HYPERSENSITIVITY DISORDERS

HYPERSENSITIVITY DISORDERS

- excessive or inappropriate activation of the immune system.

Categories of Hypersensitivity Disorders

 Type I  Type II  Type III

Rapid (i

diat )

per ensiti it

Antib d - ediated Disorders Immune complex-me iate immune isor ers T- ell- ediated disorders

 Type IV

TYPE I - api (imme iate) hypersensitivity

A.k.a.

- Atopic allergy

- Most common type of hypersensitivity

TYPE I - api (imme iate) hypersensitivity

PATHOPHYSIOLOGIC MECHANISM
Release of CYTOKINES (IL-4, IL-5, IL-13)

Allergens

Helper T cell (TH2)

IgE

IgE-producing plasma cells

Differentiation of BETA CELLS

IgE attaches to receptors on surface of mast cells and basophils

Exp sure t allergens

Sensitized mast cells and bas phils

Degranulation of SENSITIZED MAST CELLS or BASOPHILS

Release of chemical me iators (eg. Histamine)

Primary or Initial Response -Vas dilati n -Vascular leakage -Sm th muscle c ntracti n

Secondary or Late Response

-Muc sal edema -Epithelial damage -Mucus secreti n -Br nch spasm -Leuk cyte infiltrati n

TYPE I Hypersensitivity Disorders

- An intermittent an reversi le airflow o struction affecting only the airways, not the alveoli.

TYPE I Hypersensitivity Disorders

ETIOLOGY Airway o struction can occur in 2 ways: 1. Inflammation

o Specific allergens o Nonallergenic general irritants such as col air, ry air, or fine air orne particles o Microorganisms o Aspirin.

2. Airway hyperresponsiveness
o Exercise o Upper respiratory illness o Unknown reasons

TYPE I Hypersensitivity Disorders

PATHOPHYSIOLOGY
AIRWAY INFLAMMATION AIRWAY HYPERRESPONSIVENESS

Narrowing of the airway

TYPE I Hypersensitivity Disorders

CLINICAL MANIFESTATIONS
 Au i le wheeze  Increase RR  Coughing  Muscle retraction  Barrel chest

TYPE I Hypersensitivity Disorders

DIAGNOSTIC TESTS
 Arterial Blood Gas Analysis (ABG)
- shows how the client is o taining oxygen

 Elevate Eosinophil count an IgE levels

TYPE I Hypersensitivity Disorders

NURSING DIAGNOSES
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 Anxiety relate to yspnea, an situational crisis

TYPE I Hypersensitivity Disorders

ETIOLOGY & RISK FACTORS Triggere y reactions to air orne allergens, especially plant pollens, mol s, ust, animal an er, wool, foo , an air pollutants.
The ten ency to pro uce IgE in response to antigen exposure is ase 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.

TYPE I Hypersensitivity Disorders

CLINICAL MANIFESTATIONS
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.

TYPE I Hypersensitivity Disorders

DIAGNOSTIC TESTS
 CBC - Increase eosinophils - Increase

 Serum IgE levels  Skin Testing

 Intradermal Testing  Scratch Testing

TYPE I Hypersensitivity Disorders

A systemic life-threatening hypersensitivity reaction characterize y e ema in many tissues an a fall in loo pressure secon ary to vaso ilation.

TYPE I Hypersensitivity Disorders

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.

TYPE I Hypersensitivity Disorders

CLINICAL MANIFESTATIONS
 Respiratory
Bronchospasm Laryngeal e ema Inspiratory stri or Wheezing

 Car iovascular
Hypotension/circulatory shock  Dermatologic Wheal an flare reactions Urticaria Angioe ema Pruritus Flushing

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.

TYPE II Antibody-mediated Disorders

PATHOPHYSIOLOGIC MECHANISM
IgG & IgM Binding Antigen f the surface f a cell

Antib dyantigen c mplex

Activati n f MPLEME T

DESTRUCTION OF SELF CELL (thru phag cyt sis r lysis)

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.

TYPE II Hypersensitivity Disorders

PATHOPHYSIOLOGY
Pro uction of anti o ies

Attacks RBCs

RBC estruction

TYPE II Hypersensitivity Disorders

CLINICAL MANIFESTATIONS
 Integuments Pallor Cool to touch Intolerance to col temperature  Respiratory Dyspnea on exertion Decrease O2 sat  Cardiovascular Tachycar ia  Neurologic Increase somnolence Hea ache

TYPE II Hypersensitivity Disorders

DIAGNOSTIC TESTS
 Increase reticulocytes (immature RBCs)  Increase

iliru in

 Coom s test - increase anti o ies

TYPE II Hypersensitivity Disorders

ETIOLOGY

 Cause

y loo type or Rh incompati ility

TYPE II Hypersensitivity Disorders

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 cells an start inflammatory responses in the clients loo vessel walls an organs.

