Microbiology – Hypersensitivity – Flashcards
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| hypersensitivity definition ATOPIC |
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| = to allergy = exaggerated immune responses/reactivity 1. it exceeds healthy limits of intensity and/or 2. it is directed at tissues that are sensitive to the products of such responsiveness/reactivity highly allergic patients termed (blank) |
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| allergen allergic |
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| harmless antigen stimulates (blank) responses in atopic individual particularly used in reference to antigens responsible for IgE associated allergy |
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| sensitization vs. elicitation sensitization elicitization |
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| hypersensitivity diseases require initial (blank) to then be (blanked) against (blank) phase may be completed before antigen is cleared from the body - (blank) can then happen during initial allergen exposure, but usually happens after second exposure to allergen |
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| immune response vs. immune reaction immune response |
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| sensitization can be required to involve an (blank) (blank) in hypersensitivity diseases these initial (blank) (blank)s could produce potentially harmful soluble or cellular factors (blank) (blank)s happen when these responses CAUSE damage to host tissues - it is the effect of above time frame between immune response and immune reaction (pathology) may vary |
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| list types of hypersensitivity |
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| Type I - immediate hypersensitivity (IgE antibody) Type II -cytotoxic antibody (target cell-specific IgG) Type III - immune complex disease (IgG binds antigen big time and causes insoluble antibody-antigen complexes to form) Type IV - Delayed-type (effector T cells/macs attack antigen-coated host cells) |
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| Type I (Immediate) Hypersensitivity |
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| sensitization - TRANSMUCOSAL exposure, IgE antibody production; IgE bound to Fc-epsilon-R on mast cells/basophils elicitation (minutes) - second allergen exposure; allergen binds IgE "fixed" to mast cell; crosslinking and degranulation; release of pharmacologically active factors |
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| Type I hypersensitivity - sensitization |
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| [image] |
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| type I hypersensitivity - elicitation |
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| [image] |
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| allergic rhinitis |
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| minor localized irritations happens in nasopharynx and upper airway in type I hypersensitivity |
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| allergic asthma |
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| serious localized allergic reaction happens in submucosa of lower airways in type I hypersensitivity |
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| anaphylactic shock |
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| life-threatening SYSTEMIC circulatory collapse |
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| degranulation |
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| mast cells, when stimulated in type I hypersensitivity (remember, IgE hooked on to mast cells via Fc-epsilonRI and bind antigen) in this process, granules that are let out of mast cells and basophils contain anyanplyotoxins that increase vascular permeability, increased blood flow, decreased blood pressure, increased mucous secretions and smooth m contraction bridging of IgE molecules and mast cell causes influx of calcium into mast cell that results in DECREASED CYLCIC AMP this causes destabilization of membrane influx of calcium also results in MEMBRANE LIPID TURNOVER yielding via ARACHIDONIC ACID, LUEKOTRIENES and PROSTAGLANDINS |
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| examples of products released by degranulation |
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| histamine (^ vas perm and local blood flow) leukotrienes and prostaglandins (sm m. contraction and ^ vas perm) chemokines (attract leukocytes) enzymes (break down tissue matrix proteins) cytokines (promote inflammatory activities, amp of TH2 responses, ^ growth of eosinophils) |
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| wheal-and-flare reactions urticaria (hives) Urticaria (hives) |
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| skin reaction in type I HS follows local intracutaneous exposure to allergen (such as insect bite) skin tests for antigen-specific IgE hypersensitivity mimic and measure this type of localized reaction in a related condition called (blank) - allergin is ingested, but then migrates to the skin |
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| treatments of type I HS (4) |
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| Avoidance Desensitization - small to large doses changes IgE-dominated responses to IgG that doesn't bind well to mast cells inhibition of mediator release - designed to either inhibit calcium or raise levels of cAMP inhibition of mediator effects - administer epinephrine (reverse effect of anaphylotoxins), inhalation of bronchodialators and antihistamines (H receptor antagonists)..... inflammation can be treated with corticosteroids |
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| common symptoms of type I HS |
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| allergic rhinitis allergic asthma (S.O.B.) venom reactions food allergies drug allergies urticaria (hives) anaphylactic shock |
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| describe sensitization of type II hypersensitivity |
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| antibodies made that are specific to EXTRINSIC (foreign) ANTIGENS or reactive with INTRINSIC ANTIGENS (produced by target tissue itself |
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| describe elicitation of type II HS |
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| time of onset varies symptoms caused by binding of antigen-reactive antibody (IgG usually) specifically to ANTIGEN-COATED HOST CELLS; followed by direct lysis due to complement activation and further aggravated by release of active by-products of complement cascade (anaphylatoxins C3a, C5a) FcR-bearing and CR-bearing leukocytes are also recruited to the area |
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| what distinguishes type II (cytotoxic antibody) from type III (immune complex) in the biopsy? |
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| type II will demonstrate SMOOTH layer of antibody/complement coating host tissue |
