Anaphylaxis - Anaphylaxis Anaphylaxis IgE Mediated...

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Unformatted text preview: Anaphylaxis Anaphylaxis IgE Mediated Hypersensitivity What is anaphylaxis? What An acute systemic allergic reaction The result of a re-exposure to an antigen The that elicits an IgE mediated response that Usually caused by a common environmental Usually protein that is not intrinsically harmful protein Often caused by medications, foods, and Often insect stings insect It is a Type I hypersensitivity History History 1st recorded 2640BC in hieroglyphics – bee sting of a pharoah Richet & Portier – South Seas – Man-o-war – coined term anaphylaxis IgE IgE Binds irreversible to FcεRI receptors on RI mast cells, basophils, and eosinophils mast Is usually for parasitic infections E heavy chain Mast Cell Mast Has high affinity for IgE molecules (105 IgE/cell) Originates in the bone marrow, reside in Originates connective tissues connective Increases host response to parasitic infections Contain immunological mediators in granules ie. Contain Histamine, ECF-A, HMW-NCF Histamine, 2 populations that vary in granule content and populations activity activity – Connective tissue Connective – Mucosal Mucosal IgE FcRI Receptor IgE Symptoms Symptoms Peripheral vasodilation – vascular permeablility (edema) vascular Bronchospasm Cardiac arrhythmias Smooth muscle contractions Sensitization Sensitization Antigen is presented by antigen presenting Antigen cells cells TH2 cells induce B cell activation – CD40 ligand and cytokines B cells undergo isotype switching and cells produce antibody produce Serum antibody is bound by the mast cells The allergic response The Secondary presentation of antigen produces Secondary an immediate response controlled by mast immediate cells cells Granule contents are released Cell mediated response proceeds Sensitization & Response Sensitization What is happening? What Initial exposure sensitizes mast cells. Antigen specific IgE molecules attach to Antigen high affinity Fc receptors on the mast cell surface. surface. Cross linking of IgE molecules on surface Cross causes intracellular signaling pathway causes – Inflammatory mediators are released upon Inflammatory degranulation degranulation Mediators Involved Mediators Include histamine, proteases, chemotactic Include factors, leukotrienes, prostaglandin D, and cytokines cytokines Primary: released before degranulation – Interleukin 4 used by T cells induces B cell Interleukin maturation maturation – IL-3 and IL-5 released by T and mast cells are IL-3 chemo attractants for eosinophils chemo Secondary: come from granules Histamine Histamine Synthesized and stored in granules The primary mediator in the granules 3 receptors – H1: Smooth muscle & endothelium Increased IP3 & DAG – H2: Gastric mucosa, cardiac muscle, mast cells Increased cAMP – H3: Pre-synaptic brain Decreases histamine release Tissue Effects of Histamine Tissue Cardiovascular – Decreased blood pressure – Increased heart rate – Edema (separation of endothelial cells & Edema increased permeability) increased Respiratory – broncho constriction Gastrointestinal – Smooth muscle contraction and diarrhea Skin Treatments Treatments Antihistamines – Block H1 and H2 receptors Epinephrine for bronchospasms – stimulates the reformation of tight junctions stimulates between endothelial cells IV fluids to support blood pressure Desensitization Ant bites Ant Red Imported Fire Ant Venom (antigen) – Composed largely of low MW alkaloids, also Composed different proteins different – Each component is able to induce anaphylaxis Able to inject 100ng venom/bite Venom induces venom specific IgE antibody Venom production production ...
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This note was uploaded on 01/06/2012 for the course STEP 1 taught by Professor Dr.aslam during the Fall '11 term at Montgomery College.

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