Urinary2- Glomerular Disease

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Urinary2- Glomerular Disease
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2015-10-11 19:56:22
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  1. What are the components of the glomerular filtration barrier, and what selectivity does each confer?
    • Endothelium: charge selectivity (negaitve)
    • Basement Membrane: size (60kD spaces) and charge selectivity (negative)
    • Visceral Epithelium/Podocytes: size and charge selectivity (negative)
  2. Podocytes synthesize the ________ and have _________ capability.
    basement membrane; phagocytic
  3. 3 functions of the mesangium.
    structural support, contractile, phagocytic
  4. The ___________ is an early site of deposition of immune complexes and amyloid fibrils.
    mesangium
  5. Protein losing nephropathy= ____________; two types of PLN are __(2)__.
    glomerular disease; glomerulonephritis (GN) and amyloidosis
  6. What are the most common ways the glomerulus is injured, leading to glomerular disease? (3)
    increase glomerular capillary BP (hypertension), immune complex deposition on the endothelium and BM, amyloid deposition
  7. Glomerular disease eventually leads to... (3)
    inflammation, proliferation of extracellular matrix, and fibrosis.
  8. ___________ is the most common cause of glomerular disease; it results from...
    Immune complex deposition; nearly equal numbers of antigen and antibody complexes in the circulation.
  9. Immune complex GN is caused by...
    deposition of immunoglobulin or complement in the glomerular capillary wall.
  10. Factors affecting the localization of deposition of immune complexes include... (4)
    size of complexes, charge of complexes, removal of complexes by phagocytosis, and damage to the BM.
  11. Small immune complexes that are deposited under the foot processes.
    Subepithelial complexes
  12. Large or highly-negatively charged complexes that are under the endothelium (too large to pass the BM).
    Subendothelial complexes
  13. The location of immune complex deposition determines the __(2)__.
    histologic changes and severity of glomerular dysfunction
  14. Subepithelial complexes are associated with __(2)__ histologic changes and ________ proteinuria.
    BM thickening, minimal inflammatory cell infiltration; severe
  15. Subendothelial complexes are associated with __(2)__ histologic changes and _________ proteinuria.
    BM thickening, recruitment of inflammatory cells; moderate
  16. Intramembranous complex deposition is associated with _____________.
    anti-glomerular basement membrane disease
  17. Mesangial complexes are __________.
    asymptomatic
  18. Immune complex deposition in the glomerulus reduces the amount of __________, thus enhancing filtration of ____________, such as _________.
    fixed negative charge; negatively-charged circulating macromolecules; albumin
  19. Complement activation in the glomerulus results in ___(3)___.
    membrane damage, proteinuria, and recruitment of inflammatory cells
  20. Platelet activation occurring secondary to endothelial damage causes __(3)__.
    proliferation of mesangium and endothelium, vasospasm, and increased coagulation
  21. How do mesangial cells contribute to glomerular inflammation?
    increased matrix production--> fibrosis and scarring
  22. 3 consequences of immune complex deposition on glomerulus.
    reduce negative charge, activate complement, activate platelets
  23. Neutrophils and macrophages localize in the glomeruli and cause damage by...
    releasing mediators that damage and scare the glomerulus.
  24. Lesion associated with membranous GN.
    BM thickening
  25. Pathogenesis of membranous GN.
    subepithelial complexes, minimal inflammation
  26. Clinical course of membranous GN. (3)
    slowly progressive, marked proteinuria, eventual nephrotic syndrome
  27. Lesion associated with proliferative GN.
    hypercellularity
  28. Pathogenesis of proliferative GN.
    mesangial complexes with increase mesangial cells
  29. Clinical course of proliferative GN.
    no clinical disease
  30. Lesion associated with membranoproliferative GN. (2)
    BM thickening and hypercellularity
  31. Pathogenesis of membranoproliferative GN.
    subendothelial complexes with increased inflammatory cell influx
  32. Clinical course of membranoproliferative GN. (2)
    moerate proteinuria, progression to renal failure
  33. In most cases, GN is classified as ________ because...
    idiopathic; antigen source or underlying disease is not identified.
  34. The primary target for immune-mediated glomerular disease is the ___________; the primary target for non-immune mediated appears to be the ___________.
    filtration barrier; endothelial cell
  35. Damaged endothelial cells release factors that have __(3)__ effects, stimulating __________.
    vasoactive, proliferative, and pro-inflammatory; coagulation
  36. Factors that damage endothelial cells... (3)
    hemodynamic factors (hypertension), coagulation followed by platelet release, hyperlipemia
  37. Glomerular disease may induce __________ and progress to ____________.
    tubulointerstitial disease; end-stage kidney disease
  38. Obstruction of glomerular capillaries may result in ________ of the tubules and ___________.
    ischemia; tubulointerstitial disease
  39. Proteinuria leads to _____________ and _________ disease.
    interstitial immune response; tubulointerstitial disease
  40. Inflammatory mediators from damaged glomeruli may lead to ___(2)___ damage.
    tubular and interstitial
  41. GN may resolve by... (3)
    solubilization of complexes by complement, phagocytosis of complexes by macs, degradation of complexes by proteases
  42. Removal of ___________ may result in resolution of GN.
    causative agent
  43. When a large amount of protein is consumed, ___________ occurs; the _______ increases, which worsens permselectivity; this also leads to __(2)__.
    hyperfiltration; SNGFR; inflammation and injury to tubules and BM
  44. GN is classified morphologically according to the presence of... (3)
    BM thickening, hypercellularity, or both.
