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Two patterns of Type I
Atopic - familial in multiple generations
-Asthma, allergic rhinitis, atopic dermatitis
Non-atopic - occur randomly in pop
-Anaphylaxis, allergic urticaria (hives)
Diagnosis of Type I
-Skin testing w/small amts of allergen -> wheal and flare
-In vitro RAST testing detects IgE antibody
Therapy for type I
-Anti-mediator drugs (antiHS, leukotriene antagonists)
-Anti-inflam drugs (glucocorticoids)
-Immunomodulatory therapy (alergen immunotherapy)
-Cytotoxic rxns and cycolytic rxns
-Antibody (IgG or (gM) reacts w/cellular or matrix antigen
-May be autoantibodies or antibody against foreign antigen
-Antibodies produce cellular damage and tissue dysfxn
Actions against cellular antigens in Type II rxns
-Rh or ABO d/e of newborn
-Panicillin induced hemolytic anemia
-Autoimmune hemolytic anemia or ITP
Actions against tissue antigens or b.mem prot.s in Type II rxns
-Pemphigus vulgaris against epi intercellular jxns
-TSH-R in Grave's d/e leading to hyperthy
-Ach Rs in myasthenia gravis
Diagnosis of Type II
-In vitro: Coombs test for Rh or ABO sensitization, thyroid stimulating Ig in Grave's
-Immunofluorescent or immunohistochemical staining of biopsies
Therapy for Type II
-Avoid inciting antigen i.e. penicillin
-Anti-inflam/im.suppressive therapy, plasmapheresis
Type III Diagnosis
-In vitro assays for immune complexes
-Measurement of complement levels
-Im.fluorescent or im.histochemical staining of tiss biopsies
-Delayed type hypersensitivity ind of antibody fxn
-Activated T cells elaborate TH1 CKs to attract/activate monocyte/mac.p.s and initiate other inflam pathways
Type IV diagnosis
-Clinical presentation of well known d/e (Type I dia, mellitus, poison ivy)
-Im.flurescent or im.histochemical staining for T cells, mac.p.s or CK producing cells
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