Alterations in Immune Responses

8/6/2019 Alterations in Immune Responses

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HYPERSENSITIVITYDISORDERS


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HYPERSENSITIVITY DISORDERS

- excessive or inappropriate activationof the immune system.


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Categories of Hypersensitivity Disorders

Type I Rapid (i diat ) per ensiti it

Type II Antib d - ediated Disorders

Type III Immune complex-me iate immuneisor ers

Type IV T- ell- ediated disorders


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TYPE I - api (imme iate) hypersensitivity

A.k.a. - Atopic allergy

- Most common type of hypersensitivity


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TYPE I - api (imme iate) hypersensitivity

PATHOPHYSIOLOGIC MECHANISM

Allergens Helper T cell (TH2)Release of

CYTOKINES

(IL-4, IL-5, IL-13)

Differentiation of

BETA CELLS

IgE-producing

plasma cellsIgE

IgE attaches to receptors

on surface of mast cells and

basophils


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Sensitized mast cells

and bas phils

Exp sure t

allergens

Degranulation of

SENSITIZED MAST

CELLS orBASOPHILS

-Vas dilati n

-Vascular leakage

-Sm th muscle c ntracti n-Muc sal edema -Epithelial damage

-Mucus secreti n -Br nch spasm

-Leuk cyte infiltrati n

Release of chemical

me iators

(eg. Histamine)

Primary or Initial

Response

Secondary or Late

Response


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TYPE I Hypersensitivity Disorders

- An intermittent an reversi le airflow o struction

affecting only the airways, not the alveoli.


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ETIOLOGY

Airway o struction can occur in 2 ways:

2. Airway hyperresponsiveness

1. Inflammationo Specific allergens

o Nonallergenic general irritants such as col

air, ry air, or fine air orne particles

o Microorganisms

oAspirin.

o Exercise

o Upper respiratory illness

o

Unknown reasons


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PATHOPHYSIOLOGY

AIRWAY INFLAMMATION

AIRWAY

HYPERRESPONSIVENESS

Narrowing of the airway


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CLINICAL MANIFESTATIONS

Au i le wheeze

Increase RR

Coughing

Muscle retraction

Barrel chest


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DIAGNOSTIC TESTS

Elevate Eosinophil count an IgE levels

Arterial Blood Gas Analysis (ABG)

- shows how the client is o taining oxygen


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NURSING DIAGNOSES

Anxiety relate to yspnea, an situational crisis

Impaired Gas Exchange relate to re uce airway size an

excessive mucus pro uction

Ineffective Breathing pattern relate to airway o struction, (an /or

iaphragm flattening if arrel chest occurs in severe cases)

Ineffective Airway Clearance relate to excessive secretions, an

ineffective cough


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The ten ency to pro uce IgE in response to antigen exposure isase on genetic inheritance, ut no single gene has een foun

to e responsi le. Specific allergies are not inherite . A out 50%

of clients with allergic rhinitis have one parent with type I

allergies.

ETIOLOGY & RISK FACTORS

Triggere y reactions to air orne allergens,

especially plant pollens, mol s, ust, animal an er,

wool, foo , an air pollutants.


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Rhinorrhea (a runny nose)

Stuffy nose

Itchy, watery eyes

Voice has a nasal soun .

Drainage from the nose is usually clear or white.

Nasal mucosa appears swollen an pink.


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CBC

DIAGNOSTIC TESTS

- Increase eosinophils

Serum IgE levels - Increase

Skin Testing

Intradermal Testing

Scratch Testing


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A systemic life-threatening hypersensitivity reaction

characterize y e ema in many tissues an a fall in

loo pressure secon ary to vaso ilation.


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ETIOLOGY

Among the most frequent causes of anaphylactic shock

are reactions to rugs, such as penicillin; foo s, such

as nuts an shellfish; an insect venom.


