Pathophysiology Ch. 10

• Autoimmunity
• Hypersensitivity

• Primary immunodeficiency
• Secondary Immunodeficiency
• AIDS

Person's immune systems goes after self-cells, injuring body tissues

• 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

• Females are more likely to have a defect.
• Higher risk assoc. with certain cytokine patterns, MHC genes

• Viruses or bacteria trigger bad behavior in B or T cells
• Epstein-Barr virus
• Environmental or Occupational stress

• Corticosteroids
• Cytotoxins
• Cyclosporine
• Anti-rheumatic agents
• Plasmaphoresis

allergies, eczema, asthma, anaphylactic responses

• IgE response to antigens
• T cell deficiency increases mast cell degranulation
• increased histamines

• 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

• Hives
• Allergic rhinitis
• Eczema
• Throat constriction
• Localized edema
• Tachycardia
• Anaphylaxis

Antihistamines

• 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

• Transfusion reaction
• Hemolytic disease of the newborn

• Immune and phagocyctic systems fail to effectively remove antigen-antibody immune complexes
• Activation of complement
• Subsequent tissue inflammation
• Destruction of tissue

• Persistent low-grade infections
• Inhalation of antigens into alveoli
• Autoimmune production of auto-antibodies

• 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

• Rheumatoid arthritis
• Immune complex glomerulonephritis
• Lupus

• Lymphocytes
• Macrophages
• Sensitized T cells react with altered or foreign cells and initiate inflammation
• Mast cells involved in early stages
• Neutrophils not involved

• 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

May be from congenital, genetic, or acquired defects that directly affect immune cell function

• B-cell and T-cell combined disorders
• Result from embryonic defects
• Usually autosomal recessive, x-linked recessive, defective expression of MHC antigens

• DiGeorge Syndrome
• -->associated with total or partial loss of thymus gland function
• Chronic mucocutaneous candidiasis
• -->Autosomal recessive

• IgA deficiency
• -IgA bearing lymphocytes fail to become plasma cells, resulting in lack of serum and secretory IgA

• 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

• Type one- IgE mediated
• Type two- Antibody mediated (tissue specific)
• Type three- Complement mediated (immune complex)
• Type four- Cell mediated