S3M1 path2

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    • Extracellular hyaline
    • - homogenous glassy, pink appearance (H & E)
    • - old scars may appear hyalinized
    • - walls of arterioles may become hyalinized- deposition of BM material
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    • Hyaline accumulation
    • - staining with PAS and diatase digestion(hydrolyzing glycogen)
    • - hyaline droplets are distinguishable as little pink droplets
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    • Excessive IC deposits of glycogen
    • - abnormality in glucose or glycogen metabolism
    • - Best carmine stains for glycogen (rose to violet color)
    • - clear vacuoles within cytoplasm
    • - fixed with absolute alcohol
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    • Glycogen in renal tubules seen in DM (H & E stain)
    • - with DM glycogen found in renal tubular epithelial cells, liver, heart muscle and beta cells of pancreas
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    glycogen storage disease stained with PAS
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    pigment (carbon) deposition from anthrocosis or air pollution
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    • Lipofuscin deposition (yellow-brown granule)
    • - endogenous, insoluble wear and tear pigment
    • - telltale sign of free radical damage
    • - not injurious to cell or function
    • - liver and heart of aging patients
    • - also seen in severe malnutrition and cancer cachexia
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    • Hemosiderosis
    • -IC Fe accumulation
    • - Seen in increase Fe intake, hemolytic anemia, repeated blood transfusions (beta- Thal patient)
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    Prussian blue stain of hemosiderosis
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    • Psammona bodies
    • - dystrophic calcification that may form in papillary cancers
    • - IC, EC or both locations
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    • Heterotopic bone
    • - dystrophic calcification
    • - IC, EC or both
    • - basophilic, amorphous, granular, sometimes clumper appearance
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    • Metastatic calcification of the lung
    • 4 principal causes of hypercalcemia
    • - increased PTH - destruction of bone tissue
    • - vit D related issue - renal failure
  13. Major components of acute inflammation
    • - vasodilation(histamine & NO)=>increased blood flow
    • - leakage from microvasculature (exudate= plasma+proteins)
    • - leukocyte immigration (mostly n0)
  14. endothelial injury
    • - occurs in arterioles, capillaries and venules
    • - caused by burns and some microbial toxins
    • - rapid and may be long lived (hours to days)
  15. leukocyte-mediated vascular injury
    • - in venules and pulmonary capillaries
    • - associated with late stages of inflammation
    • - long lived
  16. increased transcytosis
    • occurs iin venules
    • induced by VEGF
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    • Lymphangitis
    • inflammation of lymphatics
    • red streaks seen clinically near skin wound
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    • Lymphadenitis
    • painful inflammation and enlargement of draining lymph nodes
    • hyperplasia of lymphoid follicles
    • increased lymphocytes and macrophages
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    Lymphadenitis
  20. n0 migration thru blood vessels
    • 1- rolling= P-selectin, E-selectin, (enodthelial expressed)
    • 2- integrin activation by chemokines= proteoglycan
    • 3- stable adhesion- integren:ICAM-1
    • 4- diapedisis- PECAM-1(CD31)
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    • L- n0 inflammatory infiltrate seen early in inflammation
    • M- mononuclear(lymphocytes and monocytes) seen later
  22. bactericidal/permeability increasing protein
    • binds bacterial endotoxin
    • important in defense against some G- bacteria
  23. alternatively activated macrophages
    • important in tissue repain (arginase, proline, polyaminases and TGF-beta
    • important in resolution of inflammation (IL-10, TGF-beta)
  24. abscess
    - always neutrophils
  25. prostacyclin (PGl2)
    • causes vasodilation
    • inhibits platelet aggregation

    cell derived mediator
  26. Thromboxane A2 (TXA2)
    • causes vasoconstriction
    • promotes platelet aggregation

    cell derived mediator
  27. PGD2 and PGE2
    • vasodilation
    • increased vascular permeability

    cell derived mediator
  28. Lipoxin- LXA4 and LXB4
    inhibits neutrophil adhesion and chemotaxis
  29. 5-HETE
    chemotaxis
  30. Leukotriene B4 (LTB4)
    • vasoconstriction
    • bronchospasm
    • increased vascular permeability
  31. NO
    cell derived
    • inhibits cellular component of inflammatory response
    • microbicidal
    • inhibits leukocyte recruitment
    • inhibits many features of mast cell-induced inflammation
    • causes vasodilation
    • reduced platelet aggregation and adhesion
  32. PAF
    cell derived
    • vasoconstriction and bronchoconstriction
    • vasodilation and increased vascular permeability at low concentrations
    • increased WBC adhesion to endothelium
    • chemotaxis, degranulation and oxidative burst
    • boosts eicosanoid synthesis
  33. LAP stain
    • leukocyte ALP staining
    • differentiates between leukomoid and leukemia
    • LAP+= leukomoid
    • leukemia cells are in arrested development
  34. chronic inflammation characteristics
    • infiltration with mononuclear cells (m0, lymphocytes, plasma cells)
    • tissue destruction (induced by offending agent and inflammatory cells)
    • healing by connective tissue replacement of damaged tissue (angiogenesis and scarring)
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    • Plasma cell
    • Russel bodies present (RER and proteins
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    • Eosinophil
    • IgE mediated immune reaction
    • helmith/parasitic infections
    • granules contain major basic protein
    • causes lysis of mammalian epithelial cells
    • contribute to tissue destruction in allergies
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    • serous inflammation
    • blister from burn or viral infection
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    • caseous granuloma
    • classic TB granuloma with central caseous necrosis surrounded by mutliple Langerhan cells, epitheloid cells and lymphocytes
    • - seen in TB, syphillis and cat-scratch disease
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    • non caseous granuloma
    • - leprosy, sarcoidosis and Chrons
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155721
Card Set
S3M1 path2
Description
S3M1 path2
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