Pathophysiology Ch. 10

  1. What are Excessive Immune Responses?
    • Autoimmunity
    • Hypersensitivity
  2. What are Deficient Immune Responses?
    • Primary immunodeficiency
    • Secondary Immunodeficiency
    • AIDS
  3. What is Autoimmunity?
    Person's immune systems goes after self-cells, injuring body tissues
  4. What are the theories of autoimmunity?
    • Antigenic mimicry theory
    • -->cells mimic foreign antigens
    • Sequestered antigen theory
    • -->some self-antigens are normally hidden from the immune system, revealed due to injury
    • Thymus gland defect theory
    • -->self-antigens are not present to T cells during the fetal stage due to a defect in the thymus gland
    • Defective lymphocyte theories
    • -->some lyphocytes fail to respond to suppressor cytokines
  5. What are the genetic factors for autoimmunit?
    • Females are more likely to have a defect.
    • Higher risk assoc. with certain cytokine patterns, MHC genes
  6. Environmental Factors for autoimmunity.
    • Viruses or bacteria trigger bad behavior in B or T cells
    • Epstein-Barr virus
    • Environmental or Occupational stress
  7. What are the Treatments for the Symptoms of Autoimmunity?
    • Corticosteroids
    • Cytotoxins
    • Cyclosporine
    • Anti-rheumatic agents
    • Plasmaphoresis
  8. What are examples of Type I Hypersensitivity?
    allergies, eczema, asthma, anaphylactic responses
  9. What is the Etiology of Type I Hypersensitivity?
    • IgE response to antigens
    • T cell deficiency increases mast cell degranulation
    • increased histamines
  10. What is the pathogenesis of Type I Hypersensitivity?
    • IgE binds to Fc receptors on mast cells
    • Increased intracellular calcium results in immediate, massive, local mast cell degranulation of proinflammatory mediators
    • Released mediators cause inflammatory response
  11. What are the clinical manifestations of Type I Hypersensitivity?
    • Hives
    • Allergic rhinitis
    • Eczema
    • Throat constriction
    • Localized edema
    • Tachycardia
    • Anaphylaxis
  12. What is the Pharmacological management for Type I Hypersensitivity?
  13. What is the Mechanism for Type II Hypersensitivity?
    • Exposure to antigen on foreign cell surface
    • Fab portion of IgG or IgM binds to foreign antigen -->makes antigen-antibody complex
    • Fc region of IgG or IgM stick out
    • Fc region --> bridge b/n antigen and complement or effector cell
    • Lysis mechanisms
  14. What are two examples of Type II Hypersensitivity?
    • Transfusion reaction
    • Hemolytic disease of the newborn
  15. What happens during Type III Hypersensitivity?
    • Immune and phagocyctic systems fail to effectively remove antigen-antibody immune complexes
    • Activation of complement
    • Subsequent tissue inflammation
    • Destruction of tissue
  16. What activates Type III Hypersensitivity?
    • Persistent low-grade infections
    • Inhalation of antigens into alveoli
    • Autoimmune production of auto-antibodies
  17. What is the difference between Type II and Type III?
    • Type II- response to tissue-specific antigen on direct cell eath or malfunction of antigen-antibody reactions
    • Type III- antigen-antibodies precipitate out of fluids and get into tissues
  18. What are some examples of Type III Hypersensitivity?
    • Rheumatoid arthritis
    • Immune complex glomerulonephritis
    • Lupus
  19. What are the principle effector cells in Type IV Hypersensitivity?
    • Lymphocytes
    • Macrophages
    • Sensitized T cells react with altered or foreign cells and initiate inflammation
    • Mast cells involved in early stages
    • Neutrophils not involved
  20. What are two types of Type IV Hypersensitivity?
    • Cutaneous Basophil Hypersensitivity
    • --> Most rapid type
    • -->Skin Graft reactions and rejection
    • Contact Hypersensitivity
    • -->Most familiar type, contact dermatitis
    • -->Slow reaction; hapten antigen is very small, incomplete
    • Granulomatous Hypersensitivity
    • -->Primary defense against intracellular infections
  21. What are Primary Immunodeficiency Disorders?
    May be from congenital, genetic, or acquired defects that directly affect immune cell function
  22. What is Severe combined immunodeficiency disorders?
    • B-cell and T-cell combined disorders
    • Result from embryonic defects
    • Usually autosomal recessive, x-linked recessive, defective expression of MHC antigens
  23. What are two T cell Disorders?
    • DiGeorge Syndrome
    • -->associated with total or partial loss of thymus gland function
    • Chronic mucocutaneous candidiasis
    • -->Autosomal recessive
  24. What are B cell Disorders?
    • IgA deficiency
    • -IgA bearing lymphocytes fail to become plasma cells, resulting in lack of serum and secretory IgA
  25. What is secondary Immunodeficiency Disorders?
    • Problems in neuroendocrine and immune system interaction
    • Excessive neuroendocrine response to stress; increased corticosteroid production increases susceptibility to infection
    • Immune function impaired as a result of other nonimmune system disorders that secondarily suppress immune function
    • -->Poor nutrition
    • -->Stress
    • -->Drugs
  26. What are the categories of Allergic Hypersensitivity?
    • Type one- IgE mediated
    • Type two- Antibody mediated (tissue specific)
    • Type three- Complement mediated (immune complex)
    • Type four- Cell mediated
Card Set
Pathophysiology Ch. 10
Alterations in Immune Function