indurated nodules with blackberry appearance

This type of sarcoma has been linked to herpesvirus type 8 both in HIV

and seronegatve patents (Table 3)

EPIDERMAL KAPOSIrsquoS 983080HIV983081 CLASSIC KAPOSIrsquoS

Homosexual youth (95) The elderly

Diffuse and bilateral

(frequently in palate and face)

Unilateral plaques

(lower extremities)

Frequent mucosal and visceral involvement Not so frequent

middot Precocious lymphatic invasion

middot Aggressive

Not so precocious

Table 3 Differences between epidermal and classic Kaposirsquos sarcoma

Nodular melanoma

15

Middle-aged men

middot On healthy skin

middot Any zone

middot Sudden onset

middot Uniform black nodulemiddot Rapidly invasive (vertical growth without radial)middot Frequent ulceration and bleeding

Worst histological prognosis

Lentigo malignant melanoma

10

Elderly women

90 on facephotoexposedzones of aging skins(chronic exposure)

Spot that growsduring many years (gt 10)then progresses (nodule)

Better prognosis

Acral lentinginous melanoma

5ndash10 ( 60 black and Asian race)

Elderly men

middot Sole (ankle) handsmucosa ungual bed

middot No relation to photo exposure

middot Macule with mosaic appearance (spot that grows)middot Some amelanisticmiddot Bad prognosis due to late diagnosis

Melanoma of super1047297cial extension

70

Young women

middot 30 previous nervusmiddot Intermittent exposuremiddot Men back middot Women legs

More frequent

middot Macula with mosaic appearance in colors that grows 4-5 years and then in1047297ltrates (nodule)middot Metastasis 35 to 70

Figure 33 Clinical forms of malignant melanoma

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Dermatology

Diagnosis

Diagnosis relies on clinical suspicion and histopathological confirma-

ton

Treatment

Treatment of localized forms can include surgical extrpaton radiother-

apy or intralesional vinblastne

If the sarcoma is disseminated optons involve interferon or chemo-

therapy

Mycosis Fungoides

Mycosis fungoides is a T-cell lymphoma of low-grade malignancy Its

clinical course may be very slow and surpass 50 years Three stages are

clinically diff erentated

1 Eczematous or macular phase predominantly truncular erythema-

tous macules with years of evoluton They resemble a chromic ec-

zema Histology is unspecifi

c at this stage2 Infiltratve plaque phase infiltrated erythematous plaques appear

Histology is diagnostc at this stage A dermal infiltrate of atypical

lymphocytes band forms can be observed composed of CD+4 T

lymphocytes with cerebriform nuclei There is a marked epidermo-

tropism with the presence of clusters of intraepidermal lympho-

cytes called Pautrierrsquos microabscesses (Figure 35)

Figure 35 Mycosis fungoides Infiltrative plaque phase

3 Tumoral phase erythematous exophytc plaques start to appear

(tumors) with a tendency to ulceraton They can have a large size

Histology may become unspecific again as epidermotropism disap-

pears

In more advanced stages of the disease there is aff ectaton of extra-

cutaneous organs such as lymph nodes liver spleen lungs and bone

marrow Besides there may be blastc transformaton Other possible

complicaton is sepsis by Staphylococcus aureus

These three stages usually develop consecutvely nevertheless there

may patents whose debut starts directly with the tumoral stage

Remember

Microabscesses of mycosis fungoides are due to lymphocytes and are calledPautrierrsquos abscesses Psoriasis microabscesses result from neutrophils andare labeled as Munro-Sabouraud

Seacutezary Syndrome

Seacutezary syndrome can be considered as the leukemic phase of T-cell cu-

taneous lymphoma It is defined by the triad erythroderma (Figure 36

lymphadenopathies and the existence of more than 1000 Seacutezary cellsper milliliter in peripheral blood Seacutezary cells are atypical T- lymphocyte

with cerebriform nuclei

Very intense pruritus is characteristc For many authors Seacutezary syn-

drome is an aggressive clinical form and a bad prognosis of a mycosis

fungoides

Figure 36 Erythroderma due to Seacutezary syndrome

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Dermatology

pneumonia radiologically demonstrable but clinical symptomatology is

only present in around 4 of the cases

Figure 14 Typical vesicles in patients with varicella

bull Zoster herpes thoracic zoster herpes is the most usual It sel-

dom occurs more than once throughout a personrsquos lifetime

It is characterized by vesicles on pre-existing erythema with

metameric distribution and lateral extension The most com-

mon complication is post herpetic neuralgia more frequent in

advanced age Carbamazepine or tricyclic antidepressants (Fig-

ure 15)

Figure 15 Zoster herpes

Special Clinical Forms

Special clinical forms are as follow

bull Ramsay-Hunt syndrome aff ectaton of geniculate ganglion of the

facial nerve

It produces vesicles in the outer ear external auditory canal and

pharynx homolateral facial paralysis deafness and vertgo

bull Ophthalmic involvement can result in severe keratts and requires ur-

gent referral to an ophthalmologist Suspicion should exist on patents

that present herpetc lesions on the tp of the nose) (Hutchinsonrsquos sign)

bull Disseminated zoster herpes several dermatomes are aff ected bilat-

erally Ramsay-Hunt syndrome is characteristc in the immunosup-

pressed

Remember

Affectation of the nose tip makes it necessary for ophthalmologicalexamination because the nose tip is innervated by the same nerve thatinnervates the cornea (1047297rst branch of the trigeminal nerve)

Treatment

Varicella without complicatons is treated symptomatcally Antvirals

are reserved for severe or complicated forms There is a commercial-

ized vaccine of live virus whose indicatons are stll under discussion

Zoster herpes must be treated with antvirals when detected during the

first 48-72 hours and aff ectng patents with

bull Immunosuppression

bull Age above 55

Special clinical forms previously cited

Drugs to be used are oral acyclovir and its derivatves (valacyclovir and

famciclovir) They accelerate the cure of lesions and decrease the inten-

sity of post herpetc neuralgia Patents with renal failure need a dose

adjustment as acyclovir is nephrotoxic These patents are adminis-

tered brivudine in a single daily dose

Molluscum ContagiosumDome shaped pink papules with central umbilicaton (Figure 16) Mol-

luscum contagiosum is typical of children that go to swimming pools It

is also present in the genital zone afer sexual contact and in immuno-

suppressed patents It is caused by Poxvirus

Figure 16 Molluscum contagiosum

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Amer ican Manual of Examinat ion in Medicine (2CK)

0

Lesions are asymptomatc

Diagnosis

Diagnosis is clinical Histology reveals characteristc inclusion bodies

Treatment

Lesions can resolve spontaneously

Cureage cryotherapy or local trichloroacetc acid are eff ectve meth-

ods to destroy lesions

Warts

Human papillomavirus can cause verruca vulgaris palmoplantar and

flat warts and condyloma accuminata Human papillomavirus is the

most frequent sexual transmied disease

Some subtypes of this virus (16 18) are of high risk and can cause epi-

dermoid carcinomas

Direct contact is the mechanism of contagion

Diagnosis

Diagnosis of this conditon is clinical

Staining with acetc acid can help visualize mucosal lesions

Treatment

Genital warts are treated with cryotherapy podophyllotoxin trichloro-

acetc acid imiquimod and 5-fluorouracil

Cervical lesions should be monitored by cytology and biopsy whenever

necessary to rule out cervical cancer (Figures 17 and 18)

Figure 17 Warts in HIV patient

Figure 18 Condyloma accuminata

42 Bacterial Infections

Impetigo

Impetgo is a very contagious superficial infecton without systemic re-

percussion and normally mixed etology by Gram positve cocci (strep-

tococci and staphylococci) Classically the most frequent accepted

cause was Streptococcus pyogenes However at present Staphylococcus

aureus stands out as the predominant cause

The most typical form is impetgo contagiosa (Figure 19) character-

ized by honey-colored (meliceric) scabs which normally appear on

the face and other exposed areas It is typical of children Although

infrequent poststreptococcal glomerulonephrits is a dreadful com-

plicaton

Figure 19 Impetigo contagiosa

On the contrary rheumatc fever shows no relaton to cutaneous strep-

tococcal infectons but only with pharyngeal infectons

There are other less habitual forms called bullous impetgo exclusively

of staphylococcal origin Clinical presentaton involves the presence of

blisters and erosions on the aff ected skin as a consequence of the epi-

dermolytc toxins that these bacteria contain Impetgo is treated with

topical mupirocin penicillin or oral fusidic acid

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Dermatology

Cellulitis

Cellulits is an infecton that aff ects deep dermis and subcutaneous cel-

lular tssues normally caused by streptococci (Streptococcus pyogenes

or of group A)

Community methicillin-resistant S aureus (CMRSA) is a triggering agent

that is becoming more and more frequent

Most common risk factors are diabetes chronic venous insuffi ciency

and immunosuppression

Clinical Presentation

Cellulits presents with erythematous plaques that are ill-defined pain-

ful and hot It is usually accompanied with fever and chills

Diagnosis

Diagnosis is clinical If there is an open door a culture of this area may

help see the source germ and resistance to ant

biot

cs

It is important to rule out abscesses osteomyelits and necrotzing fas-

ciits

If bacteremia is suspected blood cultures need to be performed

Treatment

Treatment implies oral antbiotcs for 7-10 days to cover Gram positve

cocci They are intravenously administered in case of lack of response

to oral treatment involvement of hands or periorbital zone diabetes or

extremes of age

Necrotizing FasciitisNecrotzing fasciits is a deep infecton up to muscular fascia that pro-

duces very intense pain and subsequent anesthesia

In 10 of the cases cellulits is due to an infecton by S pyogenes In the

remaining cases it occurs by a polymicrobial infecton caused by aerobes

and anaerobes including S aureus E coli and Clostridium perfringens

There may be prior history of trauma or surgery

Clinical Presentation

Clinical presentat

on involves pain of sudden onset and edema on theaff ected zone Pain may progress to anesthesia There appears subse-

quent erythema that progresses rapidly into necrosis

Characteristc clinical signs are tssue necrosis blisters intense pain

and gas producton

Diagnosis

Diagnosis is clinical and requires image testng X-rays or a computed

tomography CT

A biopsy of the border of the lesion helps achieve diagnosis

Treatment

Treatment entails precocious surgical debridement It is a surgical emer-

gency In additon to surgery broad-spectrum antbiotherapy will be

needed

Folliculitis

Folliculits is an infecton and inflammaton of one or several follicles

caused mainly by staphylococci

Clinical Presentation

Folliculits shows pustules with follicular distributon

When the infecton is deeper it is called furuncle

If several furuncles are infected a fluctuatng erythematous plaque forms

containing several points of suppuraton This plaque is labeled as anthrax

Diabet

c and immunosuppressed pat

ents are at higher risk

Characteristics of Folliculitis

1 Hot tub or swimming pool folliculits caused by Pseudomonas aeru-

ginosa

2 HIV associated pruritc folliculits or eosinophilic folliculits

Treatment

In mild cases treatment of choice comprises antseptcs and topic an-

tbiotcs

In more severe cases treatment of choice requires oral antbiotcs

Large sized lesions must be drained and a microbiological culture must be

performed to rule out methicillin-resistant Staphylococcus aureus MRSA

Acne Vulgaris

Acne is an inflammatory disease of the pilosebaceous follicle as a con-

sequence of an alteraton in follicular keratnizaton It aff ects adoles-

cents and young adults

Etology is multfactorial alteraton of keratnizaton of follicular infun-

dibulum quanttatve and qualitatve alteraton of sebum producton in

the sebaceous gland and alteratons of bacterial microflora (increase in

quant

ty of P acnes)

Aggravatng factors are stress androgenic oral contraceptves and the

use of cosmetc products that are not oil-free

Clinical Presentation

A comedo is the inital lesion which can be closed (whitehead) or open

(blackhead) and it evolves into inflammatory lesions that listed in as-

cending order of severity are papules pustules nodules and cysts

Lesions progress and leave scars Scars can be increased if lesions are

manipulated

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Amer ican Manual of Examinat ion in Medicine (2CK)

2

Diff erent lesions habitually combine simultaneously so acne becomes

polymorphic It is located in sebaceous areas face back shoulders and

the center thoracic region

Diagnosis

Diagnosis is clinical

Treatment

bull Comedonal acne is treated with topic retnoids and benzoyl peroxide

bull Inflammatory acne treatment requires benzoyl peroxide combined

with topic antbiotcs (erythromycin and clindamycin) Systemic

antbiotc treatment with oral tetracyclines will be prescribed if re-

sponse to topic antbiotc treatment fails

bull Severe nodular cystc acne treatment involves the use of isotret-

noin (13-cis-retnoic acid) It is a derivatve of vitamin A Isotretnoin

produces atrophy in the sebaceous gland and regulates keratniza-

ton The most frequent side eff ect is cutaneous and mucosal xero-

sis Triglycerides cholesterol and transaminases should be moni-

tored as their values may increasebull It can be associated with depression

bull It is teratogenic so pregnancy should be avoided during treatment

and untl a month afer treatment

Pilonidal Cysts

Pilonidal cysts are abscesses in the sacrococcygeal region

This type of cysts has predominance in men between 20 and 40 years

of age It is believed that repeated trauma on the aff ected area favors

their appearance

Clinical Presentation

Pilonidal cysts present with an indurated lesion that is fluctuatng hot

painful but non-adherent to deep planes in the sacrococcygeal region

Pilonidal cysts may or may not be associated to cellulits and purulent drain-

age

Diagnosis

Diagnosis is clinical and anal or perirectal abscesses should be dismissed

Treatment

Treatment implies an incision and surgical drainage

On some occasions a general surgery is required

43 Fungal Infections

Pityriasis Versicolor

Versicolor pityriasis is caused by commensal yeast called Pityrosporum

ovale which transforms into its pathogen form (Malassezia furfur) It

especially aff ects young patents (15 - 45 years of age) but it is rare

in childhood and advanced age Versicolor pityriasis relates to heat

humidity and sebaceous hypersecreton It is characterized by the ap-

pearance of hyperchromic or hypochromic macules that desquamate

on scratching (nail sign) if infecton is actve Macules usually appear on

the center thoracic region and on the back that is to say on seborrheic

zones Relapses are habitual despite treatment

Diagnosis

Diagnosis is normally clinical To that purpose the following serve as

support

bull Woodrsquos lamp emits yellow-orange fluorescence

bull Potassium hydroxide (KOH) test filaments and round elements can

be observed (ldquospaghe and meatball appearancerdquo Figure 20)

Treatment

Treatment is performed with topical azoles Oral administraton applies

for extensive cases or immunosuppressed patents Diff erental diagno-

sis includes pink pityriasis and eczemas (Figure 21)

Figure 20 Versicolor pityriasis Histological cut

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Dermatology

Figure 21 Versicolor pityriasis

Candidiasis

The most common triggering agent is Candida albicans It is normally sapro-

phyt

c although under certain condit

ons candidiasis may become patho-genic (immunosuppression humidity pregnancy and contraceptves)

Clinical Forms

bull Intertrigo erythematous plaque in cutaneous folds Atrophy and

fissures are typically deep in the skin fold as well as satellite and

peripheral lesions (papules andor pustules)

bull Mucosa involvement may cause diverse symptomatology like vul-

vovaginits glossits and white papules in the anterior region of the

oral mucosa Candidal balanits is characterized by the presence of

punctform erosions and pustules on gland and balanopreputal

sulcus Candidal balanits ofen appears afer sexual intercourse or

afer oral antbiotc intake

Remember

Almost a 100 of HIV patients suffer from muguet throughout their diseasecourse

bull Candidiasis of nail fold is usually associated with periungual inflam-

maton (perionixis) and inital proximal aff ectaton which diff erent-

ates it from tnea unguium (Figure 22)

Figure 22 Candidiasis of nail fold

Treatment

Oral Candidiasis fluconazole or nystatn

Candidiasis of the skin (intertrigo) apply topical antfungal medicaton

and keep zone clean and dry

Dermatophytosis or TineasDermatophyte infectons aff ect the skin and keratnized structures like

hair and nails (there is no mucosa involvement) Clinical diagnosis is

achieved afer performing a culture Woodrsquos lamp test normally turns

out to be negatve In general Trichophyton dermatophyte rubrum is

the most frequent dermatophyte

Non Inflammatory Tineas

Non inflammatory tneas do not produce irreversible scarring alope-

cia while inflammatory forms do Tineas are treated with azoles de-

rivatves

The types of tnea are the following

bull Ringworm of the scalp ( t nea capi t s or t nea tonsurans) is charac-

teristc of childhood It presents with alopecic plaques broken hair

and desquamaton Infectons tend to resolve spontaneously with-

out leaving scars at the onset

of puberty

bull Ringworm of the body (herpes

circinatus or t nea corporis) are

erythematous desquamatve

plaques (with more actve bor-

ders) which are also circinate

and normally pruritc (Figure

23) Plaques grow eccentrically

with less actvity in the centerand more in the borders

bull Ringworm of the foot ( t nea

pedis) the most frequent is the

ldquoathlete footrdquo with desquama-

ton in interdigital spaces

bull Tinea incognito refers to tnea

wrongly treated with cort-

coids what makes diagnosis

diffi cult as the lesion has been modified Figure 24)

Figure 24 Tinea incognito secondary to treatment with topical steroids

Figure 23 Herpes circinatus

(tinea corpis)

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Amer ican Manual of Examinat ion in Medicine (2CK)

4

bull Ringworm of the groin (t nea cruris or eczema marginatum von

hebra) formed by erythematous desquamatve plaque with more

actve borders (Figure 25)

Figure 25 Ringworm of the groin (tinea cruris)

bull Tinea unguium subungualhyperkeratosis with onychol-

ysis but without perionixis

(Figure 26)

Diagnosis

Clinical diagnosis is reached afer

performing a culture

Treatment

Treatment involves topical an-

tfungal medicaton in localized

areas

Oral antfungal medicaton is used in extensive forms nail fold or scalp

involvement

44 Parasitic Infections

Pediculosis

Pediculosis is transmied by direct contact or by contact with fomites

which release toxins that produce intense pruritus

Clinical Presentation

Pediculosis capi t s intense pruritus predominant in retroauricular and

occipital regions occasionally with excoriatons and impetginizaton

secondary to excoriatons

Pediculosis corporis intense pruritus in patents with poor hygiene or

who live in overcrowded conditons

Pediculosis pubis genital and pubic pruritus Brownish-grey macules

called maculae ceruleae are typical on underwear and skin These pig-

mentatons appear as a result of a reducton in hemoglobin by a para-

site enzyme

Diagnosis

Diagnosis is clinical and by direct visualizaton

Treatment

Pediculosis is treated with malathion lindane or topical permethrin

Scabies

Scabies is originated by an acarus known as Sarcoptes scabiei It has an

incubaton period of 1 month

Clinical Presentation

Scabies produces generalized pruritus more intense at night The pa-

tent usually catches the infestaton which is passed to the patentrsquos

relat

ves It is common tofi

nd that a recent trip to a tropical country hasbeen made Lesions appear between the fingers (Figure 27) in wrists

feet genitalia mammary areola and axilla but back and face are usu-

ally spared The most specific lesion is the acarine burrow in whose less

scaly end the advancing zone the mite lies Nodules are frequent in

axilla and genitals (nodular scabies)

bull Norwegian scabies is typical of the immunosuppressed Patents

present with generalized hyperkeratosis and scabs Norwegian sca-

bies produce lile pruritus but it is very contagious because there

are many acari

bull Nodular scabies involves the persistence of pruritc nodules despite

treatment Lesions usually appear in axilla and genitalia Pruritus is

due to a hypersensitvity phenomenon because of the acarus al-

ready dead Nodular scabies is treated with cortcoids

Figure 27 Scabies Acarine burrow

Treatment

bull Permethrin cream at 5 is the treatment of choice It is lile toxic

so it can be used in children and pregnant women

bull Topical lindane at 1 irritates and is neurotoxic therefore it is con-

traindicated in pregnant women and children

bull Oral ivermectn is utlized in cases of resistance to prior treatments

There is stll lile experience as to its use but in a first instance a

Figure 26 Tinea unguium

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Dermatology

single dose would be enough to cure scabies (already used by vet-

erinarians)

45 Ischemia

Decubitus Ulcers

Decubitus ulcers are the result of ischemic necrosis by contnuous pres-

sure on an area which restricts microcirculaton in that zone

Clinical Presentation

Decubitus ulcers are present in patents in bed with scarce mobilizaton

It is favored by bone prominences and lack of fat tssue If sensitvity

decreases there is more risk of formaton of decubitus ulcers

Diagnosis

Diagnosis is achieved based on medical records and clinical presentaton

Treatment

Preventon is of the utmost importance as well as frequent mobiliza-

ton of the patent in bed

Once ulcers have been established hydrocolloid dressings are used for

healing but sometmes surgical debridement is necessary

Gangrene

Gangrene means tssue necrosis

There are three types dry gangrene wet gangrene and gas gangrene

Clinical Presentation

Dry gangrene is due to ischemia generally secondary to atherosclero-

sis Clinical presentaton involves pain cold and paleness of extremi-

tes Once tssue is established it turns bluish-black in color and dry

Wet gangrene is owing to bacterial flora Tissue presents with an edem-

atous appearance either with blisters or pus

Gas gangrene caused by C perfringens It is normally located on re-

cent surgery Bacteria precociously destroyt

ssue producing gas It is amedical emergency

Diagnosis

Clinical diagnosis is obtained by microbiological culture

Treatment

Treatment requires surgical debridement with amputaton if necessary

and associaton of broad spectrum antbiotherapy

Gas gangrene is treated with hyperbaric oxygen

46 Miscellaneous

Acanthosis Nigricans

Acanthosis nigricans are vel-

vet-like papillomatous brown

plaques in neck axilla and groin

folds (Figure 28)

It is associated with diabetes

mellitus Cushingrsquos disease poly-

cystc ovarian syndrome and

obesity

The malignant form of acantho-

sis nigricans is a paraneoplastc

syndrome that diff erentates

from the benign form because

the laer has mucosal and pal-

moplantar involvement

Lichen Planus

Lichen planus is an inflammatory idiopathic disease that equally aff ects

both genders with higher frequency in middle age

Lichen planus has been related to diverse drugs like gold salts

anti-malarial medication and thiazides It has been also linked to

hepatitis C virus infection however this association is currently

doubtful

Clinical Presentation

Lichen planus presents with red-violaceous polygonal flat papulesquite pruritc which localizes on the flexor side of wrists forearms an-

kles and lumbosacral and flank regions On its surface a whitsh retcu-

late can be observed (Wickhamrsquos striae) About 60 - 70 of the cases

present with lesions in oral and genital mucosa oral which appear as

whitsh retculated lesions (Figures 29 and 30)

Figure 29 Lichen planus of oral mucosa with typical whitish

reticulate

Figure 28 Acanthosis nigricans

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Amer ican Manual of Examinat ion in Medicine (2CK)

6

Violaceous papules

with white stretch marks

Lichenoid lymphocyte

in1047297ltrate (band formation)

Destruction

of basal layer

Figure 30 Lymphocytic interface reaction (lichen planus)

Treatment

Mild forms are treated with topical cortcoids

Severe cases require oral cortcoids psoralens plus ultraviolet light of

the A wavelength (PUVA) or cyclosporine

Rosacea

Rosacea is a chronic disease of unknown pathogenesis characterized

by erythema and acneiform lesions on the face It aff ects middle aged

women (between 30 and 50 years of age) more

Rosacea etopathogenesis is unknown although there is involvement of

vasomotor lability infecton by Demodex folliculorum photo exposureand genetc predispositon

