74956
| 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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