The document summarizes different types of hypersensitivity and allergic reactions. It describes Type I reactions as rapid hypersensitivity reactions mediated by IgE antibodies, including seasonal allergies, food allergies, and anaphylaxis. Type II reactions are cytotoxic and involve autoantibodies against self cells. Type III reactions occur when immune complexes form in blood vessels and cause tissue damage. Type IV reactions are delayed hypersensitivity responses mediated by T cells without antibodies or complement involvement, like contact dermatitis. Type V reactions involve inappropriate stimulation of cell receptors by autoantibodies. The document also discusses specific conditions like latex allergy, allergic rhinitis, Sjogren's syndrome, and Goodpasture's syndrome

1. Peggy D. Johndrow 2009

2. Hypersensitivities/Allergies Increased or excessive response to presence of antigen to which client has been exposed Degree of reaction ranging from uncomfortable to life threatening Terms hypersensitivity and allergy used interchangeably

3. Type I: Rapid Hypersensitivity Reactions Also called atopic allergy: most common type of hypersensitivity Some reactions occur only in areas exposed to antigen Allergens contacted: Inhaled (plant pollens, fungal spores, animal dander, house dust, grass, ragweed) Ingested (foods, food additives, drugs) Injected (bee venom, drugs, biologic substances) Contacted (pollens, foods, environmental proteins) Related to increased production of IgE Examples: h ay fever, allergic rhinitis, allergic asthma, anaphylaxis, & allergies to certain foods &/or medications Anaphylaxis : severe reaction, involve all blood vessels and bronchiolar smooth muscle, causing widespread blood vessel dilation, decreased cardiac output, and bronchoconstriction IW Table 22-1 p 388

4. Allergic Rhinitis Triggered by reaction to airborne allergens Seasonal: coincides with timing of environmental exposure (i.e. spring) & lasts a short time Chronic: occurs intermittently without seasonal pattern or continuously when exposed to certain allergens Pathophysiology: initial exposure body responds by making antigen specific IgE which bind to surface of basophils & mast cells Repeat exposure to allergen results in two phase response Primary: allergen binds to IgE molecules; cell degranulates, histamine released resulting in capillary leak, mucous secretion, pruritis, & erythema Secondary: additional proteins released, increased WBC’s; more generalized reaction occurs

5. Assessment History: onset & duration symptoms: family history Clinical Manifestations: rhinorrhea, itchy/watery eyes, H/A, swollen nasal mucosa, post nasal drip, dry/scratchy throat & pharyngitis Diagnostic studies CBC: increased eosinophil count (1-2%) IgE indicates tendency to have allergic responses (>100 IU/mL) RAST: determines specific allergies by determining blood level of IgE against certain allergen Skin testing Immediate hypersensitivity reaction occurs in 15 min’ positive = redness & wheal Instruct client to stop systemic glucocorticoids & antihistamines 5 days prior to procedure Emergency equipment available Intradermal testing Performed if a specific allergen did not produce a reaction Oral food challenge Used to identify specific allergens when skin testing or food diary fails IW Table 22-2 p 391

6. Latex Allergy Allergic reaction to a protein found in processed natural latex Signs and symptoms vary in range (immediate to delayed) Increased risk for allergy seen with high exposure to latex, spina bifida, allergy to bananas or avocados Management Ask all clients about use & known reaction to latex, or specific food allergies Utilize latex free products in care of client

7. Management History Physical assessment/clinical manifestations Laboratory assessment Allergy testing including skin testing, scratch testing, intradermal testing, oral food challenge Avoidance therapy, symptomatic therapy, pharmacotherapy IW Chart 22-1 p 390

8. Pharmacotherapy Decongestant: cause vasoconstriction of inflamed tissue Examples: Neo-synepherine, Afrin Antihistamines: block histamine from binding to receptor site, prevents vasodilatation & capillary leak Examples: Benadryl, Chlor-trimeton, Zrytec, Clarinex, Allegra Corticosteroids: decrease inflammation & immune response Examples: Prednisone, Delta-cortef, Beconase, Flonase Mast cell stabilizers: prevent mast cell membrane from opening when allergen binds to IgE Example: Nasacrom Leukotriene antagonics: blocks leukotriene receptor & prevents synthesis Examples: Accolate, Zyflo, Singulair Complementary and alternative therapy (IW Chart 22-3 p 393)

