PATHOPHYSIOLOGY - MODULE 2 - EXAM 1 QUESTIONS WITH 100% CORRECT ANSWERS 2022/2023
PATHOPHYSIOLOGY - MODULE 2 - EXAM 1 QUESTIONS WITH 100% CORRECT ANSWERS 2022/2023 Answers highlighted Define hypersensitivity Altered immunologic response to an antigen that results in disease or damage to individual (strong genetic linkage) 2 alternate names for type 1 hypersensitivity Immediate hypersensitivity or IgE mediated reactions most common allergic reactions are type 1 Mechanisms of type 1 response 1. Sensitizing exposure 2. Re exposure (immediate response and longer term response) Sensitizing exposure (type 1 mechanism) - Helper 2 t cells help b lymphocytes differentiate into plasma cells which produce IgE - IgE's Fc portion (stem) binds to mast cells - When enough IgE is bound, person is sensitized to antigen Re exposure (type 1 mechanism) - 2 types Immediate response and longer term response Immediate response (re exposure) symptoms 5 mins - Antigen binds to IgE which is bound to mast cells - Mast cell release granule contents (degranulation), release histamine, which leads to inflammation Longer term response (re exposure) 8-12 hours after, lasts 24-36 hours - Mast cells generate leukotrienes/prostaglandins and platelet activating factor which lead to further inflammation. - Local/systemic effects occur (tears/mucus secretion) 3 actions of histamine 1. increases vascular permeability 2. causes vasodilation 3. contracts bronchial smooth muscle tissue What is type 2 hypersensitivity (name) Antibody dependent cytotoxic hypersensitivity Where are antigens located that react with antibodies in type 2 response Ab react to Ag fixed to surface of various body cells/specific tissues Mechanisms of type 2 response (3) 1. cell destruction 2. inflammation 3. altered cell metabolism Cell destruction (type 2 mechanism) Ab (IgG/IgM) bind to Ag on tissue cell surface and: - Cause phagocytosis (opsonization) - Activate complement (result: phagocytosis/cell lysis) - E.g., blood transfusion reaction Inflammation (type 2 mechanism) - When Ab are bound to extracellular connective tissue - Ab activate complement which cause inflammatory response (activating mast cells - releasing histamine and acting as chemokines to attract monocytes/neutrophils) - Cell injury results from release of proteases - E.g., Goodpasture syndrome Altered cell metabolism (type 2 mechanism) - Ab attach to receptors on cell surface which change cell function (2 ways) - 1. Replacing chemical that normally fits in receptor (ligand), which inappropriately stimulates cell (e.g., graves disease - thyroid gland is stimulated inappropriately to produce thyroid hormone) - 2. Blocking/destroying receptor (e.g., myasthenia gravis - acetylcholine receptors on muscle cells are blocked) Where are Ag located that react with Ab in type 3 response Ab-ag complexes formed in circulation then deposited on cell surface Type 3 hypersensitivity (name) Immune complex mediated hypersensitivity General mechanism of type 3 response with example
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