D e r m a t o l o g y American Manual of Examination in Medicine (2CK)
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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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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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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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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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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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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)
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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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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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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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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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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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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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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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
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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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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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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
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
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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
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
8182019 USMLE_01_1415_MANUAL_DMpdf
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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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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
8182019 USMLE_01_1415_MANUAL_DMpdf
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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
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
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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
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
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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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
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
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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
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
8182019 USMLE_01_1415_MANUAL_DMpdf
httpslidepdfcomreaderfullusmle011415manualdmpdf 1723
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
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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
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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
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
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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
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
8182019 USMLE_01_1415_MANUAL_DMpdf
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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
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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
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
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
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
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
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)
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
8182019 USMLE_01_1415_MANUAL_DMpdf
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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