Clinical Presentation

Rosacea symptomatology comprises facial flushing episodes that end

up by provoking a persistent erythema telangiectasias and papulopus-

tular lesions without comedos Over tme ocular lesions and hyperpla-

sia of sof tssue may develop

Treatment

Avoid vasodilator stmuli

Mild cases require topical metronidazole or azelaic acid

Moderate cases need doxycycline or oral minocyclines

Severe cases are treated with oral isotretnoin at low doses

Pink Pityriasis

Gilbertrsquos pink pityriasis is an acute self-limitng dermatosis which main-

ly aff ects young adults It is of unknown origin although a viral etology

is suspected (there is some speculaton as to links with human herpes-

virus type 7)

Clinical Presentation

Erupton starts with an erythematous plaque between 2 and 5 cm of

diameter with a desquamatve central collaree ofen localized on the

trunk (heraldic mother patch Figure 31)

Figure 31 Pink pityriasis

Around a week later oval papules appear on the trunk and extremi-

tes These papules share similar characteristcs with the mother patch

though the first ones are smaller and distributed according to skin ten-

sion lines Pink pityriasis may be asymptomatc however it is some-

tmes linked to pruritus Lesions may last between 4 and 8 weeks and

disappear without leaving scars

Diagnosis and Treatment

Diagnosis is clinical Treatment is seldom needed and recommended

therapies in the past (PUVA erythromycin or oral antvirals) have not

shown clearly favorable results

Vitiligo

Vitligo is characterized by achromic macules by melanocyte destruc-

ton

Clinical Presentation

Vitligo shows achromic macules of chronic course and variable progres-

sion

Lesions are predominant on acral and periorificial areas They also show

the Koebner phenomenon

Patents may have markers of autoimmune diseases (ie antthyroid

antbodies and diabetes) but these diseases seldom manifest them-

selves

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Dermatology

Treatment

Localized lesions require topical cortcoids

Extensive or generalized lesions are treated with ultraviolet light B

(UVB) or PUVA

Strict solar photoprotecton is indispensable (Figure 32)

Figure 32 Vitiligo

47 Neoplasias

Seborrheic Keratosis

Seborrheic keratosis is the most frequent benign tumor in human be-

ings since it is part of cutaneous aging

Clinical Presentation

Seborrheic keratosis presents with hyperkeratosic papules with an oily

or velvet-like texture crests fissures and horny plugs on their surface

These papules are normally pigmented showing a brownish-black color

Treatment

No treatment is required as lesions do not become malignant

Seborrheic keratosis can be addressed with cureage or cryotherapy

Actinic keratosis

Actnic keratosis is the most common precancerous lesion and aff ects

almost a 100 of the populaton in sunny areas

Clinical Presentation

Actnic keratosis is characterized by erythematous and desquamatve

papules which are hyperkeratosic and rough on touch developing a

chronic course

Diagnosis

Diagnosis is clinical

Treatment

Treatment entails applicaton of topical 5-fluorouracil topical imiqui-

mod cryotherapy or surgery

If underlying carcinoma is suspected a biopsy must be performed to

rule out suspicion

Epidermoid Carcinoma

Epidermoid carcinoma is the second most frequent cutaneous tumor

Solar photo exposure is the main etological factor which is why epider-

moid carcinoma appears in zones of prolonged solar exposure like the

face Most carcinomas appear over premalignant lesions (actnic kera-

tosis and leukoplakia among others)

Clinical Presentation

Clinical presentaton reveals erythematous or erythematosquamous

plaques Over tme these plaques form papules and tumors which of-

ten become ulceratve and bleed

Diagnosis

Diagnosis is based on clinical suspicion and histopathological confirmaton

Treatment

Surgery with safety margins is the treatment of choice In carcinomas

in situ cryotherapy can be used as well as topical imiquimod electro-

coagulaton or CO2 laser techniques in destructon of tumors Radio-therapy may also be used in some cases

Basal Cellular Carcinoma

Basal cellular carcinoma is the most frequent cutaneous tumor Chronic so-

lar photo exposure is the main etological factor hence most of these car-

cinomas aff ect the facial zone in patents who are 40 years of age or older

Gorlinrsquos syndrome should be considered if multple basal cellular carci-

nomas are found in non photo exposed areas

Clinical Presentation

Basal cell carcinoma shows a pearly pink papule and superficial telan-

giectasias

It is localized over healthy skin and never aff ects mucosae

Treatment

Surgery is the treatment of choice Mohs surgery is performed in zones

where surrounding healthy tssue needs to be preserved Other alter-

natves are cryotherapy imiquimod electrocoagulaton radiotherapy

photodynamic therapy and intralesional interferon Prognosis is excel-

lent as growth is slow and metastasis exceptonal

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Amer ican Manual of Examinat ion in Medicine (2CK)

8

Melanoma

Melanoma is the most aggressive cutaneous tumor given its ability to

metastasize

Risk factors comprise solar photo exposure clear phototype the pres-

ence of dysplastc nevus or a high number of melanocytc nevi Fam-

ily history is quite important as some genetc mutatons determine a

higher risk of developing the disease

Clinical Forms

See Figure 33

Diagnosis

Precocious diagnosis is essental to perform precocious surgical extrpaton

The ABCDE criteria can help patents to see if they need to seek medical

consultaton (asymmetry of lesion uneven borders color and diameter

greater than 6 mm or abnormal evolut

on)

The Breslow index is the thickness of the lesion measured in millimeters

and is the main prognosis factor

Treatment

The base of treatment is precocious surgical extrpaton If the Breslow

index is less than 1 mm margins of 1 cm will be performed If Breslow

index is greater than 1 mm margins will be of 2 cm

For melanomas with a Breslow index greater than 1 mm the sentnel

ganglion must be located This is the first draining lymph node of the

territory where the tumor is localized If the ganglion is positve re-

gional lymphadenectomy will be performed along with interferon ad-ministraton (Figure 34)

In situ Extirpation 05 cm Follow-up

Breslow lt 1 mm Extirpation 1 cm Follow-up

Lymphadenectomy

Breslow gt 4 mm Interferon

Breslow ge 1 mm Extirpation 2 cm Sentinel ganglion

+

Figure 34 Melanoma treatment

Kaposirsquos sarcoma

Kaposirsquos sarcoma is the most common cutaneous tumor in HIV patents

Clinical presentation

Kaposirsquos sarcoma has a course with violaceous fusiform macules whichovertme may evolve into indurated nodules with blackberry appearance

This type of sarcoma has been linked to herpesvirus type 8 both in HIV

and seronegatve patents (Table 3)

EPIDERMAL KAPOSIrsquoS 983080HIV983081 CLASSIC KAPOSIrsquoS

Homosexual youth (95) The elderly

Diffuse and bilateral

(frequently in palate and face)

Unilateral plaques

(lower extremities)

Frequent mucosal and visceral involvement Not so frequent

middot Precocious lymphatic invasion

middot Aggressive

Not so precocious

Table 3 Differences between epidermal and classic Kaposirsquos sarcoma

Nodular melanoma

15

Middle-aged men

middot On healthy skin

middot Any zone

middot Sudden onset

middot Uniform black nodulemiddot Rapidly invasive (vertical growth without radial)middot Frequent ulceration and bleeding

Worst histological prognosis

Lentigo malignant melanoma

10

Elderly women

90 on facephotoexposedzones of aging skins(chronic exposure)

Spot that growsduring many years (gt 10)then progresses (nodule)

Better prognosis

Acral lentinginous melanoma

5ndash10 ( 60 black and Asian race)

Elderly men

middot Sole (ankle) handsmucosa ungual bed

middot No relation to photo exposure

middot Macule with mosaic appearance (spot that grows)middot Some amelanisticmiddot Bad prognosis due to late diagnosis

Melanoma of super1047297cial extension

70

Young women

middot 30 previous nervusmiddot Intermittent exposuremiddot Men back middot Women legs

More frequent

middot Macula with mosaic appearance in colors that grows 4-5 years and then in1047297ltrates (nodule)middot Metastasis 35 to 70

Figure 33 Clinical forms of malignant melanoma

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Dermatology

Diagnosis

Diagnosis relies on clinical suspicion and histopathological confirma-

ton

Treatment

Treatment of localized forms can include surgical extrpaton radiother-

apy or intralesional vinblastne

If the sarcoma is disseminated optons involve interferon or chemo-

therapy

Mycosis Fungoides

Mycosis fungoides is a T-cell lymphoma of low-grade malignancy Its

clinical course may be very slow and surpass 50 years Three stages are

clinically diff erentated

1 Eczematous or macular phase predominantly truncular erythema-

tous macules with years of evoluton They resemble a chromic ec-

zema Histology is unspecifi

c at this stage2 Infiltratve plaque phase infiltrated erythematous plaques appear

Histology is diagnostc at this stage A dermal infiltrate of atypical

lymphocytes band forms can be observed composed of CD+4 T

lymphocytes with cerebriform nuclei There is a marked epidermo-

tropism with the presence of clusters of intraepidermal lympho-

cytes called Pautrierrsquos microabscesses (Figure 35)

Figure 35 Mycosis fungoides Infiltrative plaque phase

3 Tumoral phase erythematous exophytc plaques start to appear

(tumors) with a tendency to ulceraton They can have a large size

Histology may become unspecific again as epidermotropism disap-

pears

In more advanced stages of the disease there is aff ectaton of extra-

cutaneous organs such as lymph nodes liver spleen lungs and bone

marrow Besides there may be blastc transformaton Other possible

complicaton is sepsis by Staphylococcus aureus

These three stages usually develop consecutvely nevertheless there

may patents whose debut starts directly with the tumoral stage

Remember

Microabscesses of mycosis fungoides are due to lymphocytes and are calledPautrierrsquos abscesses Psoriasis microabscesses result from neutrophils andare labeled as Munro-Sabouraud

Seacutezary Syndrome

Seacutezary syndrome can be considered as the leukemic phase of T-cell cu-

taneous lymphoma It is defined by the triad erythroderma (Figure 36

lymphadenopathies and the existence of more than 1000 Seacutezary cellsper milliliter in peripheral blood Seacutezary cells are atypical T- lymphocyte

with cerebriform nuclei

Very intense pruritus is characteristc For many authors Seacutezary syn-

drome is an aggressive clinical form and a bad prognosis of a mycosis

fungoides

Figure 36 Erythroderma due to Seacutezary syndrome

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Amer ican Manual of Examinat ion in Medicine (2CK)

0

Lesions are asymptomatc

Diagnosis

Diagnosis is clinical Histology reveals characteristc inclusion bodies

Treatment

Lesions can resolve spontaneously

Cureage cryotherapy or local trichloroacetc acid are eff ectve meth-

ods to destroy lesions

Warts

Human papillomavirus can cause verruca vulgaris palmoplantar and

flat warts and condyloma accuminata Human papillomavirus is the

most frequent sexual transmied disease

Some subtypes of this virus (16 18) are of high risk and can cause epi-

dermoid carcinomas

Direct contact is the mechanism of contagion

Diagnosis

Diagnosis of this conditon is clinical

Staining with acetc acid can help visualize mucosal lesions

Treatment

Genital warts are treated with cryotherapy podophyllotoxin trichloro-

acetc acid imiquimod and 5-fluorouracil

Cervical lesions should be monitored by cytology and biopsy whenever

necessary to rule out cervical cancer (Figures 17 and 18)

Figure 17 Warts in HIV patient

Figure 18 Condyloma accuminata

42 Bacterial Infections

Impetigo

Impetgo is a very contagious superficial infecton without systemic re-

percussion and normally mixed etology by Gram positve cocci (strep-

tococci and staphylococci) Classically the most frequent accepted

cause was Streptococcus pyogenes However at present Staphylococcus

aureus stands out as the predominant cause

The most typical form is impetgo contagiosa (Figure 19) character-

ized by honey-colored (meliceric) scabs which normally appear on

the face and other exposed areas It is typical of children Although

infrequent poststreptococcal glomerulonephrits is a dreadful com-

plicaton

Figure 19 Impetigo contagiosa

On the contrary rheumatc fever shows no relaton to cutaneous strep-

tococcal infectons but only with pharyngeal infectons

There are other less habitual forms called bullous impetgo exclusively

of staphylococcal origin Clinical presentaton involves the presence of

blisters and erosions on the aff ected skin as a consequence of the epi-

dermolytc toxins that these bacteria contain Impetgo is treated with

topical mupirocin penicillin or oral fusidic acid

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Dermatology

Cellulitis

Cellulits is an infecton that aff ects deep dermis and subcutaneous cel-

lular tssues normally caused by streptococci (Streptococcus pyogenes

or of group A)

Community methicillin-resistant S aureus (CMRSA) is a triggering agent

that is becoming more and more frequent

Most common risk factors are diabetes chronic venous insuffi ciency

and immunosuppression

Clinical Presentation

Cellulits presents with erythematous plaques that are ill-defined pain-

ful and hot It is usually accompanied with fever and chills

Diagnosis

Diagnosis is clinical If there is an open door a culture of this area may

help see the source germ and resistance to ant

biot

cs

It is important to rule out abscesses osteomyelits and necrotzing fas-

ciits

If bacteremia is suspected blood cultures need to be performed

Treatment

Treatment implies oral antbiotcs for 7-10 days to cover Gram positve

cocci They are intravenously administered in case of lack of response

to oral treatment involvement of hands or periorbital zone diabetes or

extremes of age

Necrotizing FasciitisNecrotzing fasciits is a deep infecton up to muscular fascia that pro-

duces very intense pain and subsequent anesthesia

In 10 of the cases cellulits is due to an infecton by S pyogenes In the

remaining cases it occurs by a polymicrobial infecton caused by aerobes

and anaerobes including S aureus E coli and Clostridium perfringens

There may be prior history of trauma or surgery

Clinical Presentation

Clinical presentat

on involves pain of sudden onset and edema on theaff ected zone Pain may progress to anesthesia There appears subse-

quent erythema that progresses rapidly into necrosis

Characteristc clinical signs are tssue necrosis blisters intense pain

and gas producton

Diagnosis

Diagnosis is clinical and requires image testng X-rays or a computed

tomography CT

A biopsy of the border of the lesion helps achieve diagnosis

Treatment

Treatment entails precocious surgical debridement It is a surgical emer-

gency In additon to surgery broad-spectrum antbiotherapy will be

needed

Folliculitis

Folliculits is an infecton and inflammaton of one or several follicles

caused mainly by staphylococci

Clinical Presentation

Folliculits shows pustules with follicular distributon

When the infecton is deeper it is called furuncle

If several furuncles are infected a fluctuatng erythematous plaque forms

containing several points of suppuraton This plaque is labeled as anthrax

Diabet

c and immunosuppressed pat

ents are at higher risk

Characteristics of Folliculitis

1 Hot tub or swimming pool folliculits caused by Pseudomonas aeru-

ginosa

2 HIV associated pruritc folliculits or eosinophilic folliculits

Treatment

In mild cases treatment of choice comprises antseptcs and topic an-

tbiotcs

In more severe cases treatment of choice requires oral antbiotcs

Large sized lesions must be drained and a microbiological culture must be

performed to rule out methicillin-resistant Staphylococcus aureus MRSA

Acne Vulgaris

Acne is an inflammatory disease of the pilosebaceous follicle as a con-

sequence of an alteraton in follicular keratnizaton It aff ects adoles-

cents and young adults

Etology is multfactorial alteraton of keratnizaton of follicular infun-

dibulum quanttatve and qualitatve alteraton of sebum producton in

the sebaceous gland and alteratons of bacterial microflora (increase in

quant

ty of P acnes)

Aggravatng factors are stress androgenic oral contraceptves and the

use of cosmetc products that are not oil-free

Clinical Presentation

A comedo is the inital lesion which can be closed (whitehead) or open

(blackhead) and it evolves into inflammatory lesions that listed in as-

cending order of severity are papules pustules nodules and cysts

Lesions progress and leave scars Scars can be increased if lesions are

manipulated

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Amer ican Manual of Examinat ion in Medicine (2CK)

2

Diff erent lesions habitually combine simultaneously so acne becomes

polymorphic It is located in sebaceous areas face back shoulders and

the center thoracic region

Diagnosis

Diagnosis is clinical

Treatment

bull Comedonal acne is treated with topic retnoids and benzoyl peroxide

bull Inflammatory acne treatment requires benzoyl peroxide combined

with topic antbiotcs (erythromycin and clindamycin) Systemic

antbiotc treatment with oral tetracyclines will be prescribed if re-

sponse to topic antbiotc treatment fails

bull Severe nodular cystc acne treatment involves the use of isotret-

noin (13-cis-retnoic acid) It is a derivatve of vitamin A Isotretnoin

produces atrophy in the sebaceous gland and regulates keratniza-

ton The most frequent side eff ect is cutaneous and mucosal xero-

sis Triglycerides cholesterol and transaminases should be moni-

tored as their values may increasebull It can be associated with depression

bull It is teratogenic so pregnancy should be avoided during treatment

and untl a month afer treatment

Pilonidal Cysts

Pilonidal cysts are abscesses in the sacrococcygeal region

This type of cysts has predominance in men between 20 and 40 years

of age It is believed that repeated trauma on the aff ected area favors

their appearance

Clinical Presentation

Pilonidal cysts present with an indurated lesion that is fluctuatng hot

painful but non-adherent to deep planes in the sacrococcygeal region

Pilonidal cysts may or may not be associated to cellulits and purulent drain-

age

Diagnosis

Diagnosis is clinical and anal or perirectal abscesses should be dismissed

Treatment

Treatment implies an incision and surgical drainage

On some occasions a general surgery is required

43 Fungal Infections

Pityriasis Versicolor

Versicolor pityriasis is caused by commensal yeast called Pityrosporum

ovale which transforms into its pathogen form (Malassezia furfur) It

especially aff ects young patents (15 - 45 years of age) but it is rare

in childhood and advanced age Versicolor pityriasis relates to heat

humidity and sebaceous hypersecreton It is characterized by the ap-

pearance of hyperchromic or hypochromic macules that desquamate

on scratching (nail sign) if infecton is actve Macules usually appear on

the center thoracic region and on the back that is to say on seborrheic

zones Relapses are habitual despite treatment

Diagnosis

Diagnosis is normally clinical To that purpose the following serve as

support

bull Woodrsquos lamp emits yellow-orange fluorescence

bull Potassium hydroxide (KOH) test filaments and round elements can

be observed (ldquospaghe and meatball appearancerdquo Figure 20)

Treatment

Treatment is performed with topical azoles Oral administraton applies

for extensive cases or immunosuppressed patents Diff erental diagno-

sis includes pink pityriasis and eczemas (Figure 21)

Figure 20 Versicolor pityriasis Histological cut

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Dermatology

Figure 21 Versicolor pityriasis

Candidiasis

The most common triggering agent is Candida albicans It is normally sapro-

phyt

c although under certain condit

ons candidiasis may become patho-genic (immunosuppression humidity pregnancy and contraceptves)

Clinical Forms

bull Intertrigo erythematous plaque in cutaneous folds Atrophy and

fissures are typically deep in the skin fold as well as satellite and

peripheral lesions (papules andor pustules)

bull Mucosa involvement may cause diverse symptomatology like vul-

vovaginits glossits and white papules in the anterior region of the

oral mucosa Candidal balanits is characterized by the presence of

punctform erosions and pustules on gland and balanopreputal

sulcus Candidal balanits ofen appears afer sexual intercourse or

afer oral antbiotc intake

Remember

Almost a 100 of HIV patients suffer from muguet throughout their diseasecourse

bull Candidiasis of nail fold is usually associated with periungual inflam-

maton (perionixis) and inital proximal aff ectaton which diff erent-

ates it from tnea unguium (Figure 22)

Figure 22 Candidiasis of nail fold

Treatment

Oral Candidiasis fluconazole or nystatn

Candidiasis of the skin (intertrigo) apply topical antfungal medicaton

and keep zone clean and dry

Dermatophytosis or TineasDermatophyte infectons aff ect the skin and keratnized structures like

hair and nails (there is no mucosa involvement) Clinical diagnosis is

achieved afer performing a culture Woodrsquos lamp test normally turns

out to be negatve In general Trichophyton dermatophyte rubrum is

the most frequent dermatophyte

Non Inflammatory Tineas

Non inflammatory tneas do not produce irreversible scarring alope-

cia while inflammatory forms do Tineas are treated with azoles de-

rivatves

The types of tnea are the following

bull Ringworm of the scalp ( t nea capi t s or t nea tonsurans) is charac-

teristc of childhood It presents with alopecic plaques broken hair

and desquamaton Infectons tend to resolve spontaneously with-

out leaving scars at the onset

of puberty

bull Ringworm of the body (herpes

circinatus or t nea corporis) are

erythematous desquamatve

plaques (with more actve bor-

ders) which are also circinate

and normally pruritc (Figure

23) Plaques grow eccentrically

with less actvity in the centerand more in the borders

bull Ringworm of the foot ( t nea

pedis) the most frequent is the

ldquoathlete footrdquo with desquama-

ton in interdigital spaces

bull Tinea incognito refers to tnea

wrongly treated with cort-

coids what makes diagnosis

diffi cult as the lesion has been modified Figure 24)

Figure 24 Tinea incognito secondary to treatment with topical steroids

Figure 23 Herpes circinatus

(tinea corpis)

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Amer ican Manual of Examinat ion in Medicine (2CK)

4

bull Ringworm of the groin (t nea cruris or eczema marginatum von

hebra) formed by erythematous desquamatve plaque with more

actve borders (Figure 25)

Figure 25 Ringworm of the groin (tinea cruris)

bull Tinea unguium subungualhyperkeratosis with onychol-

ysis but without perionixis

(Figure 26)

Diagnosis

Clinical diagnosis is reached afer

performing a culture

Treatment

Treatment involves topical an-

tfungal medicaton in localized

areas

Oral antfungal medicaton is used in extensive forms nail fold or scalp

involvement

44 Parasitic Infections

Pediculosis

Pediculosis is transmied by direct contact or by contact with fomites

which release toxins that produce intense pruritus

Clinical Presentation

Pediculosis capi t s intense pruritus predominant in retroauricular and

occipital regions occasionally with excoriatons and impetginizaton

secondary to excoriatons

Pediculosis corporis intense pruritus in patents with poor hygiene or

who live in overcrowded conditons

Pediculosis pubis genital and pubic pruritus Brownish-grey macules

called maculae ceruleae are typical on underwear and skin These pig-

mentatons appear as a result of a reducton in hemoglobin by a para-

site enzyme

Diagnosis

Diagnosis is clinical and by direct visualizaton

Treatment

Pediculosis is treated with malathion lindane or topical permethrin

Scabies

Scabies is originated by an acarus known as Sarcoptes scabiei It has an

incubaton period of 1 month

Clinical Presentation

Scabies produces generalized pruritus more intense at night The pa-

tent usually catches the infestaton which is passed to the patentrsquos

relat

ves It is common tofi

nd that a recent trip to a tropical country hasbeen made Lesions appear between the fingers (Figure 27) in wrists

feet genitalia mammary areola and axilla but back and face are usu-

ally spared The most specific lesion is the acarine burrow in whose less

scaly end the advancing zone the mite lies Nodules are frequent in

axilla and genitals (nodular scabies)

bull Norwegian scabies is typical of the immunosuppressed Patents

present with generalized hyperkeratosis and scabs Norwegian sca-

bies produce lile pruritus but it is very contagious because there

are many acari

bull Nodular scabies involves the persistence of pruritc nodules despite

treatment Lesions usually appear in axilla and genitalia Pruritus is

due to a hypersensitvity phenomenon because of the acarus al-

ready dead Nodular scabies is treated with cortcoids

Figure 27 Scabies Acarine burrow

Treatment

bull Permethrin cream at 5 is the treatment of choice It is lile toxic

so it can be used in children and pregnant women

bull Topical lindane at 1 irritates and is neurotoxic therefore it is con-

traindicated in pregnant women and children

bull Oral ivermectn is utlized in cases of resistance to prior treatments

There is stll lile experience as to its use but in a first instance a

Figure 26 Tinea unguium

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Dermatology

single dose would be enough to cure scabies (already used by vet-

erinarians)