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Respiratory

Wheezing

Bronchospasm

Laryngeal e ema

Inspiratory stri or

Car iovascular

Hypotension/circulatory shock

Dermatologic

Wheal an flare reactions

Urticaria

Angioe ema

Pruritus

Flushing


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TYPE II Antibody-mediated Disorders

The o y makes special autoanti o ies irecte against

self cells that have some form of foreign protein attache

to them.


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TYPE II Antibody-mediated Disorders


IgG & IgM

Activati n f MPLEME T

DESTRUCTION OF SELF CELL

(thru phag cyt sis r lysis)

Antigen f the

surface f a cellBinding

Antib dy-

antigen c mplex


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TYPE II Hypersensitivity Disorders

Characterize y a malfunction of the immune system

that pro uces autoanti o ies, which attack RBCs as if

they were su stances foreign to the o y.


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PATHOPHYSIOLOGY

Pro uction of anti o ies

Attacks RBCs

RBC estruction


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Hea ache

Integuments

Intolerance to coltemperature

Pallor

Cool to touch

Cardiovascular

Tachycar ia

Respiratory

Dyspnea on exertion

Decrease O2 sat

Neurologic

Increase somnolence


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DIAGNOSTIC TESTS

Coom s test

Increase reticulocytes (immature RBCs)

Increase iliru in

- increase anti o ies


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ETIOLOGY

Cause y loo type orRh incompati ility


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PATHOPHYSIOLOGY

When loo containing antigens ifferent from the clients own

antigens is infuse , antigen-anti o y complexes are forme in

the clients loo . These complexes estroy the transfuse cellsan start inflammatory responses in the clients loo vessel

walls an organs.


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The reactions may e mil , with fever an chills, or life threatening, with

isseminate intravascular coagulation (DIC) an circulatory collapse.

Apprehension

Hea ache

Chest pain

Low ack pain

Tachycar ia

Tachypnea

Hypotension

Hemoglo enuria


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A chronic isease characterize y fatigue an weakness

primarily in muscles innervate y the cranial nerves, aswell as in skeletal an respiratory muscles.


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PATHOPHYSIOLOGY


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Fatigue

Motor Manifestations

Progressive muscle weakness that

usually improves with rest

Poor posture

Ptosis

Weak or incomplete eye

closure

Diplopia

Respiratory compromise

Loss of owel an la er control


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Sensory Manifestations

Muscle achiness

Paresthesia

Decrease smell an taste


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DIAGNOSTIC TESTS

Tensilon Test

Electromyography


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TYPE III IMMUNE COMPLEX REACTIONS

Involves immune complexes that are forme

when antigens in to anti o ies


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TYPE III IMMUNE COMPLEX REACTIONS


Antigens bind t

Antib dy

F rmati n f

IMMU E MPLEXES

Immune c mplex

dep siti n intissues

mplementactivati n

Acute Inflammati nTissue damage


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TYPE III Hypersensitivity Disorders

RHEUMATOID

ARTHRITIS

It is a chronic, progressive, systemic inflammatory

autoimmune isease process that primarily

affects the synovial joints.


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RHEUMATOID

ARTHRITIS

PATHOPHYSIOLOGY

AUTOANTIBODIES( heumat id Fact r [ F])

ANTIGENSBinding

IMMU E

MPLEXES

Immune c

mplex

dep

siti

n in the syn

vium mplement

activati n


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Inflammati n in the

syn vial tissues

PA US f rmati n

Articular cartilage

er si n & b ne

destructi n


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RHEUMATOID

ARTHRITIS


Early Manifestations

Joint

- Inflammation

Systemic

- Paresthesia

- Low-gra e fever

- Fatigue

- Weakness

- Anorexia


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RHEUMATOID

ARTHRITIS


Late Manifestations

Joint Deformities

BoutonniereSwan neckUlnar eviation


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RHEUMATOID

ARTHRITIS

Morning stiffness


Late Manifestations Systemic

Joint

Mo erate to severe pain

Osteoporosis

Severe fatigue

Anemia

Weight loss

Su cutaneous no ules

Peripheral neuropathy Vasculitis

Pericar itis

Fi rotic lung isease Sjogrens syn rome

Renal isease


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RHEUMATOID

ARTHRITIS

DIAGNOSTIC TESTS

La oratory tests help to support a iagnosis ofRA,

ut no single test or group of tests can confirm it.