  45. Disease characterized primarily by fibrosis of the glomeruli.
    glomerulosclerosis
  46. Chronic changes associated with glomerular disease eventually lead to _________; _________ glomeruli are not functional.
    sclerosis; sclerotic
  47. The presence of _________ on US is suggestive of glomerular disease.
    tubular protein casts
  48. Chronic GN is accompanied by...
    tubular dilatation and atrophy, interstitial lymphplasmacytic inflammation, and interstitial fibrosis.
  49. Gross changes of glomerular disease are ________.
    rare
  50. Group of diseases characterized by extracellular deposition of fibrils formed by polymerization of protein subunits with a beta-pleated sheet.
    amyloidosis
  51. Amyloid deposits are detrimental due to their __(2)__.
    insolubility and resistance to proteolysis
  52. What is the clinical diagnosis of amyloidosis based upon?
    green birefringence after Congo red staining when viewed under polarized light
  53. Renal amyloidosis in dogs and cats is... (3)
    systemic, reactive, and involves AA amyloid.
  54. Familial amyloid syndromes in __(6)__ are examples of reactive, systemic amyloidosis.
    Abyssinian, Siamese, and Oriental shorthaired cats and Shar Pei, Beagle, and English Foxhound dogs
  55. Amyloid A protein is an animal terminal fragment of ___________.
    serum amyloid A (acute phase reactant)
  56. __(2)__ are necessary pre-requisites for development of reactive amyloidosis.
    Chronic inflammation and a prolonged increase in SAA conc
  57. In the dog, AA amyloid deposits are most common in the __________ and clinical signs are due to __(2)__.
    kidney; renal failure and uremia
  58. Signalment for animals with glomerular disease.
    middle aged to older; no sex predilection in dogs, 75% male in cats
  59. __________ with a ________ and __________ is a hallmark of glomerular disease.
    Proteinuria; urine protein:cre >0.5; inactive sediment
  60. What are the 6 ways glomerular disease can present?
    proteinuria as an incidental finding during wellness exam, underlying infectious/inflammatory/neoplastic disease, chronic renal failure (anorexia,weight loss, lethargy, PU/PD, vomiting), classical nephrotic syndrome (ascites, edema), thromboembolism (dyspnea, paraparesis), sudden blindness from retinal detachment due to hypertension
  61. What is Shar Pei fever?
    episodic joint swelling (tibotarsal) and high fever that resolves within a few days
  62. What physical findings are associated with severe protein loss? (4)
    ascites, edema, poor body condition, poor haircoat
  63. What physical findings are associated with systemic hypertension? (3)
    retinal hemorrhages, vascular tortuosity, and retinal detachment
  64. Damage to the glomerulus leads to ____(2)____ loss.
    albumin (NOT globulin, as with PLE) and antithrombin III
  65. You must interpret proteinuria in light of ___________.
    urine specific gravity
  66. Isosthenuria occurs with _________ of the nephron population is non-functional; early loss of conc ability may occur in animals with ______________.
    >66%; medullary amyloid deposition (Abyssinians, etc)
  67. Biochem abnormalities with glomerular disease. (3)
    hypoalbuminemia, hypercholesterolemia, azotemia (end-stage)
  68. Why does hypercholesterolemia occur in patients with glomerular disease?
    increased hepatic synthesis secondary to chronic hypoalbuminemia
  69. ___________ can lead to chronic renal failure with the expected biochem abnormalities.
    Either GN or amyloidosis
  70. A _________ is essential in order to diagnose glomerular disease.
    urine protein:cre
  71. The presence of __(2)__ makes the urine protein:cre unreliable.
    hematuria or pyuria
  72. What is the only way to differentiate amyloidosis from GN from primary interstitial disease?
    renal biopsy
  73. ___________ and ___________ will lead to effusion into body cavities and/or peripheral edema.
    Decreased oncotic pressure in the vessels; increased hydrostatic pressure
  74. Measurement of _________ activity may help identify animals at risk for thromboembolism.
    antithrombin III
  75. The effusion seen with patients with GN/PLN is a ___________ with ______ cell count and _______ total protein conc.
    pure transudate; low; low
  76. Complications that can occur with glomerular disease. (6)
    hypoalbuminemia, hypertension, sodium retention, thromboembolism, muscle wasting, hyperlipidemia
  77. 4 major reasons for hypoalbuminemia.
    impaired liver synthesis, GI loss, renal loss, large volume blood loss
  78. Hepatic albumin synthesis is ________ with nephrotic syndrome, but...
    increase; it's insufficient to compensate for hypoalbuminemia.
