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Chapter 18 Immunological Disorders

Chapter 18 Immunological Disorders. Type I: Anaphylaxis. Allergy development Immunization sensitized to allergen produce IgE antibody Cellular response IgE binds to Fc receptor Mast cells Basophils. Figure 18.1. Type I: Anaphylaxis. Antigen binds IgE Cross-linking of IgE antibodies

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Chapter 18 Immunological Disorders

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  1. Chapter 18Immunological Disorders

  2. Type I: Anaphylaxis • Allergy development • Immunization • sensitized to allergen • produce IgE antibody • Cellular response • IgE binds to Fc receptor • Mast cells • Basophils Figure 18.1

  3. Type I: Anaphylaxis • Antigen binds IgE • Cross-linking of IgE antibodies • Degranulation • release of chemical mediators • histamine • prostaglandins • leukotrienes • Symptoms • smooth muscle contraction • vascular permeability Figure 18.1

  4. Type I: Anaphylaxis • Treatment • Short-term • anti-histamines--block histamine • prior to release of histamine • epinephrine in emergency • Long-term • desensitization (misnomer) • prolonged immunization • Antigen administered in increasing dosage • Produce High affinity IgG • react before IgE binds allergen

  5. Genetic predisposition Allergens inhaled upper respiratory allergic rhinitis lower respiratory asthma insect venoms medications ingested Testing--skin tests Causes of allergies Fig 18.2b

  6. Antibodies bind cell own cells other cells Antibodies trigger normal response alter function of cell phagocytosis activate complement lysis clumping of cells Type II: Cytotoxic Figure 18.5

  7. Type II: Cytotoxic • Examples • Autoimmune • Grave’s disease • antibodies attach thyroid cells • stimulate cells to produce thyroid hormone • increased metabolism • Goodpasture’s syndrome • antibodies bind proteins in kidney • complement activated • inflammation results

  8. Type II: Cytotoxic • Examples • Transfusion • A, B, O blood types • antigens on surface of red blood cells • produce antibodies • non-self blood antigens • incompatible blood transfusion • lysis • agglutination Fig 18.6

  9. Type II: Cytotoxic • Hemolytic Disease of the Newborn • Rh factor • RBC antigen • mother negative • baby positive • first pregnancy • no problem • no antibody produced Fig 18.7

  10. Type II: Cytotoxic • Rh+ enters mother • at or near birth • immunizes mother • produces antibodies against Rh factor Fig 18.7

  11. Type II: Cytotoxic • Next pregnancy • problem with mother’s anti-Rh antibodies • enter fetus and causes cell lysis • Prevention • injection during pregnancy • anti-Rh immune globulin Fig 18.7

  12. Type III: Immune complex • Circulating antigens • large source • combine with antibodies • form complex • macrophage remove • some deposit • blood vessels • other tissues

  13. Type III: Immune complex • Results of immune complex • complement activation and damage • leukocyte attraction • inflammation damage Fig 18.8

  14. Type III: Immune complex • Examples • Systemic lupus erythematosus (SLE) • antibodies to cell nucleus components • deposits in many areas • kidneys--most common • skin--cause butterfly rash (lupus--wolf) • joints--arthritis • brain--mental • Rheumatoid arthritis • antibodies to rheumatoid factor • joint inflammation

  15. Type IV: Cell-Mediated • T cell response • delayed • 12-48 hrs after exposure • not antibody mediated • First exposure • TD cells become sensitized • Cell proliferate Fig 18.10

  16. Type IV: Cell-Mediated • Second exposure • TD activated by antigen • release lymphokines • stimulate macrophages • inflammatory response • symptoms Fig 18.10

  17. Type IV: Cell-Mediated • Examples: • poison ivy • urushiol in sap combines with skin proteins • triggers TD response • second exposure • contact hypersensitivity • tuberculin skin test • test for exposure to tuberculosis • previous TB exposure • positive reaction Fig 18.11

  18. Immunodeficiencies • congenital deficiencies • failure to produce components of immune system • genetic basis • acquired immunodeficiencies • certain cancers • AIDS--acquired immunodeficiency syndrome • TH cells depleted

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