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16 Cards in this Set
- Front
- Back
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What is the clinical surrogate for GFR?
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Creatinine clearance
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What are the grades of renal dysfunction based on creatinine clearance?
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Cl creat 60-99 mL/min = mild impairment
Cl creat 30-59 mL/min = moderate impairment Cl creat 15-29 mL/min = severe impairment Cl creat 5-10 mL/min = ESRD |
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What are the symptoms of renal failure?
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Mild dysfunction - minimal fatigue, salt and H2O retention causing edema and hypertension
Moderate dysfunction - more fatigue and edema, mildly impaired congnition, appetite preserved. Severe - marked fatigue, loss of appetite, nausea, vomiting |
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What are the signs of severe uremia?
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Asterixis, seizures, pericardial friction rub (uremic pericarditis), prolonged bleeding time, profound anemia, low calcium and high phosphate levels, low bicarb, high potassium
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What can be done to preserve GFR?
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Tight BP control (<130/85 as opposed to 140/90), diuretics, disruption of R/A system, ACEI and ARB, plus other meds
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What is the pathogenesis of anemia in kidney disease?
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Beings with GFR < 60 mL/min; progressive hemoglobin decline as GFR falls further. The major cause of anemia is erythropoeitin deficiency.
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What is the treatment of anemia due to kidney disease?
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Recombinant epo and iron supplementation
Target Hgb is 10-11 grams, not to normal. |
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What is given to correct platelet function in patients with kidney disease?
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Desmopressin or conjugated estrogen (delayed onset but longer effect)
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What is given to treat the metabolic acidosis in kidney disease?
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Oral bicard or citrate (30-40 meq daily usually does the trick)
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What bone diseases are associated with renal disease?
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Osteitis fibrosa, low bone turn over disease, and osteomalecia
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Osteitis fibrosa
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A skeletal disorder caused by a surplus of parathyroid hormone. High PTH is due to high phosphate levels (due to decreased GFR) and low calcium (low calcitriol). This causes too rapid bone turnover and abnormal bone.
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What should be done to manage osteitis fibrosa?
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Maintain PTH at 2-3 times normal value, raise calcium level to normal, keep phosphate below 5, suppress PTH (vit-d analogues, raise calcium, lower phosphate), give cinacalcet, or kidney transplantation
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What is the MOA of cinacalcet?
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Direct inhibition of PTH release by binding calcium receptors in the parathyroid gland.
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Low bone turnover disease
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High calcium x phosphate product, low PTH. Usually results from combination of poor compliance and aggressive management of PTH, calcium, and phosphate. The result is vascular calificaiton and valvular calcification.
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Osteomalacia
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Softening of the bones due to defective bone mineralization. Heavy metal (aluminum) deposits at calcification front in bone. Don't use aluminum hydroxide as a phosphate binder.
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What has a better survival rate, cadaveric or live kidney transplant?
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Live
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