Urinary2- Renal Patho 2

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  1. Dissolution of the glycocalyx leads to __________.
  2. Viability of the glomerular endothelial cells requires _________, which comes from the _________.
    VEGF; podocytes
  3. ___________ is the hallmark of glomerular disease.
  4. What are the 4 components of nephrotic syndrome that may result from glomerular disease?
    proteinuria, hypoalbuminemia, edema/ascites, hypercholesterolemia/hyperlipidemia
  5. What is NOT a criterion for diagnosis of nephrotic syndrome?
  6. Gross lesions associated with acute glomerular disease. (3)
    swollen, smooth capsular surface, glomeruli may be red
  7. Gross lesions associated with chronic glomerular disease. (4)
    pale, firm, irregular capsular surface, granular cortex on cut surface
  8. What are the 2 large categories of glomerular disease in animals?
    imune complex mediated glomerular nephritis (ICGN), non-ICGN
  9. What 3 diseases are immune complex-mediated GN?
    membranoproliferative GN, membranous GN, mesangioproliferative GN
  10. What 4 disorders are non-ICGN?
    amyloidosis, focal segmental glomerulosclerosis, podocytopathy, GBM-opathy
  11. Disorder with immune complexes acting as aggregates of Ag and Ab in glomeruli.
    immune complex-mediated glomerulonephritis
  12. What are some examples of glomerular lesions? (5)
    hypercellularity (mesangial or endocapillary), mesangial expansion, immune deposits, deposition of fibrils, GBM remodeling
  13. With membranous GN, immune complexes are on the _________ of the glomerular BM.
  14. With membranous GN, complement is activated ___________ the capillary lumen, resulting in...
    away from (b/c IC are in abluminal surface of BM); inflammatory cells are not attracted to tuft and podocytes are damaged.
  15. Causes of secondary membranous GN. (3)
    infections, neoplasia, drugs
  16. With membranoproliferative GN, there is __________ hypercellularity due to __________.
    endocapillary; subendothelial deposits of IC
  17. 3 lesions associated with membranoproliferative GN.
    endocapillary hypercellularity, mesangial hypercellularity, glomerular BM remodeling
  18. Amyloidosis is caused by... (2)
    genetic predisposition or chronic inflammation
  19. Describe the non-genetic pathogenesis of amyloidosis.
    chronic inflammation--> increase SAA--> circulates in blood--> trapped in kidney--> fibrils deposited in glomeruli/interstitium
  20. Focal glomerulosclerosis occurs because of ___________
    podocyte injury
  21. Podocyte injury leads to... (3)
    sclerosis, fibrosis, syenchiae (adhesions b/w GBM and Bowman's capsule BM)
  22. Primary focal segmental glomerulosclerosis is assumed to be due to...
    abnormal podocyte genes/proteins.
  23. Secondary focal segmental glomerulosclerosis is due to... (3)
    podocyte injury due to systemic hypertension, obesity, or decreased nephron mass (which causes increase SNGFR).
  24. What is an example of a glomerular BM-opathy?
    Alport's syndrome- mutation in type IV collagen that leads to weaker glomerular BM
  25. Multifocal embolic nephritis in a foal is caused by septicemia with __________.
    Actinobacillus equuili
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Urinary2- Renal Patho 2
2015-10-29 02:20:58
vetmed urinary2

vetmed urinary2
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