Urinary2- Renal Dz Part 1

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Urinary2- Renal Dz Part 1
2015-10-03 19:32:46
vetmed urinary

vetmed urinary
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  1. Often, cat with chronic kidney disease have concurrent _________; this is less common with dogs.
  2. CKD cats have anemia because of decreased ___________, which is produced by the kidney; the anemia is __(3)__; when they have a normal PCV, this can be due to __(2)__.
    erythropoietin; non-regenerative, normocytic, normochromic; anemia and dehydration together
  3. Describe the WBC and platelet finding on CBC with kidney disease?
    non-specific: leukocytosis if infection, normal platelet unless infectious cause of kidney disease
  4. With kidney disease, ________ function is often decreased (cell type).
  5. Aldosterone stimulates _________ in _________, and _________ follows.
    Na+ reabsorption; principal cells; water
  6. More water intake will dilute ________, causing ________; the converse is also true.
    sodium; hyponatremia
  7. ADH causes _________ without _________.
    water loss; sodium loss
  8. Pure water deficit causes _________; causes of this include... (3)
    primary hypodipsia; DI, fever/heat, no access to water
  9. What are the 2 types of hypotonic fluid loss? What are examples of each?
    Extrarenal (GI loss, third spacing, cutaneous loss), Renal (diuresis, CKD, AKI, post renal)
  10. What are 3 causes of impermeant solute gain?
    salt poinsoning, hypertonic fluids, hyperaldosteronism/hyperadrenocorticism
  11. What are 4 GENERAL causes of hypernatremia?
    pure water deficit, extrarenal hypertonic fluid loss, renal hypertonic fluid loss, impermeant solute gain
  12. Hyponatremia with normal plasma osmolality can be caused by... (2)
    hyperlipidemia, hyperproteinemia
  13. Hyponatremia with high plasma osmolality can be caused by... (2)
    hyperglycemia (DM), mannitol
  14. Hyponatremia coupled with low plasma osmolality and hypervolemia can be caused by... (3)
    congestive heart failure, protein-losing nephropathy, liver disease
  15. Hyponatremia coupled with low plasma osmolality and normovolemia can be caused by... (1)
    psychogenic polydipsia
  16. Hyponatremia coupled with low plasma osmolality and hypovolemia can be caused by... (3)
    GI loss, third spacing, Addison's disease
  17. What is equation for comparison of chloride to sodium?
    corrected Cl- = Cl-measured = Na+normal/ Na+measured
  18. Causes of excessive loss of chloride relative to sodium through the GI. (1)
    vomiting of stomach contents
  19. Excessive loss of chloride relative to sodium through the renal route. (4)
    loop diuretics/thiazide, chronic respiratory acidosis, Cushing's, glucocorticoids
  20. Excessive loss of Cl- relative to Na+ can be caused by...
    GI loss, renal loss
  21. Renal chloride retention can be caused by... (6)
    renal failure, renal tubular acidosis, Addison's, DM, chronic respiratory alkalosis, spironolactone
  22. Potassium is filtered at the __________, reabsorbed in the __(2)__; its final control is by __(2)__ in the ________.
    glomerulus; proximal tubule and loop of Henle; principal cells (Aldosterone-secrete K+) and intercalated type A cells (reabsorb K+); distal tubule
  23. Translocation of K+ causing hypokalemia can be caused by... (5)
    alkalemia, insulin/glucose, catecholamines, hypothermia, albuterol
  24. Increased loss of potassium leading to hypokalemia can be caused by...
    GI loss, urinary loss, drugs
  25. Hyperkalemia can be caused by... (4)
    pseudohyperkalemia, translocation from ICF to ECF, increased intake, decreased urinary excretion
  26. Most phosphorous is located in ______.
  27. GI absorption of phosphorous is _________ that is _________.
    passive absorption; carrier-mediated
  28. PTH decreases the function of the __________, which enhances ___________.
    NaP cotransporter; phosphate excertion
  29. Hypophosphatemia can cause _______ of RBCs because it decreases ________, increasing _________.
    hemolysis; RBC ATP; osmotic fragility
  30. Treatment of DKA can cause _________ because insulin causes ___________.
    hypophosphatemia; translocation of Ph
  31. Causes of hypophosphatemia. (4)
    maldistribution (translocation from ICF to ECF), reduced renal reabsorption, decreased intestinal absorption, lab error
  32. Hyperphosphatemia can cause __________ as a clinical sign.
    soft tissue mineralization
  33. The active fraction of calcium is ________.
  34. The majority of calcium in the body is in _________; we measure the __________.
    bone; extracellular calcium
  35. To convert calcium in mg/dL to mmol/L,...
    divide by 4.
