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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

Insulin. Scans or angiograms . eggs. diptheria & snake venom antitoxin Treatment measures  Blood products (whole blood & components).allergic extracts . strawberries. fish. shellfish. milk.Type I: Allergens  Drugs  PCN. ants  Foods  Nuts. rabies. Chemo agents. ASA. yellow jackets. iodine –contrast media for IVP. Sulfa. bumblebees. food additives   Animal sera  Tetanus. NSAIDS  Insect venoms  WASPS. wheat. soybeans. Hornets. Local anesthetics. Tetracyclines. peanuts. chocolate. Cephalosporins.

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 .Type I   Clinical manifestations: Anaphylactic rxn Wheal & flare reaction: Localized mediator response  Characterized by “pale wheal containing edematous fld.

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

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

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Systemic Anaphylaxis .

3-0.V. if present)  Establish I. insect stinger.e. Repeat q5-15 minutes  Nebulizer tx: albuterol (Proventil)  Antihistamine: diphenhydramine (Benadryl) IM or IV  Steroids: methylprednisolone (Solumedrol) . access  EPINEPHRINE 1:1000 OF 0.5 mL) IM midanterior lateral thigh.01 Ml/KG(0.Anaphylaxis: Therapeutic Mgmt: Emergency  INITIAL:  Ensure/maintain patent AIRWAY  High-flow O2 via non-rebreather mask  Remove causative agent (i.

dopamine (Intropin) . 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. volume expanders.Anaphylaxis: Therapeutic Mgmt: Emergency  Hypotension  ONGOING Monitoring VS.e. vasopressors: i.1 mL/kg IV q2-5 minutes Maintain BP w/fluids. respiratory effort.

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

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

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

GI tract. feet.Angioedema    Localized cutaneous lesions involving deeper layers of skin & submucosa Principal areas of involvement: eyelids. abdominal pain if in GI tract . genitals Manifestation:    Swelling: starting in face. hands. tongue. outer skin may be normal or have reddish hue Lesions may burn or itch. larynx. lips. progressing to airways & other body areas No welts.

PLTs. Rh factor & drugs Disorders: ABO incompatibility transfusion rxn. Rh incompatibility transfusion rx. thrombocytopenia. autoimmune and drug related hemolytic anemia. erythroblastosis fetalis (hemolytic disease of newborn. WBC Antigens involved: ABO blood group.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. leukopenia. 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. resulting in pulmonary hemorrhage and glomerulonephritis . Deposits of IgG from complement activation.

acute glomerulonephritis  Serum sickness . blood vessels and lungs Example of type III  Rheumatoid arthritis & Systemic Lupus Erythematosus (SLE). skin.    Lead to activation of serum factors causing inflammation and lead to activation of complement cascade Common sites for deposit: kidneys.Type III: Immune Complex Reactions  Formation of antibody-antigen complexes (binding of antibody & antigen together)  Antibodies mostly being IgG and IgM. joints.

fungal and viral infections. transplant rejections .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.

poison sumac. . poison oak. cosmetics & some dyes.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.

burning or stinging Chronic contact dermatitis: lesions become thick. covered w/papules. Pruritis. scaly and lichenified Main difference b/w contact dermatitis and atopic dermatitis:   CD: localized and restricted to area exposed to allergens. edematous. vesicles and bullae.Contact Dermatitis  Acute dermatitis     Skin lesions: erythematous. 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 .

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

mucous membranes. redness. flushing. inhalation. pruritis. blood  Manifestations    .Types of Latex Allergies  Type I allergic reaction   Response to natural rubber latex proteins Occurs within minutes of contact w/proteins Rash. conjunctivitis Asthma due to full blown anaphylactic shock Systemic reactions from exposure to latex proteins via various routes: skin. rhinitis. urticaria.

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 .

asthma.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. 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 .

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. bronchial secretions tested for eosinophils PFTS: if asthma suspected . nasal.Diagnostic Studies       CBC w/diff.

Skin Test   Used to identify specific allergens that are causing allergic symptoms 3 different methods    Scratch or prick test Intradermal test Patch test .

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  Results      Positive reactions: hypersensitive to test within minutes after insertion in the skin and may last for 8-12 hours.

EPI injection may be necessary .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.

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

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 .

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

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. .

 High risk for INFECTION .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.

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 .

Neoral. Gengraf] Tacrolimus [Prograf] Cyclophosphamide [Cytoxan] Azathiopine [Imuran] Sirolimus [Rapamune]  Cytotoxic    .Immunosuppressive therapy   Corticosteroids-prednisone. methylprednisolone [Solumedrol] Calcineurin inhibitors   Cyclosporine [Sandimmune.

Immunosuppressive therapy   Monoclonal antibodies Polyclonal antibody .

neurotoxic: tremors. liver toxicity.Immunosuppressive therapy   Calcineurin inhibitors Cyclosporine [Sandimunne]. seizures. IV A/E: Nephrotoxicity. leukopenia. gingival hyperplasia . increase risk for infection. HTN. tacrolimus [Prograf}   PO. hirsutism. lymphoma.

Immunosuppressive therapy   Cytotoxic Cyclophosphamide [Cytoxan]   HEMORRHAGIC CYSTITIS. thrombocytopenia. diarrhea. althralgia. neutropenia High cholesterol. NEUTROPENIA Nsg: FORCE FLUIDS Bone marrow suppression. Increases incidence of malignancies  Azathiopine [Imuran]   Sirolimus [Rapamune]: renal transplant pts  . Not used in liver or lung. leuko/thrombopenia. anemia. anemia.

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 .

Host or recipient rejects tissue Onset: 7 to 30 days post transplant Target organs: skin. Radiation. 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. liver. .Graft versus host disease         Immunoincompetent patient is transfused with immunocompetent cells.