45 Ischemia

Decubitus Ulcers

Decubitus ulcers are the result of ischemic necrosis by contnuous pres-

sure on an area which restricts microcirculaton in that zone

Clinical Presentation

Decubitus ulcers are present in patents in bed with scarce mobilizaton

It is favored by bone prominences and lack of fat tssue If sensitvity

decreases there is more risk of formaton of decubitus ulcers

Diagnosis

Diagnosis is achieved based on medical records and clinical presentaton

Treatment

Preventon is of the utmost importance as well as frequent mobiliza-

ton of the patent in bed

Once ulcers have been established hydrocolloid dressings are used for

healing but sometmes surgical debridement is necessary

Gangrene

Gangrene means tssue necrosis

There are three types dry gangrene wet gangrene and gas gangrene

Clinical Presentation

Dry gangrene is due to ischemia generally secondary to atherosclero-

sis Clinical presentaton involves pain cold and paleness of extremi-

tes Once tssue is established it turns bluish-black in color and dry

Wet gangrene is owing to bacterial flora Tissue presents with an edem-

atous appearance either with blisters or pus

Gas gangrene caused by C perfringens It is normally located on re-

cent surgery Bacteria precociously destroyt

ssue producing gas It is amedical emergency

Diagnosis

Clinical diagnosis is obtained by microbiological culture

Treatment

Treatment requires surgical debridement with amputaton if necessary

and associaton of broad spectrum antbiotherapy

Gas gangrene is treated with hyperbaric oxygen

46 Miscellaneous

Acanthosis Nigricans

Acanthosis nigricans are vel-

vet-like papillomatous brown

plaques in neck axilla and groin

folds (Figure 28)

It is associated with diabetes

mellitus Cushingrsquos disease poly-

cystc ovarian syndrome and

obesity

The malignant form of acantho-

sis nigricans is a paraneoplastc

syndrome that diff erentates

from the benign form because

the laer has mucosal and pal-

moplantar involvement

Lichen Planus

Lichen planus is an inflammatory idiopathic disease that equally aff ects

both genders with higher frequency in middle age

Lichen planus has been related to diverse drugs like gold salts

anti-malarial medication and thiazides It has been also linked to

hepatitis C virus infection however this association is currently

doubtful

Clinical Presentation

Lichen planus presents with red-violaceous polygonal flat papulesquite pruritc which localizes on the flexor side of wrists forearms an-

kles and lumbosacral and flank regions On its surface a whitsh retcu-

late can be observed (Wickhamrsquos striae) About 60 - 70 of the cases

present with lesions in oral and genital mucosa oral which appear as

whitsh retculated lesions (Figures 29 and 30)

Figure 29 Lichen planus of oral mucosa with typical whitish

reticulate

Figure 28 Acanthosis nigricans

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Amer ican Manual of Examinat ion in Medicine (2CK)

6

Violaceous papules

with white stretch marks

Lichenoid lymphocyte

in1047297ltrate (band formation)

Destruction

of basal layer

Figure 30 Lymphocytic interface reaction (lichen planus)

Treatment

Mild forms are treated with topical cortcoids

Severe cases require oral cortcoids psoralens plus ultraviolet light of

the A wavelength (PUVA) or cyclosporine

Rosacea

Rosacea is a chronic disease of unknown pathogenesis characterized

by erythema and acneiform lesions on the face It aff ects middle aged

women (between 30 and 50 years of age) more

Rosacea etopathogenesis is unknown although there is involvement of

vasomotor lability infecton by Demodex folliculorum photo exposureand genetc predispositon

Clinical Presentation

Rosacea symptomatology comprises facial flushing episodes that end

up by provoking a persistent erythema telangiectasias and papulopus-

tular lesions without comedos Over tme ocular lesions and hyperpla-

sia of sof tssue may develop

Treatment

Avoid vasodilator stmuli

Mild cases require topical metronidazole or azelaic acid

Moderate cases need doxycycline or oral minocyclines

Severe cases are treated with oral isotretnoin at low doses

Pink Pityriasis

Gilbertrsquos pink pityriasis is an acute self-limitng dermatosis which main-

ly aff ects young adults It is of unknown origin although a viral etology

is suspected (there is some speculaton as to links with human herpes-

virus type 7)

Clinical Presentation

Erupton starts with an erythematous plaque between 2 and 5 cm of

diameter with a desquamatve central collaree ofen localized on the

trunk (heraldic mother patch Figure 31)

Figure 31 Pink pityriasis

Around a week later oval papules appear on the trunk and extremi-

tes These papules share similar characteristcs with the mother patch

though the first ones are smaller and distributed according to skin ten-

sion lines Pink pityriasis may be asymptomatc however it is some-

tmes linked to pruritus Lesions may last between 4 and 8 weeks and

disappear without leaving scars

Diagnosis and Treatment

Diagnosis is clinical Treatment is seldom needed and recommended

therapies in the past (PUVA erythromycin or oral antvirals) have not

shown clearly favorable results

Vitiligo

Vitligo is characterized by achromic macules by melanocyte destruc-

ton

Clinical Presentation

Vitligo shows achromic macules of chronic course and variable progres-

sion

Lesions are predominant on acral and periorificial areas They also show

the Koebner phenomenon

Patents may have markers of autoimmune diseases (ie antthyroid

antbodies and diabetes) but these diseases seldom manifest them-

selves

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Dermatology

Treatment

Localized lesions require topical cortcoids

Extensive or generalized lesions are treated with ultraviolet light B

(UVB) or PUVA

Strict solar photoprotecton is indispensable (Figure 32)

Figure 32 Vitiligo

47 Neoplasias

Seborrheic Keratosis

Seborrheic keratosis is the most frequent benign tumor in human be-

ings since it is part of cutaneous aging

Clinical Presentation

Seborrheic keratosis presents with hyperkeratosic papules with an oily

or velvet-like texture crests fissures and horny plugs on their surface

These papules are normally pigmented showing a brownish-black color

Treatment

No treatment is required as lesions do not become malignant

Seborrheic keratosis can be addressed with cureage or cryotherapy

Actinic keratosis

Actnic keratosis is the most common precancerous lesion and aff ects

almost a 100 of the populaton in sunny areas

Clinical Presentation

Actnic keratosis is characterized by erythematous and desquamatve

papules which are hyperkeratosic and rough on touch developing a

chronic course

Diagnosis

Diagnosis is clinical

Treatment

Treatment entails applicaton of topical 5-fluorouracil topical imiqui-

mod cryotherapy or surgery

If underlying carcinoma is suspected a biopsy must be performed to

rule out suspicion

Epidermoid Carcinoma

Epidermoid carcinoma is the second most frequent cutaneous tumor

Solar photo exposure is the main etological factor which is why epider-

moid carcinoma appears in zones of prolonged solar exposure like the

face Most carcinomas appear over premalignant lesions (actnic kera-

tosis and leukoplakia among others)

Clinical Presentation

Clinical presentaton reveals erythematous or erythematosquamous

plaques Over tme these plaques form papules and tumors which of-

ten become ulceratve and bleed

Diagnosis

Diagnosis is based on clinical suspicion and histopathological confirmaton

Treatment

Surgery with safety margins is the treatment of choice In carcinomas

in situ cryotherapy can be used as well as topical imiquimod electro-

coagulaton or CO2 laser techniques in destructon of tumors Radio-therapy may also be used in some cases

Basal Cellular Carcinoma

Basal cellular carcinoma is the most frequent cutaneous tumor Chronic so-

lar photo exposure is the main etological factor hence most of these car-

cinomas aff ect the facial zone in patents who are 40 years of age or older

Gorlinrsquos syndrome should be considered if multple basal cellular carci-

nomas are found in non photo exposed areas

Clinical Presentation

Basal cell carcinoma shows a pearly pink papule and superficial telan-

giectasias

It is localized over healthy skin and never aff ects mucosae

Treatment

Surgery is the treatment of choice Mohs surgery is performed in zones

where surrounding healthy tssue needs to be preserved Other alter-

natves are cryotherapy imiquimod electrocoagulaton radiotherapy

photodynamic therapy and intralesional interferon Prognosis is excel-

lent as growth is slow and metastasis exceptonal

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Amer ican Manual of Examinat ion in Medicine (2CK)

8

Melanoma

Melanoma is the most aggressive cutaneous tumor given its ability to

metastasize

Risk factors comprise solar photo exposure clear phototype the pres-

ence of dysplastc nevus or a high number of melanocytc nevi Fam-

ily history is quite important as some genetc mutatons determine a

higher risk of developing the disease

Clinical Forms

See Figure 33

Diagnosis

Precocious diagnosis is essental to perform precocious surgical extrpaton

The ABCDE criteria can help patents to see if they need to seek medical

consultaton (asymmetry of lesion uneven borders color and diameter

greater than 6 mm or abnormal evolut

on)

The Breslow index is the thickness of the lesion measured in millimeters

and is the main prognosis factor

Treatment

The base of treatment is precocious surgical extrpaton If the Breslow

index is less than 1 mm margins of 1 cm will be performed If Breslow

index is greater than 1 mm margins will be of 2 cm

For melanomas with a Breslow index greater than 1 mm the sentnel

ganglion must be located This is the first draining lymph node of the

territory where the tumor is localized If the ganglion is positve re-

gional lymphadenectomy will be performed along with interferon ad-ministraton (Figure 34)

In situ Extirpation 05 cm Follow-up

Breslow lt 1 mm Extirpation 1 cm Follow-up

Lymphadenectomy

Breslow gt 4 mm Interferon

Breslow ge 1 mm Extirpation 2 cm Sentinel ganglion

+

Figure 34 Melanoma treatment

Kaposirsquos sarcoma

Kaposirsquos sarcoma is the most common cutaneous tumor in HIV patents

Clinical presentation

Kaposirsquos sarcoma has a course with violaceous fusiform macules whichovertme may evolve into indurated nodules with blackberry appearance

This type of sarcoma has been linked to herpesvirus type 8 both in HIV

and seronegatve patents (Table 3)

EPIDERMAL KAPOSIrsquoS 983080HIV983081 CLASSIC KAPOSIrsquoS

Homosexual youth (95) The elderly

Diffuse and bilateral

(frequently in palate and face)

Unilateral plaques

(lower extremities)

Frequent mucosal and visceral involvement Not so frequent

middot Precocious lymphatic invasion

middot Aggressive

Not so precocious

Table 3 Differences between epidermal and classic Kaposirsquos sarcoma

Nodular melanoma

15

Middle-aged men

middot On healthy skin

middot Any zone

middot Sudden onset

middot Uniform black nodulemiddot Rapidly invasive (vertical growth without radial)middot Frequent ulceration and bleeding

Worst histological prognosis

Lentigo malignant melanoma

10

Elderly women

90 on facephotoexposedzones of aging skins(chronic exposure)

Spot that growsduring many years (gt 10)then progresses (nodule)

Better prognosis

Acral lentinginous melanoma

5ndash10 ( 60 black and Asian race)

Elderly men

middot Sole (ankle) handsmucosa ungual bed

middot No relation to photo exposure

middot Macule with mosaic appearance (spot that grows)middot Some amelanisticmiddot Bad prognosis due to late diagnosis

Melanoma of super1047297cial extension

70

Young women

middot 30 previous nervusmiddot Intermittent exposuremiddot Men back middot Women legs

More frequent

middot Macula with mosaic appearance in colors that grows 4-5 years and then in1047297ltrates (nodule)middot Metastasis 35 to 70

Figure 33 Clinical forms of malignant melanoma

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Dermatology

Diagnosis

Diagnosis relies on clinical suspicion and histopathological confirma-

ton

Treatment

Treatment of localized forms can include surgical extrpaton radiother-

apy or intralesional vinblastne

If the sarcoma is disseminated optons involve interferon or chemo-

therapy

Mycosis Fungoides

Mycosis fungoides is a T-cell lymphoma of low-grade malignancy Its

clinical course may be very slow and surpass 50 years Three stages are

clinically diff erentated

1 Eczematous or macular phase predominantly truncular erythema-

tous macules with years of evoluton They resemble a chromic ec-

zema Histology is unspecifi

c at this stage2 Infiltratve plaque phase infiltrated erythematous plaques appear

Histology is diagnostc at this stage A dermal infiltrate of atypical

lymphocytes band forms can be observed composed of CD+4 T

lymphocytes with cerebriform nuclei There is a marked epidermo-

tropism with the presence of clusters of intraepidermal lympho-

cytes called Pautrierrsquos microabscesses (Figure 35)

Figure 35 Mycosis fungoides Infiltrative plaque phase

3 Tumoral phase erythematous exophytc plaques start to appear

(tumors) with a tendency to ulceraton They can have a large size

Histology may become unspecific again as epidermotropism disap-

pears

In more advanced stages of the disease there is aff ectaton of extra-

cutaneous organs such as lymph nodes liver spleen lungs and bone

marrow Besides there may be blastc transformaton Other possible

complicaton is sepsis by Staphylococcus aureus

These three stages usually develop consecutvely nevertheless there

may patents whose debut starts directly with the tumoral stage

Remember

Microabscesses of mycosis fungoides are due to lymphocytes and are calledPautrierrsquos abscesses Psoriasis microabscesses result from neutrophils andare labeled as Munro-Sabouraud

Seacutezary Syndrome

Seacutezary syndrome can be considered as the leukemic phase of T-cell cu-

taneous lymphoma It is defined by the triad erythroderma (Figure 36

lymphadenopathies and the existence of more than 1000 Seacutezary cellsper milliliter in peripheral blood Seacutezary cells are atypical T- lymphocyte

with cerebriform nuclei

Very intense pruritus is characteristc For many authors Seacutezary syn-

drome is an aggressive clinical form and a bad prognosis of a mycosis

fungoides

Figure 36 Erythroderma due to Seacutezary syndrome

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Dermatology

Cellulitis

Cellulits is an infecton that aff ects deep dermis and subcutaneous cel-

lular tssues normally caused by streptococci (Streptococcus pyogenes

or of group A)

Community methicillin-resistant S aureus (CMRSA) is a triggering agent

that is becoming more and more frequent

Most common risk factors are diabetes chronic venous insuffi ciency

and immunosuppression

Clinical Presentation

Cellulits presents with erythematous plaques that are ill-defined pain-

ful and hot It is usually accompanied with fever and chills

Diagnosis

Diagnosis is clinical If there is an open door a culture of this area may

help see the source germ and resistance to ant

biot

cs

It is important to rule out abscesses osteomyelits and necrotzing fas-

ciits

If bacteremia is suspected blood cultures need to be performed

Treatment

Treatment implies oral antbiotcs for 7-10 days to cover Gram positve

cocci They are intravenously administered in case of lack of response

to oral treatment involvement of hands or periorbital zone diabetes or

extremes of age

Necrotizing FasciitisNecrotzing fasciits is a deep infecton up to muscular fascia that pro-

duces very intense pain and subsequent anesthesia

In 10 of the cases cellulits is due to an infecton by S pyogenes In the

remaining cases it occurs by a polymicrobial infecton caused by aerobes

and anaerobes including S aureus E coli and Clostridium perfringens

There may be prior history of trauma or surgery

Clinical Presentation

Clinical presentat

on involves pain of sudden onset and edema on theaff ected zone Pain may progress to anesthesia There appears subse-

quent erythema that progresses rapidly into necrosis

Characteristc clinical signs are tssue necrosis blisters intense pain

and gas producton

Diagnosis

Diagnosis is clinical and requires image testng X-rays or a computed

tomography CT

A biopsy of the border of the lesion helps achieve diagnosis

Treatment

Treatment entails precocious surgical debridement It is a surgical emer-

gency In additon to surgery broad-spectrum antbiotherapy will be

needed

Folliculitis

Folliculits is an infecton and inflammaton of one or several follicles

caused mainly by staphylococci

Clinical Presentation

Folliculits shows pustules with follicular distributon

When the infecton is deeper it is called furuncle

If several furuncles are infected a fluctuatng erythematous plaque forms

containing several points of suppuraton This plaque is labeled as anthrax

Diabet

c and immunosuppressed pat

ents are at higher risk

Characteristics of Folliculitis

1 Hot tub or swimming pool folliculits caused by Pseudomonas aeru-

ginosa

2 HIV associated pruritc folliculits or eosinophilic folliculits

Treatment

In mild cases treatment of choice comprises antseptcs and topic an-

tbiotcs

In more severe cases treatment of choice requires oral antbiotcs

Large sized lesions must be drained and a microbiological culture must be

performed to rule out methicillin-resistant Staphylococcus aureus MRSA

Acne Vulgaris

Acne is an inflammatory disease of the pilosebaceous follicle as a con-

sequence of an alteraton in follicular keratnizaton It aff ects adoles-

cents and young adults

Etology is multfactorial alteraton of keratnizaton of follicular infun-

dibulum quanttatve and qualitatve alteraton of sebum producton in

the sebaceous gland and alteratons of bacterial microflora (increase in

quant

ty of P acnes)

Aggravatng factors are stress androgenic oral contraceptves and the

use of cosmetc products that are not oil-free

Clinical Presentation

A comedo is the inital lesion which can be closed (whitehead) or open

(blackhead) and it evolves into inflammatory lesions that listed in as-

cending order of severity are papules pustules nodules and cysts

Lesions progress and leave scars Scars can be increased if lesions are

manipulated

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Amer ican Manual of Examinat ion in Medicine (2CK)

2

Diff erent lesions habitually combine simultaneously so acne becomes

polymorphic It is located in sebaceous areas face back shoulders and

the center thoracic region

Diagnosis

Diagnosis is clinical

Treatment

bull Comedonal acne is treated with topic retnoids and benzoyl peroxide

bull Inflammatory acne treatment requires benzoyl peroxide combined

with topic antbiotcs (erythromycin and clindamycin) Systemic

antbiotc treatment with oral tetracyclines will be prescribed if re-

sponse to topic antbiotc treatment fails

bull Severe nodular cystc acne treatment involves the use of isotret-

noin (13-cis-retnoic acid) It is a derivatve of vitamin A Isotretnoin

produces atrophy in the sebaceous gland and regulates keratniza-

ton The most frequent side eff ect is cutaneous and mucosal xero-

sis Triglycerides cholesterol and transaminases should be moni-

tored as their values may increasebull It can be associated with depression

bull It is teratogenic so pregnancy should be avoided during treatment

and untl a month afer treatment

Pilonidal Cysts

Pilonidal cysts are abscesses in the sacrococcygeal region

This type of cysts has predominance in men between 20 and 40 years

of age It is believed that repeated trauma on the aff ected area favors

their appearance

Clinical Presentation

Pilonidal cysts present with an indurated lesion that is fluctuatng hot

painful but non-adherent to deep planes in the sacrococcygeal region

Pilonidal cysts may or may not be associated to cellulits and purulent drain-

age

Diagnosis

Diagnosis is clinical and anal or perirectal abscesses should be dismissed

Treatment

Treatment implies an incision and surgical drainage

On some occasions a general surgery is required

43 Fungal Infections

Pityriasis Versicolor

Versicolor pityriasis is caused by commensal yeast called Pityrosporum

ovale which transforms into its pathogen form (Malassezia furfur) It

especially aff ects young patents (15 - 45 years of age) but it is rare

in childhood and advanced age Versicolor pityriasis relates to heat

humidity and sebaceous hypersecreton It is characterized by the ap-

pearance of hyperchromic or hypochromic macules that desquamate

on scratching (nail sign) if infecton is actve Macules usually appear on

the center thoracic region and on the back that is to say on seborrheic

zones Relapses are habitual despite treatment

Diagnosis

Diagnosis is normally clinical To that purpose the following serve as

support

bull Woodrsquos lamp emits yellow-orange fluorescence

bull Potassium hydroxide (KOH) test filaments and round elements can

be observed (ldquospaghe and meatball appearancerdquo Figure 20)

Treatment

Treatment is performed with topical azoles Oral administraton applies

for extensive cases or immunosuppressed patents Diff erental diagno-

sis includes pink pityriasis and eczemas (Figure 21)

Figure 20 Versicolor pityriasis Histological cut

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Dermatology

Figure 21 Versicolor pityriasis

Candidiasis

The most common triggering agent is Candida albicans It is normally sapro-

phyt

c although under certain condit

ons candidiasis may become patho-genic (immunosuppression humidity pregnancy and contraceptves)

Clinical Forms

bull Intertrigo erythematous plaque in cutaneous folds Atrophy and

fissures are typically deep in the skin fold as well as satellite and

peripheral lesions (papules andor pustules)

bull Mucosa involvement may cause diverse symptomatology like vul-

vovaginits glossits and white papules in the anterior region of the

oral mucosa Candidal balanits is characterized by the presence of

punctform erosions and pustules on gland and balanopreputal

sulcus Candidal balanits ofen appears afer sexual intercourse or

afer oral antbiotc intake

Remember

Almost a 100 of HIV patients suffer from muguet throughout their diseasecourse

bull Candidiasis of nail fold is usually associated with periungual inflam-

maton (perionixis) and inital proximal aff ectaton which diff erent-

ates it from tnea unguium (Figure 22)

Figure 22 Candidiasis of nail fold

Treatment

Oral Candidiasis fluconazole or nystatn

Candidiasis of the skin (intertrigo) apply topical antfungal medicaton

and keep zone clean and dry

Dermatophytosis or TineasDermatophyte infectons aff ect the skin and keratnized structures like

hair and nails (there is no mucosa involvement) Clinical diagnosis is

achieved afer performing a culture Woodrsquos lamp test normally turns

out to be negatve In general Trichophyton dermatophyte rubrum is

the most frequent dermatophyte

Non Inflammatory Tineas

Non inflammatory tneas do not produce irreversible scarring alope-

cia while inflammatory forms do Tineas are treated with azoles de-

rivatves

The types of tnea are the following

bull Ringworm of the scalp ( t nea capi t s or t nea tonsurans) is charac-

teristc of childhood It presents with alopecic plaques broken hair

and desquamaton Infectons tend to resolve spontaneously with-

out leaving scars at the onset

of puberty

bull Ringworm of the body (herpes

circinatus or t nea corporis) are

erythematous desquamatve

plaques (with more actve bor-

ders) which are also circinate

and normally pruritc (Figure

23) Plaques grow eccentrically

with less actvity in the centerand more in the borders

bull Ringworm of the foot ( t nea

pedis) the most frequent is the

ldquoathlete footrdquo with desquama-

ton in interdigital spaces

bull Tinea incognito refers to tnea

wrongly treated with cort-

coids what makes diagnosis

diffi cult as the lesion has been modified Figure 24)

Figure 24 Tinea incognito secondary to treatment with topical steroids

Figure 23 Herpes circinatus

(tinea corpis)

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Amer ican Manual of Examinat ion in Medicine (2CK)

4

bull Ringworm of the groin (t nea cruris or eczema marginatum von

hebra) formed by erythematous desquamatve plaque with more

actve borders (Figure 25)

Figure 25 Ringworm of the groin (tinea cruris)

bull Tinea unguium subungualhyperkeratosis with onychol-

ysis but without perionixis

(Figure 26)