TYPE II Hypersensitivity Disorders

CLINICAL MANIFESTATIONS
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

TYPE II Hypersensitivity Disorders

A chronic isease characterize y fatigue an weakness primarily in muscles innervate y the cranial nerves, as well as in skeletal an respiratory muscles.

TYPE II Hypersensitivity Disorders

PATHOPHYSIOLOGY

TYPE II Hypersensitivity Disorders

CLINICAL MANIFESTATIONS
 Motor Manifestations
Progressive muscle weakness that usually improves with rest Poor posture Loss of owel an Ptosis Weak or incomplete eye closure Fatigue la er control Diplopia Respiratory compromise

TYPE II Hypersensitivity Disorders

CLINICAL MANIFESTATIONS
 Sensory Manifestations
Muscle achiness Paresthesia Decrease smell an taste

TYPE II Hypersensitivity Disorders

DIAGNOSTIC TESTS Tensilon Test Electromyography

TYPE III IMMUNE COMPLEX REACTIONS

Involves immune complexes that are forme when antigens in to anti o ies

TYPE III IMMUNE COMPLEX REACTIONS

PATHOPHYSIOLOGIC MECHANISM
Antigens bind t Antib dy F rmati n f IMMU E MPLEXES Immune c mplex dep siti n in tissues

Tissue damage

Acute Inflammati n

mplement activati n

TYPE III Hypersensitivity Disorders

RHEUMATOID ARTHRITIS

It is a chronic, progressive, systemic inflammatory autoimmune isease process that primarily affects the synovial joints.

TYPE III Hypersensitivity Disorders

RHEUMATOID ARTHRITIS
AUTOANTIBODIES
( heumat id Fact r [ F])

PATHOPHYSIOLOGY

Binding

ANTIGENS

IMMU E MPLEXES
Immune c mplex dep siti n in the syn vium

mplement activati n

Inflammati n in the syn vial tissues

PA

US f rmati n

Articular cartilage er si n & b ne destructi n

TYPE III Hypersensitivity Disorders

RHEUMATOID ARTHRITIS
Early Manifestations  Joint
- Inflammation

CLINICAL MANIFESTATIONS

 Systemic
- Low-gra e fever - Fatigue - Weakness - Anorexia - Paresthesia

TYPE III Hypersensitivity Disorders

RHEUMATOID ARTHRITIS
Late Manifestations  Joint Deformities

CLINICAL MANIFESTATIONS

Ulnar eviation

Swan neck

Boutonniere

TYPE III Hypersensitivity Disorders

RHEUMATOID ARTHRITIS
Late Manifestations  Joint
 Mo erate to severe pain  Morning stiffness

CLINICAL MANIFESTATIONS
 Systemic
 Osteoporosis  Severe fatigue  Anemia  Weight loss  Su cutaneous no ules  Peripheral neuropathy  Vasculitis  Pericar itis  Fi rotic lung isease  Sjogren s syn rome  Renal isease

TYPE III Hypersensitivity Disorders

RHEUMATOID ARTHRITIS
DIAGNOSTIC TESTS
La oratory tests help to support a iagnosis of RA, ut no single test or group of tests can confirm it.

Test for Rheumatoid Factor Antinuclear Antibody Titer Erythrocyte sedimentation Rate Arthrocentesis

TYPE III Hypersensitivity Disorders

RHEUMATOID ARTHRITIS
NURSING DIAGNOSES

Acute Pain relate to joint inflammation an tissue amage

Impaired Physical Mobility relate to pain on movement an range in motion ecrease

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

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 releasing chemical me iators an triggering macrophages to estroy the antigen. A type IV response typically occurs hours to exposure. ays after

HIV/AI S

HI TRANSMISSION
During unprotecte sex Bloo transfusion Sharing nee les Fro other to chil

PATHOPHYSIOLOGY

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

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 singlestran e messenger DNA (mRNA), which uil s new viruses

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

PATHOPHYSIOLOGY

HIV replication involves estruction of CD4 T cell

Gra ual in CD4 cell count

PATHOPHYSIOLOGY
STAGES OF HI DISEASE

HI Asymptomatic (CDC Category A: > 500 CD4 T cell)

HI Symptomatic (CDC Category B: 200 499 CD4 T cell)

AIDS (CDC Category C: < 200 CD4 T cell)

CLI ICAL MA IFESTATI

The symptoms of HIV an AIDS vary, epen ing on the phase of infection. WITHIN THE FIRST FEW WEEKS 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

CLI ICAL MA IFESTATI

YEARS LATER

You may remain symptom-free for years. But as the virus continues to 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

CLI ICAL MA IFESTATI

PROGRESSION TO AIDS

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 to opportunistic 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 mouth Headaches Persistent, unexplained fatigue Blurred and distorted vision Weight loss Skin rashes or umps