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33 Cards in this Set
- Front
- Back
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passive immunization vs active |
PASSIVE -antibodies / antiserum -immediate but short lived protection ACTIVE -sensitized lymphocytes memory cells that can be turned in future (booster) *give at separate sites to allow antigen/toxoid to get to lymph nodes before passive Ab binds |
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passive immunization w/ heterologous antitoxin |
-risk of serious anaphylactic rxn -heterologous antiserum- stimulate production of Ab to foreign protein ---> serum sickness -before giving, check history passive immunizations bc if given before, host may have developed Ab against horse proteins |
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toxin |
-nonimmune response - death -takes more toxin to stimulate Ab production than to kill a person -IF SURVIVE from tetanus - no developed immunity |
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toxoid |
-toxins that are detoxified by moderate heat + treatment w/ chemical -intact antigenic (ability to bind Ab OR ability to induce Ab synthesis) + immunogenic (ability to induce Ab synthesis) properties |
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DPT |
-diptheria, pertussis, tetanus -primary immunization should be given to everyone |
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anamnestic response |
-antigen Ab rxn based off memory cells |
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in patient who have been active immunized |
-and have risk - don't need to give passive (expensive) + just active... (to activate memory cells) |
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give passive immunization |
-only if no previous active immunizations -if have active immunizations - then just give booster or none if recent boosters (within 5 years) |
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erythroblastosis fetalis |
-extravascular hemolysis due to uptake by phagocytic cells mediated by Fc receptors - recognize RBC associated IgG antibodies |
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prozone phenomena |
-in agglutination tests, when dilution is too high and there is aggutination in more dilute sera, would expect agglutination at higher sera -BUT appears negative because so much Ab present that it coats all the antigenic sites on all the particles, no antigen sites available for bridging antibodies |
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what is a titer |
reciprocal of highest dilution resulting in positive rxn (highest dilution - most dilute 1:640 over 1:40) |
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immunodiffusion assay |
-use dilated value ex 1:2 (1500) and multiply by 2= 3000 since logarithmic scale for square diameter vs IgG concentration -larger ring diameter, more % IgG |
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immunofixation electrophoresis |
-serum/urine proteins separated by electrophoresis (check conc of album+chains) -same serum applied to gel, sep by electrophoresis -Ab against whole serum proteins layered on each lane + soluble proteins washed out -precipitated proteins stained to reveal patterns |
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why do you see lambda chains in urine of multiple myeloma |
-IgG too big for glomerlus, light chain can pass - called bence-jones proteins |
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when does polyclonal hypergammalglobulinemia occr |
-monoclonal - multiple myeloma -polyclonal - response to complex Ag -tetanus toxoid, malaria |
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3 causes of anemia |
-blood loss -blood destruction (direct Coombs) -decreased RBC formation |
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multiple myeloma can result in |
-anemia (dec hematrocrit)- plasma cells replace normal bone marrow and dec RBC production -increased susceptibility to infection- lower levels of relevant Ab production -pathlogic fracture of L3- can destroy bone/ fractures + skulls |
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one way to check T cell activity |
-candidal antigen or PPD - checks cell mediated immunity |
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cytokines released by TH1 VS TH2 |
-th1 - IL-2 + those that activate macrophages - INF-gamma, TNF-alpha -th2 - cytokines that activate B cells - IL-4, IL-5, IL-10 *presence of polyclonal hypergammaglobulinemia consistent w/ high IL-4 levels |
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ways to measure cytokine exp |
-ELISA- can be used to measure cytokine exp using peripheral blood lymphocytes -RT-PCR - measure mRNA for cytokines |
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cd4+:cd8 |
2:1 |
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RAST assay |
-insolubilized allergen + radiolabeled anti-IgE -skin test measures in vivo activity of Ab - susceptible to additional factors like antihistamine therapy, blocking antibody concentrations, #/activity of mast cells *fairly good correlation b/w skin + RAST -if antihistamine/IgE melanoma-affect ALL skin tests |
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cromolyn sodium vs blocking antibody |
-stabilized mast cell membranes + reduces release of histamine -inhibits degranulation + too late in emergency -blocking antibody binds Ag, prevents from binding to IgE on mast cells |
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asthma vs allergic rhinitis |
-asthma - lower resp tract -allergic rhinitis - upper resp tract |
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IL-4 in allergies |
-cytokine primary determinant of vigorous IgE response to allergen -responsible for switch from IgM to IgE |
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wheal + flare |
-wheal occurs 1-15 mins after injection -multivalent antigen required to fire off mast cell -hapten is univalent |
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previous insect sting + allergy |
-previous causes Th2 --> IL-4 --> IgE -allergen binds to IgE - mast cell degranulation -histamine, PAF, chemotactic factors --> bronchoconstriction, hypotension -later stages, leukotrines + PAF * can be worst next time |
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allergy shots |
-stimulate production of IgG antibody - binds to antigen before getting to IgE antibody on mast cells -change in Ab isotype - takes time -resp allergies - try to switch to IgA isotype (mucosal) |
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glucocorticoids for allergies |
-inhibit eosinophil degranulation + progression late phase of immediate hypersensitivity rxns (asthma) -down regulation of pro-inflam cytokines, reduced exp of CAMs on vessel wall, synthesis of phospholiase A2 downregulated, upregulate lipocortin-1 (anti-inflammatory, inhibit A2) |
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RAST ASSAY |
-allergen + sepharose beads (activated w/ CNBr to covalently link antigen) -add specific IgE (patient serum added) -beads are washed to remove unbound IgE + radiolabeled anti-IgE added + measured |
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univalent |
-two IgE close together must bind same antigen |
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chronic asthma treatment |
-glucocorticoids |
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desensitiztation for ragweed allergic rhinitis vs bee sting allergy |
--less effective for ragweed blocking Ab is less likely to bind allergen -beed venom travel via blood from site of sting to target tissue - resp tract - combine w/ IgG in blood -ragweed get mast cells in nasal submucosa w/ less exposure to IgG |