  79. What is the primary stimulus for increased hepatic synthesis of albumin in nephrotic syndrome?
    low plasma oncotic pressure
  80. _____________ is increased in nephrotic syndrome due to increased resorption of filtered protein.
    Renal catabolism of albumin
  81. The ___________ pool of albumin is more depleted than the ___________ pool with nephrotic syndrome.
    extravascular; intravascular
  82. An increase in dietary protein dietary protein stimulates __________ and increases __________.
    hepatic albumin synthesis; urinary loss of protein
  83. Hypoalbuminemia is treated with ___________ to reduce intraglomerular pressure.
    ACE inhibitors
  84. Systemic hypertension occurs due to... (3)
    sodium retention, activation of the RAAS system, and impaired release of normal renal vasodilator substances.
  85. Systemic hypertension has been associated with __(3)__.
    GN, glomerulosclerosis, and amyloidosis
  86. ___________ measurements should be obtained in all dogs and cats with suspected glomerular disease because control can slow its progression.
    Blood pressure
  87. What is the mainstay of hypertensive treatment b/c is it an arteriovasodilator.
    Ca2+ channel blocker Amlodipine
  88. The underfill hypothesis is premised on the fact that hypoalbuminemia leads to decreased ___________; decreased circulating volume leads to __________; both of these cause ___________.
    oncotic pressure; activation of RAAS; sodium and water retention
  89. The overfill hypothesis states that the primary intrarenal sodium retention in nephrotic syndrome occurs in the ________ and contributes to ___________.
    distal tubule; extracellular fluid volume/edema
  90. In patients with adequate serum albumin conc and intravascular oncotic pressure, intrarenal sodium retention leads to...
    expansion of circulating volume and suppression of RAAS.
  91. In patients with severe hypoalbuminemia and low circulating volume, intrarenal sodium retention leads to...
    activation of RAAS.
  92. _________ is the most common site for thromboembolism.
    Pulmonary artery
  93. Dogs with pulmonary thromboembolism are __(2)__.
    dyspneic and hypoxic
  94. Hypoalbuminemia causes ________ and ________, which result in increased platelet adhesion and aggregation (and can contribute to thromboembolism).
    mild thrombocytosis; platelet hypersensitivity
  95. Loss of _________ in the urine contributes to hypercoagulability, contributing to thromboembolism risk.
    Antithrombin III
  96. Increased ________ conc and decreased _________ contribute to hypercoagulability; animals with _________ conc greater than _______ and __________ conc less than ________ of normal are considered at risk for thromboembolism and should be treated as such.
    fibrinogen; fibrinolysis; fibrinogen; 300 mg/dL; Antithrombin III; 70%
  97. ____________ lead to cachexia, which involves __(3)__.
    Inflammatory mediators; reduced food intake, muscle wasting, and suppressed muscle regeneration
  98. In nephrotic patients, plasma albumin concs are inversely correlated with plasma ____________ conc; and ___________ tends to increase as albumin decreases.
    cholesterol/TG; cholesterol/lipid
  99. How can you slow the progression of glomerular damage?
    add Omega-3 fatty acids to suppress glomerular inflammation and coagulation by interfering with production of pro-inflammatory prostanoids
  100. Goals of treatment of glomerular disease. (6)
    slow progression, reduce proteinuria, manage hypertension, ID/treat underlying conditions, consider immunosuppression, prevent thromboembolism
  101. How do you reduce proteinuria? (3)
    ACE inhibitors (Enalapril or benasepril), Ang receptor blockers (Telmisartan)
  102. ACE inhibitors decrease protein by partially blocking _______ and _________ the ________ arteriole, thus reducing __________.
    RAAS; dilating; efferent; intraglomerular pressure
  103. How do you manage hypertension? (2)
    Ca2+ channel blockers (Amlodipine), ACE inhibitors
  104. Ca2+ channel blockers reduce hypertension by _____________.
    vasodilation of arterioles
  105. ACE inhibitors aid in management of hypertension by...
    decreasing sodium and water retention.
  106. When managing hypertension and proteinuria, monitor for __(2)__.
    reduction in GFR and increase in K+
  107. If the decision is made not to biopsy, immunosuppressive therapy can be started if... (3)
    standard therapy is already being given AND Cre>3mg/dL, azotemia is rapidly progressive, or hypoalbuminemia is severe
  108. If the decision is made to start immunosuppressive therapy, give ________ at the __________ dose; ___________ is an immunosuppressive drug used in dogs.
    glucocorticoids; immunosuppressive; Mycophenalate
  109. How do you prevent thromboembolism in animals that are determined to be at risk?
    low-dose aspirin (prevents platelet aggregation)
  110. Drug that blockades ADP-mediated platelet activation.
    Clopidogrel (Plavix)
  111. Treatment of amyloidosis.
    no treatment has shown to be beneficial
  112. Amyloidosis prognosis.
    progressive disease with poor prognosis; less than 1 year
  113. Prognosis of GN.
    variable course; can end with: spontaneous remission, stable course with ongoing proteinuria for months to years, or progression to chronic renal failure over months to years

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