Immuno- Type III and IV HS.txt

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  1. Type III hypersensitivity is also known as _________________.
    immune complex disease
  2. Type III hypersensitivity is the result of...
    deposition of antibody/antigen complexes.
  3. What are the 2 categories of Type III hypersensitivity?
    antibody excess (local) and antigen excess (generalized)
  4. Small amount of _________ are always forming under normal circumstances; they are either __________ or ___________.
    immune complexes; soluble; insoluble
  5. Under normal circumstances, insoluble immune complexes are removed by the ________________.
    mononuclear phagocyte system
  6. Under normal circumstances, soluble immune complexes are removed when they _____________, which then bind to ___________, where the complex is stripped off.
    complement receptors on erythrocytes or platelets; phagocytes
  7. A localized Type III hypersensitivity reaction is called ___________.
    an arthus reaction
  8. With a local Type III, there is an excess of _________; repeated exposure to an Ag results in high concentrations of ______.
    antibody; IgG
  9. With a local Type III HS, ___________ is activated, __________ are recruited and activated, and a localized ___________ is incited.
    complement; neutrophils; inflammatory response
  10. What are 3 clinical examples of local Type III HS?
    blue eye, hypersensitivity pneumonitis, staphylococcal hypersensitivity
  11. Blue eye is a result of infection with ____________; there is immune complex deposition in the _____________.
    infectious canine hepatitis (adenovirus 1); anterior uvea
  12. With hypersensitivity pneumonitis, small allergens reach __________ and induce ________________; then Ab in the _________ complex with Ag.
    alveoli; chronic antigenic sensitization; alveolar walls
  13. Staphylococcal hypersensitivity is also called _____________, and it results in ___________.
    juvenile cellulitis; pruritic pustular dermatitis
  14. Staphylococcal hypersensitivity involves what hypersensitivity type(s)?
    Types I, III, and IV
  15. Generalized Type III HS occurs when there are very high concentrations of _________ present, which complex in the ________ and result in... (6)
    antigens; blood; glomerulonephritis, vasculitis, arthritis, anemia, leukopenia, and thrombocytopenia.
  16. With generalized Type III HS, high levels of _______ persist, increasing _______ production and thus increasing the potential for the production of __________, which deposit in _________________.
    antigen; antibody; immune complexes; vessel walls of various organs
  17. 3 organs that are commonly affected by generalized type III HS.
    glomerulus, vasculature, synovium
  18. With generalized type III HS, deposition site for immune complexes is influenced by... (3)
    capillary blood flow dynamics, pre-existing lesions in endothelium, and the nature of the antigens.
  19. With generalized type III HS, once immune complexes bind in vessel walls, they induce ________________ and _______________.
    neutrophil accumulation; endothelial proliferation
  20. How does generalized type III HS induce anemia, leukopenia, and thrombocytopenia?
    immune complexes bind to circulating cells and the Ab laden cells are removed via Fc binding by macrophages
  21. With a generalized type III HS, the altered BM environment and.or binding and destruction in blood results in... (2)
    non-regenerative anemia and thrombocytopenia
  22. With generalized type III HS, chronic antigenic stimulation results in... (1)
    marked hyperglobulinemia
  23. With generalized type III HS, Ag-Ab complex deposition results in... (2)
    proteinuria (glomerulus), suppurative arthritis (synovium)
  24. Membranoproliferative glomerulonephritis (MPGN) is a _____________HS, in which immune complexes are deposited in the _____________ on the __________ side of the basement membrane. These complexes stimulate ____________________.
    generalized Type III; glomerular vessels; endothelial; mesangial cell and endothelial proliferation
  25. With MPGN, increased _______ and _______ induce mesangial and endothelial proliferation and fibrosis.
    IL-6; TGFβ
  26. 4 chronic viral disease that can cause MPGN.
    equine infectious anemia, infectious canine hepatitis, aleutian disease, african swine fever
  27. Chronic parasitic disease that can cause MPGN.
  28. 3 chronic bacterial diseases that can cause MPGN.
    lyme disease, ehrlichiosis, and anaplasmosis
  29. MPGN can cause proteinuria, and _________ will be lost before ________ because it is smaller.
    albumin; globulins
  30. 8 clinical signs associated with MPGN.
    proteinuria, hypoalbuminemia, edema, sodium retention, azotemia, renal failure, thromboembolic disease, vasculitis
  31. Vasculitis associated with MPGN may results in __________ on the skin and __________.
    target lesions; tissue sloughing (ears)
  32. Purpura hemorrhagic is a ____________ HS seen in horses 2-4 weeks after _____________; it results in... (3)
    generalized Type III; strep equi infection or vaccination; vasculitis, edema, and MPGN.
