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What are Excessive Immune Responses?
What are Deficient Immune Responses?
- Primary immunodeficiency
- Secondary Immunodeficiency
What is Autoimmunity?
Person's immune systems goes after self-cells, injuring body tissues
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
What are the genetic factors for autoimmunit?
- Females are more likely to have a defect.
- Higher risk assoc. with certain cytokine patterns, MHC genes
Environmental Factors for autoimmunity.
- Viruses or bacteria trigger bad behavior in B or T cells
- Epstein-Barr virus
- Environmental or Occupational stress
What are the Treatments for the Symptoms of Autoimmunity?
- Anti-rheumatic agents
What are examples of Type I Hypersensitivity?
allergies, eczema, asthma, anaphylactic responses
What is the Etiology of Type I Hypersensitivity?
- IgE response to antigens
- T cell deficiency increases mast cell degranulation
- increased histamines
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
What are the clinical manifestations of Type I Hypersensitivity?
- Allergic rhinitis
- Throat constriction
- Localized edema
What is the Pharmacological management for Type I Hypersensitivity?
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
What are two examples of Type II Hypersensitivity?
- Transfusion reaction
- Hemolytic disease of the newborn
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
What activates Type III Hypersensitivity?
- Persistent low-grade infections
- Inhalation of antigens into alveoli
- Autoimmune production of auto-antibodies
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
What are some examples of Type III Hypersensitivity?
- Rheumatoid arthritis
- Immune complex glomerulonephritis
What are the principle effector cells in Type IV Hypersensitivity?
- Sensitized T cells react with altered or foreign cells and initiate inflammation
- Mast cells involved in early stages
- Neutrophils not involved
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
What are Primary Immunodeficiency Disorders?
May be from congenital, genetic, or acquired defects that directly affect immune cell function
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
What are two T cell Disorders?
- DiGeorge Syndrome
- -->associated with total or partial loss of thymus gland function
- Chronic mucocutaneous candidiasis
- -->Autosomal recessive
What are B cell Disorders?
- IgA deficiency
- -IgA bearing lymphocytes fail to become plasma cells, resulting in lack of serum and secretory IgA
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
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