Urinary2- Renal Dz Part 2

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Mawad
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308615
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Urinary2- Renal Dz Part 2
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2015-10-03 19:32:56
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vetmed urinary AKI
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vetmed urinary
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  1. What is the most important part of treating AKI?
    fluid therapy
  2. Major sources of insensible fluid loss. (3)
    respiratory, sweat, stool
  3. Major source of sensible fluid loss.
    urine
  4. Insensible fluid loss is _______/day.
    22mL/kg
  5. What strategy do you use for fluid therapy?
    • 1. restore effective circulating volume
    • 2. maintain intravascular fluid volume
    • 3. remove excess fluid
  6. What is a major pitfall of the old way of fluid therapy?
    push for diuresis, which is not effective and tends to overhydrate (we now understand that overhydration is just as bad)
  7. With shock, immediate __________ is imperative; rate of fluids for a dog should be ___________, for cats ___________; a bolus should be __________ and repeated as needed.
    resuscitation; 60-90 mL/kg; 45-60 mL/kg; 1/4 the rate value IV
  8. How do you determine the fluid deficit in a patient?
    body weight (kg) x estimated % dehydration = fluid deficit in L
  9. Maintenance fluid therapy is less useful in __________; is presumes normal ________, which is usually altered with renal failure.
    renal failure; urine volume
  10. During the recovery phase, _______ fluids, assess _________ and __________.
    taper; hydration; renal values
  11. What are some examples if crystalloid fluids? (3)
    LRS, 0.9% saline, plasmalyte
  12. Crystalloid fluids provide... (2)
    volume and sodium.
  13. What are some examples of colloid fluids? (2)
    vetstarch, hetastarch
  14. What is the purpose of giving colloid fluids? (3)
    provide colloid oncotic pressure; synthetic start acts like protein; replaces part of crystalloid voume
  15. How do you treat oliguria and anuria? (3)
    ensure adequate hydration, ensure adequate blood pressure, exclude blockage/leakage
  16. It is not advised to give _________ to treat oliguria.
    diuretics (def don't give fluids)
  17. Give _________ to treat volume overload, and DON'T GIVE TOO MUCH FLUIDS AGAIN.
    diuretics
  18. Early EKG changes with hyperkalemia. (3)
    tall T waves, shortened QT interval, reflects rapid repolarization
  19. Later EKG changes associated with hyperkalemia. (3)
    wide QRS, small/absent P wave, reflects delayed depolarization
  20. Severe EKG changes associated with hyperkalemia. (3)
    sine wave, ventricular fibrillation, standstill
  21. To treat hyperkalemia, ... (3)
    translocated K+ intracellularly (insulin, dextrose, bicarb), stabilize membranes (Ca2+), (if possible) remove K+ from body (unblock urethra, dialysis)
  22. Normochloremia high anion gap metabolic acidosis is a failure to _________ and __________; if dehydrated _________ can contribute.
    reabsorb bicarb; fixed acids; lactic acid
  23. An abrupt decrease in GFR causes increase in __________, leading to a decrease in ________.
    phosphate; Ca2+
  24. Amlodipine is a ___________ that is fast, effective treatment for _____________.
    Ca2+ channel blocker; hypertension
  25. GI signs associated with AKI. (4)
    vomiting, nausea, anorexia, ileus
  26. AKI is highly _________; therefore, you should start _________ early.
    catabolic; nutritional support
  27. What are some types of nutritional support used with AKI?
    appetite stimulants, feeding tube, total parenteral nutrition (if ileus or vomiting is severe)
  28. Severity of azotemia is __________ for prognosis of AKI.
    not predictive
  29. Oliguria/anuria is ___________ for prognosis of AKI.
    predictive
  30. Best outcome for azotemia results from _____________; middle outcome for prognosis of azotemia results from __________; the worst outcome for azotemia is usually due to _________.
    obstruction/infection; ischemia/hemodynamic; toxin
  31. ______________ increases risk of death due to AKI by 3 times.
