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Hypersensitive Reactions Allergies

Hypersensitive Reactions Allergies. Hugh B. Fackrell. Hypersensitive Reactions. Assigned Reading Content Outline Performance Objectives Key terms Key Concepts Short Answer Questions. Assigned Reading. Chapter: 17 pp 413-439 Janis Kuby’s Immunology 3rd Ed.

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Hypersensitive Reactions Allergies

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  1. Hypersensitive ReactionsAllergies Hugh B. Fackrell

  2. Hypersensitive Reactions • Assigned Reading • Content Outline • Performance Objectives • Key terms • Key Concepts • Short Answer Questions

  3. Assigned Reading • Chapter: 17 pp 413-439 • Janis Kuby’s Immunology 3rd Ed

  4. Gell & Coombs Classification Type I Hypersensitivity: IgE mediatiated Type II Hypersensitivity: Antibody mediated cytotoxic Type III Hypersensitivity: Complex mediated cytotoxic Type IV Hypersensitivity: DTH mediated Content Outline

  5. Type I Hypersensitivity: IgE mediatiated • Components • Mechanisms • Mediators • Consequences • Regulation • Detection • Therapy

  6. Components • Allergens • IgE • Mast cells & basophils • IgE binding receptors

  7. House dust mite • Mite fecal pellets are the major source of the allergen in house dust

  8. Cat Hair • Major cause of allergies

  9. Pollen

  10. Type I Hypersensitivity

  11. Mechanisms • receptor cross linkage • Intracellular events

  12. Mechanism of Latex Allergy • 3 step process • sensitization • Activation of mast cells • Prolonged immune activity

  13. Sensitization to Latex Proteins • Macrophage presents Ag to T cells • T cells activate B cells via IL-4 • B cells become plasma cells make IgE • IgE attaches to mast cell receptors

  14. Activation of Mast cells • Allergen binds to IgE on mast cell • Intracellular enzyme cascade • immediate release of histamines cytokines • Induction of intracellular lipids • Prostoglandins, arachadonic acid

  15. Prolongation of Immune Activity Chemical released by activated mast cells induce basophils and other cells in the bloodstream to migrate into the tissue. These cells sustain immune activity which leads to tissue damage

  16. Allergen Activation

  17. Mediators • histamine • leukotriens & prostoglandins • cytokines

  18. Consequences • systemic anaphylaxis • localized anaphylaxis • late phase reaction

  19. Atopic Eczema

  20. Anaphylatic Response to Bee venom

  21. Early vs late Response

  22. Detection

  23. Skin Patch Test

  24. Positive History RAST positive Avoid latex Rast Negative Patch tests Positive Identify allergen Patch tests Negative Treat dermatitis Negative History RAST positive Latex test positive Avoid latex latex test negative powder free gloves Rast negative Safe to use latex Latex Questionaire

  25. Therapy • Hyposensitization • IgG as blocking antibody • repeated subcutaneous injections • T cell anergy • soluble antigens • Antihistamines

  26. Drugs for Type I hypersenstivity • Antihistamines blocks receptors • Cromolyn sodium blocks Ca++ influx • Theophylline • inhibits phosphodiesterase • [cAMP] kept high • Epinephrine • stimulates cAMP via beta adrenergic receptors • Cortisone • blocks conversion of histidine to histamine

  27. Performance Objectives

  28. Key Terms • allergen, allergy, anaphylactic shock,anaphylaxis, anergy, atopy, basophils, • contact sensitivity, degranulation, delayed type hypersensitivity, • desenstization, granulomas, homocytotropic antibodies, hypersensitivity,

  29. hyposensitivity, immediate hypersensitivity, late phase reaction, mast cells, • sensitization, senstizing dose, shocking dose, systemic anaphlyaxis, triple response: edema, erythema, wheal and flare, • tubercles, tuberculin skine reaction, tuberculosis, Type I hypersensitivity, • Type II hypersensitivity, Type II hypersensitivity, Type IV hypersensitivity.

  30. Key Concepts • List the Gell & Coombs classification for hypersensitivity reactions; give examples of each type. • Describe stimulatory hypersensitivity and give a specific example • Discuss the difference between primary and secondary exposure to antigen in imunity and in hypersensitivity

  31. Describe the structural and functional characteristics of IgE. • Discuss the cytotropic nature of IgE • Differentiate betweeen the cyclooxygenase and lipoxygenase pathways of mediator production

  32. Describe the role of mast cells in immediate hypersensitivity reactions. • Distinguish between release of preformed and newly formed mediators from mast cells and give examples of each type of mediator • Discuss the hallmarks of delayed type hypersensitivity

  33. Explain the mechanisms of Delayed Type Hypersensitivity induction and development • Distinguish between different types of Delayed type hypersensitivity. • Describe tuberculosis in terms of hypersensitivity reactions.

  34. Short Answer Questions

  35. By derivation, what does allergy mean and what does hypersensitivity mean? Are they synonymous? • The main difference between immediate and delayed types of hypersensivitiy is the time of appearance of the reactions. True/False? If false, name the main differences. • What is the type II reaction described by Gell & Cooombs? Does this reaction require complement?

  36. Is there a tendency to immediate hypersenstivity reactions? Explain? • Differentiate between antigen and allergen. • What immune and nonimmune cells are involved in immediate hypersensivity?

  37. What class of antibody in responsible for immediate hypersenstivity? Describe some structural and biological characteristics of this antibody? • What do we mean by homocytotropic antibodies? • Briefly describe the result of the interaction of IgE, with mast cells • a) in the presence of allergen. • b) in the absence of allergen.

  38. What are the chemical mediators of immediate hypersentivity reactions? • Some effector molecules of immediate hypersensitivity reactions are preformed mediators; others are newly synthesized mediators. Distinguish between the two. • Briefly describe the two pathways for the production of newly synthesized mediators.

  39. How can you determine whether a person is allergic to a foreign protein? • What is the triple response? Name two "in vitro" tests. • What is the mechanism for desensitization for immediate hypersensitivities? Is this desensitization lifelong? If not speculate on the reasons. What are some other modes of treatment for immediate hypersensitivity?

  40. Describe the differences between systemic anahylaxis and atopy? • Are the mechanisms of cell-mediated immunity and DTH the same? • Name the effector cells in DTH. • What are some of the hallmarks of DTH reactions?

  41. Describe contact sensitivity. • How does contact sensitivity differ from the tuberculin skin reaction? • What is the mechanism of the tuberculin skin test? If the test is positive what causes the induration (hardening) of the test site? What substances are used in this test?

  42. DONE!!!

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