Term
| How is type I hypersensitivity (immediate hypersensitivity) enacted? |
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Definition
| Th2 cells activated by antigen which induces B cells to switch to IgE, production of IgE and binding of secreted IgE to mast cell FceR, undergoes activation, degranulation, and tissue damage by mast cells upon secondary exposure to antigen |
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Term
| Th2 differentiation requires what factores? |
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Definition
| Protein antigen and the presence of IL-4 |
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Term
| How do mast cells develop? |
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Definition
| Produced in the bone marrow and released as immature cells that mature in the tissues |
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Term
| What causes the release of granules in type I hypersensitivity? |
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Definition
| Crosslinking/antigen binding of FceR and IgE |
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Term
| What occurs in mast cells that have just released exocytic vesicles upon activation? |
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Definition
| Same compounds are synthesized again as well as a new compound each for immediate release |
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Term
| What causes the "wheal and flare" immediate response? |
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Definition
| Histamine release is the primary toxic mediator initially released by mast cells |
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Term
| What is synthesized after the initial activation and release of vesicles in mast cells during type I hypersensitivity? |
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Definition
| Cytokines (IL-4, IL-3, IL-5, TNF-alpja_ lipid mediators (leukotriens) and chemokines |
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Term
| What is the effect of leukotriens in the late phase of type I hypersensitivity? |
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Definition
| Similar effects as immediate response but larger in magnitude |
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Term
| When are eosinophils expressed in type I hypersensitivity? |
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Definition
| Acts as a cell mediator in limited numbers expressed after the FceRI activation, can do more damage to self than mast cell immediate secretions |
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Term
| What is the function of basophils in type I hypersensitivity? |
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Definition
| Similar to mast cells, recruited to mucosal tissues, secretes histamines (less than mast cells), can do toxic damage |
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Term
| Histamine causes what response through H-1 and H-2 receptors? |
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Definition
| Arteriolar vasodilation, venous constriction in some vascular beds, increased capillary permeability, causes tissue edema, stimulation of gastric secretions, contraction of smooth muscle (except in blood vessels), cardiac stimulation, increased vascular permeability |
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Term
| What are some examples of classic type I reactions? |
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Definition
| Allergic asthma, allergic rhinitis (hay fever), food allergies, insect sting alergies |
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Term
| What causes systemic anaphylaxis? |
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Definition
| Extreme case of type I hypersensitivity caused by allergen being introduced into the blood stream and disseminating throughout the body, mast cells throughout the body respond with degranulation |
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Term
| What is the emergent treatment (within 20 minutes) to systemic anaphylaxis? |
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Definition
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Term
| How can you diagnose type I reactions? |
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Definition
| Serum IgE levels, skin prick testing for specific IgE responses, periodicity of symptoms |
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Term
| What causes type II hypersensitivity? |
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Definition
| IgM or IgG is generated against "self" cell surface or ECM protein antigens, is antibody mediated |
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Term
| What are the primary targets for damage in type II hypersensitivity? |
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Definition
| Erythrocytes and platelets, antibody and complement can lead to cell destruction alone or with the aid of phagocytes |
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Term
| What can induce type II hypersensitivity? |
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Definition
| Drug-induced anemia or thrombocytopenia most commonly via penicillin, quinidine, or methyldopa |
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Term
| How does type III hypersensitivity occur? |
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Definition
| Antibody is generated against soluble antigen, antigen-IgG complexes are insufficient to fix complement and clear antigen, incomplete complexes sediment in vessels/tubules and collectively activates inflammation |
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Term
| What is necessary to fix complement and clear antigens in a type III hypersensitivity reaction? |
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Definition
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Term
| What are some classic type III hypersensitivity reactions? |
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Definition
| Arthus reaction and serum sickness |
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Term
| What are the symptoms involved in type III hypersensitivity? |
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Definition
| Variable but mainly involves arthritis, nephritis, and vasculitis |
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Term
| How does type IV hypersensitivity occur? |
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Definition
| T cell activation by APCs, production of cytokines which results in inflammation with direct or indirect damage to tissues |
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Term
| What is involved in delayed type IV hypersensitivity? |
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Definition
| Predominantly involves Th1 cells (an macrophage activation), can also involve Th2, uses secondary mediators IFN-gamma, TNF-alpha, and IL-4 (with Th2 involvement) |
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Term
| A TB skin test is an example of what kind of hypersensitivity? |
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Definition
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Term
| What is the process of initiating a type IV hypersensitivity response? |
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Definition
| Antigen introduced in subcutatneous tissue, processed by antigen-presenting cells, Th1 effector cell recognizes antigen and releases cytokines that act on vascular endothelium via recruited T cells, phagocytes, fluid, and proteins |
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Term
| What are some examples of contact type IV hypersensitivity? |
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Definition
| Poison ivy, metal allergies, etc. |
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Term
| Type I diabetes is associated with what type of hypersensitivity response? |
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Definition
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Term
| Penicillin can cause what type of hypersensitivity response? |
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Definition
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Term
| Which hypersensitivity reaction is likely to be organ specific? Which is not? |
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Definition
| Type IV is organ specific, Type III is not |
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