Hypersensitivity - PPT NO. 7 PDF

HYPERSENSITIVITY – DR. HUSSEIN (7TH PPT) 1. What is allergy? A: A disease caused by an immune response to an antigen (allergen). 2. What is anaphylaxis? A: A severe, life-threatening systemic allergic reaction characterized by bronchioconstriction and hypotension. 3. What is atopy? A: A genetic...

HYPERSENSITIVITY – DR. HUSSEIN (7TH PPT) 1. What is allergy? A: A disease caused by an immune response to an antigen (allergen). 2. What is anaphylaxis? A: A severe, life-threatening systemic allergic reaction characterized by bronchioconstriction and hypotension. 3. What is atopy? A: A genetic predisposition to develop allergic reactions such as asthma, hay fever, and eczema. 4. What is sensitization? A: The process where the first contact with an antigen induces antibody formation without an immediate allergic response. 5. What is desensitization? A: A method used to reduce or eliminate an allergic response by administering increasing amounts of an allergen over time. 6. What is a shocking dose? A: The dose of allergen that causes an allergic reaction in a sensitized individual. 7. What are the four types of hypersensitivity reactions? A: Type I (immediate), Type II (cytotoxic), Type III (immune complex-mediated), and Type IV (cell- mediated). 8. What immune component mediates Type I hypersensitivity? A: IgE antibodies. 9. What immune component mediates Type II hypersensitivity? A: IgG or IgM antibodies. 10. What mediates Type III hypersensitivity reactions? A: Immune complexes of antibodies and antigens that deposit in tissues. 11. What characterizes Type IV hypersensitivity? A: Delayed T-cell-mediated immune responses. 12. What is the role of mast cells in immediate hypersensitivity? A: Mast cells release mediators like histamine upon activation by IgE, leading to allergic symptoms. 13. What is degranulation? A: The process by which mast cells release preformed mediators such as histamine upon activation. 14. What is the primary mediator released during a Type I hypersensitivity reaction? A: Histamine. 15. What are preformed mediators in Type I hypersensitivity? A: Histamine, heparin, ECF-A, and serotonin. 16. What are newly synthesized mediators in Type I hypersensitivity? A: Prostaglandins, leukotrienes, thromboxanes, and slow-reacting substances of anaphylaxis (SRS-A). 17. What is the role of IgE in hypersensitivity? A: IgE binds to mast cells and basophils, triggering degranulation when allergens cross-link the IgE molecules. 18. What are the clinical manifestations of Type I hypersensitivity? A: Urticaria, eczema, conjunctivitis, rhinitis, asthma, and anaphylaxis. 19. What is the function of epinephrine in treating hypersensitivity reactions? A: It increases cAMP levels in cells, which inhibits the release of allergic mediators and relaxes smooth muscle. 20. What is the role of corticosteroids in treating hypersensitivity? A: They reduce inflammation by inhibiting cytokine production and stabilizing immune cells. 21. What is SRS-A (slow-reacting substance of anaphylaxis)? A: A group of leukotrienes that cause prolonged smooth muscle contraction and increased vascular permeability. 22. What is the role of eosinophils in Type I hypersensitivity? A: Eosinophils release histaminase and arylsulfatase, which degrade histamine and SRS-A, potentially reducing the severity of allergic reactions. 23. What is serotonin's role in anaphylaxis? A: It causes vasoconstriction of large blood vessels and vasodilation of capillaries, contributing to the allergic response. 24. How do leukotrienes contribute to asthma? A: They cause bronchoconstriction, increased vascular permeability, and inflammation. 25. What is an anaphylactoid reaction? A: A reaction similar to anaphylaxis but not mediated by IgE; it occurs when certain drugs directly induce mast cell degranulation. 26. What is the Prausnitz-Küstner reaction? A: A historical test for determining allergic sensitivity by injecting serum from an allergic person into a non-allergic individual. 27. What are the common clinical symptoms of drug hypersensitivity? A: Rashes, fever, local or systemic anaphylaxis, and varying severity. 28. How do Type II hypersensitivity reactions occur? A: Antibodies (IgG or IgM) bind to cell surface antigens, leading to complement-mediated lysis or antibody-dependent cellular cytotoxicity (ADCC). 29. What is an example of a Type II hypersensitivity reaction? A: Hemolytic anemia or ABO transfusion reactions. 30. What is the mechanism behind Type III hypersensitivity? A: Immune complexes form and deposit in tissues, activating complement and causing inflammation and tissue damage. 31. What is a common autoimmune disease caused by Type III hypersensitivity? A: Systemic lupus erythematosus (SLE). 32. What is the effector mechanism of Type III hypersensitivity? A: Complement activation and recruitment of neutrophils that cause tissue injury. 33. What is an example of a Type IV hypersensitivity reaction? A: Contact dermatitis or the tuberculin test. 34. What cells mediate Type IV hypersensitivity? A: CD4+ helper T cells and CD8+ cytotoxic T cells. 35. What is the role of macrophages in Type IV hypersensitivity? A: They are activated by T cells to produce cytokines and cause inflammation at the site of antigen exposure. 36. What is the tuberculin skin test used for? A: It tests for previous exposure or infection with Mycobacterium tuberculosis. 37. What is contact allergy? A: A delayed hypersensitivity reaction caused by skin contact with certain chemicals, plant material, or cosmetics. 38. What is the allergen in poison ivy? A: Urushiol, which acts as a hapten and causes contact dermatitis. 39. What is the role of T cells in autoimmune diseases like rheumatoid arthritis? A: T cells attack self-antigens in tissues, leading to inflammation and tissue damage. 40. What is Myasthenia gravis? A: An autoimmune disease where antibodies block acetylcholine receptors, leading to muscle weakness. 41. What is Graves' disease? A: An autoimmune disorder where antibodies stimulate the thyroid, causing hyperthyroidism. 42. What is the mechanism of immune complex-mediated diseases? A: Immune complexes deposit in tissues, causing inflammation and tissue damage through complement activation. 43. What is Goodpasture's syndrome? A: An autoimmune disease where antibodies attack the basement membranes of the kidneys and lungs, causing organ damage. 44. How does rheumatic fever relate to hypersensitivity? A: Antibodies against streptococcal bacteria cross-react with heart tissue, leading to tissue damage. 45. What is pemphigus? A: An autoimmune skin disease characterized by blisters due to antibodies attacking skin cells. 46. What is the role of histamine in allergic reactions? A: Histamine increases vascular permeability, vasodilation, and smooth muscle contraction. 47. What is the significance of leukotrienes in asthma? A: They are the main mediators of bronchoconstriction and are not treatable by antihistamines. 48. What is the role of complement in antibody-mediated hypersensitivity? A: Complement is activated by antibodies bound to antigens, leading to inflammation and cell lysis. 49. What is immune complex disease? A: A condition where immune complexes persist and deposit in tissues, causing diseases like arthritis and nephritis. 50. What happens during chronic desensitization therapy? A: Long-term administration of an allergen leads to the production of IgG-blocking antibodies, preventing allergic reactions.