Urinary2- Renal Patho 1

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Mawad
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310319
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Urinary2- Renal Patho 1
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2015-10-28 22:01:48
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  1. Grossly, "focal" means...
    one lesion
  2. Histologically, "focal" means...
    <50% of nephrons/glomeruli are involved
  3. Grossly, "diffuse" means...
    entire organ
  4. Histologically, "diffuse" means...
    >50% of nephrons/glomeruli are involved
  5. Grossly, "segmental" means...
    has distinct geometric shape
  6. Histologically, "segmental" means...
    <50% of the glomerular tuft is involved; or only part of the nephron is involved
  7. Grossly, "global" means...
    it is not used to describe gross lesions
  8. Histologically, "global" means...
    >50% of the glomerular tuft is involved
  9. Grossly, "multifocal" means...
    multiple discrete lesions
  10. Histologically, "multifocal" means...
    tubulointerstitial lesions (NOT glomerular lesions)
  11. Words used to describe distribution of lesions in the kidney.
    diffuse, random. miliary, multifocal, focal
  12. Lesions scattered throughout, not associated with any specific structure.
    random
  13. Small, scattered foci throughout the organ, too numerous to count.
    miliary
  14. Lesions tracking along a vessel.
    serpiginous
  15. How can you describe demarcation? (4)
    well demarcated vs poorly demarcated [can you see the border?], encapsulated vs unencapsulated
  16. Degree of elevation or depression.
    contour
  17. Describe the usual contour of acute necrosis and inflammation.
    bulge due to intracellular and extracellular edema
  18. Describe the usual contour with chronic lesions.
    depressed and contracted due to atrophy and fibrosis
  19. Red color can be indicative of...
    hemoglobin or blood; congestion vs hemorrhage
  20. Grey, white tan, or yellow color can be indicative of... (5)
    necrosis, degeneration, fat, inflammatory exudate, neoplasms
  21. Green color can be indicative of... (2)
    bile, rotten
  22. Black color can be indicative of... (3)
    pseudomelanosis (b/c kidney is close to gall bladder), in sheep can be true melanosis, heavy metal intoxication
  23. Consistency/texture can be... (3)
    amorphous (cream cheese), solid (maintains shape), cystic (fluid filled)
  24. Abscesses/ suppurative inflammation in the cortex only are usually of _________ origin.
    embolic
  25. Abscesses/suppurative inflammation in the medulla and cortex usually originates from __________.
    ascending pyelonephritis
  26. [Differentials] White/tan foci. (6)
    abscess/suppurative inflammation, neoplasia, granuloma, FIP [cat], halicephalobus gingivalis [equine], multifocal tubulointerstitial nephritis [cattle]
  27. How does a parasitic/fungal granuloma arise?
    aberrant migration- visceral larval migrans
  28. With grossly multifocal to coalescing suppurative pyelonephritis, histologically you will see...
    bacteria and neutrophils
  29. Grossly multifocal embolic tubulointerstitial nephritis due to __________; histopathologically, you will see ____________.
    neonatal septicemia; lymphocytic inflammation
  30. [Differentials] Red foci. (4)
    hemangiosarcoma (older dogs), vasculitis (tracks along vessels), acute hemorrhagic infarcts, glomerulonephritis (red spots in cortex)
  31. [Differentials] renal cysts. (1)
    polycystic kidney disease (Persians, bull terriers, westies, prerendale sheep)
  32. [Differentials] Lesions in renal pelvis. (4)
    hydronephrosis (expanded renal pelvis due to obstruction), pyonephrosis (hydronephrosis with pus), pyelonephritis, nephrolithiasis
  33. Unilateral hydronephrosis means the obstruction is in... (3)
    ureteropelvic junction, ureter, or ureterocystic orifice.
  34. Bilateral hydronephrosis means the obstruction is in... (3)
    urinary bladder, urethra, or both ureters.
