← All CSR Flashcard Decks

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
  1. A hemodialysis patient consistently has pre-dialysis serum bicarbonate of 17 mEq/L. What dietary intervention, in addition to oral sodium bicarbonate supplementation, can help correct metabolic acidosis?

    Answer: Increasing intake of base-producing foods: fruits and vegetables (with attention to potassium content)

    Fruits and vegetables produce bicarbonate precursors (organic anions like citrate, malate) when metabolized. A diet rich in plant foods increases dietary alkali load, helping correct metabolic acidosis in CKD. Potassium content must be monitored in HD patients.

  2. Which statement BEST describes the management of hypermagnesemia in an end-stage renal disease patient on hemodialysis?

    Answer: Avoid magnesium-containing medications (antacids, laxatives) and foods excessively high in magnesium; dialysate magnesium concentration can be adjusted for severe cases

    In ESRD, the kidney cannot excrete excess magnesium, so magnesium-containing medications (Maalox, Milk of Magnesia, magnesium-containing laxatives) are the most common cause of dangerous hypermagnesemia. Dietary and medication restriction plus dialysate concentration adjustment are the management strategies.

  3. In dialysis patients, 'rebound hyperkalemia' can occur within hours after dialysis. Which physiological mechanism PRIMARILY explains this phenomenon?

    Answer: Shift of potassium from the intracellular compartment back to the extracellular space following removal of dialysis-induced alkalosis effects

    During dialysis, potassium is removed rapidly from plasma, but intracellular potassium equilibrates slowly. Post-dialysis, the electrochemical gradient drives K+ back from the intracellular compartment to plasma (rebound). Correction of dialysis-induced alkalosis also shifts K+ back extracellularly.

  4. Which phosphate binder is MOST appropriate for a CKD Stage 5D patient with both hyperphosphatemia AND iron-deficiency anemia?

    Answer: Sucroferric oxyhydroxide (Velphoro) or ferric citrate (Auryxia)

    Ferric citrate (Auryxia) and sucroferric oxyhydroxide (Velphoro) are iron-based phosphate binders that simultaneously bind dietary phosphate and provide systemic iron (via absorption of released iron), addressing both hyperphosphatemia and iron-deficiency anemia.

  5. A dialysis patient develops sudden onset swelling of the tongue and difficulty swallowing. Serum calcium is 6.8 mg/dL (corrected). Which nutritional intervention is MOST urgently indicated?

    Answer: Ensure adequate calcium and vitamin D supplementation, and alert the medical team for IV calcium gluconate if severe hypocalcemia is causing tetany/laryngospasm

    Corrected serum calcium of 6.8 mg/dL represents severe hypocalcemia. Hypocalcemia can cause laryngospasm and tetany (emergency). The immediate response is to alert the medical team and provide calcium support; IV calcium gluconate is the emergency treatment.

  6. In the context of CKD mineral and bone disorder (CKD-MBD), fibroblast growth factor 23 (FGF-23) plays a key role in mineral metabolism. Which of the following correctly describes FGF-23's action?

    Answer: FGF-23 inhibits 1α-hydroxylase (reducing calcitriol) and promotes phosphaturia; elevated in CKD as a compensatory response to phosphate retention

    FGF-23 is secreted by osteocytes in response to phosphate loading. It inhibits renal 1α-hydroxylase (reducing calcitriol), reduces sodium-phosphate cotransporter expression in the proximal tubule (promoting phosphaturia), and is markedly elevated in CKD as kidneys fail to respond.