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Anaphylaxis

Anaphylaxis. IgE Mediated Hypersensitivity. What is anaphylaxis?. An acute systemic allergic reaction The result of a re-exposure to an antigen that elicits an IgE mediated response Usually caused by a common environmental protein that is not intrinsically harmful

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Anaphylaxis

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  1. Anaphylaxis IgE Mediated Hypersensitivity

  2. What is anaphylaxis? • An acute systemic allergic reaction • The result of a re-exposure to an antigen that elicits an IgE mediated response • Usually caused by a common environmental protein that is not intrinsically harmful • Often caused by medications, foods, and insect stings • It is a Type I hypersensitivity

  3. History • 1st recorded 2640BC in hieroglyphics • bee sting of a pharoah • Richet & Portier • South Seas • Man-o-war • coined term anaphylaxis

  4. IgE • Binds irreversible to FcεRI receptors on mast cells, basophils, and eosinophils • Is usually for parasitic infections • E heavy chain

  5. Mast Cell • Has high affinity for IgE molecules (105 IgE/cell) • Originates in the bone marrow, reside in connective tissues • Increases host response to parasitic infections • Contain immunological mediators in granules ie. Histamine, ECF-A, HMW-NCF • 2 populations that vary in granule content and activity • Connective tissue • Mucosal

  6. IgE FcRI Receptor

  7. Symptoms • Peripheral vasodilation • vascular permeablility (edema) • Bronchospasm • Cardiac arrhythmias • Smooth muscle contractions

  8. Sensitization • Antigen is presented by antigen presenting cells • TH2 cells induce B cell activation • CD40 ligand and cytokines • B cells undergo isotype switching and produce antibody • Serum antibody is bound by the mast cells

  9. The allergic response • Secondary presentation of antigen produces an immediate response controlled by mast cells • Granule contents are released • Cell mediated response proceeds

  10. Sensitization & Response

  11. What is happening? • Initial exposure sensitizes mast cells. • Antigen specific IgE molecules attach to high affinity Fc receptors on the mast cell surface. • Cross linking of IgE molecules on surface causes intracellular signaling pathway • Inflammatory mediators are released upon degranulation

  12. Mediators Involved • Include histamine, proteases, chemotactic factors, leukotrienes, prostaglandin D, and cytokines • Primary: released before degranulation • Interleukin 4 used by T cells induces B cell maturation • IL-3 and IL-5 released by T and mast cells are chemo attractants for eosinophils • Secondary: come from granules

  13. 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

  14. Tissue Effects of Histamine • Cardiovascular • Decreased blood pressure • Increased heart rate • Edema (separation of endothelial cells & increased permeability) • Respiratory • broncho constriction • Gastrointestinal • Smooth muscle contraction and diarrhea • Skin • Urticaria

  15. Treatments • Antihistamines • Block H1 and H2 receptors • Epinephrine for bronchospasms • stimulates the reformation of tight junctions between endothelial cells • IV fluids to support blood pressure • Desensitization

  16. Ant bites • Red Imported Fire Ant • Venom (antigen) • Composed largely of low MW alkaloids, also different proteins • Each component is able to induce anaphylaxis • Able to inject 100ng venom/bite • Venom induces venom specific IgE antibody production

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