  35. Nephrolithiasis can be caused by... (3)
    stone, blood lot, or necrotic papilla
  36. What gross lesions are expected with acute azotemia? (4)
    papillary necrosis, subtle parenchymal swelling, pallor (glomerular disease), smaller (if chronic is presenting acutely)
  37. Gross lesions expected with proteinuria/glomerular disease. (3)
    normal shape acutely, cortex pallor, small/shrunken with chronic
  38. What stain do you use to detect amyloid in the kidney?
    Lugols iodine
  39. Gross lesions expected with chronic kidney disease. (3)
    small, bumpy, if only one kidney the contralateral may undergo compensatory hypertrophy
  40. What is a pathognomonic lesion for canine herpes virus 1?
    red petechiae in puppies younger than 2 weeks
  41. What is a large worm you see in the renal pelvis of dogs?
    Dioctophyma renale
  42. What is a small worm that is grossly evident in the kidneys of infected foals?
    Actinobacillus equuli
  43. Lesion that occurs in the kidney with vitamin D toxicity?
    mineralization of corticomedullary junction
  44. What are the gross lesions in the kidney with FIP?
    multifocal perivascular pyogranulomatous nephritis
  45. Causes of acute renal disease. (5)
    acute tubular epithelial injury, infectious tubulointerstitial nephritis, ascending pyelonephritis, vascular disease/acute infarcts, acute glomerulonephritis
  46. What are 3 causes of acute tubular epithelial injury?
    toxic, ischemic, obstructive
  47. What is the gross appearance of acute infarcts in the kidney?
    red, wedge-shaped foci, especially in the cortex
  48. What is important to remember when evaluating any animal for acute kidney injury?
    chronic disease can present acutely
  49. What is the basis for why AKI can sometimes be reversible?
    --> normal tubule--> proximal tubule simplification: lose their apical brush border--> scattered tubule epithelial cells die and detach--> dead cells/fragments obstruct lumens of distal nephrons-->neighboring cells stretch to cover denuded BM--> normal tubule
  50. What is imperative for AKI to be reversible?
    basement membrane must be intact!!
  51. Tubular epithelial cell vacuolation is associated with __________.
    proteinuria
  52. Histological lesions of acute kidney injury. (8)
    loss of apical brush border, singly dead epithelial cells, fragments of cells in tubules,stretched out simplified cells, congestion, interstitial hemorrhage, acute inflammation, crystals in tubules
  53. If AKI insult is severe and/or prolonged, ___________ may develop.
    coagulative and liquefactive necrosis
  54. What are the determinants of the outcome of AKI? (3)
    timely removal of inciting cause, maintenance of intact tubular basement membranes, cytokine expression of tubular epithelial cells
  55. Mechanisms of acute tubular epithelial injury? (8)
    interference with oxidative phosphorylation, vascular effects, lipid peroxidation, membrane damage, calcium homeostasis, protein synthesis, cytoskeletal toxins, induction of apoptosis
  56. Causes of ischemic acute tubular epithelial injury. (5)
    hypovolemic shock, neurogenic shock, cardiogenic shock, septic shock, DIC
  57. What portion of the tubule is most susceptible to ischemic ATEI?
    striaght portion of the proximal tubule (pars recta)
  58. What other tubular injury has so many of the same lesions as ischemic ATEI that you cannot definitively tell them apart histologically?
    nephrotoxic acute tubular injury
  59. Aminoglycosides cause ___________ tubular injury; they are eliminated mostly by __________, but some is taken up by the __________, where it complexes with _______ and forms _________---> ________.
    acute ischemic; glomerular filtration; proximal tubule; iron; reactive oxygen species; apoptosis
  60. What gross lesion is classically associated with NSAID nephrotoxicity?
    papillary necrosis
  61. How do NSAIDs cause nephrotoxicity?
    inhibit COX--> decrease renal PGE and PGI (vasodilatory)--> vasconstriction--> decreased GFR--> renal ischemia
  62. Ethylene glycol is rapidly absorbed from the GI and metabolized in the liver by _________ into __________; ___________ precipitate in the tubules.
    alcohol dehydrogenase; nephrotoxic metabolites; calcium oxalate crystals
  63. Differentials for oxalate crystals in the tubules. (4)
    ethylene glycol, cruciferous vegetables, philadendron plants, high amounts of ascorbic acid (vit C)
  64. Oak nephrotoxicity occurs in _______; the toxic principal is _________; grossly, kidneys are __(3)__, and there is accompanying... (3)
    ruminants; tannins; swollen, pale, and cortical petechiae; colitis, perirenal edema, and anasarca.