    Hospital-acquired AKI (stages 2-5)
  32. Risk factors for developing CKD. (3-cat, dog, both)
    cats >9yrs,  smaller dogs, both- dental disease
  33. Damage to one nephron will eventually cause...
    the entire nephron to become non-functional.
  34. When the number of functional nephrons drops below the critical level of _______, then global renal function...
    25%; is insufficient to maintain homeostasis and azotemia occurs.
  35. At less than 33% function, ___________ is impaired and _________ occurs.
    ability to conc urine; polyuria
  36. What is the leading cause of CKD in dogs?
    glomerulonephritis
  37. If glomerulonephritis is the leading cause of CKD in dogs, why is there a higher percentage of dogs with tubulointerstitial nephritis on necropsy?
    TIN is an end-stage change; therefore, it is seen on almost all necropsies, BUT the initial cause is usually GN
  38. What is the leading cause of CKD in cats?
    tubulointerstitial disease (unknown etiology usually)
  39. What are some less likely causes of CKD in dogs and cats? (6)
    amyloidosis, renal dysplasia, chronic pyelonephritis, neoplasia, obstruction, AKI
  40. Most common causes of CKD in horses. (2- 1 more common)
    (most common) chronic glomerulonephritis, chronic interstitial nephritis
  41. Most common cause of CKD in cattle.
    chronic pyelonephritis
  42. What are the most common etiologies of pyelonephritis-causing CKD in cattle? (2)
    E. coli, Cornyebacterium renale
  43. Cause of CKD in hamsters.
    amyloidosis
  44. Cause of CKD in rats.
    chronic progressive nephrosis
  45. CKD is a _________ disease, meaning...
    progressive; once it starts, it inevitably gets worse.
  46. Progression of CKD is mediated by... (4)
    tubulointerstitial inflammation, fibrosis, hyperfiltration, and mineralization.
  47. Why is proteinuria so damaging?
    it elicits an inflammatory response
  48. __(2)__ are common findings with CKD, regardless of the inciting cause.
    Tubulointerstitial inflammation and fibrosis
  49. ____________ increases the amount of protein in the UF; protein is reabsorbed and causes...
    Glomerular damage; damage to the tubular cells and interstitium.
  50. As nephron mass decreases with CKD, _______________, leading to ___________.
    nephrons hypertrophy; tubulointerstitial disease
  51. Damage to nephrons that occurs with CKD leads to transition of __________ to __________.
    epithelial tubular cells; mesenchymal fibroblasts
  52. __________ is one of the most important contributors to tubulointerstitial disease in CKD.
    Chronic hypoxia
  53. Decreased nephron mass with CKD leads to __________, causing ___________ as compensation with ____________, ultimately causing ___________.
    increased SNGFR; afferent arteriolar dilation; glomerular hypertrophy (no hyperplasia); glomerular scelrosis
  54. ____________ leads to glomerular hyperfiltration.
    Intraglomerular hypertension
  55. __________ retention occurs in early CKD; __________ occurs when the ________ product is over 70.
    Phosphate; calcium x phosphate product
  56. Mineral deposits in the kidneys incite...
    an inflammatory reaction that further worsens renal function, worsening hyperphosphatemia, thus worsening renal function, vicious cycle
