S3M1 path2

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sweetlu
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155721
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S3M1 path2
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2012-06-05 18:41:01
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S3M1 path2
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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
    • Hyaline accumulation
    • - staining with PAS and diatase digestion(hydrolyzing glycogen)
    • - hyaline droplets are distinguishable as little pink droplets
    • 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
    • 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
  1. glycogen storage disease stained with PAS
  2. pigment (carbon) deposition from anthrocosis or air pollution
    • 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
    • Hemosiderosis
    • -IC Fe accumulation
    • - Seen in increase Fe intake, hemolytic anemia, repeated blood transfusions (beta- Thal patient)
  3. Prussian blue stain of hemosiderosis
    • Psammona bodies
    • - dystrophic calcification that may form in papillary cancers
    • - IC, EC or both locations
    • Heterotopic bone
    • - dystrophic calcification
    • - IC, EC or both
    • - basophilic, amorphous, granular, sometimes clumper appearance
    • Metastatic calcification of the lung
    • 4 principal causes of hypercalcemia
    • - increased PTH - destruction of bone tissue
    • - vit D related issue - renal failure
  4. Major components of acute inflammation
    • - vasodilation(histamine & NO)=>increased blood flow
    • - leakage from microvasculature (exudate= plasma+proteins)
    • - leukocyte immigration (mostly n0)
  5. endothelial injury
    • - occurs in arterioles, capillaries and venules
    • - caused by burns and some microbial toxins
    • - rapid and may be long lived (hours to days)
  6. leukocyte-mediated vascular injury
    • - in venules and pulmonary capillaries
    • - associated with late stages of inflammation
    • - long lived
  7. increased transcytosis
    • occurs iin venules
    • induced by VEGF
    • Lymphangitis
    • inflammation of lymphatics
    • red streaks seen clinically near skin wound
    • Lymphadenitis
    • painful inflammation and enlargement of draining lymph nodes
    • hyperplasia of lymphoid follicles
    • increased lymphocytes and macrophages
  8. Lymphadenitis
  9. 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)
    • L- n0 inflammatory infiltrate seen early in inflammation
    • M- mononuclear(lymphocytes and monocytes) seen later
  10. bactericidal/permeability increasing protein
    • binds bacterial endotoxin
    • important in defense against some G- bacteria
  11. alternatively activated macrophages
    • important in tissue repain (arginase, proline, polyaminases and TGF-beta
    • important in resolution of inflammation (IL-10, TGF-beta)
  12. abscess
    - always neutrophils
  13. prostacyclin (PGl2)
    • causes vasodilation
    • inhibits platelet aggregation

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

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

    cell derived mediator
  16. Lipoxin- LXA4 and LXB4
    inhibits neutrophil adhesion and chemotaxis
  17. 5-HETE
    chemotaxis
  18. Leukotriene B4 (LTB4)
    • vasoconstriction
    • bronchospasm
    • increased vascular permeability
  19. 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
  20. 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
  21. LAP stain
    • leukocyte ALP staining
    • differentiates between leukomoid and leukemia
    • LAP+= leukomoid
    • leukemia cells are in arrested development
  22. 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)
    • Plasma cell
    • Russel bodies present (RER and proteins
    • 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
    • serous inflammation
    • blister from burn or viral infection
    • 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
    • non caseous granuloma
    • - leprosy, sarcoidosis and Chrons

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