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BIO170 - Obj 18
BIO170 - Obj 18 - Hypersensitivity
| Question | Answer |
|---|---|
| What is hypersensitivity? | because of an altered immune response to an initial exposure to an antigen, subsequent exposure to the same antigen results in a pathological over-reaction of the immune response |
| What are the 3 types of hypersensitivity? | allergies (exaggerated immunte response to an environmental antigen), alloimmunity (immune response against beneficial non-self antigens; ex: organ transplant rejection, blood transfusion reactions), and autoimmunity |
| What is autoimmunity? What are some examples? | a misdirected immune response against self antigens' a loss of self-tolerance tp body's own self antigens; examples: Grave's disease, systemic lupus erythematosis, rheumatoid arthritis, myasthenia gravis, Crohn's disease |
| What are the 4 theories of why autoimmune disease occurs? | sequestered antigen, neoantigen, infectious disease, suppressor T cell dysfunction |
| Explain the sequestered antigen theory: | certain self antigens develope in areas of body never exposed to developing immune system (ex in eyes, testes); trauma exposes these antigens to immune system resulting in an immune response |
| What is an example of a hypersensitivity disorder related to the sequestered antigen antigen theory? | uveitis - an autoimmune disease of the eye; frequently occurs in response to eye trauma |
| Explain the neoantigen theory and an example: | simple molecules called haptens are too small to elicit an immune response; they bind to larger host protein becoming immunogenic (hapten-carrier complex); ex: thyroiditis - autoimmune disease of the thyroid gland |
| What are examples of the infectious disease theory? | systemic streptococcus microorganisms complex with antibody and precipitate in tissue; esp effects kidney->glomerulonephritis & heart valves where strep mimics self antigens->immune response attacks strep & self antigens (mechanism for Rheumatic fever) |
| Explain the suppressor T cell dysfunction theory: | T cells initiate an immune response against a self-antigen due to the maturation of forbidden clones of lymphocytes which are reactive to self antigens; normally these forbidden clones do not mature because of the inhibition of suppressor T cells |
| What causes suppressor T cell dysfunction? | probably due to the mechanism of the autoimmune disorder systemic lupus erythematosis and/or advancing age (depressed T cell function) |
| How many mechanisms of hypersensitivity are there? What are they? | 4: Type I - IgE mediated (anaphylactic); Type II - Tissue specific (cytolytic); Type III - Immune complex; and type IV - cell-mediated |
| What is the etiology of anaphylactic hypersensitivity? | aka IgE mediated or Type I, etiology is asthma, drug reactions (ex: penicillin), bee stings, and food (milk, chocolate, citrus, eggs, wheat, nuts, fish) |
| What is the pathogenesis of Type I hypersensitivity? | Ag stimulates IgE secretion; IgE binds to mast cells in mucous membranes causing degranulation, esp of histamine; may be genetic component to IgE over-secretion |
| What is anaphylactic shock? | a severe, often fatal form of shock, characterized by smooth muscled contraction and capillary dilation initiated by IgE class antibodies |
| How quickly do manifestations of anaphylactic shock appear? Which body systems are affected? | manifestations occurs within minutes; effects on blood vessels, skin, respiratory tract, and digestive tract |
| What are the effects of IgE mediated hypersensitivity on the blood vessels? | histamine increases vascular permeability, causing edema as blood plasma leaves blood vessels for interstitial fluid; also vasodilation, increasing blood flow -> hypotension & further edema |
| What are the effects of IgE mediated hypersensitivity on the skin? | increased blood flow & blood vessel permeability in cutaneous blood vessels causes urticaria (hives) in the skin |
| What are the effects of IgE mediated hypersensitivity on the respiratory tract? | blood vessel effects; bronchoconstriction due to histamine-> smooth muscle contraction of smooth muscle of bronchioles (esp w/asthma); increased mucous secretion (-> rhinitis, conjunctivitis) |
| What are the effects of IgE mediated hypersensitivity on the digestive tract? | food allergies cause nausea, vomiting, diarrhea, abdominal cramps, and malabsorption |
| What is the etiology of tissue specific hypersensitivity? | aka Type II or cytolytic; etiology is due to transfusion reactions, erythroblastosis fetalis, myasthenia gravis, hyperthyroid |
| What is the pathogenesis of cytolytic hypersensitivity? | IgG or IgM is inappropriately formed against membrane antigens, triggering macrophages and NK cells to phagocytosize boyd cells; the Ab-Ag complex (including the body cell) activates the complement system which lyses the cell |
| What are the manifestations of Type II hypersensitivity? How quickly do they appear? | phagocytosis of cells with specific self antigen; cell lysis of cells with specific self antigen |
| What is the etiology of immune complex hypersensitivity? | aka Type III; chronic low-grade infections, glomerulonephritis, systemic lupus erythematosis, rheumatoid arthritis, vaccine reactions |
| What is the pathogenesis of Type III hypersensitivity? | IgG forms soluble complex w/antigen which can deposit into tissues->releasing chemotactic factors-1)attracts neutrophils which attempt to phagocytize Ab-Ag complex & release lysosomal enzymes & 2)activates complement system leading to tissue inflammation |
| What are the manifestations of immune complex hypersensitivity? When do they occur? | manifestations occur within hours and include inflammation, tissue destruction (phagocytosis, complement activation), arthus reaction in the blood vessels, and serum sickness |
| Describe the arthus reaction in the blood vessels manifested in Type III hypersensitivity: | inflammation of blood vessels in some Type III hypersensitivity disease causes edema, hemorrhage, and blood clotting |
| Describe serum sickness manifested in Type III hypersensitivity | inflammation is particularly elevated in blood vessels, joints, kidneys, & lymph nodes; only occurs in certain type III hypersensitivity diseases; fever, rash, and pain are common symptoms |
| What is the etiology of Type IV hypersensitivity? | aka cell mediated, includes contact dermatitis (poison ivy, metals), tuberculin reactions (Ag injections reacts w/circulating Ab in skin test), and transplant rejections |
| What is the pathogenesis of cell mediated hypersensitivity? | Tc and Td cells are sensitized to antigen; these secrete lymphokines to recruit macrophages through chemotaxis which release lysosomal enzymes during phaocytosis of body cells; destruction of body cells->oxidized products |
| What causes inflammation in Type IV hypersensitivity? | both lysosomal enzymes and oxidized products of tissue destruction |
| What are the manifestations of cell mediated hypersensitivity? | inflammation, T cell lymphokine secretion and macrophage mediator secretion |
| If IgE is present, what type of hypersensitivity? IgG? IgM? Tc and Td cells? | IgE - Type I (anaphylactic); IgG could be either Type II or Type III; IgM is type II; Tc and Td cells are cell mediated |
Created by:
debmurph
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