Diagnosis

Clinical diagnosis is reached afer

performing a culture

Treatment

Treatment involves topical an-

tfungal medicaton in localized

areas

Oral antfungal medicaton is used in extensive forms nail fold or scalp

involvement

44 Parasitic Infections

Pediculosis

Pediculosis is transmied by direct contact or by contact with fomites

which release toxins that produce intense pruritus

Clinical Presentation

Pediculosis capi t s intense pruritus predominant in retroauricular and

occipital regions occasionally with excoriatons and impetginizaton

secondary to excoriatons

Pediculosis corporis intense pruritus in patents with poor hygiene or

who live in overcrowded conditons

Pediculosis pubis genital and pubic pruritus Brownish-grey macules

called maculae ceruleae are typical on underwear and skin These pig-

mentatons appear as a result of a reducton in hemoglobin by a para-

site enzyme

Diagnosis

Diagnosis is clinical and by direct visualizaton

Treatment

Pediculosis is treated with malathion lindane or topical permethrin

Scabies

Scabies is originated by an acarus known as Sarcoptes scabiei It has an

incubaton period of 1 month

Clinical Presentation

Scabies produces generalized pruritus more intense at night The pa-

tent usually catches the infestaton which is passed to the patentrsquos

relat

ves It is common tofi

nd that a recent trip to a tropical country hasbeen made Lesions appear between the fingers (Figure 27) in wrists

feet genitalia mammary areola and axilla but back and face are usu-

ally spared The most specific lesion is the acarine burrow in whose less

scaly end the advancing zone the mite lies Nodules are frequent in

axilla and genitals (nodular scabies)

bull Norwegian scabies is typical of the immunosuppressed Patents

present with generalized hyperkeratosis and scabs Norwegian sca-

bies produce lile pruritus but it is very contagious because there

are many acari

bull Nodular scabies involves the persistence of pruritc nodules despite

treatment Lesions usually appear in axilla and genitalia Pruritus is

due to a hypersensitvity phenomenon because of the acarus al-

ready dead Nodular scabies is treated with cortcoids

Figure 27 Scabies Acarine burrow

Treatment

bull Permethrin cream at 5 is the treatment of choice It is lile toxic

so it can be used in children and pregnant women

bull Topical lindane at 1 irritates and is neurotoxic therefore it is con-

traindicated in pregnant women and children

bull Oral ivermectn is utlized in cases of resistance to prior treatments

There is stll lile experience as to its use but in a first instance a

Figure 26 Tinea unguium

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Dermatology

single dose would be enough to cure scabies (already used by vet-

erinarians)

45 Ischemia

Decubitus Ulcers

Decubitus ulcers are the result of ischemic necrosis by contnuous pres-

sure on an area which restricts microcirculaton in that zone

Clinical Presentation

Decubitus ulcers are present in patents in bed with scarce mobilizaton

It is favored by bone prominences and lack of fat tssue If sensitvity

decreases there is more risk of formaton of decubitus ulcers

Diagnosis

Diagnosis is achieved based on medical records and clinical presentaton

Treatment

Preventon is of the utmost importance as well as frequent mobiliza-

ton of the patent in bed

Once ulcers have been established hydrocolloid dressings are used for

healing but sometmes surgical debridement is necessary

Gangrene

Gangrene means tssue necrosis

There are three types dry gangrene wet gangrene and gas gangrene

Clinical Presentation

Dry gangrene is due to ischemia generally secondary to atherosclero-

sis Clinical presentaton involves pain cold and paleness of extremi-

tes Once tssue is established it turns bluish-black in color and dry

Wet gangrene is owing to bacterial flora Tissue presents with an edem-

atous appearance either with blisters or pus

Gas gangrene caused by C perfringens It is normally located on re-

cent surgery Bacteria precociously destroyt

ssue producing gas It is amedical emergency

Diagnosis

Clinical diagnosis is obtained by microbiological culture

Treatment

Treatment requires surgical debridement with amputaton if necessary

and associaton of broad spectrum antbiotherapy

Gas gangrene is treated with hyperbaric oxygen

46 Miscellaneous

Acanthosis Nigricans

Acanthosis nigricans are vel-

vet-like papillomatous brown

plaques in neck axilla and groin

folds (Figure 28)

It is associated with diabetes

mellitus Cushingrsquos disease poly-

cystc ovarian syndrome and

obesity

The malignant form of acantho-

sis nigricans is a paraneoplastc

syndrome that diff erentates

from the benign form because

the laer has mucosal and pal-

moplantar involvement

Lichen Planus

Lichen planus is an inflammatory idiopathic disease that equally aff ects

both genders with higher frequency in middle age

Lichen planus has been related to diverse drugs like gold salts

anti-malarial medication and thiazides It has been also linked to

hepatitis C virus infection however this association is currently

doubtful

Clinical Presentation

Lichen planus presents with red-violaceous polygonal flat papulesquite pruritc which localizes on the flexor side of wrists forearms an-

kles and lumbosacral and flank regions On its surface a whitsh retcu-

late can be observed (Wickhamrsquos striae) About 60 - 70 of the cases

present with lesions in oral and genital mucosa oral which appear as

whitsh retculated lesions (Figures 29 and 30)

Figure 29 Lichen planus of oral mucosa with typical whitish

reticulate

Figure 28 Acanthosis nigricans

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Amer ican Manual of Examinat ion in Medicine (2CK)

6

Violaceous papules

with white stretch marks

Lichenoid lymphocyte

in1047297ltrate (band formation)

Destruction

of basal layer

Figure 30 Lymphocytic interface reaction (lichen planus)

Treatment

Mild forms are treated with topical cortcoids

Severe cases require oral cortcoids psoralens plus ultraviolet light of

the A wavelength (PUVA) or cyclosporine

Rosacea

Rosacea is a chronic disease of unknown pathogenesis characterized

by erythema and acneiform lesions on the face It aff ects middle aged

women (between 30 and 50 years of age) more

Rosacea etopathogenesis is unknown although there is involvement of

vasomotor lability infecton by Demodex folliculorum photo exposureand genetc predispositon

Clinical Presentation

Rosacea symptomatology comprises facial flushing episodes that end

up by provoking a persistent erythema telangiectasias and papulopus-

tular lesions without comedos Over tme ocular lesions and hyperpla-

sia of sof tssue may develop

Treatment

Avoid vasodilator stmuli

Mild cases require topical metronidazole or azelaic acid

Moderate cases need doxycycline or oral minocyclines

Severe cases are treated with oral isotretnoin at low doses

Pink Pityriasis

Gilbertrsquos pink pityriasis is an acute self-limitng dermatosis which main-

ly aff ects young adults It is of unknown origin although a viral etology

is suspected (there is some speculaton as to links with human herpes-

virus type 7)

Clinical Presentation

Erupton starts with an erythematous plaque between 2 and 5 cm of

diameter with a desquamatve central collaree ofen localized on the

trunk (heraldic mother patch Figure 31)

Figure 31 Pink pityriasis

Around a week later oval papules appear on the trunk and extremi-

tes These papules share similar characteristcs with the mother patch

though the first ones are smaller and distributed according to skin ten-

sion lines Pink pityriasis may be asymptomatc however it is some-

tmes linked to pruritus Lesions may last between 4 and 8 weeks and

disappear without leaving scars

Diagnosis and Treatment

Diagnosis is clinical Treatment is seldom needed and recommended

therapies in the past (PUVA erythromycin or oral antvirals) have not

shown clearly favorable results

Vitiligo

Vitligo is characterized by achromic macules by melanocyte destruc-

ton

Clinical Presentation

Vitligo shows achromic macules of chronic course and variable progres-

sion

Lesions are predominant on acral and periorificial areas They also show

the Koebner phenomenon

Patents may have markers of autoimmune diseases (ie antthyroid

antbodies and diabetes) but these diseases seldom manifest them-

selves

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Dermatology

Treatment

Localized lesions require topical cortcoids

Extensive or generalized lesions are treated with ultraviolet light B

(UVB) or PUVA

Strict solar photoprotecton is indispensable (Figure 32)

Figure 32 Vitiligo

47 Neoplasias

Seborrheic Keratosis

Seborrheic keratosis is the most frequent benign tumor in human be-

ings since it is part of cutaneous aging

Clinical Presentation

Seborrheic keratosis presents with hyperkeratosic papules with an oily

or velvet-like texture crests fissures and horny plugs on their surface

These papules are normally pigmented showing a brownish-black color

Treatment

No treatment is required as lesions do not become malignant

Seborrheic keratosis can be addressed with cureage or cryotherapy

Actinic keratosis

Actnic keratosis is the most common precancerous lesion and aff ects

almost a 100 of the populaton in sunny areas

Clinical Presentation

Actnic keratosis is characterized by erythematous and desquamatve

papules which are hyperkeratosic and rough on touch developing a

chronic course

Diagnosis

Diagnosis is clinical

Treatment

Treatment entails applicaton of topical 5-fluorouracil topical imiqui-

mod cryotherapy or surgery

If underlying carcinoma is suspected a biopsy must be performed to

rule out suspicion

Epidermoid Carcinoma

Epidermoid carcinoma is the second most frequent cutaneous tumor

Solar photo exposure is the main etological factor which is why epider-

moid carcinoma appears in zones of prolonged solar exposure like the

face Most carcinomas appear over premalignant lesions (actnic kera-

tosis and leukoplakia among others)

Clinical Presentation

Clinical presentaton reveals erythematous or erythematosquamous

plaques Over tme these plaques form papules and tumors which of-

ten become ulceratve and bleed

Diagnosis

Diagnosis is based on clinical suspicion and histopathological confirmaton

Treatment

Surgery with safety margins is the treatment of choice In carcinomas

in situ cryotherapy can be used as well as topical imiquimod electro-

coagulaton or CO2 laser techniques in destructon of tumors Radio-therapy may also be used in some cases

Basal Cellular Carcinoma

Basal cellular carcinoma is the most frequent cutaneous tumor Chronic so-

lar photo exposure is the main etological factor hence most of these car-

cinomas aff ect the facial zone in patents who are 40 years of age or older

Gorlinrsquos syndrome should be considered if multple basal cellular carci-

nomas are found in non photo exposed areas

Clinical Presentation

Basal cell carcinoma shows a pearly pink papule and superficial telan-

giectasias

It is localized over healthy skin and never aff ects mucosae

Treatment

Surgery is the treatment of choice Mohs surgery is performed in zones

where surrounding healthy tssue needs to be preserved Other alter-

natves are cryotherapy imiquimod electrocoagulaton radiotherapy

photodynamic therapy and intralesional interferon Prognosis is excel-

lent as growth is slow and metastasis exceptonal

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Amer ican Manual of Examinat ion in Medicine (2CK)

8

Melanoma

Melanoma is the most aggressive cutaneous tumor given its ability to

metastasize

Risk factors comprise solar photo exposure clear phototype the pres-

ence of dysplastc nevus or a high number of melanocytc nevi Fam-

ily history is quite important as some genetc mutatons determine a

higher risk of developing the disease

Clinical Forms

See Figure 33

Diagnosis

Precocious diagnosis is essental to perform precocious surgical extrpaton

The ABCDE criteria can help patents to see if they need to seek medical

consultaton (asymmetry of lesion uneven borders color and diameter

greater than 6 mm or abnormal evolut

on)

The Breslow index is the thickness of the lesion measured in millimeters

and is the main prognosis factor

Treatment

The base of treatment is precocious surgical extrpaton If the Breslow

index is less than 1 mm margins of 1 cm will be performed If Breslow

index is greater than 1 mm margins will be of 2 cm

For melanomas with a Breslow index greater than 1 mm the sentnel

ganglion must be located This is the first draining lymph node of the

territory where the tumor is localized If the ganglion is positve re-

gional lymphadenectomy will be performed along with interferon ad-ministraton (Figure 34)

In situ Extirpation 05 cm Follow-up

Breslow lt 1 mm Extirpation 1 cm Follow-up

Lymphadenectomy

Breslow gt 4 mm Interferon

Breslow ge 1 mm Extirpation 2 cm Sentinel ganglion

+

Figure 34 Melanoma treatment

Kaposirsquos sarcoma

Kaposirsquos sarcoma is the most common cutaneous tumor in HIV patents

Clinical presentation

Kaposirsquos sarcoma has a course with violaceous fusiform macules whichovertme may evolve into indurated nodules with blackberry appearance

This type of sarcoma has been linked to herpesvirus type 8 both in HIV

and seronegatve patents (Table 3)

EPIDERMAL KAPOSIrsquoS 983080HIV983081 CLASSIC KAPOSIrsquoS

Homosexual youth (95) The elderly

Diffuse and bilateral

(frequently in palate and face)

Unilateral plaques

(lower extremities)

Frequent mucosal and visceral involvement Not so frequent

middot Precocious lymphatic invasion

middot Aggressive

Not so precocious

Table 3 Differences between epidermal and classic Kaposirsquos sarcoma

Nodular melanoma

15

Middle-aged men

middot On healthy skin

middot Any zone

middot Sudden onset

middot Uniform black nodulemiddot Rapidly invasive (vertical growth without radial)middot Frequent ulceration and bleeding

Worst histological prognosis

Lentigo malignant melanoma

10

Elderly women

90 on facephotoexposedzones of aging skins(chronic exposure)

Spot that growsduring many years (gt 10)then progresses (nodule)

Better prognosis

Acral lentinginous melanoma

5ndash10 ( 60 black and Asian race)

Elderly men

middot Sole (ankle) handsmucosa ungual bed

middot No relation to photo exposure

middot Macule with mosaic appearance (spot that grows)middot Some amelanisticmiddot Bad prognosis due to late diagnosis

Melanoma of super1047297cial extension

70

Young women

middot 30 previous nervusmiddot Intermittent exposuremiddot Men back middot Women legs

More frequent

middot Macula with mosaic appearance in colors that grows 4-5 years and then in1047297ltrates (nodule)middot Metastasis 35 to 70

Figure 33 Clinical forms of malignant melanoma

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Dermatology

Diagnosis

Diagnosis relies on clinical suspicion and histopathological confirma-

ton

Treatment

Treatment of localized forms can include surgical extrpaton radiother-

apy or intralesional vinblastne

If the sarcoma is disseminated optons involve interferon or chemo-

therapy

Mycosis Fungoides

Mycosis fungoides is a T-cell lymphoma of low-grade malignancy Its

clinical course may be very slow and surpass 50 years Three stages are

clinically diff erentated

1 Eczematous or macular phase predominantly truncular erythema-

tous macules with years of evoluton They resemble a chromic ec-

zema Histology is unspecifi

c at this stage2 Infiltratve plaque phase infiltrated erythematous plaques appear

Histology is diagnostc at this stage A dermal infiltrate of atypical

lymphocytes band forms can be observed composed of CD+4 T

lymphocytes with cerebriform nuclei There is a marked epidermo-

tropism with the presence of clusters of intraepidermal lympho-

cytes called Pautrierrsquos microabscesses (Figure 35)

Figure 35 Mycosis fungoides Infiltrative plaque phase

3 Tumoral phase erythematous exophytc plaques start to appear

(tumors) with a tendency to ulceraton They can have a large size

Histology may become unspecific again as epidermotropism disap-

pears

In more advanced stages of the disease there is aff ectaton of extra-

cutaneous organs such as lymph nodes liver spleen lungs and bone

marrow Besides there may be blastc transformaton Other possible

complicaton is sepsis by Staphylococcus aureus

These three stages usually develop consecutvely nevertheless there

may patents whose debut starts directly with the tumoral stage

Remember

Microabscesses of mycosis fungoides are due to lymphocytes and are calledPautrierrsquos abscesses Psoriasis microabscesses result from neutrophils andare labeled as Munro-Sabouraud

Seacutezary Syndrome

Seacutezary syndrome can be considered as the leukemic phase of T-cell cu-

taneous lymphoma It is defined by the triad erythroderma (Figure 36

lymphadenopathies and the existence of more than 1000 Seacutezary cellsper milliliter in peripheral blood Seacutezary cells are atypical T- lymphocyte

with cerebriform nuclei

Very intense pruritus is characteristc For many authors Seacutezary syn-

drome is an aggressive clinical form and a bad prognosis of a mycosis

fungoides

Figure 36 Erythroderma due to Seacutezary syndrome

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Amer ican Manual of Examinat ion in Medicine (2CK)

2

Diff erent lesions habitually combine simultaneously so acne becomes

polymorphic It is located in sebaceous areas face back shoulders and

the center thoracic region

Diagnosis

Diagnosis is clinical

Treatment

bull Comedonal acne is treated with topic retnoids and benzoyl peroxide

bull Inflammatory acne treatment requires benzoyl peroxide combined

with topic antbiotcs (erythromycin and clindamycin) Systemic

antbiotc treatment with oral tetracyclines will be prescribed if re-

sponse to topic antbiotc treatment fails

bull Severe nodular cystc acne treatment involves the use of isotret-

noin (13-cis-retnoic acid) It is a derivatve of vitamin A Isotretnoin

produces atrophy in the sebaceous gland and regulates keratniza-

ton The most frequent side eff ect is cutaneous and mucosal xero-

sis Triglycerides cholesterol and transaminases should be moni-

tored as their values may increasebull It can be associated with depression

bull It is teratogenic so pregnancy should be avoided during treatment

and untl a month afer treatment

Pilonidal Cysts

Pilonidal cysts are abscesses in the sacrococcygeal region

This type of cysts has predominance in men between 20 and 40 years

of age It is believed that repeated trauma on the aff ected area favors

their appearance

Clinical Presentation

Pilonidal cysts present with an indurated lesion that is fluctuatng hot

painful but non-adherent to deep planes in the sacrococcygeal region

Pilonidal cysts may or may not be associated to cellulits and purulent drain-

age

Diagnosis

Diagnosis is clinical and anal or perirectal abscesses should be dismissed

Treatment

Treatment implies an incision and surgical drainage

On some occasions a general surgery is required

43 Fungal Infections

Pityriasis Versicolor

Versicolor pityriasis is caused by commensal yeast called Pityrosporum

ovale which transforms into its pathogen form (Malassezia furfur) It

especially aff ects young patents (15 - 45 years of age) but it is rare

in childhood and advanced age Versicolor pityriasis relates to heat

humidity and sebaceous hypersecreton It is characterized by the ap-

pearance of hyperchromic or hypochromic macules that desquamate

on scratching (nail sign) if infecton is actve Macules usually appear on

the center thoracic region and on the back that is to say on seborrheic

zones Relapses are habitual despite treatment

Diagnosis

Diagnosis is normally clinical To that purpose the following serve as

support

bull Woodrsquos lamp emits yellow-orange fluorescence

bull Potassium hydroxide (KOH) test filaments and round elements can

be observed (ldquospaghe and meatball appearancerdquo Figure 20)

Treatment

Treatment is performed with topical azoles Oral administraton applies

for extensive cases or immunosuppressed patents Diff erental diagno-

sis includes pink pityriasis and eczemas (Figure 21)

Figure 20 Versicolor pityriasis Histological cut

8182019 USMLE_01_1415_MANUAL_DMpdf

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Dermatology

Figure 21 Versicolor pityriasis

Candidiasis

The most common triggering agent is Candida albicans It is normally sapro-

phyt

c although under certain condit

ons candidiasis may become patho-genic (immunosuppression humidity pregnancy and contraceptves)

Clinical Forms

bull Intertrigo erythematous plaque in cutaneous folds Atrophy and

fissures are typically deep in the skin fold as well as satellite and

peripheral lesions (papules andor pustules)

bull Mucosa involvement may cause diverse symptomatology like vul-

vovaginits glossits and white papules in the anterior region of the

oral mucosa Candidal balanits is characterized by the presence of

punctform erosions and pustules on gland and balanopreputal

sulcus Candidal balanits ofen appears afer sexual intercourse or

afer oral antbiotc intake

Remember

Almost a 100 of HIV patients suffer from muguet throughout their diseasecourse

bull Candidiasis of nail fold is usually associated with periungual inflam-

maton (perionixis) and inital proximal aff ectaton which diff erent-

ates it from tnea unguium (Figure 22)

Figure 22 Candidiasis of nail fold

Treatment

Oral Candidiasis fluconazole or nystatn

Candidiasis of the skin (intertrigo) apply topical antfungal medicaton

and keep zone clean and dry

Dermatophytosis or TineasDermatophyte infectons aff ect the skin and keratnized structures like

hair and nails (there is no mucosa involvement) Clinical diagnosis is

achieved afer performing a culture Woodrsquos lamp test normally turns

out to be negatve In general Trichophyton dermatophyte rubrum is

the most frequent dermatophyte

Non Inflammatory Tineas

Non inflammatory tneas do not produce irreversible scarring alope-

cia while inflammatory forms do Tineas are treated with azoles de-

rivatves

The types of tnea are the following

bull Ringworm of the scalp ( t nea capi t s or t nea tonsurans) is charac-

teristc of childhood It presents with alopecic plaques broken hair

and desquamaton Infectons tend to resolve spontaneously with-

out leaving scars at the onset

of puberty

bull Ringworm of the body (herpes

circinatus or t nea corporis) are

erythematous desquamatve

plaques (with more actve bor-

ders) which are also circinate

and normally pruritc (Figure

23) Plaques grow eccentrically

with less actvity in the centerand more in the borders

bull Ringworm of the foot ( t nea

pedis) the most frequent is the

ldquoathlete footrdquo with desquama-

ton in interdigital spaces

bull Tinea incognito refers to tnea

wrongly treated with cort-

coids what makes diagnosis

diffi cult as the lesion has been modified Figure 24)

Figure 24 Tinea incognito secondary to treatment with topical steroids

Figure 23 Herpes circinatus

(tinea corpis)

8182019 USMLE_01_1415_MANUAL_DMpdf

httpslidepdfcomreaderfullusmle011415manualdmpdf 1823

Amer ican Manual of Examinat ion in Medicine (2CK)

4

bull Ringworm of the groin (t nea cruris or eczema marginatum von

hebra) formed by erythematous desquamatve plaque with more

actve borders (Figure 25)

Figure 25 Ringworm of the groin (tinea cruris)

bull Tinea unguium subungualhyperkeratosis with onychol-

ysis but without perionixis

(Figure 26)

Diagnosis

Clinical diagnosis is reached afer

performing a culture

Treatment

Treatment involves topical an-

tfungal medicaton in localized

areas

Oral antfungal medicaton is used in extensive forms nail fold or scalp

involvement

44 Parasitic Infections

Pediculosis

Pediculosis is transmied by direct contact or by contact with fomites

which release toxins that produce intense pruritus

Clinical Presentation

Pediculosis capi t s intense pruritus predominant in retroauricular and

occipital regions occasionally with excoriatons and impetginizaton

secondary to excoriatons

Pediculosis corporis intense pruritus in patents with poor hygiene or

who live in overcrowded conditons

Pediculosis pubis genital and pubic pruritus Brownish-grey macules

called maculae ceruleae are typical on underwear and skin These pig-

mentatons appear as a result of a reducton in hemoglobin by a para-

site enzyme

Diagnosis

Diagnosis is clinical and by direct visualizaton

Treatment

Pediculosis is treated with malathion lindane or topical permethrin

Scabies

Scabies is originated by an acarus known as Sarcoptes scabiei It has an

incubaton period of 1 month

Clinical Presentation

Scabies produces generalized pruritus more intense at night The pa-

tent usually catches the infestaton which is passed to the patentrsquos

relat

ves It is common tofi

nd that a recent trip to a tropical country hasbeen made Lesions appear between the fingers (Figure 27) in wrists

feet genitalia mammary areola and axilla but back and face are usu-

ally spared The most specific lesion is the acarine burrow in whose less

scaly end the advancing zone the mite lies Nodules are frequent in

axilla and genitals (nodular scabies)

bull Norwegian scabies is typical of the immunosuppressed Patents

present with generalized hyperkeratosis and scabs Norwegian sca-

bies produce lile pruritus but it is very contagious because there

are many acari

bull Nodular scabies involves the persistence of pruritc nodules despite

treatment Lesions usually appear in axilla and genitalia Pruritus is

due to a hypersensitvity phenomenon because of the acarus al-

ready dead Nodular scabies is treated with cortcoids

Figure 27 Scabies Acarine burrow

Treatment

bull Permethrin cream at 5 is the treatment of choice It is lile toxic

so it can be used in children and pregnant women

bull Topical lindane at 1 irritates and is neurotoxic therefore it is con-

traindicated in pregnant women and children

bull Oral ivermectn is utlized in cases of resistance to prior treatments

There is stll lile experience as to its use but in a first instance a

Figure 26 Tinea unguium

8182019 USMLE_01_1415_MANUAL_DMpdf

httpslidepdfcomreaderfullusmle011415manualdmpdf 1923

Dermatology

single dose would be enough to cure scabies (already used by vet-

erinarians)

