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Immune System Alterations: Hypersensitivities

Chapter 14

Hypersensitivity Reactions

Hypersensitivity reactions

Overreaction of immune system against foreign antigens; or reaction against its own tissue leading to tissue damage Classified according to

source of antigen, time sequence (immediate or delayed) or basic immunologic mechanisms causing injury Body fails to recognize self-proteins and reacts against self-antigens

Autoimmune diseases

Allergic Reaction

Type I: IgE Mediated Reaction

ALLERGIC REACTIONS ANAPHYLACTIC reactions Occurs to susceptible people who are highly sensitized to specific allergen Antigen: exogenous pollen, food, dust, drugs Antibody produced: IgE: produced on 1st exposure to allergen & (bind to mast cells & basophils) Chemical mediators released

Histamine, mast cells, leukotrienes,prostaglandins

When released attack target tissue= allergic symptoms

Type I: Allergens

Drugs

PCN, Sulfa, Insulin, ASA, Tetracyclines, Local anesthetics, Chemo agents, Cephalosporins, NSAIDS

Insect venoms

WASPS, Hornets, yellow jackets, bumblebees, ants

Foods

Nuts, peanuts, eggs, milk, shellfish, fish, chocolate, strawberries, wheat, soybeans, food additives

Animal sera

Tetanus, rabies, diptheria & snake venom antitoxin

Treatment measures

Blood products (whole blood & components), iodine contrast media for IVP, Scans or angiograms .allergic extracts

Type I

Clinical manifestations: Anaphylactic rxn Wheal & flare reaction: Localized mediator response

Characterized by pale wheal containing edematous fld. surrounded by red flare from hyperema

Classic example: Mosquito bite Serves as diagnostic purpose as means of demonstrating allergic reactions to specific allergies during skin tests

Anaphylaxis

Overview

Sudden severe allergic rxn from massive histamine release from cells-Life threatening Common causes: foods: nuts, shellfish; drugs, latex, insect bites & stings Can lead to shock & or death if untreated Onset: within minutes to an hour; severe episode: more rapid onset

Anaphylaxis: Manifestations/Nsg Assessment

Initial: angioedema (face, lips, tongue & or neck), urticaria (hives) w/pruritis @ site of exposure Dyspnea, wheezing, respiratory obstruction Dysphagia Skin erythema, flushing Weak, rapid pulse, hypotension, dilated pupils Syncope, shock Circulatory shock; death (untreated)

Systemic Anaphylaxis

Anaphylaxis: Therapeutic Mgmt: Emergency

INITIAL: Ensure/maintain patent AIRWAY High-flow O2 via non-rebreather mask Remove causative agent (i.e. insect stinger, if present) Establish I.V. access EPINEPHRINE 1:1000 OF 0.01 Ml/KG(0.3-0.5 mL) IM midanterior lateral thigh, Repeat q5-15 minutes Nebulizer tx: albuterol (Proventil) Antihistamine: diphenhydramine (Benadryl) IM or IV Steroids: methylprednisolone (Solumedrol)

Anaphylaxis: Therapeutic Mgmt: Emergency

Hypotension

ONGOING Monitoring
VS, respiratory effort, cardiac rhythm O2 saturation LOC Anticipate intubation w/severe distress Anticipate cricothyrotomy or tracheostomy w/severe laryngeal spasm

Position: recumbent & elevate legs [modified Trendelenberg] EPINEPHRINE 1:1000 OF 0.1 mL/kg IV q2-5 minutes Maintain BP w/fluids, volume expanders, vasopressors: i.e. dopamine (Intropin)

Patient Teaching

Avoid future contact w/allergen Wear Medic-alert identification listing allergy Notify all caregivers Learn how to use Epinephrine auto-injector pens. Teach others how to use Epi pen.

Type I: Atopic Reactions

Inherited tendency to become sensitized to environmental allergens Atopic diseases


Allergic rhinitis Asthma Atopic dermatitis Urticaria angioedema

Atopic dermatitis

Eczema Chronic, inherited skin disorder Characterized by exacerbations & remissions Cause: several environmental allergens, often difficult to identify IgE: elevated; Skin test: + Skin lesions: generalized, vasodilation of blood vessels leading to interstitial edema w/vesicle formation

Urticaria

Hives Transient wheals :pink, raised, edematous,pruritic areas body Local vasodilation (erythema), wheal & flaring: due to histamine release Pruritis and lesions (WELTS): due to histamine

Angioedema

Localized cutaneous lesions involving deeper layers of skin & submucosa Principal areas of involvement: eyelids, lips, tongue, larynx, hands, feet, GI tract, genitals Manifestation:

Swelling: starting in face, progressing to airways & other body areas No welts; outer skin may be normal or have reddish hue Lesions may burn or itch; abdominal pain if in GI tract

Type II:Cytotoxic & Cytotoxic Rxns


Involves activation of complement by antigen-antibody Involve direct binding of IgG or IgM antibodies to an antigen on cell surface Production of autoantibodies that destroy own cells or tissues Target cells destroyed: RBCs, PLTs, WBC Antigens involved: ABO blood group, Rh factor & drugs Disorders: ABO incompatibility transfusion rxn, Rh incompatibility transfusion rx, autoimmune and drug related hemolytic anemia, leukopenia, thrombocytopenia, erythroblastosis fetalis (hemolytic disease of newborn, Good Pasture syndrome

Type II: Hemolytic Transfusion Reaction

Receiving ABO incompatible blood from a donor MISMATCHED BLOOD TRANSFUSION: Transfused with incompatible blood, antibodies immediately coat foreign RBC causing agglutination (clumping).

