Pathology- Deposits and Pigments.txt

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Mawad
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300120
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Pathology- Deposits and Pigments.txt
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2015-04-06 21:31:44
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  1. Extracellular deposition of insoluble masses of glycoprotein fibrils.
    amyoloidosis
  2. Tissues undergoing accumulation of amyloid typically have concurrent _____________ and sometimes ___________.
    degeneration; necrosis
  3. Amyloid has a positive _______ reaction.
    PAS
  4. What are amyloid precursor proteins (APP)? (3)
    Ig V-regions of light chains, CRP, hormone precursor molecues
  5. Amyloidosis in the brain occurs in the __________ and ___________.
    cerebral cortex; hippocampus
  6. Amyloidosis in the kidney occurs in the ___________ due to filtering of ________ and leads to ___________.
    glomerulus; serum proteins; protein-losing nephropathy
  7. Amyloidosis in the liver occurs in the ___________, first by the _________.
    space of Disse; Kupffer cells
  8. Amyloidosis in the lymph nodes occurs in __________ and ____________.
    lymphoid follicles; subcapsular sinusoids
  9. Amyloidosis occurs in pancreatic islets in ______[species] only.
    cats
  10. Amyloidosis occurs in the ________ and ________ of skin in _________ [species].
    dermis; subcutis; horses
  11. Amyloidosis occurs in the __________ of the small intestine and is apparently incidental.
    lamina propria
  12. Amyloidosis of the spleen occurs around ___________.
    central arterioles
  13. At a gross level, amyloidosis causes tissues to be... (3)
    pale, tan, and swollen.
  14. Microscopically, amyloidosis does not affect tissues ______________.
    uniformly throughout
  15. Amyloidosis results in the deposit of ____(3)____ material.
    extracellular, homogeneous, eosinophilic
  16. With amyloidosis, there is _________ of inflammation near or in amyloid deposits.
    no evidence
  17. What special stains are used to diagnose amyloidosis?
    Congo red, PAS
  18. __________ with Congo red stain causes amyloid to glow (birefringent).
    polarized light
  19. Amyloidosis is typically a secondary disease with primary....
    chronic systemic inflammation
  20. Amyloid precursor proteins are ___________ by __________; then, indigestible fragments are ____________, _____________ and ___________; there is gradual accretion of __________, leading to secondary ___________ and ___________.
    phagocytosed; macrophages; regurgitated; re-phagocytosed; re-regurgitated; fibril masses; degeneration; necrosis
  21. Amyloid can be lethal, usually due to _________ leading to _________.
    glomerular lesions; kidney failure
  22. Amyloid deposits act as ____________ and can damage adjacent tissue by... (2)
    apace-occupying masses; direct cytotoxicity or reduced capillary perfusion.
  23. What are the 2 types of morphologic changes associated with lipidosis?
    macrovesicular and microvesicular
  24. With macrovesicular lipidosis, there is...
    a large single lipid vacuole displacing the cell contents to the periphery.
  25. With microvesicular lipidosis, there is...
    small, discrete round lipid vacuoles.
  26. The pathogenesis of lipidosis involves ____________ accumulation associated with ________________.
    triglyceride; cell metabolic disturbances
  27. With lipidosis, there is retention of triglycerides due to ____(2)____ and lipid metabolites due to __________.
    excessive uptake or decreased export; incomplete degradation
  28. Lipidosis may occur because of reduced triglyceride utilization due to ________________.
    mitochondrial injury
  29. Mineralization is the deposition of _________ in _______.
    insoluble materials; life
  30. Deposition of mineral into necrotic foci with an adjacent blood supply.
    dystrophic mineralization
  31. Deposition of mineral into normal tissues due to altered calcium metabolism.
    metastatic mineralization
  32. The pathogenesis of dystrophic mineralization involves minerals binding to _________ and _________ released from ______________.
    denatured proteins; lipids; dead cells
  33. The pathogenesis of metastatic mineralization involves ______________.
    hypercalcemia
  34. Humoral hypercalcemia of malignancy is a __________ syndrome associated with ____________.
    paraneoplastic; metastatic mineralization
  35. The gross morphologic features of mineralization include.... (3)
    firm, white/gray, grates when cut
  36. The microscopic morphologic features of mineralization are... (3)
    pale to dark, blue to purple, irregular crystals
  37. At the cellular level, the pathogenesis of mineralization involves free _______________ precipitating in mitochondrial leaves as _________; the mineral deposits damage mitochondria and inhibit ______________.