45 Ischemia

Decubitus Ulcers

Decubitus ulcers are the result of ischemic necrosis by contnuous pres-

sure on an area which restricts microcirculaton in that zone

Clinical Presentation

Decubitus ulcers are present in patents in bed with scarce mobilizaton

It is favored by bone prominences and lack of fat tssue If sensitvity

decreases there is more risk of formaton of decubitus ulcers

Diagnosis

Diagnosis is achieved based on medical records and clinical presentaton

Treatment

Preventon is of the utmost importance as well as frequent mobiliza-

ton of the patent in bed

Once ulcers have been established hydrocolloid dressings are used for

healing but sometmes surgical debridement is necessary

Gangrene

Gangrene means tssue necrosis

There are three types dry gangrene wet gangrene and gas gangrene

Clinical Presentation

Dry gangrene is due to ischemia generally secondary to atherosclero-

sis Clinical presentaton involves pain cold and paleness of extremi-

tes Once tssue is established it turns bluish-black in color and dry

Wet gangrene is owing to bacterial flora Tissue presents with an edem-

atous appearance either with blisters or pus

Gas gangrene caused by C perfringens It is normally located on re-

cent surgery Bacteria precociously destroyt

ssue producing gas It is amedical emergency

Diagnosis

Clinical diagnosis is obtained by microbiological culture

Treatment

Treatment requires surgical debridement with amputaton if necessary

and associaton of broad spectrum antbiotherapy

Gas gangrene is treated with hyperbaric oxygen

46 Miscellaneous

Acanthosis Nigricans

Acanthosis nigricans are vel-

vet-like papillomatous brown

plaques in neck axilla and groin

folds (Figure 28)

It is associated with diabetes

mellitus Cushingrsquos disease poly-

cystc ovarian syndrome and

obesity

The malignant form of acantho-

sis nigricans is a paraneoplastc

syndrome that diff erentates

from the benign form because

the laer has mucosal and pal-

moplantar involvement

Lichen Planus

Lichen planus is an inflammatory idiopathic disease that equally aff ects

both genders with higher frequency in middle age

Lichen planus has been related to diverse drugs like gold salts

anti-malarial medication and thiazides It has been also linked to

hepatitis C virus infection however this association is currently

doubtful

Clinical Presentation

Lichen planus presents with red-violaceous polygonal flat papulesquite pruritc which localizes on the flexor side of wrists forearms an-

kles and lumbosacral and flank regions On its surface a whitsh retcu-

late can be observed (Wickhamrsquos striae) About 60 - 70 of the cases

present with lesions in oral and genital mucosa oral which appear as

whitsh retculated lesions (Figures 29 and 30)

Figure 29 Lichen planus of oral mucosa with typical whitish

reticulate

Figure 28 Acanthosis nigricans

8182019 USMLE_01_1415_MANUAL_DMpdf

httpslidepdfcomreaderfullusmle011415manualdmpdf 2023

Amer ican Manual of Examinat ion in Medicine (2CK)

6

Violaceous papules

with white stretch marks

Lichenoid lymphocyte

in1047297ltrate (band formation)

Destruction

of basal layer

Figure 30 Lymphocytic interface reaction (lichen planus)

Treatment

Mild forms are treated with topical cortcoids

Severe cases require oral cortcoids psoralens plus ultraviolet light of

the A wavelength (PUVA) or cyclosporine

Rosacea

Rosacea is a chronic disease of unknown pathogenesis characterized

by erythema and acneiform lesions on the face It aff ects middle aged

women (between 30 and 50 years of age) more

Rosacea etopathogenesis is unknown although there is involvement of

vasomotor lability infecton by Demodex folliculorum photo exposureand genetc predispositon

Clinical Presentation

Rosacea symptomatology comprises facial flushing episodes that end

up by provoking a persistent erythema telangiectasias and papulopus-

tular lesions without comedos Over tme ocular lesions and hyperpla-

sia of sof tssue may develop

Treatment

Avoid vasodilator stmuli

Mild cases require topical metronidazole or azelaic acid

Moderate cases need doxycycline or oral minocyclines

Severe cases are treated with oral isotretnoin at low doses

Pink Pityriasis

Gilbertrsquos pink pityriasis is an acute self-limitng dermatosis which main-

ly aff ects young adults It is of unknown origin although a viral etology

is suspected (there is some speculaton as to links with human herpes-

virus type 7)

Clinical Presentation

Erupton starts with an erythematous plaque between 2 and 5 cm of

diameter with a desquamatve central collaree ofen localized on the

trunk (heraldic mother patch Figure 31)

Figure 31 Pink pityriasis

Around a week later oval papules appear on the trunk and extremi-

tes These papules share similar characteristcs with the mother patch

though the first ones are smaller and distributed according to skin ten-

sion lines Pink pityriasis may be asymptomatc however it is some-

tmes linked to pruritus Lesions may last between 4 and 8 weeks and

disappear without leaving scars

Diagnosis and Treatment

Diagnosis is clinical Treatment is seldom needed and recommended

therapies in the past (PUVA erythromycin or oral antvirals) have not

shown clearly favorable results

Vitiligo

Vitligo is characterized by achromic macules by melanocyte destruc-

ton

Clinical Presentation

Vitligo shows achromic macules of chronic course and variable progres-

sion

Lesions are predominant on acral and periorificial areas They also show

the Koebner phenomenon

Patents may have markers of autoimmune diseases (ie antthyroid

antbodies and diabetes) but these diseases seldom manifest them-

selves

8182019 USMLE_01_1415_MANUAL_DMpdf

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Dermatology

Treatment

Localized lesions require topical cortcoids

Extensive or generalized lesions are treated with ultraviolet light B

(UVB) or PUVA

Strict solar photoprotecton is indispensable (Figure 32)

Figure 32 Vitiligo

47 Neoplasias

Seborrheic Keratosis

Seborrheic keratosis is the most frequent benign tumor in human be-

ings since it is part of cutaneous aging

Clinical Presentation

Seborrheic keratosis presents with hyperkeratosic papules with an oily

or velvet-like texture crests fissures and horny plugs on their surface

These papules are normally pigmented showing a brownish-black color

Treatment

No treatment is required as lesions do not become malignant

Seborrheic keratosis can be addressed with cureage or cryotherapy

Actinic keratosis

Actnic keratosis is the most common precancerous lesion and aff ects

almost a 100 of the populaton in sunny areas

Clinical Presentation

Actnic keratosis is characterized by erythematous and desquamatve

papules which are hyperkeratosic and rough on touch developing a

chronic course

Diagnosis

Diagnosis is clinical

Treatment

Treatment entails applicaton of topical 5-fluorouracil topical imiqui-

mod cryotherapy or surgery

If underlying carcinoma is suspected a biopsy must be performed to

rule out suspicion

Epidermoid Carcinoma

Epidermoid carcinoma is the second most frequent cutaneous tumor

Solar photo exposure is the main etological factor which is why epider-

moid carcinoma appears in zones of prolonged solar exposure like the

face Most carcinomas appear over premalignant lesions (actnic kera-

tosis and leukoplakia among others)

Clinical Presentation

Clinical presentaton reveals erythematous or erythematosquamous

plaques Over tme these plaques form papules and tumors which of-

ten become ulceratve and bleed

Diagnosis

Diagnosis is based on clinical suspicion and histopathological confirmaton

Treatment

Surgery with safety margins is the treatment of choice In carcinomas

in situ cryotherapy can be used as well as topical imiquimod electro-

coagulaton or CO2 laser techniques in destructon of tumors Radio-therapy may also be used in some cases

Basal Cellular Carcinoma

Basal cellular carcinoma is the most frequent cutaneous tumor Chronic so-

lar photo exposure is the main etological factor hence most of these car-

cinomas aff ect the facial zone in patents who are 40 years of age or older

Gorlinrsquos syndrome should be considered if multple basal cellular carci-

nomas are found in non photo exposed areas

Clinical Presentation

Basal cell carcinoma shows a pearly pink papule and superficial telan-

giectasias

It is localized over healthy skin and never aff ects mucosae

Treatment

Surgery is the treatment of choice Mohs surgery is performed in zones

where surrounding healthy tssue needs to be preserved Other alter-

natves are cryotherapy imiquimod electrocoagulaton radiotherapy

photodynamic therapy and intralesional interferon Prognosis is excel-

lent as growth is slow and metastasis exceptonal

8182019 USMLE_01_1415_MANUAL_DMpdf

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Amer ican Manual of Examinat ion in Medicine (2CK)

8

Melanoma

Melanoma is the most aggressive cutaneous tumor given its ability to

metastasize

Risk factors comprise solar photo exposure clear phototype the pres-

ence of dysplastc nevus or a high number of melanocytc nevi Fam-

ily history is quite important as some genetc mutatons determine a

higher risk of developing the disease

Clinical Forms

See Figure 33

Diagnosis

Precocious diagnosis is essental to perform precocious surgical extrpaton

The ABCDE criteria can help patents to see if they need to seek medical

consultaton (asymmetry of lesion uneven borders color and diameter

greater than 6 mm or abnormal evolut

on)

The Breslow index is the thickness of the lesion measured in millimeters

and is the main prognosis factor

Treatment

The base of treatment is precocious surgical extrpaton If the Breslow

index is less than 1 mm margins of 1 cm will be performed If Breslow

index is greater than 1 mm margins will be of 2 cm

For melanomas with a Breslow index greater than 1 mm the sentnel

ganglion must be located This is the first draining lymph node of the

territory where the tumor is localized If the ganglion is positve re-

gional lymphadenectomy will be performed along with interferon ad-ministraton (Figure 34)

In situ Extirpation 05 cm Follow-up

Breslow lt 1 mm Extirpation 1 cm Follow-up

Lymphadenectomy

Breslow gt 4 mm Interferon

Breslow ge 1 mm Extirpation 2 cm Sentinel ganglion

+

Figure 34 Melanoma treatment

Kaposirsquos sarcoma

Kaposirsquos sarcoma is the most common cutaneous tumor in HIV patents

Clinical presentation

Kaposirsquos sarcoma has a course with violaceous fusiform macules whichovertme may evolve into indurated nodules with blackberry appearance

This type of sarcoma has been linked to herpesvirus type 8 both in HIV

and seronegatve patents (Table 3)

EPIDERMAL KAPOSIrsquoS 983080HIV983081 CLASSIC KAPOSIrsquoS

Homosexual youth (95) The elderly

Diffuse and bilateral

(frequently in palate and face)

Unilateral plaques

(lower extremities)

Frequent mucosal and visceral involvement Not so frequent

middot Precocious lymphatic invasion

middot Aggressive

Not so precocious

Table 3 Differences between epidermal and classic Kaposirsquos sarcoma

Nodular melanoma

15

Middle-aged men

middot On healthy skin

middot Any zone

middot Sudden onset

middot Uniform black nodulemiddot Rapidly invasive (vertical growth without radial)middot Frequent ulceration and bleeding

Worst histological prognosis

Lentigo malignant melanoma

10

Elderly women

90 on facephotoexposedzones of aging skins(chronic exposure)

Spot that growsduring many years (gt 10)then progresses (nodule)

Better prognosis

Acral lentinginous melanoma

5ndash10 ( 60 black and Asian race)

Elderly men

middot Sole (ankle) handsmucosa ungual bed

middot No relation to photo exposure

middot Macule with mosaic appearance (spot that grows)middot Some amelanisticmiddot Bad prognosis due to late diagnosis

Melanoma of super1047297cial extension

70

Young women

middot 30 previous nervusmiddot Intermittent exposuremiddot Men back middot Women legs

More frequent

middot Macula with mosaic appearance in colors that grows 4-5 years and then in1047297ltrates (nodule)middot Metastasis 35 to 70

Figure 33 Clinical forms of malignant melanoma

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Dermatology

Diagnosis

Diagnosis relies on clinical suspicion and histopathological confirma-

ton

Treatment

Treatment of localized forms can include surgical extrpaton radiother-

apy or intralesional vinblastne

If the sarcoma is disseminated optons involve interferon or chemo-

therapy

Mycosis Fungoides

Mycosis fungoides is a T-cell lymphoma of low-grade malignancy Its

clinical course may be very slow and surpass 50 years Three stages are

clinically diff erentated

1 Eczematous or macular phase predominantly truncular erythema-

tous macules with years of evoluton They resemble a chromic ec-

zema Histology is unspecifi

c at this stage2 Infiltratve plaque phase infiltrated erythematous plaques appear

Histology is diagnostc at this stage A dermal infiltrate of atypical

lymphocytes band forms can be observed composed of CD+4 T

lymphocytes with cerebriform nuclei There is a marked epidermo-

tropism with the presence of clusters of intraepidermal lympho-

cytes called Pautrierrsquos microabscesses (Figure 35)

Figure 35 Mycosis fungoides Infiltrative plaque phase

3 Tumoral phase erythematous exophytc plaques start to appear

(tumors) with a tendency to ulceraton They can have a large size

Histology may become unspecific again as epidermotropism disap-

pears

In more advanced stages of the disease there is aff ectaton of extra-

cutaneous organs such as lymph nodes liver spleen lungs and bone

marrow Besides there may be blastc transformaton Other possible

complicaton is sepsis by Staphylococcus aureus

These three stages usually develop consecutvely nevertheless there

may patents whose debut starts directly with the tumoral stage

Remember

Microabscesses of mycosis fungoides are due to lymphocytes and are calledPautrierrsquos abscesses Psoriasis microabscesses result from neutrophils andare labeled as Munro-Sabouraud

Seacutezary Syndrome

Seacutezary syndrome can be considered as the leukemic phase of T-cell cu-

taneous lymphoma It is defined by the triad erythroderma (Figure 36

lymphadenopathies and the existence of more than 1000 Seacutezary cellsper milliliter in peripheral blood Seacutezary cells are atypical T- lymphocyte

with cerebriform nuclei

Very intense pruritus is characteristc For many authors Seacutezary syn-

drome is an aggressive clinical form and a bad prognosis of a mycosis

fungoides

Figure 36 Erythroderma due to Seacutezary syndrome

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Dermatology

Figure 21 Versicolor pityriasis

Candidiasis

The most common triggering agent is Candida albicans It is normally sapro-

phyt

c although under certain condit

ons candidiasis may become patho-genic (immunosuppression humidity pregnancy and contraceptves)

Clinical Forms

bull Intertrigo erythematous plaque in cutaneous folds Atrophy and

fissures are typically deep in the skin fold as well as satellite and

peripheral lesions (papules andor pustules)

bull Mucosa involvement may cause diverse symptomatology like vul-

vovaginits glossits and white papules in the anterior region of the

oral mucosa Candidal balanits is characterized by the presence of

punctform erosions and pustules on gland and balanopreputal

sulcus Candidal balanits ofen appears afer sexual intercourse or

afer oral antbiotc intake

Remember

Almost a 100 of HIV patients suffer from muguet throughout their diseasecourse

bull Candidiasis of nail fold is usually associated with periungual inflam-

maton (perionixis) and inital proximal aff ectaton which diff erent-

ates it from tnea unguium (Figure 22)

Figure 22 Candidiasis of nail fold

Treatment

Oral Candidiasis fluconazole or nystatn

Candidiasis of the skin (intertrigo) apply topical antfungal medicaton

and keep zone clean and dry

Dermatophytosis or TineasDermatophyte infectons aff ect the skin and keratnized structures like

hair and nails (there is no mucosa involvement) Clinical diagnosis is

achieved afer performing a culture Woodrsquos lamp test normally turns

out to be negatve In general Trichophyton dermatophyte rubrum is

the most frequent dermatophyte

Non Inflammatory Tineas

Non inflammatory tneas do not produce irreversible scarring alope-

cia while inflammatory forms do Tineas are treated with azoles de-

rivatves

The types of tnea are the following

bull Ringworm of the scalp ( t nea capi t s or t nea tonsurans) is charac-

teristc of childhood It presents with alopecic plaques broken hair

and desquamaton Infectons tend to resolve spontaneously with-

out leaving scars at the onset

of puberty

bull Ringworm of the body (herpes

circinatus or t nea corporis) are

erythematous desquamatve

plaques (with more actve bor-

ders) which are also circinate

and normally pruritc (Figure

23) Plaques grow eccentrically

with less actvity in the centerand more in the borders

bull Ringworm of the foot ( t nea

pedis) the most frequent is the

ldquoathlete footrdquo with desquama-

ton in interdigital spaces

bull Tinea incognito refers to tnea

wrongly treated with cort-

coids what makes diagnosis

diffi cult as the lesion has been modified Figure 24)

Figure 24 Tinea incognito secondary to treatment with topical steroids

Figure 23 Herpes circinatus

(tinea corpis)

8182019 USMLE_01_1415_MANUAL_DMpdf

httpslidepdfcomreaderfullusmle011415manualdmpdf 1823

Amer ican Manual of Examinat ion in Medicine (2CK)

4

bull Ringworm of the groin (t nea cruris or eczema marginatum von

hebra) formed by erythematous desquamatve plaque with more

actve borders (Figure 25)

Figure 25 Ringworm of the groin (tinea cruris)

bull Tinea unguium subungualhyperkeratosis with onychol-

ysis but without perionixis

(Figure 26)

Diagnosis

Clinical diagnosis is reached afer

performing a culture

Treatment

Treatment involves topical an-

tfungal medicaton in localized

areas

Oral antfungal medicaton is used in extensive forms nail fold or scalp

involvement

44 Parasitic Infections

Pediculosis

Pediculosis is transmied by direct contact or by contact with fomites

which release toxins that produce intense pruritus

Clinical Presentation

Pediculosis capi t s intense pruritus predominant in retroauricular and

occipital regions occasionally with excoriatons and impetginizaton

secondary to excoriatons

Pediculosis corporis intense pruritus in patents with poor hygiene or

who live in overcrowded conditons

Pediculosis pubis genital and pubic pruritus Brownish-grey macules

called maculae ceruleae are typical on underwear and skin These pig-

mentatons appear as a result of a reducton in hemoglobin by a para-

site enzyme

Diagnosis

Diagnosis is clinical and by direct visualizaton

Treatment

Pediculosis is treated with malathion lindane or topical permethrin

Scabies

Scabies is originated by an acarus known as Sarcoptes scabiei It has an

incubaton period of 1 month

Clinical Presentation

Scabies produces generalized pruritus more intense at night The pa-

tent usually catches the infestaton which is passed to the patentrsquos

relat

ves It is common tofi

nd that a recent trip to a tropical country hasbeen made Lesions appear between the fingers (Figure 27) in wrists

feet genitalia mammary areola and axilla but back and face are usu-

ally spared The most specific lesion is the acarine burrow in whose less

scaly end the advancing zone the mite lies Nodules are frequent in

axilla and genitals (nodular scabies)

bull Norwegian scabies is typical of the immunosuppressed Patents

present with generalized hyperkeratosis and scabs Norwegian sca-

bies produce lile pruritus but it is very contagious because there

are many acari

bull Nodular scabies involves the persistence of pruritc nodules despite

treatment Lesions usually appear in axilla and genitalia Pruritus is

due to a hypersensitvity phenomenon because of the acarus al-

ready dead Nodular scabies is treated with cortcoids

Figure 27 Scabies Acarine burrow

Treatment

bull Permethrin cream at 5 is the treatment of choice It is lile toxic

so it can be used in children and pregnant women

bull Topical lindane at 1 irritates and is neurotoxic therefore it is con-

traindicated in pregnant women and children

bull Oral ivermectn is utlized in cases of resistance to prior treatments

There is stll lile experience as to its use but in a first instance a

Figure 26 Tinea unguium

8182019 USMLE_01_1415_MANUAL_DMpdf

httpslidepdfcomreaderfullusmle011415manualdmpdf 1923

Dermatology

single dose would be enough to cure scabies (already used by vet-

erinarians)

45 Ischemia

Decubitus Ulcers

Decubitus ulcers are the result of ischemic necrosis by contnuous pres-

sure on an area which restricts microcirculaton in that zone

Clinical Presentation

Decubitus ulcers are present in patents in bed with scarce mobilizaton

It is favored by bone prominences and lack of fat tssue If sensitvity

decreases there is more risk of formaton of decubitus ulcers

Diagnosis

Diagnosis is achieved based on medical records and clinical presentaton

Treatment

Preventon is of the utmost importance as well as frequent mobiliza-

ton of the patent in bed

Once ulcers have been established hydrocolloid dressings are used for

healing but sometmes surgical debridement is necessary

Gangrene

Gangrene means tssue necrosis

There are three types dry gangrene wet gangrene and gas gangrene

Clinical Presentation

Dry gangrene is due to ischemia generally secondary to atherosclero-

sis Clinical presentaton involves pain cold and paleness of extremi-

tes Once tssue is established it turns bluish-black in color and dry

Wet gangrene is owing to bacterial flora Tissue presents with an edem-

atous appearance either with blisters or pus

Gas gangrene caused by C perfringens It is normally located on re-

cent surgery Bacteria precociously destroyt

ssue producing gas It is amedical emergency

Diagnosis

Clinical diagnosis is obtained by microbiological culture

Treatment

Treatment requires surgical debridement with amputaton if necessary

and associaton of broad spectrum antbiotherapy

Gas gangrene is treated with hyperbaric oxygen

46 Miscellaneous

Acanthosis Nigricans

Acanthosis nigricans are vel-

vet-like papillomatous brown

plaques in neck axilla and groin

folds (Figure 28)

It is associated with diabetes

mellitus Cushingrsquos disease poly-

cystc ovarian syndrome and

obesity

The malignant form of acantho-

sis nigricans is a paraneoplastc

syndrome that diff erentates

from the benign form because

the laer has mucosal and pal-

moplantar involvement

Lichen Planus

Lichen planus is an inflammatory idiopathic disease that equally aff ects

both genders with higher frequency in middle age

Lichen planus has been related to diverse drugs like gold salts

anti-malarial medication and thiazides It has been also linked to

hepatitis C virus infection however this association is currently

doubtful

Clinical Presentation

Lichen planus presents with red-violaceous polygonal flat papulesquite pruritc which localizes on the flexor side of wrists forearms an-

kles and lumbosacral and flank regions On its surface a whitsh retcu-

late can be observed (Wickhamrsquos striae) About 60 - 70 of the cases

present with lesions in oral and genital mucosa oral which appear as

whitsh retculated lesions (Figures 29 and 30)

Figure 29 Lichen planus of oral mucosa with typical whitish

reticulate

Figure 28 Acanthosis nigricans

8182019 USMLE_01_1415_MANUAL_DMpdf

httpslidepdfcomreaderfullusmle011415manualdmpdf 2023

Amer ican Manual of Examinat ion in Medicine (2CK)

6

Violaceous papules

with white stretch marks

Lichenoid lymphocyte

in1047297ltrate (band formation)

Destruction

of basal layer

Figure 30 Lymphocytic interface reaction (lichen planus)