Type II: Good Pasture Syndrome


Anti-glomerular basement antibody disease Disorder involving lungs and kidneys Autoimmune reaction involving glomerular and alveolar basement membranes. Deposits of IgG from complement activation, resulting in pulmonary hemorrhage and glomerulonephritis

Type III: Immune Complex Reactions

Formation of antibody-antigen complexes (binding of antibody & antigen together)

Antibodies mostly being IgG and IgM.

Lead to activation of serum factors causing inflammation and lead to activation of complement cascade Common sites for deposit: kidneys, skin, joints, blood vessels and lungs Example of type III

Rheumatoid arthritis & Systemic Lupus Erythematosus (SLE), acute glomerulonephritis

Serum sickness

Type IV: Delayed Hypersensitivity Reactions

Cell-mediated response involving T lymphocytes Involve recognition and response of T lymphocytes to foreign substances Manifestations

Contact dermatitis Hypersensitivity reactions to bacterial, fungal and viral infections; transplant rejections

Contact Dermatitis

Allergic contact dermatitis Delayed hypersensitivity reaction involving the skin Eczematous lesions develop within 48 h Most common antigenic substances encountered:

Metal compounds (nickel containing),rubber compounds, catechols present in poison ivy, poison oak,poison sumac, cosmetics & some dyes.

Contact Dermatitis

Acute dermatitis

Skin lesions: erythematous, edematous, covered w/papules, vesicles and bullae. Pruritis, burning or stinging Chronic contact dermatitis: lesions become thick, scaly and lichenified Main difference b/w contact dermatitis and atopic dermatitis:

CD: localized and restricted to area exposed to allergens; Atopic: widespread

Latex Allergies

Allergy as a result of exposure to latex product More frequent & prolonged exposure, the greater the likelihood of developing allergy Latex proteins become aerosolized through powder on gloves and can result in serious reaction when inhaled by sensitized individuals

Recommendation: USE OF POWDER FREE GLOVES IN HEALTHCARE FACILITIES to avoid respiratory exposure to latex proteins

Latex Allergies:Who is at Risk?


Healthcare workers: HIGHEST RISK Food handlers Hairdressers Industrial workers Housekeepers

Types of Latex Allergies

Type IV contact dermatitis

Due to chemicals used in manufacturing process of gloves Delayed reaction: occurs within 6-48 hours

Manifestations:

Initially: dryness, pruritis, fissuring and cracking of skin followed by Redness & crusting at 24 to 48h Chronic exposure: lichenification, scaly, hyperpigmentation

Types of Latex Allergies

Type I allergic reaction


Response to natural rubber latex proteins Occurs within minutes of contact w/proteins Rash, pruritis, flushing, redness, urticaria, rhinitis, conjunctivitis Asthma due to full blown anaphylactic shock Systemic reactions from exposure to latex proteins via various routes: skin, mucous membranes, inhalation, blood

Manifestations

Latex Food Syndrome

Foods: may cause an allergic rxn in people who are allergic to latex due to proteins in rubber being similar to food proteins-Latex food syndrome Most common foods:

BANANA AVOCADO KIWI CHESTNUT WATER CHESTNUT GUAVA HAZELNUTS POTATOES PEACHES GRAPES APRICOTS

Nursing and Collaborative Management: Latex Allergies

Identification of patients and HCW at risk Thorough health hx Thorough allergy hx Greatest risk factor

Long term multiple exposures to latex products: HCW Patients w/multiple surgeries

Rubber industry workers

Additional: hx hay fever, asthma, allergies to certain foods

Nursing and Collaborative Management: Latex Allergies

Nursing and Collaborative Management: Latex Allergies

Latex protection protocols for latex + allergic patients or hx s/s related to latex exposure Latex-free products Teach patients to avoid certain foods Medic-alert bracelet Epi pen at all times

Assessment

Complete health and allergy hx Note past & present hx Note allergen and type of reaction to allergen Food allergy: maintain daily food dairy Screen for medication allergy Comprehensive head to toe exam

Diagnostic Studies

CBC w/diff, absolute lymphocyte count and esosinophil count Esosinophil count: elevated w/type involving IgE immunoglobulin Serum IgE: elevated w/type I: diagnostic indicator of atopic diseases Radioallergosobent test [RAST]: invitro test for IgE antibodies to specific allergens Sputum, nasal, bronchial secretions tested for eosinophils PFTS: if asthma suspected

Skin Test

Used to identify specific allergens that are causing allergic symptoms 3 different methods

Scratch or prick test Intradermal test Patch test

Skin Test

Results

Positive reactions: hypersensitive to test within minutes after insertion in the skin and may last for 8-12 hours. Positive reaction manifested: local wheal and flare response. Means person is sensitized to that allergen Precautions Highly sensitive person is always at risk for developing anaphylactic reaction to skin tests. NEVER LEAVE PT ALONE DURING TESTING PERIOD.