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| two examples of type II (cytotoxic antibody) HS |
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| Hemolytic Disease of the Newborn (HDN) - mom is Rh(neg) and fetus is Rh(pos); mom is sensitized after first Rh(pos) birth; next pregnancy, she elicits type II HS to Rh(pos) antigens in fetus (IgG antibodies can cross into placenta); causes SEVERE ANEMIA in fetus; RhoGam can be used to avoid these complications Goodpasture's Syndrome - antibodies produced that attack BASEMENT MEMBRANES of renal glomeruli and (in some cases) pulmonary alveoli; binding occurs specifically to alpha-3 chain of type IV collagen of BM |
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| goodpasture's syndrome... tell me about it |
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| type II (cytotoxic antibody) HS antibodies produced that attack BASEMENT MEMBRANES of renal glomeruli and (in some cases) pulmonary alveoli; binding occurs specifically to alpha-3 chain of type IV collagen of BM |
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| hemolytic disease of the newborn |
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| mom is Rh(neg) and fetus is Rh(pos); mom is sensitized after first Rh(pos) birth; next pregnancy, she elicits type II HS to Rh(pos) antigens in fetus (IgG antibodies can cross into placenta); causes SEVERE ANEMIA in fetus; RhoGam can be used to avoid these complications |
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| describe sensitization in type III HS (immune complex disease) |
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| initial antigen exposure = activation of antigen-specific B cells specific IgG antibodies reactive with antigen; antigen is soluble and freely circulating |
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| describe elicitation in type III HS (immune complex disease) |
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| no need for additional antigen exposures! this response is direct many molecules of antibody bind to many molecules of antigen forming multiple crosslinks to each other - eventually form LARGE INSOLUBLE ANTIBODY-ANTIGEN COMPLEXES normally, phagocytes eat up these immune complexes, but this reaction builds up so fast that they can't keep up deposition of the complexes can occur in/on filtering organs such as kidneys or areas rich in capillary beds (lungs) |
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| what are symptoms of type III (immune complex disease) HS |
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| ** symptoms caused by non-specific deposition of immune complexes serum sickness farmers lung syndrome rheumatoid arthritis systemic lupus erythematosus |
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| arthus reaction |
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| test of type III hypersensitivity inject antigen into skin; if it attracts circulating IgG (forms immune complexes) then this patient has type III HS to that antigen |
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| serum sickness |
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| happens when large quantities of foreign antigen are given to a patient to treat infects or intoxications (snake bite) |
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| describe sensitization process of type IV hypersensitivity (delayed-type) |
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| activate CD4+ TH1/TH17cells (not TH2s) 10-14 days antigen covalently attaches to host tissue membranes - effector activities then directed against host tissues CD8+ cells can also be activated if antigen is lipid soluble and crosses PM of host cells |
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| describe elicitation process of type IV hypersensitivity (delayed-type) |
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| type 4 HS (DTH) is exaggerated form of cell-mediated immunity symptoms caused by T cell derived cytokines (chemokines, IFN-gama, TNF-alpha, TNF-beta, IL-3/GM-CSF) nonspecific T cells significant EDEMA and INDURATION (hardness) |
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| what are the 3 different variants of DTH (delayed type hypersensitivity) |
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| contact hypersensitivity - langerhans' cell is APC to T cells in EPIDERMIS; 24-48 hrs; POISON IVY tuberculin hypersensitivty - intradermal reaction; macrophages present antigen to T cells; TB tests with purified protein derivative (PPD) of tubercule bacilli granulomatous hypersensitivity - 21-28 days; antigens within macrophage difficult to degrade; GRANULOMA FORMATION; make multi-nucleated giant cells (from T cell cuff around a core of macs); EPITHELIOD CELLS also present inside these cuffs; size/mass of granulomas keep growing |
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| contact hypersensitivity |
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| langerhans' cell is APC to T cells in EPIDERMIS; 24-48 hrs; POISON IVY |
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| tuberculin hypersensitivity |
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| intradermal reaction; macrophages present antigen to T cells; TB tests with purified protein derivative (PPD) of tubercule bacilli |
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| granulomatous hypersensitivity |
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| 21-28 days; antigens within macrophage difficult to degrade; GRANULOMA FORMATION - make multi-nucleated giant cells (from T cell cuff around a core of macs); EPITHELIOD CELLS also present inside these cuffs; size/mass of granulomas keep growing |
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| type II HS goodpasture's syndrome alpha-3 chain type IV collagen of basement membrane triggers complement cascade type II HS called CYTOTOXIC ANTIBODY hypersensitivity |
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| this is an example of type (blank) HS (blank) (blank) - antibodies produced that attack BASEMENT MEMBRANES of renal glomeruli and (in some cases) pulmonary alveoli antibody binding triggers (blank) cascade, resulting in cell death = reason why type (blank) HS is called (blank) (blank) hypersensitivity binding occurs specifically to (blank) chain of type (blank) collagen of (blank) |
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| type II HS goodpasture's syndrome alpha-3 chain type IV collagen of basement membrane triggers complement cascade type II HS called CYTOTOXIC ANTIBODY hypersensitivity |
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| this is an example of type (blank) HS (blank) (blank) - antibodies produced that attack BASEMENT MEMBRANES of renal glomeruli and (in some cases) pulmonary alveoli antibody binding triggers (blank) cascade, resulting in cell death = reason why type (blank) HS is called (blank) (blank) hypersensitivity binding occurs specifically to (blank) chain of type (blank) collagen of (blank) |