Treatment

Mild forms are treated with topical cortcoids

Severe cases require oral cortcoids psoralens plus ultraviolet light of

the A wavelength (PUVA) or cyclosporine

Rosacea

Rosacea is a chronic disease of unknown pathogenesis characterized

by erythema and acneiform lesions on the face It aff ects middle aged

women (between 30 and 50 years of age) more

Rosacea etopathogenesis is unknown although there is involvement of

vasomotor lability infecton by Demodex folliculorum photo exposureand genetc predispositon

Clinical Presentation

Rosacea symptomatology comprises facial flushing episodes that end

up by provoking a persistent erythema telangiectasias and papulopus-

tular lesions without comedos Over tme ocular lesions and hyperpla-

sia of sof tssue may develop

Treatment

Avoid vasodilator stmuli

Mild cases require topical metronidazole or azelaic acid

Moderate cases need doxycycline or oral minocyclines

Severe cases are treated with oral isotretnoin at low doses

Pink Pityriasis

Gilbertrsquos pink pityriasis is an acute self-limitng dermatosis which main-

ly aff ects young adults It is of unknown origin although a viral etology

is suspected (there is some speculaton as to links with human herpes-

virus type 7)

Clinical Presentation

Erupton starts with an erythematous plaque between 2 and 5 cm of

diameter with a desquamatve central collaree ofen localized on the

trunk (heraldic mother patch Figure 31)

Figure 31 Pink pityriasis

Around a week later oval papules appear on the trunk and extremi-

tes These papules share similar characteristcs with the mother patch

though the first ones are smaller and distributed according to skin ten-

sion lines Pink pityriasis may be asymptomatc however it is some-

tmes linked to pruritus Lesions may last between 4 and 8 weeks and

disappear without leaving scars

Diagnosis and Treatment

Diagnosis is clinical Treatment is seldom needed and recommended

therapies in the past (PUVA erythromycin or oral antvirals) have not

shown clearly favorable results

Vitiligo

Vitligo is characterized by achromic macules by melanocyte destruc-

ton

Clinical Presentation

Vitligo shows achromic macules of chronic course and variable progres-

sion

Lesions are predominant on acral and periorificial areas They also show

the Koebner phenomenon

Patents may have markers of autoimmune diseases (ie antthyroid

antbodies and diabetes) but these diseases seldom manifest them-

selves

8182019 USMLE_01_1415_MANUAL_DMpdf

httpslidepdfcomreaderfullusmle011415manualdmpdf 2123

Dermatology

Treatment

Localized lesions require topical cortcoids

Extensive or generalized lesions are treated with ultraviolet light B

(UVB) or PUVA

Strict solar photoprotecton is indispensable (Figure 32)

Figure 32 Vitiligo

47 Neoplasias

Seborrheic Keratosis

Seborrheic keratosis is the most frequent benign tumor in human be-

ings since it is part of cutaneous aging

Clinical Presentation

Seborrheic keratosis presents with hyperkeratosic papules with an oily

or velvet-like texture crests fissures and horny plugs on their surface

These papules are normally pigmented showing a brownish-black color

Treatment

No treatment is required as lesions do not become malignant

Seborrheic keratosis can be addressed with cureage or cryotherapy

Actinic keratosis

Actnic keratosis is the most common precancerous lesion and aff ects

almost a 100 of the populaton in sunny areas

Clinical Presentation

Actnic keratosis is characterized by erythematous and desquamatve

papules which are hyperkeratosic and rough on touch developing a

chronic course

Diagnosis

Diagnosis is clinical

Treatment

Treatment entails applicaton of topical 5-fluorouracil topical imiqui-

mod cryotherapy or surgery

If underlying carcinoma is suspected a biopsy must be performed to

rule out suspicion

Epidermoid Carcinoma

Epidermoid carcinoma is the second most frequent cutaneous tumor

Solar photo exposure is the main etological factor which is why epider-

moid carcinoma appears in zones of prolonged solar exposure like the

face Most carcinomas appear over premalignant lesions (actnic kera-

tosis and leukoplakia among others)

Clinical Presentation

Clinical presentaton reveals erythematous or erythematosquamous

plaques Over tme these plaques form papules and tumors which of-

ten become ulceratve and bleed

Diagnosis

Diagnosis is based on clinical suspicion and histopathological confirmaton

Treatment

Surgery with safety margins is the treatment of choice In carcinomas

in situ cryotherapy can be used as well as topical imiquimod electro-

coagulaton or CO2 laser techniques in destructon of tumors Radio-therapy may also be used in some cases

Basal Cellular Carcinoma

Basal cellular carcinoma is the most frequent cutaneous tumor Chronic so-

lar photo exposure is the main etological factor hence most of these car-

cinomas aff ect the facial zone in patents who are 40 years of age or older

Gorlinrsquos syndrome should be considered if multple basal cellular carci-

nomas are found in non photo exposed areas

Clinical Presentation

Basal cell carcinoma shows a pearly pink papule and superficial telan-

giectasias

It is localized over healthy skin and never aff ects mucosae

Treatment

Surgery is the treatment of choice Mohs surgery is performed in zones

where surrounding healthy tssue needs to be preserved Other alter-

natves are cryotherapy imiquimod electrocoagulaton radiotherapy

photodynamic therapy and intralesional interferon Prognosis is excel-

lent as growth is slow and metastasis exceptonal

8182019 USMLE_01_1415_MANUAL_DMpdf

httpslidepdfcomreaderfullusmle011415manualdmpdf 2223

Amer ican Manual of Examinat ion in Medicine (2CK)

8

Melanoma

Melanoma is the most aggressive cutaneous tumor given its ability to

metastasize

Risk factors comprise solar photo exposure clear phototype the pres-

ence of dysplastc nevus or a high number of melanocytc nevi Fam-

ily history is quite important as some genetc mutatons determine a

higher risk of developing the disease

Clinical Forms

See Figure 33

Diagnosis

Precocious diagnosis is essental to perform precocious surgical extrpaton

The ABCDE criteria can help patents to see if they need to seek medical

consultaton (asymmetry of lesion uneven borders color and diameter

greater than 6 mm or abnormal evolut

on)

The Breslow index is the thickness of the lesion measured in millimeters

and is the main prognosis factor

Treatment

The base of treatment is precocious surgical extrpaton If the Breslow

index is less than 1 mm margins of 1 cm will be performed If Breslow

index is greater than 1 mm margins will be of 2 cm

For melanomas with a Breslow index greater than 1 mm the sentnel

ganglion must be located This is the first draining lymph node of the

territory where the tumor is localized If the ganglion is positve re-

gional lymphadenectomy will be performed along with interferon ad-ministraton (Figure 34)

In situ Extirpation 05 cm Follow-up

Breslow lt 1 mm Extirpation 1 cm Follow-up

Lymphadenectomy

Breslow gt 4 mm Interferon

Breslow ge 1 mm Extirpation 2 cm Sentinel ganglion

+

Figure 34 Melanoma treatment

Kaposirsquos sarcoma

Kaposirsquos sarcoma is the most common cutaneous tumor in HIV patents

Clinical presentation

Kaposirsquos sarcoma has a course with violaceous fusiform macules whichovertme may evolve into indurated nodules with blackberry appearance

This type of sarcoma has been linked to herpesvirus type 8 both in HIV

and seronegatve patents (Table 3)

EPIDERMAL KAPOSIrsquoS 983080HIV983081 CLASSIC KAPOSIrsquoS

Homosexual youth (95) The elderly

Diffuse and bilateral

(frequently in palate and face)

Unilateral plaques

(lower extremities)

Frequent mucosal and visceral involvement Not so frequent

middot Precocious lymphatic invasion

middot Aggressive

Not so precocious

Table 3 Differences between epidermal and classic Kaposirsquos sarcoma

Nodular melanoma

15

Middle-aged men

middot On healthy skin

middot Any zone

middot Sudden onset

middot Uniform black nodulemiddot Rapidly invasive (vertical growth without radial)middot Frequent ulceration and bleeding

Worst histological prognosis

Lentigo malignant melanoma

10

Elderly women

90 on facephotoexposedzones of aging skins(chronic exposure)

Spot that growsduring many years (gt 10)then progresses (nodule)

Better prognosis

Acral lentinginous melanoma

5ndash10 ( 60 black and Asian race)

Elderly men

middot Sole (ankle) handsmucosa ungual bed

middot No relation to photo exposure

middot Macule with mosaic appearance (spot that grows)middot Some amelanisticmiddot Bad prognosis due to late diagnosis

Melanoma of super1047297cial extension

70

Young women

middot 30 previous nervusmiddot Intermittent exposuremiddot Men back middot Women legs

More frequent

middot Macula with mosaic appearance in colors that grows 4-5 years and then in1047297ltrates (nodule)middot Metastasis 35 to 70

Figure 33 Clinical forms of malignant melanoma

8182019 USMLE_01_1415_MANUAL_DMpdf

httpslidepdfcomreaderfullusmle011415manualdmpdf 2323

Dermatology

Diagnosis

Diagnosis relies on clinical suspicion and histopathological confirma-

ton

Treatment

Treatment of localized forms can include surgical extrpaton radiother-

apy or intralesional vinblastne

If the sarcoma is disseminated optons involve interferon or chemo-

therapy

Mycosis Fungoides

Mycosis fungoides is a T-cell lymphoma of low-grade malignancy Its

clinical course may be very slow and surpass 50 years Three stages are

clinically diff erentated

1 Eczematous or macular phase predominantly truncular erythema-

tous macules with years of evoluton They resemble a chromic ec-

zema Histology is unspecifi

c at this stage2 Infiltratve plaque phase infiltrated erythematous plaques appear

Histology is diagnostc at this stage A dermal infiltrate of atypical

lymphocytes band forms can be observed composed of CD+4 T

lymphocytes with cerebriform nuclei There is a marked epidermo-

tropism with the presence of clusters of intraepidermal lympho-

cytes called Pautrierrsquos microabscesses (Figure 35)

Figure 35 Mycosis fungoides Infiltrative plaque phase

3 Tumoral phase erythematous exophytc plaques start to appear

(tumors) with a tendency to ulceraton They can have a large size

Histology may become unspecific again as epidermotropism disap-

pears

In more advanced stages of the disease there is aff ectaton of extra-

cutaneous organs such as lymph nodes liver spleen lungs and bone

marrow Besides there may be blastc transformaton Other possible

complicaton is sepsis by Staphylococcus aureus

These three stages usually develop consecutvely nevertheless there

may patents whose debut starts directly with the tumoral stage

Remember

Microabscesses of mycosis fungoides are due to lymphocytes and are calledPautrierrsquos abscesses Psoriasis microabscesses result from neutrophils andare labeled as Munro-Sabouraud

Seacutezary Syndrome

Seacutezary syndrome can be considered as the leukemic phase of T-cell cu-

taneous lymphoma It is defined by the triad erythroderma (Figure 36

lymphadenopathies and the existence of more than 1000 Seacutezary cellsper milliliter in peripheral blood Seacutezary cells are atypical T- lymphocyte

with cerebriform nuclei

Very intense pruritus is characteristc For many authors Seacutezary syn-

drome is an aggressive clinical form and a bad prognosis of a mycosis

fungoides

Figure 36 Erythroderma due to Seacutezary syndrome

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Amer ican Manual of Examinat ion in Medicine (2CK)

4

bull Ringworm of the groin (t nea cruris or eczema marginatum von

hebra) formed by erythematous desquamatve plaque with more

actve borders (Figure 25)

Figure 25 Ringworm of the groin (tinea cruris)

bull Tinea unguium subungualhyperkeratosis with onychol-

ysis but without perionixis

(Figure 26)

Diagnosis

Clinical diagnosis is reached afer

performing a culture

Treatment

Treatment involves topical an-

tfungal medicaton in localized

areas

Oral antfungal medicaton is used in extensive forms nail fold or scalp

involvement

44 Parasitic Infections

Pediculosis

Pediculosis is transmied by direct contact or by contact with fomites

which release toxins that produce intense pruritus

Clinical Presentation

Pediculosis capi t s intense pruritus predominant in retroauricular and

occipital regions occasionally with excoriatons and impetginizaton

secondary to excoriatons

Pediculosis corporis intense pruritus in patents with poor hygiene or

who live in overcrowded conditons

Pediculosis pubis genital and pubic pruritus Brownish-grey macules

called maculae ceruleae are typical on underwear and skin These pig-

mentatons appear as a result of a reducton in hemoglobin by a para-

site enzyme

Diagnosis

Diagnosis is clinical and by direct visualizaton

Treatment

Pediculosis is treated with malathion lindane or topical permethrin

Scabies

Scabies is originated by an acarus known as Sarcoptes scabiei It has an

incubaton period of 1 month

Clinical Presentation

Scabies produces generalized pruritus more intense at night The pa-

tent usually catches the infestaton which is passed to the patentrsquos

relat

ves It is common tofi

nd that a recent trip to a tropical country hasbeen made Lesions appear between the fingers (Figure 27) in wrists

feet genitalia mammary areola and axilla but back and face are usu-

ally spared The most specific lesion is the acarine burrow in whose less

scaly end the advancing zone the mite lies Nodules are frequent in

axilla and genitals (nodular scabies)

bull Norwegian scabies is typical of the immunosuppressed Patents

present with generalized hyperkeratosis and scabs Norwegian sca-

bies produce lile pruritus but it is very contagious because there

are many acari

bull Nodular scabies involves the persistence of pruritc nodules despite

treatment Lesions usually appear in axilla and genitalia Pruritus is

due to a hypersensitvity phenomenon because of the acarus al-

ready dead Nodular scabies is treated with cortcoids

Figure 27 Scabies Acarine burrow

Treatment

bull Permethrin cream at 5 is the treatment of choice It is lile toxic

so it can be used in children and pregnant women

bull Topical lindane at 1 irritates and is neurotoxic therefore it is con-

traindicated in pregnant women and children

bull Oral ivermectn is utlized in cases of resistance to prior treatments

There is stll lile experience as to its use but in a first instance a

Figure 26 Tinea unguium

8182019 USMLE_01_1415_MANUAL_DMpdf

httpslidepdfcomreaderfullusmle011415manualdmpdf 1923

Dermatology

single dose would be enough to cure scabies (already used by vet-

erinarians)

45 Ischemia

Decubitus Ulcers

Decubitus ulcers are the result of ischemic necrosis by contnuous pres-

sure on an area which restricts microcirculaton in that zone

Clinical Presentation

Decubitus ulcers are present in patents in bed with scarce mobilizaton

It is favored by bone prominences and lack of fat tssue If sensitvity

decreases there is more risk of formaton of decubitus ulcers

Diagnosis

Diagnosis is achieved based on medical records and clinical presentaton

Treatment

Preventon is of the utmost importance as well as frequent mobiliza-

ton of the patent in bed

Once ulcers have been established hydrocolloid dressings are used for

healing but sometmes surgical debridement is necessary

Gangrene

Gangrene means tssue necrosis

There are three types dry gangrene wet gangrene and gas gangrene

Clinical Presentation

Dry gangrene is due to ischemia generally secondary to atherosclero-

sis Clinical presentaton involves pain cold and paleness of extremi-

tes Once tssue is established it turns bluish-black in color and dry

Wet gangrene is owing to bacterial flora Tissue presents with an edem-

atous appearance either with blisters or pus

Gas gangrene caused by C perfringens It is normally located on re-

cent surgery Bacteria precociously destroyt

ssue producing gas It is amedical emergency

Diagnosis

Clinical diagnosis is obtained by microbiological culture

Treatment

Treatment requires surgical debridement with amputaton if necessary

and associaton of broad spectrum antbiotherapy

Gas gangrene is treated with hyperbaric oxygen

46 Miscellaneous

Acanthosis Nigricans

Acanthosis nigricans are vel-

vet-like papillomatous brown

plaques in neck axilla and groin

folds (Figure 28)

It is associated with diabetes

mellitus Cushingrsquos disease poly-

cystc ovarian syndrome and

obesity

The malignant form of acantho-

sis nigricans is a paraneoplastc

syndrome that diff erentates

from the benign form because

the laer has mucosal and pal-

moplantar involvement

Lichen Planus

Lichen planus is an inflammatory idiopathic disease that equally aff ects

both genders with higher frequency in middle age

Lichen planus has been related to diverse drugs like gold salts

anti-malarial medication and thiazides It has been also linked to

hepatitis C virus infection however this association is currently

doubtful

Clinical Presentation

Lichen planus presents with red-violaceous polygonal flat papulesquite pruritc which localizes on the flexor side of wrists forearms an-

kles and lumbosacral and flank regions On its surface a whitsh retcu-

late can be observed (Wickhamrsquos striae) About 60 - 70 of the cases

present with lesions in oral and genital mucosa oral which appear as

whitsh retculated lesions (Figures 29 and 30)

Figure 29 Lichen planus of oral mucosa with typical whitish

reticulate

Figure 28 Acanthosis nigricans

8182019 USMLE_01_1415_MANUAL_DMpdf

httpslidepdfcomreaderfullusmle011415manualdmpdf 2023

Amer ican Manual of Examinat ion in Medicine (2CK)

6

Violaceous papules

with white stretch marks

Lichenoid lymphocyte

in1047297ltrate (band formation)

Destruction

of basal layer

Figure 30 Lymphocytic interface reaction (lichen planus)

Treatment

Mild forms are treated with topical cortcoids

Severe cases require oral cortcoids psoralens plus ultraviolet light of

the A wavelength (PUVA) or cyclosporine

Rosacea

Rosacea is a chronic disease of unknown pathogenesis characterized

by erythema and acneiform lesions on the face It aff ects middle aged

women (between 30 and 50 years of age) more

Rosacea etopathogenesis is unknown although there is involvement of

vasomotor lability infecton by Demodex folliculorum photo exposureand genetc predispositon

Clinical Presentation

Rosacea symptomatology comprises facial flushing episodes that end

up by provoking a persistent erythema telangiectasias and papulopus-

tular lesions without comedos Over tme ocular lesions and hyperpla-

sia of sof tssue may develop

Treatment

Avoid vasodilator stmuli

Mild cases require topical metronidazole or azelaic acid

Moderate cases need doxycycline or oral minocyclines

Severe cases are treated with oral isotretnoin at low doses

Pink Pityriasis

Gilbertrsquos pink pityriasis is an acute self-limitng dermatosis which main-

ly aff ects young adults It is of unknown origin although a viral etology

is suspected (there is some speculaton as to links with human herpes-

virus type 7)

Clinical Presentation

Erupton starts with an erythematous plaque between 2 and 5 cm of

diameter with a desquamatve central collaree ofen localized on the

trunk (heraldic mother patch Figure 31)

Figure 31 Pink pityriasis

Around a week later oval papules appear on the trunk and extremi-

tes These papules share similar characteristcs with the mother patch

though the first ones are smaller and distributed according to skin ten-

sion lines Pink pityriasis may be asymptomatc however it is some-

tmes linked to pruritus Lesions may last between 4 and 8 weeks and

disappear without leaving scars

Diagnosis and Treatment

Diagnosis is clinical Treatment is seldom needed and recommended

therapies in the past (PUVA erythromycin or oral antvirals) have not

shown clearly favorable results

Vitiligo

Vitligo is characterized by achromic macules by melanocyte destruc-

ton

Clinical Presentation

Vitligo shows achromic macules of chronic course and variable progres-

sion

Lesions are predominant on acral and periorificial areas They also show

the Koebner phenomenon

Patents may have markers of autoimmune diseases (ie antthyroid

antbodies and diabetes) but these diseases seldom manifest them-

selves

8182019 USMLE_01_1415_MANUAL_DMpdf

httpslidepdfcomreaderfullusmle011415manualdmpdf 2123

Dermatology

Treatment

Localized lesions require topical cortcoids

Extensive or generalized lesions are treated with ultraviolet light B

(UVB) or PUVA

Strict solar photoprotecton is indispensable (Figure 32)

Figure 32 Vitiligo

47 Neoplasias

Seborrheic Keratosis

Seborrheic keratosis is the most frequent benign tumor in human be-

ings since it is part of cutaneous aging

Clinical Presentation

Seborrheic keratosis presents with hyperkeratosic papules with an oily

or velvet-like texture crests fissures and horny plugs on their surface

These papules are normally pigmented showing a brownish-black color

Treatment

No treatment is required as lesions do not become malignant

Seborrheic keratosis can be addressed with cureage or cryotherapy

Actinic keratosis

Actnic keratosis is the most common precancerous lesion and aff ects

almost a 100 of the populaton in sunny areas

Clinical Presentation

Actnic keratosis is characterized by erythematous and desquamatve

papules which are hyperkeratosic and rough on touch developing a

chronic course

Diagnosis

Diagnosis is clinical

Treatment

Treatment entails applicaton of topical 5-fluorouracil topical imiqui-

mod cryotherapy or surgery

If underlying carcinoma is suspected a biopsy must be performed to

rule out suspicion

Epidermoid Carcinoma

Epidermoid carcinoma is the second most frequent cutaneous tumor

Solar photo exposure is the main etological factor which is why epider-

moid carcinoma appears in zones of prolonged solar exposure like the

face Most carcinomas appear over premalignant lesions (actnic kera-

tosis and leukoplakia among others)

Clinical Presentation

Clinical presentaton reveals erythematous or erythematosquamous

plaques Over tme these plaques form papules and tumors which of-

ten become ulceratve and bleed

Diagnosis

Diagnosis is based on clinical suspicion and histopathological confirmaton

Treatment

Surgery with safety margins is the treatment of choice In carcinomas

in situ cryotherapy can be used as well as topical imiquimod electro-

coagulaton or CO2 laser techniques in destructon of tumors Radio-therapy may also be used in some cases

Basal Cellular Carcinoma

Basal cellular carcinoma is the most frequent cutaneous tumor Chronic so-

lar photo exposure is the main etological factor hence most of these car-

cinomas aff ect the facial zone in patents who are 40 years of age or older

Gorlinrsquos syndrome should be considered if multple basal cellular carci-

nomas are found in non photo exposed areas

Clinical Presentation

Basal cell carcinoma shows a pearly pink papule and superficial telan-

giectasias

It is localized over healthy skin and never aff ects mucosae

Treatment

Surgery is the treatment of choice Mohs surgery is performed in zones

where surrounding healthy tssue needs to be preserved Other alter-

natves are cryotherapy imiquimod electrocoagulaton radiotherapy

photodynamic therapy and intralesional interferon Prognosis is excel-

lent as growth is slow and metastasis exceptonal

8182019 USMLE_01_1415_MANUAL_DMpdf

httpslidepdfcomreaderfullusmle011415manualdmpdf 2223

Amer ican Manual of Examinat ion in Medicine (2CK)

8

Melanoma

Melanoma is the most aggressive cutaneous tumor given its ability to

metastasize

Risk factors comprise solar photo exposure clear phototype the pres-

ence of dysplastc nevus or a high number of melanocytc nevi Fam-

ily history is quite important as some genetc mutatons determine a

higher risk of developing the disease

Clinical Forms

See Figure 33

Diagnosis

Precocious diagnosis is essental to perform precocious surgical extrpaton

The ABCDE criteria can help patents to see if they need to seek medical

consultaton (asymmetry of lesion uneven borders color and diameter

greater than 6 mm or abnormal evolut

on)

The Breslow index is the thickness of the lesion measured in millimeters

and is the main prognosis factor

Treatment

The base of treatment is precocious surgical extrpaton If the Breslow

index is less than 1 mm margins of 1 cm will be performed If Breslow

index is greater than 1 mm margins will be of 2 cm

For melanomas with a Breslow index greater than 1 mm the sentnel

ganglion must be located This is the first draining lymph node of the

territory where the tumor is localized If the ganglion is positve re-

gional lymphadenectomy will be performed along with interferon ad-ministraton (Figure 34)

