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25 Cards in this Set
- Front
- Back
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quick 1/2 words: the 4 types of hypersensitivity reactions
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1- immediate (IgE)
2- cytotoxic/ direct killing 3- immune-complex 4- delayed cell-mediated |
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what are the key features of type 2 hyper sensitivity reactions
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cytotoxic/ direct cell killing
AUTO-abs to surface antigens --> activate: - complement - phagocytosis |
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in type 2 hypersensitivity (cytotoxic), what antibodies do Bcells secrete against cell surface antigens
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IgM, IgG
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4 effects of complement (involved in type 2 hypersensitivity)
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solubilise immune complexes
opsonins ↑ vasc permeability & chemotactic lysis (Membrane attack complex- MAC) |
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what are anaphylotoxins
released by what |
fragments of complement which ↑vasc permeability
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three types of opsonins
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ab's
acute phase proteins complement |
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what causes complement activation in type 2 cytotoxic hypersensitivity
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auto-ab : surface antigen binding (RBC/ platelet)
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examples of types 2 cytotoxic hypersensitivity (auto-ab's to RBC/ platelets)
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transfusion reactions
autoimmune haemolytic anaemia Goodpasture's syndrome (ab's to golmerular basement membrane) Myasthenia gravis Guillan Barre syndrome Grave's disease |
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2 types management for type 2 cytotoxic hypersensitivity
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immunosuppression
Plasmapheresis (remove pathogenic ab) |
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key features of type 3 hypersensitivity reactions
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immune-complex mediated
ab's to foreign bug BOUND to innate (human) cell deposit complexes in vessels/ tissues activate COMPLEMENT...INFLAMMATION (neutrophils) |
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autoimmune reactions to RBCs/ platelets show what type off hypersensitivity reaction
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type 2 cytotoxic/ direct killing
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which hypersensitivity reaction shows inflammation (influx of neutrophils) and complement activation
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type 3 immune complex mediated
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examples of type 3 immune-complex mediated hypersensitivity
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hypersensitivity pneumonitis (e.g Farmer's lung)
glomerulnephritis vasculitis RA SLE |
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which cells characterise type 3 hypersensitivity
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immune complexes
complement NEUTROPHILS (inflammation where complexes deposit) |
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most important drug in management of type 3 immune-complex mediated hypersensitivity
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CORTICOSTEROIDS (anti-inflam)
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3 main actions of CORTICOSTEROIDS
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anti-inflam
metabolic immunosuppressive |
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what protein does corticosteroid activate to reduce the synthesis of leukotrienes
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ANNEXIN-1
→ inhibits phospholipase A2 → ↓arachidonic acid → ↓prostaglandins, PAF, leukotrienes, chemotaxins |
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what drug inhibits: cytokine expression,T-cell prolif, ab's
and reduces lymphocytes |
corticosteroids
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key features of type 4 hypersensitivity
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DELAYED Tcell-mediated:
sensitise T cells → cytokines → macrophages/ CD8 → direct cell damage Persistent INFLAMMATION! |
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which hypersensitivity reaction shows infiltration of activated T-cells and persistent inflammation
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type 4 delayed T-cell mediated hypersensitivity
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in type 4 delayed T-cell mediated hypersensitivity, collection of macrophages and lymphocytes leads to what
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persistent inflammation
GRANULOMA |
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autoimmune & non-autoimmune conditions associated with type 4 delayed T-cell mediated hypersensitivity
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type 1 DM, psoriasis
nickel hypersensitivity (contact dermatitis), TB, leprosy, SARCOIDOSIS, GRAFT rejection |
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what type of hypersensitivity is sarcoidosis (,multi-system non-caseating granulomatous disease)
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type 4 delayed T-cell mediated hypersensitivity
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what's a granuloma
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organised collection of ACTIVATED lymphocytes & macrophages
non-specific inflam response triggered by DIVERSE range antigens (foreign or innate) fail to remove stimulus = persistent prod activated cytokines & lymphocytes |
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management of type 4 hypersensitivity (delayed T-cell mediated)
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wait
NSAIDs- acute onset corticosteroids- systemic |