Arthrocentesis

Test for Rheumatoid Factor

Antinuclear Antibody Titer

Erythrocyte sedimentation Rate


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RHEUMATOID

ARTHRITIS

NURSING DIAGNOSES

Acute Pain relate to joint inflammation an tissue amage

Impaired Physical Mobility relate to pain on movement an ecrease

range in motion

Self-care Deficit relate to contractures, fatigue, or loss of motion


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TYPE I DELAYED HYPERSENSITI ITY REACTIONS

The reactive cell is the T-lymphocyte (T-cell). Anti o ies an

complement are not involve . Sensitize T-cells (from

previous exposure) respon to an antigen y releasingchemical me iators an triggering macrophages to estroy

the antigen.

A type IV response typically occurs hours to ays afterexposure.


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HIV/AI S


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HI TRANSMISSION During unprotecte sex

Bloo tr ansfusion

Sharing nee les

Fro other to chil


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PATHOPHYSIOLOGY


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PATHOPHYSIOLOGY

HIV enters the o y

HIV attaches to CD4

- T cell

Viral envelope

pepti es fuse to CD4-T

cell mem rane

Contents of the viral

core enter the host

cells


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PATHOPHYSIOLOGY

RNA transforms into

DNA

The new DNA enters

the nucleus of the CD4

T cell & inserte into

the cells original DNA

ou le stran e viral

DNA forms into single-

stran e messenger

DNA (mRNA), which

uil s new viruses


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PATHOPHYSIOLOGY

mRNA creates a chain of

proteins & enzymes

(polyprotein)

HIV enzymes protease

cuts the polyprotein

chain into the

in ivi ual proteins that

make up the new virus.

Assem ly & release

of the new virus from

the host cells


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PATHOPHYSIOLOGY

HIV replication involves

estruction ofCD4 T cell

Gra ual in CD4 cell

count


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PATHOPHYSIOLOGY

STAGES OF HI

DISEASE

HI Asymptomatic(CDCCategory A: > 500 CD4 T cell)

HI Symptomatic

(CDCCategory B: 200 499CD4 T cell)

AIDS

(CDCCategory C: < 200 CD4 T cell)


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CLI ICAL MA IFESTATI S

The symptoms of HIV an AIDS vary, epen ing on the phase of

infection.

When first infecte with HIV, you may have no signs or symptoms at

all, although you're still a le to transmit the virus to others. Many

people evelop a rief flu-like illness two to four weeks after ecoming

infecte . Signs an symptoms may inclu e:

Fever

Hea ache

Sore throat

Swollen lymph glan s

Rash

WITHIN THE FIRST FEWWEEKS


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You may remain symptom-free for years. But as the virus continuesto multiply an estroy immune cells, you may evelop mil

infections or chronic symptoms such as:

Swollen lymph no es often one of the first signs of HIV infection

Diarrhea

Weight loss

Fever

Cough an shortness of reath

YEARS LATER


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If you receive no treatment for your HIV infection, the isease typically

progresses to AIDS in a out 10 years. By the time AIDS develops, your

immune system has een severely damaged, making you suscepti le toopportunistic infections diseases that wouldn't trou le a person with a

healthy immune system. The signs and symptoms of some of these infections

may include:Soaking night sweats

Shaking chills or fever higher than 100 F (38 C) for several weeks

Cough and shortness of reath

Chronic diarrhea

Persistent white spots or unusual lesions on your tongue or in your mouthHeadaches

Persistent, unexplained fatigue

Blurred anddistorted vision

Weight loss

Skin rashes or umps

PROGRESSION TO AIDS

Alterations in Immune Responses

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