Hypersensitivity

Descripción

Immunopathology Fichas sobre Hypersensitivity, creado por lumen7 el 07/05/2013.
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Fichas por lumen7, actualizado hace más de 1 año
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Creado por lumen7 hace más de 11 años
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Resumen del Recurso

Pregunta Respuesta
transfusion reactions= type II rare today. if transfusion done incorectly massive hemolysis
autoantigens= type II breakdown of tolerance of self, causes tissue damage, examples: goodpastures, myasthenia gravis
delayed hypersensitivy (delayed) 24 hours after contact, T cell mediated, chronic antigen results in granulomas, skin contact
production of granulomas T cells cannot kill off antigen so they "wall off" with cytokines
contact sensitivity (type IV) skin reactions, go away when irritant removed
tuberculin reaction= type IV tb under skin, processed and presented by DC, memory T cells produce cytokines, edema, swelling= +ve skin test
hypersensitivity heightened response to antigen with clinical symptoms
three factors leading to development of HS age, environment, genetics
type I immediate IgE mediated, allergies most common, mild-fatal, allergic rhinitis, asthma, increasing incidence from pollution and hygeine,
type I sensitisation phase Th2 cells secrete IL-4 for b cell growth and class switching to IgE
type I effector phase IgE antibodies produced following initial contact bind to receptors on mast cells, basophils and eosinophils. cross linking results in rapid degranulation causing inflamation
tx of allergy drugs inhibiting the production release or action of granules-diphenhydramine
type II sensitivity IgG and IgM mediated aka cytotoxic directed at celular antigens, damage via opsonisation lysis or ab dependent toxicity, rhesus incompatibility, transfusion reactions, auto antigens
rhesus incompatibility= type II rh- mothers carrying rh+ babies sensitise to rh+, subsequent pregnancies can trigger memory response and IgG passes throg placenta to kill fetal rbs (hemolytic disease)
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