  36. With hypoalbuminemia, the protein-bound fraction of ________, which is reflected as low _________; in this case, __________ is not reflected and might still be normal.
    calcium; total calcium; ionized calcium
  37. With renal failure, calcium is decreased because of decreased _________; consequently, _________ is increased due to the Law of _______.
    calcitriol; phosphate; Mass Action
  38. Common causes of hypocalcemia include... (5)
    hypoalbuminemia, CKD, AKI, eclampsia, acute pancreatitis
  39. Clinical signs of hypercalcemia. (6)
    PU/PD, anorexia, dehydration,lethargy, weakness, vomiting
  40. Hypercalcemia causes _________ azotemia.
  41. What are the renal effects of hypercalcemia in acute kidney injury? (1)
    intrarenal vasoconstriction that can be rapidly reversed
  42. What are the renal effects of hypercalcemia in CKD? (1)
    mineralization of tissue
  43. Hypocalcemia can lead to increased ___________ and may culminate in ___________.
    excitability of nerves; hypocalcemic tetany or seizures
  44. Hypercalcemia can depress ____________ and lead to ___________.
    neuromuscular excitability; cardiac arrhythmias
  45. Hypercalcemia impairs the action of ________, which can lead to __________.
    ADH; calcium oxalate stones
  46. Causes of hypercalcemia. (8)
    HARD IONS- Hyperparathyroidism, Addison's, Renal Dz, D Vitamin excess, Idiopathic, Osteolytic, Neoplasia, Spurious
  47. Ionized calcium causes intrarenal __________, which can lead to intrinsic acute kidney injury.
  48. What are the 2 mechanisms by which hypercalcemia impairs urine concentrating ability?
    Ca++ reabsorption in the LoH decreases Na+ reabsorption; Ca++ impairs action of ADH on the collecting duct
  49. If total hypercalcemia is mild, measure __________ to help determine if...
    ionized calcium; it is clinically significant.
  50. In late CKD, there is decreased _______, leading to decreased _________ clearance; this causes increased plasma _______ and decreased __(2)__; all of this causes an increase in _______ and.. (3)
    GFR; phosphate ion; phosphorous; calcitriol; ionized calcium; PTH; decreased survival, soft tissue mineralization, and demineralization of bone.
  51. Renal secondary hyperparathyroidism occurs with _________.
    chronic kidney disease
  52. Refractory hypokalemia or persistent hypocalcemia should prompt evaluation for __________.
    Magnesium deficiency
  53. Hyperalbuminemia causes ________ and increased ________.
    dehydration; hematocrit
  54. Hypoalbuminemia can be caused by __(2)__.
    protein-losing nephropathy, GI loss, liver disease (decreased production), or vasculitis (redistribution).
  55. When renal loss is the cause of hypoalbuminemia, albumin is ________ and globulin is ________.
    low; normal
  56. When GI loss is the cause of hypoalbuminemia, albumin is _________ and globulin is ________.
    low; low
  57. When liver failure is the cause of hypoalbuminemia, albumin is ________ and globulin is _________.
    low; normal to high
  58. When vasculitis is the cause of hypoalbuminemia, albumin is ________ and globulin is _______.
    low; normal
  59. Metabolic acidosis = ________.
    low bicarb
  60. What is the equation for anion gap?
    (Na+ + K+) - (Cl- + HCO3-)
  61. What are the 3 steps to evaluating blood gas results?
    • 1. Determine if pH is normal, low (acidosis), or high (alkalosis)
    • 2. Determine is bicarb supports metabolic cause: low (acidosis), high (alkalosis); if not, it is respiratory, look to PCO2.
    • 3. Determine if compensation is present (ex. metabolic acidosis, bicarb is low, PCO2 should also be low for compensation)
  62. When ________ goes up, bicarb goes down; ________ increases.
    lactate; anion gap
  63. Loss of bicarb without a corresponding loss of Cl leads to _________; there is a(n) __________ anion gap.
    acidosis; normal
  64. With CKD, prothrombin time is _________, aPTT is __________, platelet count is __________; patient runs risk of __________, which is detected through __________.