9. Avoidance and Desensitization Therapy Avoidance therapy Instruct client to avoid direct or close contact w/ known allergens Desensitization therapy Used when identified allergens can't be easily avoided Decrease allergic response by competition

10. Anaphylaxis Systemic reaction; occurs rapidly after exposure (in seconds) Initial feelings of uneasiness, apprehension, weakness & impending doom Pruritus & urticaria Erythema and sometimes angioedema eyes, lips, tongue Histamine causes capillary leak bronchoconstriction, mucosal edema & excess mucus secretion Congestion, rhinorrhea, dyspnea & increasing respiratory distress with audible wheezing result Potentially fatal IW Chart 22-2 p 392

11. Cascade Itching, urticaria  angioedema  dyspnea, increased salivation, audible wheezing  laryngeal edema, stridor, hypoxia  hypotension, dysrhythmias, shock  cardiopulmonary arrest

12. Interventions Initially assess respiratory function; must always establish and maintain an airway Prepare for emergency intubation or tracheostomy Oxygen reduces hypoxemia: O2 via NC 2 2-6L/min to maintain SAO2 >90% Pharmacotherapy: (IW Chart 22-3 p 393) Epinephrine (1:1000) .03-0.5 mL SQ; with initial symptoms Antihistamines (25-100mg) IM, IV or PO; treat angioedema & urticaria Theophylline (6mg/kg) IV over 20-30 min: bronchodilator Inhaled beta-adrenergic agonist via small volume (high flow) nebulizer Q2-4 hrs; bronchodilator Corticosteroids; decrease inflammation Dopamine, Levophed; increase B/P May require CPR

13. Type II: Cytotoxic Reactions Body makes special autoantibodies directed against self cells that have some form of foreign protein attached Clinical examples include hemolytic anemias, thrombocytopenic purpura, hemolytic transfusion reactions, Goodpasture’s syndrome, and drug-induced hemolytic anemia Management D/C medication or blood product Hemolytic crisis or renal failure can occur Treatment usually symptomatic May require plasmapheresis

14. Type III: Immune Complex Reactions Excess antigens cause immune complexes to form in blood; these circulating complexes usually lodge in small blood vessels Usual sites include kidneys, skin, joints & small blood vessels Lodge in the small vessel walls, trigger inflammation & cause tissue or vessel damage Deposited complexes trigger inflammation, resulting in tissue or vessel damage Examples: rheumatoid arthritis, systemic lupus erythematosus & serum sickness IW Table 22-3 & Women Health p 396

15. Type IV: Delayed Hypersensitivity Reactions Reactive cell T-lymphocyte (T-cell) Antibodies & complement not involved Local collection of lymphocytes & macrophages causes edema, induration, ischemia & tissue damage at site within hours to days after exposure Examples: Tb test (positive purified protein derivative), contact dermatitis, poison ivy skin rashes, insect stings, tissue transplant rejection & sarcoidosis

16. Management Intervention Identification and removal of allergen Client preparation Procedure Follow-up care Reaction self-limiting & treated symptomatically

17. Type V: Stimulatory Reactions Inappropriate stimulation of a normal cell surface receptor by an autoantibody, resulting in a continuous “turned-on” state for the cell Example: Graves’ disease, form of hyperthyroidism IW Table 22-3 p 396 Management One organ: removal of enough tissue to return function to normal Widespread involvement: decrease autoantibody production with immunosupression

18. Sjögren’s Syndrome Group of problems often appear with other autoimmune disorders Dry eyes, dry mucous membranes of nose/mouth (xerostomia) & vaginal dryness Insufficient tears causing inflammation & ulceration of cornea Treatment: immunomodulation & symptomatic therapy

19. Goodpasture’s Syndrome Autoimmune disorder in which autoantibodies made against glomerular basement membrane & neutrophils Lungs and kidneys Shortness of breath, hemoptysis, decreased urine output, weight gain, edema, hypertension & tachycardia Treatment: high-dose corticosteroids

20. Therapies Pharmacotherapy: Rheumatrex (methotrexate) Cytoxan (cyclophosphamide) Corticosteroids Sandimmune (cyclosporine) Plaquenil (hydroxchloroquine) Symptomatic Artificial tears, saliva Lubricants Pain control Renal support: hemodialysis, peritoneal dialysis Other Plasmapheresis (filter plasma, remove proteins)