  65. Histologically, you will see __________ of the proximal tubules in ruminants with oak nephrotoxicity.
    coagulative necrosis
  66. Malemine and cyanuric acid crystallize in the kidneys of _________ and cause production of _________ in the ________ nephron.
    small animals; yellow-brown crystals; distal
  67. Toxin in cats that causes overt necrosis of the entire proximal tubule.
    Lilies (all parts of the plant are toxic)
  68. What do heavy metals cause to form in the tubules?
    inclusions in tubular epithelial cells
  69. Describe the pathophysiology of pigment nephropathy.
    RBC lysis--> anemia and hemoglobin release--> ischemic necrosis and hemoglobin is toxic to tubules
  70. 3 main patterns of inflammatory lesions in the kidney. (3)
    embolic, pyelonephritis, interstitial
  71. What are some gross lesions that can be present with embolic nephritis? (3)
    multifocal**(always) miliary/larger lesions, bilateral*, usually cortical
  72. What are the most common causes of embolic nephritis? (4)
    bacterial, mycobacterial, fungal, viral (FIP)
  73. Bacterial infection causes __(3)__ [adjectives] nephritis.
    acute suppurative embolic
  74. Mycobacterial embolic nephritis causes what lesions?
    chronic multifocal granulomas
  75. 2 types of lesions that can be caused by fungal embolic nephritis.
    chronic granulomatous or vascular with infarcts
  76. Pyelonephritis can cause loss of ____________ due to ___________.
    concentrating ability; renal papillary necrosis
  77. Predisposing causes to pyelonephritis. (5)
    cystitis, vesiculoureteral reflux, young, female, poor urogenital anatomy
  78. Gross lesions of acute pyelonephritis.
    suppuration, necrosis focused on renal pelvis, +/- papillary necrosis
  79. Gross lesions of chronic pyelonephritis. (3)
    radiating bands of fibrosis, atrophy of cortex, hydronephrosis
  80. With Acute Tubulointerstitial Nephritis (ATIN), tubular damage results from compression of peritubular capillaries by __(2)__.
    interstitial edema and inflammatory cells
  81. Interstitial inflammation that injures tubules.
    acute tubulointerstitial nephritis (ATIN)
  82. Gross lesions of ATIN are similar to those of __________, and you need to use __________ to tell the difference.
    acute tubuloepithelial injury (ATEI); histology
  83. Leptospiral organisms like to live in the __________; gross lesions are _________; lesions are a good example of __(2)__.
    proximal tubules; non-specific; interstitial pattern or tubulointerstitial pattern
  84. Tubular disease can be secondary to... (2)
    proteinuria, bile cast nephropathy from liver failure
  85. Disorder in which epithelial cells don't resorb glucose or AA, leading to glucosuria with normoglycemia.
    Fanconi's-like syndrome (genetic in Basenjis)
  86. Why do biopsy with AKI?
    will help determine if the kidneys can be saved or not (are lesions reversible?)
  87. Chronic irreversible lesions. (4)
    interstitial fibrosis, tubular atrophy (thicken BM), glomerulosclerosis, arteriosclerosis
  88. What is the hallmark of chronic kidney disease?
    interstitial fibrosis
  89. Why do you see depressions on the surface of the kidney with interstitial fibrosis?
    collagen contracts (like a scar)
  90. What will you see on histopath with interstitial fibrosis?
    collagen physically separates tubules from peritubular capilaries; TUBULES SHOULD BE BACK-TO-BACK
  91. Describe histopath of tubular atrophy. (2)
    thickened/hyalinized BM, attenuated epithelium (due to hypoxia)
  92. Describe mechanistic progression of renal disease.
    nephron loss-> other nephrons hypertrophy to compensate-> increased SNGFR-> tubules have increase workload-> interstitial fibrosis and tubular atrophy-> glomeruli have extra workload as well
  93. Pro-fibrotic molecules. (3)
    TGF-β, smads, CTGF (connective tissue growth factor)
  94. Describe the results of pathologic activation of RAAS. (3)
    hypertrophy, fibrosis through TGF-β, oxidative stress on cells
  95. Anti-fibrotic mediators. (2)
    hepatocyte growth factor, bone morphologic protein-7

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