Chapter 18 Immunological Disorders

Type I: Anaphylaxis Allergy development Immunization Cellular response 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 Degranulation release of chemical mediators histamine prostaglandins leukotrienes Symptoms smooth muscle contraction vascular permeability Figure 18.1

Type I: Anaphylaxis Treatment Short-term Long-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

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

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

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

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

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

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

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

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

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

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

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

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

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

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