Skin Test

Precautions

Highly sensitive person is always at risk for anaphylactic reaction to skin test Never leave patient alone during testing period If skin testing contraindicated, use RAST test If severe reaction: remove extract immediately apply anti-inflammatory cream to site Intradermal testing: arm is used so that a tourniquet can be applied during a severe reaction. EPI injection may be necessary

Drug Therapy

Antihistamines Allergic rhinitis, urticaria Sympathomimetic/Decongestants EPINEPHRINE[ADRENALIN]: DOC FOR ANAPHYLAXIS IV/IM PO: Phenylephrine [Neo-synephrine]. Pseudoephedrine [Sudafed]: allergic rhinitis Corticosteroids:Nasal sprays: allergic rhinitis Antipruritics: topical agents Mast cell stabilizers: intal [Cromolyn] Leukotriene receptor antagonists:montelukast [Singular]

Autoimmune diseases

Grouped according to organ specific and systemic diseases. SLE: systemic lupus erythematosus Lyme disease Apheresis

Platepheresis: remove plts Leukocytapheresis: remove WBC Lymphocytapheresis: used to decrease high lymphocyte counts

Plasmapheresis

Transplant Rejection

Major problem following organ transplantation Will occur as a normal immune response to foreign tissue. Controlled by immunosuppressive therapy, ABO, HLA matching and ensuring that crossmatching is negative. Prevention, early diagnosis and tx of rejection are essential for long-term graft function

Hyperacute Rejection

Antibody mediated humoral Occurs in minutes to hours after transplant Vessels are rapidly destroyed Occurs due to person having preexisting antibodies against transplanted tissue or organ. No treatment and transplanted organ must be removed Most susceptible organ is kidney.

Acute Rejection

Most common Manifested in first six months post transplant Mediated by recipients lymphocytes which have been activated against donated [foreign] tissue or organ PT will require LIFE LONG IMMUNOSUPPRESSIVE THERAPY.

High risk for INFECTION

Chronic Rejection

Occurs over months or years\ Irreversible Occurs for unknown reasons or from repeated episodes from acute rejection Transplanted organ is infiltrated with large numbers of T and B cells Chronic rejection results in fibrosis and scarring No definitive therapy Tx is supportive Transplant list for retransplant

Immunosuppressive therapy

Corticosteroids-prednisone, methylprednisolone [Solumedrol] Calcineurin inhibitors


Cyclosporine [Sandimmune,Neoral, Gengraf] Tacrolimus [Prograf] Cyclophosphamide [Cytoxan] Azathiopine [Imuran] Sirolimus [Rapamune]

Cytotoxic

Immunosuppressive therapy

Monoclonal antibodies Polyclonal antibody

Immunosuppressive therapy

Calcineurin inhibitors Cyclosporine [Sandimunne], tacrolimus [Prograf}


PO, IV A/E: Nephrotoxicity, increase risk for infection, neurotoxic: tremors, seizures, liver toxicity, lymphoma, HTN, hirsutism, leukopenia, gingival hyperplasia

Immunosuppressive therapy

Cytotoxic Cyclophosphamide [Cytoxan]


HEMORRHAGIC CYSTITIS, NEUTROPENIA Nsg: FORCE FLUIDS Bone marrow suppression, thrombocytopenia, anemia, neutropenia High cholesterol, leuko/thrombopenia, anemia, diarrhea, althralgia. Not used in liver or lung. Increases incidence of malignancies

Azathiopine [Imuran]

Sirolimus [Rapamune]: renal transplant pts

Immunosuppressive therapy

Mycophenolate mofetil [Cellcept] Lymphocyte specific inhibitor of purine synthesis with suppressive effects on both T and B lymphocytres Most effective when used in combo w/tacrolimus and cyclosporine Many GI toxicities making it a major limitation

Graft versus host disease

Immunoincompetent patient is transfused with immunocompetent cells. Host or recipient rejects tissue Onset: 7 to 30 days post transplant Target organs: skin, liver, GI tract Biggest problem: Infection Bacterial and fungal infections: predominate immediately after transplant when granulocytopenia exists Interstitial pneumonitis: primary concern later in disease Corticosteroids, immunosuppressive drugs used as preventive rather than tx measure. Radiation.

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