    normal; normal; normal; bleeding; buccal mucosal bleeding time
  65. With protein-losing nephropathy, there is an ___________ deficiency.
    antithrombin III
  66. What are indications for renal biopsy? (3)
    proteinuria, suspected neoplasia, FIP
  67. What are contra-indications for renal biopsy? (3)
    end-stage CKD, severe uremia (bleeding risk), hypertension (bleeding risk)
  68. When performing a renal biopsy, avoid...
    entering the medulla
  69. Creatinine is ________ correlated to GFR.
  70. Grade I AKI grading: _________ blood Cre, __________ clinical description.
    <1.6 (increase of >0.3); non-azotemic AKI
  71. Grade II AKI grading: _________ blood Cre, __________ clinical description.
    1.7-2.5; mild AKI
  72. Grade III AKI grading: _________ blood Cre, __________ clinical description.
    2.6-5.0; mod to severe AKI
  73. Grade IV AKI grading: _________ blood Cre, __________ clinical description.
    5.1-10.0; mod to severe AKI
  74. Grade V AKI grading: _________ blood Cre, __________ clinical description.
    >10.0; mod to severe AKI
  75. What are 3 etiologies of AKI?
    hemodynamic (aka. volume-responsive), intrinsic (renal), post-renal
  76. What are 6 causes of volume-responsive azotemia?
    dehydration, hypotension, hypovolemia (or decreased effective circulating volume), anesthesia, shock, renal hypoperfusion (NSAIDs)
  77. Volume-responsive azotemia is usually coupled with a __________; it is potentially rapidly _________.
    high USG; reversible
  78. What are the 2 most common causes of intrinsic AKI? What are 2 less common causes?
    ischemia and nephrotoxins; inflammatory/infectious, systemic
  79. What are some infectious causes of AKI? (4)
    pyelonephritis from an ascending E. coli infection, Lepto, Borrelia (Lyme disease), Ehrlichia (the list goes on and on)
  80. What are some systemic diseases that can cause AKI? (4)
    FIP, pancreatitis, sepsis, DIC (and the list goes on..)
  81. What is a short list of the most common nephrotoxins causing AKI? (6)
    ethylene glycol, Rimadyl, rodenticides, lillies, grapes/raisins, venom (bee stings, snake bites)
  82. 2 causes of post-renal AKI.
    nephro-/urolithiasis, bladder rupture
  83. Which types of AKI are reversible?
    both pre- and post-renal damage are reversible, but will lead to intrinsic kidney damaged is not addressed properly
  84. What are the 5 stages of AKI?
    insult--> initiation--> extension--> maintenance--> repair
  85. When is it ideal to recognize kidney damage and why?
    in the insult phase because you are more likely to be able to reverse it before you enter initiation and extension of the damage (caveat: it is HARD to recognize AKI in this stage)
  86. What are the 2 major cellular mechanisms of decreased GFR?
    intrarenal vasoconstriction, tubular dysfunction
  87. In the normal renal tubule cytoskeleton __________ hold cells together, __________ on the basolateral side anchor the cell to the basement membrane, and ________ help make the barrier.
    adherens junctions (zonula adhrerens); adhesion molecules (integrins); tight junctions
  88. In AKI, the cytoskeleton disruption leads to... (3)
    blood leaks into the UF and bypasses glomerulus, the Na+K+ATPase pump moves to luminal side and orientation is backward
  89. Describe how cytoskeleton disruption leads to cast formation.
    epithelial cells are not anchored and fall off the basement membrane into the UF; these bind together to form casts
  90. What are  categories of risk factors for AKI?
    community acquired, hospital acquired
  91. Renal blood flow is determined by... (3)
    cardiac output, intravascular volume, real perfusion pressure
  92. Risk factors for volume depletion. (6)
    anesthesia, electrolyte disorders, hyperglycemia, expired tetracycline, penicillin, sulfa drugs (cause crystals)
  93. How can you avoid nephrotoxicity associated with aminoglycosides? (3)
    give once daily, maintain adequate hydration, monitor fresh urine daily for casts
  94. Aminoglycosides cause nephrotoxicity because...
    they concentrate in renal epithelial cells and cause damage and cast formation
  95. Toxicity is more likely to occur with NSAID use when...
    renal blood flow is decreased.
  96. Prevention of AKI involves...
    avoiding or ameliorating risk factors and use of renoprotective drugs
  97. How do you monitor hydration?
    skin turgor, mucous membranes, weight (changes in weight over days to weeks is usually fluid changes)
  98. Monitoring AKI involves... (4)
    weight, blood pressure, PCV and total solids
  99. What patients should you not give fluids to and why?
    patients with oliguria and anuria because you can cause volume overload and congestive heart failure
  100. Litterpan dry vs wet- the difference in weight can calculate the urine volume by the conversion ________ (assuming they haven't dumped litter out).
  101. What is the most accurate method of monitoring urine output?
    urinary catheter
  102. When monitoring blood values of an AKI patient, it is most important to look at... (4)
    BUN, creatinine, electrolytes, PCV