patho hypersensitivity

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  1. Four main categories of immune system dysfunction
    •Hypersensitivity Disorders (type I, II, III, IV)

    •Autoimmune disorders

    •Transplant rejection

    •Immunodeficiency Disorders (primary, acquired)
  2. Type I Hypersensitivity
    •Commonly called “allergic reactions”

    •Systemic or anaphylactic reactions

    •Local or atopic reactions (genetic)

    –Rhinitis (hay fever)

    –Food allergies

    –Bronchial asthma


    –Atopic dermatitis
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  4. Type II Hypersensitivity

    •IgG or IgM attack antigens on surfaces of cells or other tissue components

    • –Usually
    • involves antigens on red or white blood cells

    –Transfusion reactions

    –Rh disease

    –Drug reactions
  5. Type III Hypersensitivity
    •Free-floating antigen + antibody ->circulating immune complex

    Autoimmune vasculitis:

    Glomerulonephritis: inflammation of kidney

    • Serum sickness: Serum sickness is a systemic immune complex disorder that is triggered by the deposition of insoluble antigen–antibody (IgM, IgG, and occasionally IgA) complexes in blood vessels, joints, and heart and kidney tissue.2,3 The deposited complexes activate complement, increase vascular permeability, and recruit phagocytic cells, all of which can promote local tissue damage and edema. The term serum sickness was originally coined to describe a syndrome consisting of rash, lymphadenopathy, arthralgias, and occasionally neurologic disorders that appeared 7 or more days after injections of horse antiserum (tetanus).
    • Arthus reaction : The Arthus reaction is a term used by pathologists and immunologists to describe localized tissue necrosis (usually in the skin) caused by immune complexes. In the laboratory, an Arthus reaction can be produced by injecting an antigen preparation into the skin of an immune animal with high levels of circulating antibody. Within 4 to 10 hours, a red, raised lesion appears on the skin at the site of the injection
  6. Type
    IV Hypersensitivity
    • Cell-mediated: sensitized T cells attack antigen
    • Delayed-type hypersensitivity :Delayed-type hypersensitivity (DTH) reactions (Fig. 16-4B) occur in response to soluble protein antigens and primarily involve antigen-presenting cells such as macrophages and CD4+ helper T cells of the TH1 type. During the reaction TH1 cells are activated and secrete an array of cytokines that recruit and activate macrophages, lymphocytes, fibroblasts, and other inflammatory cells.7 These T-cell–mediated responses require the synthesis of effector molecules and take 24 to 72 hours to develop, which is why they are called “delayed-type” hypersensitivity disorders
    • Tuberculin test: The best-known DTH response is the reaction to the tuberculin test, in which inactivated tuberculin or purified protein derivative is injected under the skin. In a person who has been sensitized by previous infection, a local area of redness and induration develops within 8 to 12 hours, reaching a peak in 24 to 72 hours
    • Allergic contact dermatitis: Allergic contact dermatitis denotes an inflammatory response confined to the skin that is initiated by reexposure to an allergen to which a person had previously become sensitized (e.g., cosmetics, hair dyes, metals, topical drugs).15 The most common form of this condition is the dermatitis that follows an intimate encounter with poison ivy or poison oak antigens, although many other substances can trigger a reaction
    • •Hypersensitivity pneumonitis: Hypersensitivity pneumonitis, which is associated with exposure to inhaled organic dusts or related occupational antigens, is another example of a DTH reaction.16 The disorder is thought to involve a susceptible host and activation of pulmonary T cells, followed by the release of cytokine mediators of inflammation. The inflammatory response that ensues (usually several hours after exposure) produces labored breathing, dry cough, chills and fever, headache, and malaise. The symptoms usually subside within hours after the sensitizing antigens are removed.(

    • Direct cell-mediated cytotoxicity: In direct cell-mediated cytotoxicity (Fig. 16-4A), CD8+ cytotoxic T lymphocytes (CTLs) directly kill target cells that express peptides derived from cytosolic antigens that are presented in association with class I major histocompatibility complex (MHC) molecules
    • Viral reactions:: In viral infections, CTL responses can lead to tissue injury by killing infected target cells even if the virus itself has no cytotoxic effects.2 Some viruses directly injure infected cells and are said to be cytopathic, whereas other, noncytopathic viruses do not. Because CTLs cannot distinguish between cytopathic and noncytopathic viruses, they kill virtually all infected cells regardless of whether the infection is harmful. In certain forms of hepatitis, for example, the destruction of liver cells is due to the host CTL response and not the virus.
  7. Hypersensitivity reactions
    •Type I: IgE, mast cells

    •Type II: IgG, IgM

    •Type III: IgG, IgM, immune complexes

    • •Type IV: T-cell mediated (CD8+ cells)
    • delayed type (CD4+)
    • no immunoglobulin involvement
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patho hypersensitivity
2011-11-07 03:23:59
patho hypersensitivity

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