  57. Risk factors for progression of CKD. (4)
    proteinuria, hypertension, hyperphosphatemia, metabolic acidosis
  58. By what mechanisms does proteinuria  mediate progression of CKD? (2)
    mesangial toxicity, tubular injury due to inflammation
  59. In health, the kidneys excrete excess _______, but with CKD, _______ excretion is impaired and __________ develops.
    acid; acid; metabolic acidosis
  60. Predictors in mortality due to CKD inc cats. (4)
    plasma Cre, urine protein:cre ratio, leukocytosis, hyperphosphatemia
  61. Predictors of mortality due to CKD in dogs. (4)
    urine protein:cre ratio, hypoalbuminemia, hypertension, low BCS
  62. All uremic patients are ________.
    azotemic (NOT ALL AZOTEMIC PATIENTS ARE UREMIC)
  63. What is uremia?
    clinical signs of kidney failure
  64. Functional damage readily progresses to __________, and vice versa.
    structural damage
  65. What 2 types of insults can cause CDK?
    structural damage, functional damage
  66. Common clinical signs of CKD. (12)
    PU/PD, anorexia, weight loss, lethargy, vomiting, halitosis, oral ulcers, poor hair coat, heart murmur, bleeding, small kidneys, dehydration
  67. What is normal water intake?
    60mL/kg/day
  68. What clinical signs are present with CKD, but not AKI? (4)
    small kidneys, poor hair coat, thin, pale
  69. The severity of biochemical changes tends to become greater with _________.
    CKD progression
  70. What changes are on a biochem profile of a CKD patient? (4)
    increased BUN/Cre, increased phosphate, decreased bicarb
  71. Cre is determined largely by __________.
    individual muscle mass (greyhounds have higher normally)
  72. Cre excretion is achieved almost exclusively by __________.
    glomerular filtration
  73. What is the basis for staging CKD?
    plasma Cre conc
  74. Plasma Cre should be evaluated when the patient is ___________.
    well-hydrated
  75. Decreased BUN can be attributed to... (3)
    liver failure, porto-systemic shunt, low-protein diet
  76. Increased BUN can be attributed to... (5)
    dehydration, decreased GFR, high protein diet, GI bleed, increased protein catabolism
  77. Cre is not a sensitive indicator of renal disease if...
    disease is early on in progression.
  78. Why is there an increased anion gap with CKD?
    kidney fails to resorb bicarb and fails to excrete acid (like lactic acid)
  79. What is adequately concentrated urine for dogs and for cats?
    • dogs USG>1.030
    • cats USG>1.035
  80. There is inadequate concentration when there is less than ________ renal function.
    66%
  81. Which came first: PU or PD?
    PU
  82. In dogs with suspected CKD, negative proteinuria dipstick is __________, positive proteinuria dipstick is __________.
    negative; not reliable-confirm all positives with UPC
  83. How do you confirm proteinuria?
    urine protein:cre ratio
  84. 66% of older cats with a UTI have _______.
    CKD
  85. What is the best way to get urine for culture in a CKD patient?
    cysto
  86. What do you usually see on abdominal ultrasound of a CKD patient?
    small irregular kidneys with hyperechoic cortices and decreased corticomedullary distinction
  87. __________ on renal biopsy confirms CKD.
    Fibrosis
  88. What must you do before you stage CKD? (2)
    definitively diagnose CKD, stabilize the patient
  89. IRIS Stage I CKD:
    Cat: _____
    Dog: _____
    • Cre <1.6
    • Cre<1.4
    • Non-azotemic
  90. IRIS Stage II CKD:
    Cat: _____
    Dog: _____
    • Cre 1.6-2.8
    • Cre 1.4-2.0
    • Mild or absent clinical signs
  91. IRIS Stage III CKD:
    Cat: _____
    Dog: _____
    • Cre 2.9-5
    • Cre 2.1-5
    • with or without uremia
  92. IRIS Stage IV CKD:
    Cat: _____
    Dog: _____
    • Cre >5
    • Cre >5
    • uremia
  93. IRIS Proteinuric:
    Cats:
    Dogs:
    • UPC>0.4
    • UPC>0.5
  94. IRIS Borderline Proteinuria:
    Cats:
    Dogs:
    • UPC 0.2-0.4
    • UPC 0.2-0.5
  95. IRIS Non-proteinuric:
    Cats:
    Dogs:
    • UPC<0.2
    • UPC<0.2
  96. 2 differences b/w prognosis for AKI and CKD.
    AKI is potentially reversible, AKI has worse short-term survival

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