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15 Cards in this Set
- Front
- Back
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Characteristics of Type I hypersensitivity
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Initiated by IgE against soluble allergens, combat parasites, rxn in a few seconds to minutes by mast cell activation
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Characteristics of Type II hypersensitivity
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IgG/IgM binding on cell membranes presenting exogenous antigens, combat cell pathogens via complement recruitment and phagocytosis, take minutes to hours
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Characteristics of Type III hypersensitivity
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Aggregations of Ab-Ag complexes, that in turn recruit complement and phagocytes in an attempt to remove those complexes, but are trapped by lysosomal enzymes and O radicals, takes hours to days
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Characteristics of Type IV hypersensitivity
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T cell mediated (TH1 usually, TH2 in chronic asthma, CD8 recruited by active macrophages) , attack intracellular pathogens, often takes days
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Physiological results of Type I hypersensitivity rxn
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Vascular dilation -> edema
Smooth muscle contraction Mucus production Inflammation |
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The three stages of Type I rxns
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Sensitization: (TH2 presents to B cell)
Immediate response: (B cells activate mast cells) Late response: (physiological results: edema, smooth muscle, mucus, inflammation) |
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Physiological results of Type II hypersensitivity rxn
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Cell lysis
Inflammation |
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Physiological results of Type III hypersensitivity rxn
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Inflammation leading to necrosis and fibrosis
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Physiological results of Type IV hypersensitivity rxn
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Cell infiltration -> edema
Cell destruction Granuloma formation |
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Wheal and Flare
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Sequelae of Type I:
Wheal: redness/edema from vasodilation from mast cells Flare: later dilated redness: eosinophil recruitment |
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Atopy
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Genetic predisposition to Type I hypersensitivity rxns - increased affinity of Class II molecules for allergen peptides. The manifestation is any one of several allergic responses not in the initial inoculation site
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Characteristics of anaphylactic shock
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Vascular leakage -> edema
Swelling (airway) Hypotension Hypoxia Rapid Pulse Loss of consciousness |
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ABO incompatibility
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Type II -- Ex: O or B patient has A-presenting blood cells in plasma (baby different from mother, or transfusion). Agglutination of foreign A cells results with antibodies, complement is activated = tissue damage
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Penicillin reactivity rxn
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Type II (remember, Type II is from exogenous source): Penicillin fights both bacterial transpeptidase AND complexes with patient's RBCs to form neotopes that look, to the body, like the "wrong" blood cell. Agglutination, complement, inflammation result
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Serum sickness
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Foreign blood is introduced (blood-borne antigen) to human body, the body makes antibodies to it, they aggregate in complexes. Symptoms are: fever, nephritis, arthritis, vasculitis
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