In situ Extirpation 05 cm Follow-up

Breslow lt 1 mm Extirpation 1 cm Follow-up

Lymphadenectomy

Breslow gt 4 mm Interferon

Breslow ge 1 mm Extirpation 2 cm Sentinel ganglion

+

Figure 34 Melanoma treatment

Kaposirsquos sarcoma

Kaposirsquos sarcoma is the most common cutaneous tumor in HIV patents

Clinical presentation

Kaposirsquos sarcoma has a course with violaceous fusiform macules whichovertme may evolve into indurated nodules with blackberry appearance

This type of sarcoma has been linked to herpesvirus type 8 both in HIV

and seronegatve patents (Table 3)

EPIDERMAL KAPOSIrsquoS 983080HIV983081 CLASSIC KAPOSIrsquoS

Homosexual youth (95) The elderly

Diffuse and bilateral

(frequently in palate and face)

Unilateral plaques

(lower extremities)

Frequent mucosal and visceral involvement Not so frequent

middot Precocious lymphatic invasion

middot Aggressive

Not so precocious

Table 3 Differences between epidermal and classic Kaposirsquos sarcoma

Nodular melanoma

15

Middle-aged men

middot On healthy skin

middot Any zone

middot Sudden onset

middot Uniform black nodulemiddot Rapidly invasive (vertical growth without radial)middot Frequent ulceration and bleeding

Worst histological prognosis

Lentigo malignant melanoma

10

Elderly women

90 on facephotoexposedzones of aging skins(chronic exposure)

Spot that growsduring many years (gt 10)then progresses (nodule)

Better prognosis

Acral lentinginous melanoma

5ndash10 ( 60 black and Asian race)

Elderly men

middot Sole (ankle) handsmucosa ungual bed

middot No relation to photo exposure

middot Macule with mosaic appearance (spot that grows)middot Some amelanisticmiddot Bad prognosis due to late diagnosis

Melanoma of super1047297cial extension

70

Young women

middot 30 previous nervusmiddot Intermittent exposuremiddot Men back middot Women legs

More frequent

middot Macula with mosaic appearance in colors that grows 4-5 years and then in1047297ltrates (nodule)middot Metastasis 35 to 70

Figure 33 Clinical forms of malignant melanoma

8182019 USMLE_01_1415_MANUAL_DMpdf

httpslidepdfcomreaderfullusmle011415manualdmpdf 2323

Dermatology

Diagnosis

Diagnosis relies on clinical suspicion and histopathological confirma-

ton

Treatment

Treatment of localized forms can include surgical extrpaton radiother-

apy or intralesional vinblastne

If the sarcoma is disseminated optons involve interferon or chemo-

therapy

Mycosis Fungoides

Mycosis fungoides is a T-cell lymphoma of low-grade malignancy Its

clinical course may be very slow and surpass 50 years Three stages are

clinically diff erentated

1 Eczematous or macular phase predominantly truncular erythema-

tous macules with years of evoluton They resemble a chromic ec-

zema Histology is unspecifi

c at this stage2 Infiltratve plaque phase infiltrated erythematous plaques appear

Histology is diagnostc at this stage A dermal infiltrate of atypical

lymphocytes band forms can be observed composed of CD+4 T

lymphocytes with cerebriform nuclei There is a marked epidermo-

tropism with the presence of clusters of intraepidermal lympho-

cytes called Pautrierrsquos microabscesses (Figure 35)

Figure 35 Mycosis fungoides Infiltrative plaque phase

3 Tumoral phase erythematous exophytc plaques start to appear

(tumors) with a tendency to ulceraton They can have a large size

Histology may become unspecific again as epidermotropism disap-

pears

In more advanced stages of the disease there is aff ectaton of extra-

cutaneous organs such as lymph nodes liver spleen lungs and bone

marrow Besides there may be blastc transformaton Other possible

complicaton is sepsis by Staphylococcus aureus

These three stages usually develop consecutvely nevertheless there

may patents whose debut starts directly with the tumoral stage

Remember

Microabscesses of mycosis fungoides are due to lymphocytes and are calledPautrierrsquos abscesses Psoriasis microabscesses result from neutrophils andare labeled as Munro-Sabouraud

Seacutezary Syndrome

Seacutezary syndrome can be considered as the leukemic phase of T-cell cu-

taneous lymphoma It is defined by the triad erythroderma (Figure 36

lymphadenopathies and the existence of more than 1000 Seacutezary cellsper milliliter in peripheral blood Seacutezary cells are atypical T- lymphocyte

with cerebriform nuclei

Very intense pruritus is characteristc For many authors Seacutezary syn-

drome is an aggressive clinical form and a bad prognosis of a mycosis

fungoides

Figure 36 Erythroderma due to Seacutezary syndrome

Page 19: USMLE_01_1415_MANUAL_DM.pdf

8182019 USMLE_01_1415_MANUAL_DMpdf

httpslidepdfcomreaderfullusmle011415manualdmpdf 1923

Dermatology

single dose would be enough to cure scabies (already used by vet-

erinarians)

45 Ischemia

Decubitus Ulcers

Decubitus ulcers are the result of ischemic necrosis by contnuous pres-

sure on an area which restricts microcirculaton in that zone

Clinical Presentation

Decubitus ulcers are present in patents in bed with scarce mobilizaton

It is favored by bone prominences and lack of fat tssue If sensitvity

decreases there is more risk of formaton of decubitus ulcers

Diagnosis

Diagnosis is achieved based on medical records and clinical presentaton

Treatment

Preventon is of the utmost importance as well as frequent mobiliza-

ton of the patent in bed

Once ulcers have been established hydrocolloid dressings are used for

healing but sometmes surgical debridement is necessary

Gangrene

Gangrene means tssue necrosis

There are three types dry gangrene wet gangrene and gas gangrene

Clinical Presentation

Dry gangrene is due to ischemia generally secondary to atherosclero-

sis Clinical presentaton involves pain cold and paleness of extremi-

tes Once tssue is established it turns bluish-black in color and dry

Wet gangrene is owing to bacterial flora Tissue presents with an edem-

atous appearance either with blisters or pus

Gas gangrene caused by C perfringens It is normally located on re-

cent surgery Bacteria precociously destroyt

ssue producing gas It is amedical emergency

Diagnosis

Clinical diagnosis is obtained by microbiological culture

Treatment

Treatment requires surgical debridement with amputaton if necessary

and associaton of broad spectrum antbiotherapy

Gas gangrene is treated with hyperbaric oxygen

46 Miscellaneous

Acanthosis Nigricans

Acanthosis nigricans are vel-

vet-like papillomatous brown

plaques in neck axilla and groin

folds (Figure 28)

It is associated with diabetes

mellitus Cushingrsquos disease poly-

cystc ovarian syndrome and

obesity

The malignant form of acantho-

sis nigricans is a paraneoplastc

syndrome that diff erentates

from the benign form because

the laer has mucosal and pal-

moplantar involvement

Lichen Planus

Lichen planus is an inflammatory idiopathic disease that equally aff ects

both genders with higher frequency in middle age

Lichen planus has been related to diverse drugs like gold salts

anti-malarial medication and thiazides It has been also linked to

hepatitis C virus infection however this association is currently

doubtful

Clinical Presentation

Lichen planus presents with red-violaceous polygonal flat papulesquite pruritc which localizes on the flexor side of wrists forearms an-

kles and lumbosacral and flank regions On its surface a whitsh retcu-

late can be observed (Wickhamrsquos striae) About 60 - 70 of the cases

present with lesions in oral and genital mucosa oral which appear as

whitsh retculated lesions (Figures 29 and 30)

Figure 29 Lichen planus of oral mucosa with typical whitish

reticulate

Figure 28 Acanthosis nigricans

8182019 USMLE_01_1415_MANUAL_DMpdf

httpslidepdfcomreaderfullusmle011415manualdmpdf 2023

Amer ican Manual of Examinat ion in Medicine (2CK)

6

Violaceous papules

with white stretch marks

Lichenoid lymphocyte

in1047297ltrate (band formation)

Destruction

of basal layer

Figure 30 Lymphocytic interface reaction (lichen planus)

Treatment

Mild forms are treated with topical cortcoids

Severe cases require oral cortcoids psoralens plus ultraviolet light of

the A wavelength (PUVA) or cyclosporine

Rosacea

Rosacea is a chronic disease of unknown pathogenesis characterized

by erythema and acneiform lesions on the face It aff ects middle aged

women (between 30 and 50 years of age) more

Rosacea etopathogenesis is unknown although there is involvement of

vasomotor lability infecton by Demodex folliculorum photo exposureand genetc predispositon

Clinical Presentation

Rosacea symptomatology comprises facial flushing episodes that end

up by provoking a persistent erythema telangiectasias and papulopus-

tular lesions without comedos Over tme ocular lesions and hyperpla-

sia of sof tssue may develop

Treatment

Avoid vasodilator stmuli

Mild cases require topical metronidazole or azelaic acid

Moderate cases need doxycycline or oral minocyclines

Severe cases are treated with oral isotretnoin at low doses

Pink Pityriasis

Gilbertrsquos pink pityriasis is an acute self-limitng dermatosis which main-

ly aff ects young adults It is of unknown origin although a viral etology

is suspected (there is some speculaton as to links with human herpes-

virus type 7)

Clinical Presentation

Erupton starts with an erythematous plaque between 2 and 5 cm of

diameter with a desquamatve central collaree ofen localized on the

trunk (heraldic mother patch Figure 31)

Figure 31 Pink pityriasis

Around a week later oval papules appear on the trunk and extremi-

tes These papules share similar characteristcs with the mother patch

though the first ones are smaller and distributed according to skin ten-

sion lines Pink pityriasis may be asymptomatc however it is some-

tmes linked to pruritus Lesions may last between 4 and 8 weeks and

disappear without leaving scars

Diagnosis and Treatment

Diagnosis is clinical Treatment is seldom needed and recommended

therapies in the past (PUVA erythromycin or oral antvirals) have not

shown clearly favorable results

Vitiligo

Vitligo is characterized by achromic macules by melanocyte destruc-

ton

Clinical Presentation

Vitligo shows achromic macules of chronic course and variable progres-

sion

Lesions are predominant on acral and periorificial areas They also show

the Koebner phenomenon

Patents may have markers of autoimmune diseases (ie antthyroid

antbodies and diabetes) but these diseases seldom manifest them-

selves

8182019 USMLE_01_1415_MANUAL_DMpdf

httpslidepdfcomreaderfullusmle011415manualdmpdf 2123

Dermatology

Treatment

Localized lesions require topical cortcoids

Extensive or generalized lesions are treated with ultraviolet light B

(UVB) or PUVA

Strict solar photoprotecton is indispensable (Figure 32)

Figure 32 Vitiligo

47 Neoplasias

Seborrheic Keratosis

Seborrheic keratosis is the most frequent benign tumor in human be-

ings since it is part of cutaneous aging

Clinical Presentation

Seborrheic keratosis presents with hyperkeratosic papules with an oily

or velvet-like texture crests fissures and horny plugs on their surface

These papules are normally pigmented showing a brownish-black color

Treatment

No treatment is required as lesions do not become malignant

Seborrheic keratosis can be addressed with cureage or cryotherapy

Actinic keratosis

Actnic keratosis is the most common precancerous lesion and aff ects

almost a 100 of the populaton in sunny areas

Clinical Presentation

Actnic keratosis is characterized by erythematous and desquamatve

papules which are hyperkeratosic and rough on touch developing a

chronic course

Diagnosis

Diagnosis is clinical

Treatment

Treatment entails applicaton of topical 5-fluorouracil topical imiqui-

mod cryotherapy or surgery

If underlying carcinoma is suspected a biopsy must be performed to

rule out suspicion

Epidermoid Carcinoma

Epidermoid carcinoma is the second most frequent cutaneous tumor

Solar photo exposure is the main etological factor which is why epider-

moid carcinoma appears in zones of prolonged solar exposure like the

face Most carcinomas appear over premalignant lesions (actnic kera-

tosis and leukoplakia among others)

Clinical Presentation

Clinical presentaton reveals erythematous or erythematosquamous

plaques Over tme these plaques form papules and tumors which of-

ten become ulceratve and bleed

Diagnosis

Diagnosis is based on clinical suspicion and histopathological confirmaton

Treatment

Surgery with safety margins is the treatment of choice In carcinomas

in situ cryotherapy can be used as well as topical imiquimod electro-

coagulaton or CO2 laser techniques in destructon of tumors Radio-therapy may also be used in some cases

Basal Cellular Carcinoma

Basal cellular carcinoma is the most frequent cutaneous tumor Chronic so-

lar photo exposure is the main etological factor hence most of these car-

cinomas aff ect the facial zone in patents who are 40 years of age or older

Gorlinrsquos syndrome should be considered if multple basal cellular carci-

nomas are found in non photo exposed areas

Clinical Presentation

Basal cell carcinoma shows a pearly pink papule and superficial telan-

giectasias

It is localized over healthy skin and never aff ects mucosae

Treatment

Surgery is the treatment of choice Mohs surgery is performed in zones

where surrounding healthy tssue needs to be preserved Other alter-

natves are cryotherapy imiquimod electrocoagulaton radiotherapy

photodynamic therapy and intralesional interferon Prognosis is excel-

lent as growth is slow and metastasis exceptonal

8182019 USMLE_01_1415_MANUAL_DMpdf

httpslidepdfcomreaderfullusmle011415manualdmpdf 2223

Amer ican Manual of Examinat ion in Medicine (2CK)

8

Melanoma

Melanoma is the most aggressive cutaneous tumor given its ability to

metastasize

Risk factors comprise solar photo exposure clear phototype the pres-

ence of dysplastc nevus or a high number of melanocytc nevi Fam-

ily history is quite important as some genetc mutatons determine a

higher risk of developing the disease

Clinical Forms

See Figure 33

Diagnosis

Precocious diagnosis is essental to perform precocious surgical extrpaton

The ABCDE criteria can help patents to see if they need to seek medical

consultaton (asymmetry of lesion uneven borders color and diameter

greater than 6 mm or abnormal evolut

on)

The Breslow index is the thickness of the lesion measured in millimeters

and is the main prognosis factor

Treatment

The base of treatment is precocious surgical extrpaton If the Breslow

index is less than 1 mm margins of 1 cm will be performed If Breslow

index is greater than 1 mm margins will be of 2 cm

For melanomas with a Breslow index greater than 1 mm the sentnel

ganglion must be located This is the first draining lymph node of the

territory where the tumor is localized If the ganglion is positve re-

gional lymphadenectomy will be performed along with interferon ad-ministraton (Figure 34)

In situ Extirpation 05 cm Follow-up

Breslow lt 1 mm Extirpation 1 cm Follow-up

Lymphadenectomy

Breslow gt 4 mm Interferon

Breslow ge 1 mm Extirpation 2 cm Sentinel ganglion

+

Figure 34 Melanoma treatment

Kaposirsquos sarcoma

Kaposirsquos sarcoma is the most common cutaneous tumor in HIV patents

Clinical presentation

Kaposirsquos sarcoma has a course with violaceous fusiform macules whichovertme may evolve into indurated nodules with blackberry appearance

This type of sarcoma has been linked to herpesvirus type 8 both in HIV

and seronegatve patents (Table 3)

EPIDERMAL KAPOSIrsquoS 983080HIV983081 CLASSIC KAPOSIrsquoS

Homosexual youth (95) The elderly

Diffuse and bilateral

(frequently in palate and face)

Unilateral plaques

(lower extremities)

Frequent mucosal and visceral involvement Not so frequent

middot Precocious lymphatic invasion

middot Aggressive

Not so precocious

Table 3 Differences between epidermal and classic Kaposirsquos sarcoma

Nodular melanoma

15

Middle-aged men

middot On healthy skin

middot Any zone

middot Sudden onset

middot Uniform black nodulemiddot Rapidly invasive (vertical growth without radial)middot Frequent ulceration and bleeding

Worst histological prognosis

Lentigo malignant melanoma

10

Elderly women

90 on facephotoexposedzones of aging skins(chronic exposure)

Spot that growsduring many years (gt 10)then progresses (nodule)

Better prognosis

Acral lentinginous melanoma

5ndash10 ( 60 black and Asian race)

Elderly men

middot Sole (ankle) handsmucosa ungual bed

middot No relation to photo exposure

middot Macule with mosaic appearance (spot that grows)middot Some amelanisticmiddot Bad prognosis due to late diagnosis

Melanoma of super1047297cial extension

70

Young women

middot 30 previous nervusmiddot Intermittent exposuremiddot Men back middot Women legs

More frequent

middot Macula with mosaic appearance in colors that grows 4-5 years and then in1047297ltrates (nodule)middot Metastasis 35 to 70

Figure 33 Clinical forms of malignant melanoma

8182019 USMLE_01_1415_MANUAL_DMpdf

httpslidepdfcomreaderfullusmle011415manualdmpdf 2323

Dermatology

Diagnosis

Diagnosis relies on clinical suspicion and histopathological confirma-

ton

Treatment

Treatment of localized forms can include surgical extrpaton radiother-

apy or intralesional vinblastne

If the sarcoma is disseminated optons involve interferon or chemo-

therapy

Mycosis Fungoides

Mycosis fungoides is a T-cell lymphoma of low-grade malignancy Its

clinical course may be very slow and surpass 50 years Three stages are

clinically diff erentated

1 Eczematous or macular phase predominantly truncular erythema-

tous macules with years of evoluton They resemble a chromic ec-

zema Histology is unspecifi

c at this stage2 Infiltratve plaque phase infiltrated erythematous plaques appear

Histology is diagnostc at this stage A dermal infiltrate of atypical

lymphocytes band forms can be observed composed of CD+4 T

lymphocytes with cerebriform nuclei There is a marked epidermo-

tropism with the presence of clusters of intraepidermal lympho-

cytes called Pautrierrsquos microabscesses (Figure 35)

Figure 35 Mycosis fungoides Infiltrative plaque phase

3 Tumoral phase erythematous exophytc plaques start to appear

(tumors) with a tendency to ulceraton They can have a large size

Histology may become unspecific again as epidermotropism disap-

pears

In more advanced stages of the disease there is aff ectaton of extra-

cutaneous organs such as lymph nodes liver spleen lungs and bone

marrow Besides there may be blastc transformaton Other possible

complicaton is sepsis by Staphylococcus aureus

These three stages usually develop consecutvely nevertheless there

may patents whose debut starts directly with the tumoral stage

Remember

Microabscesses of mycosis fungoides are due to lymphocytes and are calledPautrierrsquos abscesses Psoriasis microabscesses result from neutrophils andare labeled as Munro-Sabouraud

Seacutezary Syndrome

Seacutezary syndrome can be considered as the leukemic phase of T-cell cu-

taneous lymphoma It is defined by the triad erythroderma (Figure 36

lymphadenopathies and the existence of more than 1000 Seacutezary cellsper milliliter in peripheral blood Seacutezary cells are atypical T- lymphocyte

with cerebriform nuclei

Very intense pruritus is characteristc For many authors Seacutezary syn-

drome is an aggressive clinical form and a bad prognosis of a mycosis

fungoides

Figure 36 Erythroderma due to Seacutezary syndrome

Page 20: USMLE_01_1415_MANUAL_DM.pdf

8182019 USMLE_01_1415_MANUAL_DMpdf

httpslidepdfcomreaderfullusmle011415manualdmpdf 2023

Amer ican Manual of Examinat ion in Medicine (2CK)

6

Violaceous papules

with white stretch marks

Lichenoid lymphocyte

in1047297ltrate (band formation)

Destruction

of basal layer

Figure 30 Lymphocytic interface reaction (lichen planus)

Treatment

Mild forms are treated with topical cortcoids

Severe cases require oral cortcoids psoralens plus ultraviolet light of

the A wavelength (PUVA) or cyclosporine

Rosacea

Rosacea is a chronic disease of unknown pathogenesis characterized

by erythema and acneiform lesions on the face It aff ects middle aged

women (between 30 and 50 years of age) more

Rosacea etopathogenesis is unknown although there is involvement of

vasomotor lability infecton by Demodex folliculorum photo exposureand genetc predispositon

Clinical Presentation

Rosacea symptomatology comprises facial flushing episodes that end

up by provoking a persistent erythema telangiectasias and papulopus-

tular lesions without comedos Over tme ocular lesions and hyperpla-

sia of sof tssue may develop

Treatment

Avoid vasodilator stmuli

Mild cases require topical metronidazole or azelaic acid

Moderate cases need doxycycline or oral minocyclines

Severe cases are treated with oral isotretnoin at low doses

Pink Pityriasis

Gilbertrsquos pink pityriasis is an acute self-limitng dermatosis which main-

ly aff ects young adults It is of unknown origin although a viral etology

is suspected (there is some speculaton as to links with human herpes-

virus type 7)

Clinical Presentation

Erupton starts with an erythematous plaque between 2 and 5 cm of

diameter with a desquamatve central collaree ofen localized on the

trunk (heraldic mother patch Figure 31)

Figure 31 Pink pityriasis

Around a week later oval papules appear on the trunk and extremi-

tes These papules share similar characteristcs with the mother patch

though the first ones are smaller and distributed according to skin ten-

sion lines Pink pityriasis may be asymptomatc however it is some-

tmes linked to pruritus Lesions may last between 4 and 8 weeks and

disappear without leaving scars

Diagnosis and Treatment

Diagnosis is clinical Treatment is seldom needed and recommended

therapies in the past (PUVA erythromycin or oral antvirals) have not

shown clearly favorable results

Vitiligo

Vitligo is characterized by achromic macules by melanocyte destruc-

ton

Clinical Presentation

Vitligo shows achromic macules of chronic course and variable progres-

sion

Lesions are predominant on acral and periorificial areas They also show

the Koebner phenomenon

Patents may have markers of autoimmune diseases (ie antthyroid

antbodies and diabetes) but these diseases seldom manifest them-

selves

8182019 USMLE_01_1415_MANUAL_DMpdf

httpslidepdfcomreaderfullusmle011415manualdmpdf 2123

Dermatology

Treatment

Localized lesions require topical cortcoids

Extensive or generalized lesions are treated with ultraviolet light B

(UVB) or PUVA

Strict solar photoprotecton is indispensable (Figure 32)

Figure 32 Vitiligo

47 Neoplasias

Seborrheic Keratosis

Seborrheic keratosis is the most frequent benign tumor in human be-

ings since it is part of cutaneous aging

Clinical Presentation

Seborrheic keratosis presents with hyperkeratosic papules with an oily

or velvet-like texture crests fissures and horny plugs on their surface

These papules are normally pigmented showing a brownish-black color

Treatment

No treatment is required as lesions do not become malignant

Seborrheic keratosis can be addressed with cureage or cryotherapy

Actinic keratosis

Actnic keratosis is the most common precancerous lesion and aff ects

almost a 100 of the populaton in sunny areas

Clinical Presentation

Actnic keratosis is characterized by erythematous and desquamatve

papules which are hyperkeratosic and rough on touch developing a

chronic course

Diagnosis

Diagnosis is clinical

Treatment

Treatment entails applicaton of topical 5-fluorouracil topical imiqui-

mod cryotherapy or surgery

If underlying carcinoma is suspected a biopsy must be performed to

rule out suspicion

Epidermoid Carcinoma

Epidermoid carcinoma is the second most frequent cutaneous tumor

Solar photo exposure is the main etological factor which is why epider-

moid carcinoma appears in zones of prolonged solar exposure like the

face Most carcinomas appear over premalignant lesions (actnic kera-

tosis and leukoplakia among others)

Clinical Presentation

Clinical presentaton reveals erythematous or erythematosquamous

plaques Over tme these plaques form papules and tumors which of-

ten become ulceratve and bleed

Diagnosis

Diagnosis is based on clinical suspicion and histopathological confirmaton

Treatment

Surgery with safety margins is the treatment of choice In carcinomas

in situ cryotherapy can be used as well as topical imiquimod electro-

coagulaton or CO2 laser techniques in destructon of tumors Radio-therapy may also be used in some cases