    intracellular calcium; phosphate salts; ATP production
  38. At the tissue level, the pathogenesis of mineralization involves free ___________ from blood precipitates on ___________ and __________.
    extracellular calcium; coagulated proteins; lipids
  39. Mineral deposits associated with mineralization are ___________; dystrophic calcification is often associated with _____________ indicative of an ____________.
    permanent; localized secondary changes; underlying disease process
  40. Metabolic disease associated with systemic mineralization of connective tissues at many sites is characteristic of __________; affected sites include... (3)
    uremia; digestive tract (stomach), kidney, and lung.
  41. Crystalline mineral deposits may incite additional tissue damage due to _________ and thereby invoke a ___________.
    mechanical irritation; secondary inflammatory reaction
  42. Metaplastic tissue change in which true bone is formed in extra-skeletal tissues.
    ossification
  43. hat is the morphologic change associated with pathologic ossification?
    bone in extra-skeletal tissues
  44. Sites of abnormal ossification in animals: (5)
    articular cartilage of joints, lateral cartilage of hooves (sidebone), skeletal muscle, spinal cord dura matter, tumors
  45. What is the term for ossification at sites of severe traumatic muscle injury?
    myositis ossificans
  46. Deposition of insoluble uric acid/urate crystals in soft tissue.
    gout
  47. What is the species predilection for gout?
    humans, birds, reptiles
  48. Grossly, gout is associated with what morphological changes?
    chalky white nodules (tophi)
  49. What are the 2 gross forms of gout?
    articular form, visceral form
  50. The pathogenesis of gout involves __________ that incite mechanical irritation; then, there is an infiltration of _________ and __________.
    urate crystals; neutrophils; macrophages
  51. What are the etiologies of gout in birds and reptiles? (3)
    dehydration, high-protein diets, or renal failure
  52. 4 particulates that are exogenous pigments.
    asbestos, carbon, dust, silica
  53. Dust, especially coal, causes ____________, which is ___________ pigment deposition.
    pneumoconiosis; black/dark brown
  54. 6 non-particulates that are exogenous pigments.
    barium, carotenoids, drugs, lead, silver, tattoo ink
  55. 5 endogenous pigments.
    blood pigments, ceroid, iron sulfide, lipofuscin, melanin
  56. Blood pigments result from ___________ to _____________; iron-containing pigments stain positive for ___________.
    blood cell degradation; conserve iron; Prussian blue
  57. Hemoglobin imparts ______ pigment; hemosidern imparts a _________ pigment with ___________; ferritin imparts ________________; biliverdin imparts a _________ pigment; bilirubin imparts a _________ pigment; urobilin imparts a __________.
    red; golden brown; globular cytoplasmic granules; dark brown cytoplasmic granules; green; yellow-brown; yellow color to urine
  58. Main iron storage form in blood.
    ferritin
  59. Heme-transporting form to carry water-insoluble heme in blood.
    biliverdin
  60. Main porphyrin excretion form.
    bilirubin
  61. Product of microbial processing of excreted porphyrin rings.
    urobilin
  62. Excessive accumulation of hemosiderin occurs in what pathologic states? (2)
    heart failure, intravascular hemolysis
  63. Ceroid results from _________ and _________.
    lipid peroxidation; fat necrosis
  64. Lipofuscin is the __________ pigment in ___________.
    "old-age"; post-mitotic cells
  65. Icterus results from ____________.
    abnormal retention of hemes
  66. Pre-hepatic icterus results from __________________.
    excess hemoglobin breakdown (hemolysis)
  67. Hepatic icterus results from ___________, leading to a failure in ___________________.
    organic liver disease; processing and excreting bilirubin
  68. Post-hepatic icterus results from ____________.
    blocked bile excretion
  69. The test to discriminate the bilirubin forms; works best in humans.
    Van den Bergh test
  70. Describe the Van den Bergh test.
    clinical chemistry analysis demonstrating increased unconjugated (water-insoluble) bilirubin in serum

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