Electrolyte Management in Renal Disease Flashcards
6 cards from real CSR practice questions. Tap to flip, then mark Knew It or Still Learning — missed cards come back until you master them.
Read the first 6 Electrolyte Management in Renal Disease flashcards as text
A CKD patient on a low-potassium diet is advised to use leaching techniques for vegetables. Which step is MOST critical for effective potassium reduction?
Answer: Peel, cut into small pieces, soak in large volume of water for at least 2 hours, and boil in fresh water (discarding cooking water)
Leaching maximizes potassium removal: peeling removes the high-potassium skin, cutting small increases surface area for diffusion, soaking in large volume of water for ≥2 hours allows passive diffusion, and boiling in fresh water (not soaking water) with subsequent discarding removes the leached potassium.
A hemodialysis patient has serum calcium of 10.8 mg/dL (corrected) and serum phosphorus of 7.5 mg/dL. Which combination of interventions is MOST appropriate?
Answer: Switch to non-calcium-containing phosphate binders (sevelamer or lanthanum), intensify dietary phosphorus restriction, review vitamin D analog doses, and consider cinacalcet if PTH elevated
With both hypercalcemia AND hyperphosphatemia, calcium-containing binders are contraindicated (worsen hypercalcemia). Non-calcium binders are preferred. Active vitamin D analogs (which raise calcium) should be reviewed or reduced. Cinacalcet lowers both calcium and PTH.
Which of the following electrolyte abnormalities is MOST commonly seen in the early post-kidney transplant period and requires dietary management?
Answer: Hyperkalemia from calcineurin inhibitor use and hypophosphatemia from urinary phosphate wasting
Post-transplant, calcineurin inhibitors (tacrolimus, cyclosporine) impair renal potassium excretion → hyperkalemia. High GFR post-transplant combined with post-hyperparathyroidism → phosphate wasting → hypophosphatemia. These are the most common electrolyte issues in the early post-transplant period.
Salt substitutes (potassium chloride-based products) are commonly recommended as a 'healthy' alternative to table salt for the general population. Why are they CONTRAINDICATED in most CKD patients?
Answer: They contain 2500–3000 mg of potassium per teaspoon, posing a serious hyperkalemia risk in patients with impaired renal potassium excretion
Potassium chloride-based salt substitutes (NoSalt, Nu-Salt, Morton Salt Substitute) provide 2500–3000 mg potassium per teaspoon. In CKD patients with reduced potassium excretion capacity, even modest use can rapidly cause life-threatening hyperkalemia.
Which of the following BEST describes 'calciphylaxis' (calcific uremic arteriolopathy) and its nutritional relevance in dialysis patients?
Answer: A life-threatening condition of small vessel calcification and skin necrosis in uremic patients, associated with high calcium-phosphate product; requires elimination of calcium-containing phosphate binders and vitamin D analogs
Calciphylaxis is a severe, potentially fatal condition (mortality >50%) of calcification in small dermal arterioles causing ischemia and necrotic skin wounds. Management includes: stopping calcium-containing binders, switching to sodium thiosulfate, strict phosphorus restriction, and optimizing dialysis.
A hemodialysis patient has a predialysis serum sodium of 148 mEq/L (hypernatremia). Which dietary/fluid management approach addresses this finding?
Answer: Assess sodium and fluid intake together — hypernatremia in HD patients is usually from insufficient fluid intake relative to sodium intake; counsel on adequate fluid intake within prescription and reducing sodium intake
True hypernatremia in HD patients is uncommon and usually reflects insufficient free water intake relative to sodium intake (hypertonic state) or excessive sodium intake without adequate fluid. Management involves balanced counseling on sodium reduction AND ensuring fluid intake meets prescription volume.