Basal Cellular Carcinoma

Basal cellular carcinoma is the most frequent cutaneous tumor Chronic so-

lar photo exposure is the main etological factor hence most of these car-

cinomas aff ect the facial zone in patents who are 40 years of age or older

Gorlinrsquos syndrome should be considered if multple basal cellular carci-

nomas are found in non photo exposed areas

Clinical Presentation

Basal cell carcinoma shows a pearly pink papule and superficial telan-

giectasias

It is localized over healthy skin and never aff ects mucosae

Treatment

Surgery is the treatment of choice Mohs surgery is performed in zones

where surrounding healthy tssue needs to be preserved Other alter-

natves are cryotherapy imiquimod electrocoagulaton radiotherapy

photodynamic therapy and intralesional interferon Prognosis is excel-

lent as growth is slow and metastasis exceptonal

8182019 USMLE_01_1415_MANUAL_DMpdf

httpslidepdfcomreaderfullusmle011415manualdmpdf 2223

Amer ican Manual of Examinat ion in Medicine (2CK)

8

Melanoma

Melanoma is the most aggressive cutaneous tumor given its ability to

metastasize

Risk factors comprise solar photo exposure clear phototype the pres-

ence of dysplastc nevus or a high number of melanocytc nevi Fam-

ily history is quite important as some genetc mutatons determine a

higher risk of developing the disease

Clinical Forms

See Figure 33

Diagnosis

Precocious diagnosis is essental to perform precocious surgical extrpaton

The ABCDE criteria can help patents to see if they need to seek medical

consultaton (asymmetry of lesion uneven borders color and diameter

greater than 6 mm or abnormal evolut

on)

The Breslow index is the thickness of the lesion measured in millimeters

and is the main prognosis factor

Treatment

The base of treatment is precocious surgical extrpaton If the Breslow

index is less than 1 mm margins of 1 cm will be performed If Breslow

index is greater than 1 mm margins will be of 2 cm

For melanomas with a Breslow index greater than 1 mm the sentnel

ganglion must be located This is the first draining lymph node of the

territory where the tumor is localized If the ganglion is positve re-

gional lymphadenectomy will be performed along with interferon ad-ministraton (Figure 34)

In situ Extirpation 05 cm Follow-up

Breslow lt 1 mm Extirpation 1 cm Follow-up

Lymphadenectomy

Breslow gt 4 mm Interferon

Breslow ge 1 mm Extirpation 2 cm Sentinel ganglion

+

Figure 34 Melanoma treatment

Kaposirsquos sarcoma

Kaposirsquos sarcoma is the most common cutaneous tumor in HIV patents

Clinical presentation

Kaposirsquos sarcoma has a course with violaceous fusiform macules whichovertme may evolve into indurated nodules with blackberry appearance

This type of sarcoma has been linked to herpesvirus type 8 both in HIV

and seronegatve patents (Table 3)

EPIDERMAL KAPOSIrsquoS 983080HIV983081 CLASSIC KAPOSIrsquoS

Homosexual youth (95) The elderly

Diffuse and bilateral

(frequently in palate and face)

Unilateral plaques

(lower extremities)

Frequent mucosal and visceral involvement Not so frequent

middot Precocious lymphatic invasion

middot Aggressive

Not so precocious

Table 3 Differences between epidermal and classic Kaposirsquos sarcoma

Nodular melanoma

15

Middle-aged men

middot On healthy skin

middot Any zone

middot Sudden onset

middot Uniform black nodulemiddot Rapidly invasive (vertical growth without radial)middot Frequent ulceration and bleeding

Worst histological prognosis

Lentigo malignant melanoma

10

Elderly women

90 on facephotoexposedzones of aging skins(chronic exposure)

Spot that growsduring many years (gt 10)then progresses (nodule)

Better prognosis

Acral lentinginous melanoma

5ndash10 ( 60 black and Asian race)

Elderly men

middot Sole (ankle) handsmucosa ungual bed

middot No relation to photo exposure

middot Macule with mosaic appearance (spot that grows)middot Some amelanisticmiddot Bad prognosis due to late diagnosis

Melanoma of super1047297cial extension

70

Young women

middot 30 previous nervusmiddot Intermittent exposuremiddot Men back middot Women legs

More frequent

middot Macula with mosaic appearance in colors that grows 4-5 years and then in1047297ltrates (nodule)middot Metastasis 35 to 70

Figure 33 Clinical forms of malignant melanoma

8182019 USMLE_01_1415_MANUAL_DMpdf

httpslidepdfcomreaderfullusmle011415manualdmpdf 2323

Dermatology

Diagnosis

Diagnosis relies on clinical suspicion and histopathological confirma-

ton

Treatment

Treatment of localized forms can include surgical extrpaton radiother-

apy or intralesional vinblastne

If the sarcoma is disseminated optons involve interferon or chemo-

therapy

Mycosis Fungoides

Mycosis fungoides is a T-cell lymphoma of low-grade malignancy Its

clinical course may be very slow and surpass 50 years Three stages are

clinically diff erentated

1 Eczematous or macular phase predominantly truncular erythema-

tous macules with years of evoluton They resemble a chromic ec-

zema Histology is unspecifi

c at this stage2 Infiltratve plaque phase infiltrated erythematous plaques appear

Histology is diagnostc at this stage A dermal infiltrate of atypical

lymphocytes band forms can be observed composed of CD+4 T

lymphocytes with cerebriform nuclei There is a marked epidermo-

tropism with the presence of clusters of intraepidermal lympho-

cytes called Pautrierrsquos microabscesses (Figure 35)

Figure 35 Mycosis fungoides Infiltrative plaque phase

3 Tumoral phase erythematous exophytc plaques start to appear

(tumors) with a tendency to ulceraton They can have a large size

Histology may become unspecific again as epidermotropism disap-

pears

In more advanced stages of the disease there is aff ectaton of extra-

cutaneous organs such as lymph nodes liver spleen lungs and bone

marrow Besides there may be blastc transformaton Other possible

complicaton is sepsis by Staphylococcus aureus

These three stages usually develop consecutvely nevertheless there

may patents whose debut starts directly with the tumoral stage

Remember

Microabscesses of mycosis fungoides are due to lymphocytes and are calledPautrierrsquos abscesses Psoriasis microabscesses result from neutrophils andare labeled as Munro-Sabouraud

Seacutezary Syndrome

Seacutezary syndrome can be considered as the leukemic phase of T-cell cu-

taneous lymphoma It is defined by the triad erythroderma (Figure 36

lymphadenopathies and the existence of more than 1000 Seacutezary cellsper milliliter in peripheral blood Seacutezary cells are atypical T- lymphocyte

with cerebriform nuclei

Very intense pruritus is characteristc For many authors Seacutezary syn-

drome is an aggressive clinical form and a bad prognosis of a mycosis

fungoides

Figure 36 Erythroderma due to Seacutezary syndrome

Page 21: USMLE_01_1415_MANUAL_DM.pdf

8182019 USMLE_01_1415_MANUAL_DMpdf

httpslidepdfcomreaderfullusmle011415manualdmpdf 2123

Dermatology

Treatment

Localized lesions require topical cortcoids

Extensive or generalized lesions are treated with ultraviolet light B

(UVB) or PUVA

Strict solar photoprotecton is indispensable (Figure 32)

Figure 32 Vitiligo

47 Neoplasias

Seborrheic Keratosis

Seborrheic keratosis is the most frequent benign tumor in human be-

ings since it is part of cutaneous aging

Clinical Presentation

Seborrheic keratosis presents with hyperkeratosic papules with an oily

or velvet-like texture crests fissures and horny plugs on their surface

These papules are normally pigmented showing a brownish-black color

Treatment

No treatment is required as lesions do not become malignant

Seborrheic keratosis can be addressed with cureage or cryotherapy

Actinic keratosis

Actnic keratosis is the most common precancerous lesion and aff ects

almost a 100 of the populaton in sunny areas

Clinical Presentation

Actnic keratosis is characterized by erythematous and desquamatve

papules which are hyperkeratosic and rough on touch developing a

chronic course

Diagnosis

Diagnosis is clinical

Treatment

Treatment entails applicaton of topical 5-fluorouracil topical imiqui-

mod cryotherapy or surgery

If underlying carcinoma is suspected a biopsy must be performed to

rule out suspicion

Epidermoid Carcinoma

Epidermoid carcinoma is the second most frequent cutaneous tumor

Solar photo exposure is the main etological factor which is why epider-

moid carcinoma appears in zones of prolonged solar exposure like the

face Most carcinomas appear over premalignant lesions (actnic kera-

tosis and leukoplakia among others)

Clinical Presentation

Clinical presentaton reveals erythematous or erythematosquamous

plaques Over tme these plaques form papules and tumors which of-

ten become ulceratve and bleed

Diagnosis

Diagnosis is based on clinical suspicion and histopathological confirmaton

Treatment

Surgery with safety margins is the treatment of choice In carcinomas

in situ cryotherapy can be used as well as topical imiquimod electro-

coagulaton or CO2 laser techniques in destructon of tumors Radio-therapy may also be used in some cases

Basal Cellular Carcinoma

Basal cellular carcinoma is the most frequent cutaneous tumor Chronic so-

lar photo exposure is the main etological factor hence most of these car-

cinomas aff ect the facial zone in patents who are 40 years of age or older

Gorlinrsquos syndrome should be considered if multple basal cellular carci-

nomas are found in non photo exposed areas

Clinical Presentation

Basal cell carcinoma shows a pearly pink papule and superficial telan-

giectasias

It is localized over healthy skin and never aff ects mucosae

Treatment

Surgery is the treatment of choice Mohs surgery is performed in zones

where surrounding healthy tssue needs to be preserved Other alter-

natves are cryotherapy imiquimod electrocoagulaton radiotherapy

photodynamic therapy and intralesional interferon Prognosis is excel-

lent as growth is slow and metastasis exceptonal

8182019 USMLE_01_1415_MANUAL_DMpdf

httpslidepdfcomreaderfullusmle011415manualdmpdf 2223

Amer ican Manual of Examinat ion in Medicine (2CK)

8

Melanoma

Melanoma is the most aggressive cutaneous tumor given its ability to

metastasize

Risk factors comprise solar photo exposure clear phototype the pres-

ence of dysplastc nevus or a high number of melanocytc nevi Fam-

ily history is quite important as some genetc mutatons determine a

higher risk of developing the disease

Clinical Forms

See Figure 33

Diagnosis

Precocious diagnosis is essental to perform precocious surgical extrpaton

The ABCDE criteria can help patents to see if they need to seek medical

consultaton (asymmetry of lesion uneven borders color and diameter

greater than 6 mm or abnormal evolut

on)

The Breslow index is the thickness of the lesion measured in millimeters

and is the main prognosis factor

Treatment

The base of treatment is precocious surgical extrpaton If the Breslow

index is less than 1 mm margins of 1 cm will be performed If Breslow

index is greater than 1 mm margins will be of 2 cm

For melanomas with a Breslow index greater than 1 mm the sentnel

ganglion must be located This is the first draining lymph node of the

territory where the tumor is localized If the ganglion is positve re-

gional lymphadenectomy will be performed along with interferon ad-ministraton (Figure 34)

In situ Extirpation 05 cm Follow-up

Breslow lt 1 mm Extirpation 1 cm Follow-up

Lymphadenectomy

Breslow gt 4 mm Interferon

Breslow ge 1 mm Extirpation 2 cm Sentinel ganglion

+

Figure 34 Melanoma treatment

Kaposirsquos sarcoma

Kaposirsquos sarcoma is the most common cutaneous tumor in HIV patents

Clinical presentation

Kaposirsquos sarcoma has a course with violaceous fusiform macules whichovertme may evolve into indurated nodules with blackberry appearance

This type of sarcoma has been linked to herpesvirus type 8 both in HIV

and seronegatve patents (Table 3)

EPIDERMAL KAPOSIrsquoS 983080HIV983081 CLASSIC KAPOSIrsquoS

Homosexual youth (95) The elderly

Diffuse and bilateral

(frequently in palate and face)

Unilateral plaques

(lower extremities)

Frequent mucosal and visceral involvement Not so frequent

middot Precocious lymphatic invasion

middot Aggressive

Not so precocious

Table 3 Differences between epidermal and classic Kaposirsquos sarcoma

Nodular melanoma

15

Middle-aged men

middot On healthy skin

middot Any zone

middot Sudden onset

middot Uniform black nodulemiddot Rapidly invasive (vertical growth without radial)middot Frequent ulceration and bleeding

Worst histological prognosis

Lentigo malignant melanoma

10

Elderly women

90 on facephotoexposedzones of aging skins(chronic exposure)

Spot that growsduring many years (gt 10)then progresses (nodule)

Better prognosis

Acral lentinginous melanoma

5ndash10 ( 60 black and Asian race)

Elderly men

middot Sole (ankle) handsmucosa ungual bed

middot No relation to photo exposure

middot Macule with mosaic appearance (spot that grows)middot Some amelanisticmiddot Bad prognosis due to late diagnosis

Melanoma of super1047297cial extension

70

Young women

middot 30 previous nervusmiddot Intermittent exposuremiddot Men back middot Women legs

More frequent

middot Macula with mosaic appearance in colors that grows 4-5 years and then in1047297ltrates (nodule)middot Metastasis 35 to 70

Figure 33 Clinical forms of malignant melanoma

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Dermatology

Diagnosis

Diagnosis relies on clinical suspicion and histopathological confirma-

ton

Treatment

Treatment of localized forms can include surgical extrpaton radiother-

apy or intralesional vinblastne

If the sarcoma is disseminated optons involve interferon or chemo-

therapy

Mycosis Fungoides

Mycosis fungoides is a T-cell lymphoma of low-grade malignancy Its

clinical course may be very slow and surpass 50 years Three stages are

clinically diff erentated

1 Eczematous or macular phase predominantly truncular erythema-

tous macules with years of evoluton They resemble a chromic ec-

zema Histology is unspecifi

c at this stage2 Infiltratve plaque phase infiltrated erythematous plaques appear

Histology is diagnostc at this stage A dermal infiltrate of atypical

lymphocytes band forms can be observed composed of CD+4 T

lymphocytes with cerebriform nuclei There is a marked epidermo-

tropism with the presence of clusters of intraepidermal lympho-

cytes called Pautrierrsquos microabscesses (Figure 35)

Figure 35 Mycosis fungoides Infiltrative plaque phase

3 Tumoral phase erythematous exophytc plaques start to appear

(tumors) with a tendency to ulceraton They can have a large size

Histology may become unspecific again as epidermotropism disap-

pears

In more advanced stages of the disease there is aff ectaton of extra-

cutaneous organs such as lymph nodes liver spleen lungs and bone

marrow Besides there may be blastc transformaton Other possible

complicaton is sepsis by Staphylococcus aureus

These three stages usually develop consecutvely nevertheless there

may patents whose debut starts directly with the tumoral stage

Remember

Microabscesses of mycosis fungoides are due to lymphocytes and are calledPautrierrsquos abscesses Psoriasis microabscesses result from neutrophils andare labeled as Munro-Sabouraud

Seacutezary Syndrome

Seacutezary syndrome can be considered as the leukemic phase of T-cell cu-

taneous lymphoma It is defined by the triad erythroderma (Figure 36

lymphadenopathies and the existence of more than 1000 Seacutezary cellsper milliliter in peripheral blood Seacutezary cells are atypical T- lymphocyte

with cerebriform nuclei

Very intense pruritus is characteristc For many authors Seacutezary syn-

drome is an aggressive clinical form and a bad prognosis of a mycosis

fungoides

Figure 36 Erythroderma due to Seacutezary syndrome

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Amer ican Manual of Examinat ion in Medicine (2CK)

8

Melanoma

Melanoma is the most aggressive cutaneous tumor given its ability to

metastasize

Risk factors comprise solar photo exposure clear phototype the pres-

ence of dysplastc nevus or a high number of melanocytc nevi Fam-

ily history is quite important as some genetc mutatons determine a

higher risk of developing the disease

Clinical Forms

See Figure 33

Diagnosis

Precocious diagnosis is essental to perform precocious surgical extrpaton

The ABCDE criteria can help patents to see if they need to seek medical

consultaton (asymmetry of lesion uneven borders color and diameter

greater than 6 mm or abnormal evolut

on)

The Breslow index is the thickness of the lesion measured in millimeters

and is the main prognosis factor

Treatment

The base of treatment is precocious surgical extrpaton If the Breslow

index is less than 1 mm margins of 1 cm will be performed If Breslow

index is greater than 1 mm margins will be of 2 cm

For melanomas with a Breslow index greater than 1 mm the sentnel

ganglion must be located This is the first draining lymph node of the

territory where the tumor is localized If the ganglion is positve re-

gional lymphadenectomy will be performed along with interferon ad-ministraton (Figure 34)

In situ Extirpation 05 cm Follow-up

Breslow lt 1 mm Extirpation 1 cm Follow-up

Lymphadenectomy

Breslow gt 4 mm Interferon

Breslow ge 1 mm Extirpation 2 cm Sentinel ganglion

+

Figure 34 Melanoma treatment

Kaposirsquos sarcoma

Kaposirsquos sarcoma is the most common cutaneous tumor in HIV patents

Clinical presentation

Kaposirsquos sarcoma has a course with violaceous fusiform macules whichovertme may evolve into indurated nodules with blackberry appearance

This type of sarcoma has been linked to herpesvirus type 8 both in HIV

and seronegatve patents (Table 3)

EPIDERMAL KAPOSIrsquoS 983080HIV983081 CLASSIC KAPOSIrsquoS

Homosexual youth (95) The elderly

Diffuse and bilateral

(frequently in palate and face)

Unilateral plaques

(lower extremities)

Frequent mucosal and visceral involvement Not so frequent

middot Precocious lymphatic invasion

middot Aggressive

Not so precocious

Table 3 Differences between epidermal and classic Kaposirsquos sarcoma

Nodular melanoma

15

Middle-aged men

middot On healthy skin

middot Any zone

middot Sudden onset

middot Uniform black nodulemiddot Rapidly invasive (vertical growth without radial)middot Frequent ulceration and bleeding

Worst histological prognosis

Lentigo malignant melanoma

10

Elderly women

90 on facephotoexposedzones of aging skins(chronic exposure)

Spot that growsduring many years (gt 10)then progresses (nodule)

Better prognosis

Acral lentinginous melanoma

5ndash10 ( 60 black and Asian race)

Elderly men

middot Sole (ankle) handsmucosa ungual bed

middot No relation to photo exposure

middot Macule with mosaic appearance (spot that grows)middot Some amelanisticmiddot Bad prognosis due to late diagnosis

Melanoma of super1047297cial extension

70

Young women

middot 30 previous nervusmiddot Intermittent exposuremiddot Men back middot Women legs

More frequent

middot Macula with mosaic appearance in colors that grows 4-5 years and then in1047297ltrates (nodule)middot Metastasis 35 to 70

Figure 33 Clinical forms of malignant melanoma

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Dermatology

Diagnosis

Diagnosis relies on clinical suspicion and histopathological confirma-

ton

Treatment

Treatment of localized forms can include surgical extrpaton radiother-

apy or intralesional vinblastne

If the sarcoma is disseminated optons involve interferon or chemo-

therapy

Mycosis Fungoides

Mycosis fungoides is a T-cell lymphoma of low-grade malignancy Its

clinical course may be very slow and surpass 50 years Three stages are

clinically diff erentated

1 Eczematous or macular phase predominantly truncular erythema-

tous macules with years of evoluton They resemble a chromic ec-

zema Histology is unspecifi

c at this stage2 Infiltratve plaque phase infiltrated erythematous plaques appear

Histology is diagnostc at this stage A dermal infiltrate of atypical

lymphocytes band forms can be observed composed of CD+4 T

lymphocytes with cerebriform nuclei There is a marked epidermo-

tropism with the presence of clusters of intraepidermal lympho-

cytes called Pautrierrsquos microabscesses (Figure 35)

Figure 35 Mycosis fungoides Infiltrative plaque phase

3 Tumoral phase erythematous exophytc plaques start to appear

(tumors) with a tendency to ulceraton They can have a large size

Histology may become unspecific again as epidermotropism disap-

pears

In more advanced stages of the disease there is aff ectaton of extra-

cutaneous organs such as lymph nodes liver spleen lungs and bone

marrow Besides there may be blastc transformaton Other possible

complicaton is sepsis by Staphylococcus aureus

These three stages usually develop consecutvely nevertheless there

may patents whose debut starts directly with the tumoral stage

Remember

Microabscesses of mycosis fungoides are due to lymphocytes and are calledPautrierrsquos abscesses Psoriasis microabscesses result from neutrophils andare labeled as Munro-Sabouraud

Seacutezary Syndrome

Seacutezary syndrome can be considered as the leukemic phase of T-cell cu-

taneous lymphoma It is defined by the triad erythroderma (Figure 36

lymphadenopathies and the existence of more than 1000 Seacutezary cellsper milliliter in peripheral blood Seacutezary cells are atypical T- lymphocyte

with cerebriform nuclei

Very intense pruritus is characteristc For many authors Seacutezary syn-

drome is an aggressive clinical form and a bad prognosis of a mycosis

fungoides

Figure 36 Erythroderma due to Seacutezary syndrome

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Dermatology

Diagnosis

Diagnosis relies on clinical suspicion and histopathological confirma-

ton

Treatment

Treatment of localized forms can include surgical extrpaton radiother-

apy or intralesional vinblastne

If the sarcoma is disseminated optons involve interferon or chemo-

therapy

Mycosis Fungoides

Mycosis fungoides is a T-cell lymphoma of low-grade malignancy Its

clinical course may be very slow and surpass 50 years Three stages are

clinically diff erentated

1 Eczematous or macular phase predominantly truncular erythema-

tous macules with years of evoluton They resemble a chromic ec-

zema Histology is unspecifi

c at this stage2 Infiltratve plaque phase infiltrated erythematous plaques appear

Histology is diagnostc at this stage A dermal infiltrate of atypical

lymphocytes band forms can be observed composed of CD+4 T

lymphocytes with cerebriform nuclei There is a marked epidermo-

tropism with the presence of clusters of intraepidermal lympho-

cytes called Pautrierrsquos microabscesses (Figure 35)

Figure 35 Mycosis fungoides Infiltrative plaque phase

3 Tumoral phase erythematous exophytc plaques start to appear

(tumors) with a tendency to ulceraton They can have a large size

Histology may become unspecific again as epidermotropism disap-

pears

In more advanced stages of the disease there is aff ectaton of extra-

cutaneous organs such as lymph nodes liver spleen lungs and bone

marrow Besides there may be blastc transformaton Other possible

complicaton is sepsis by Staphylococcus aureus

These three stages usually develop consecutvely nevertheless there

may patents whose debut starts directly with the tumoral stage

Remember

Microabscesses of mycosis fungoides are due to lymphocytes and are calledPautrierrsquos abscesses Psoriasis microabscesses result from neutrophils andare labeled as Munro-Sabouraud

Seacutezary Syndrome

Seacutezary syndrome can be considered as the leukemic phase of T-cell cu-

taneous lymphoma It is defined by the triad erythroderma (Figure 36

lymphadenopathies and the existence of more than 1000 Seacutezary cellsper milliliter in peripheral blood Seacutezary cells are atypical T- lymphocyte

with cerebriform nuclei

Very intense pruritus is characteristc For many authors Seacutezary syn-

drome is an aggressive clinical form and a bad prognosis of a mycosis

fungoides

Figure 36 Erythroderma due to Seacutezary syndrome