  33. Dietary HS and drug HS are types of ___________ HS.
    generalized type III
  34. Type IV HS is also called ____________.
    delayed hypersensitivity
  35. Type IV HS is a __________ immune response to ___________ or _________.
    slowly developing; injected Ag; uncleared Ag
  36. Type IV HS is mediated by _________ and _________.
    T cells; NK cells
  37. Pathological consequences of a type IV HS response include... (3)
    tubercle formation, granuloma or granulomatous inflammation.
  38. With a Type IV HS response, Ag is injected into dermis and picked up by __________, which interact with ________ in the ________.
    langerhans cells; memory T cells; regional lymph node
  39. Type IV HS induces _____________, which migrate to the dermis and secrete cytokines, of which ________ is the most important.
    Th1 memory cells; IFNγ
  40. With a Type IV HS response, IFNγ produced by memory Th1 cells draws in _________ to create _________; these accumulate in a ____________.
    macrophages; inflammatory reactions; perivascular formation
  41. Comparative mycobacterial testing in cattle makes use of a ______________ HS response.
    type IV
  42. False negatives can be seen on a comparative mycobacterium test in cattle if... (4)
    infection is in early stages, advanced disease, recent post-partum, and very old animals
  43. False positive can be seen on comparative mycobacterium test in cattle if... (1)
    the animal is infected with other types of mycobacterium.
  44. With short thermal testing for mycobacterium in cattle, you inject ______________ and examine the animal's ________ 4-8 hours later.
    a large volume of tuberculin solution SQ; temperature
  45. With the stertmont test, you administer ________ of tuberculin at the ________, 7 days apart.
    2 doses; same site
  46. You can test for mycobacterium by stimulating lymphocytes in vitro with mycobacterial Ag and then measuring the production of ______.
  47. Tubercle formation occurs with ________ HS and results in _____________; it can be caused by... (3)
    Type IV; granuloma/granulomatous inflammation; tuberculosis, brucellosis, certain fungi
  48. Allergic contact dermatitis occurs with __________ HS; it is induced by ________ to chemicals, or other Ag and _________ bind the Ag directly to stimulate a _______ immune response and _______ production.
    type IV; topical exposure; langerhans cells; Th1; IFNγ
  49. With allergic contact dermatitis, once IFNγ production is stimulated, _______ and ________ migrate to the epidermis and attack sensitized epidermal cells to create ________.
    CTLs; NKT cells; cutaneous vesicles
  50. Atopic dermatitis (Type I HS) presents as... (3)
    In contrast, allergic contact dermatitis (Type IV HS) presents as... (4)
    hyperemia, urticaria, pruritis; hyperemia, vesiculation, alopecia, eryhtrema
  51. Atopic dermatitis (Type I HS) is located on the... (3)
    In contrast, allergic contact dermatitis (Type IV HS) is located on the...
    face, feet perineum; less haired areas
  52. Atopic dermatitis (Type I HS) is induced by... (3)
    In contrast, allergic contact dermatitis (Type IV HS) is induced by... (2)
    foods, pollens, fleas; chemicals, substances
  53. The histopathology of atopic dermatitis (Type I HS) shows... (2)
    In contrast, the histopath of allergic contact dermatitis (Type IV HS) shows... (1)
    eosinophils and edema; mononuclear cell infiltrate
  54. Epidermal necrolysis variants are a _________ HS, and they are often associated with _________.
    Type IV; drug administration
  55. Epidermal necrolysis variants are due to a __________ HS when drugs bind to __________ and upregulate _______, which react with ________ to induce __________.
    T-cell mediated HS; keratinocytes; CD95L; CTLs; apoptosis
  56. 3 typical disorders associated with epidermal necrolysis.
    erythrema multiforme, stevens johnson (<10% skin loss), toxic epidermal necrolysis (>30% skin loss)
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Immuno- Type III and IV HS.txt
2015-03-02 23:06:20

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