In addition to aggressive refeeding, which places a patient at risk for hypophosphatemia?

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Multiple Choice

In addition to aggressive refeeding, which places a patient at risk for hypophosphatemia?

Explanation:
Phosphate moves into cells when the body shifts from a catabolic to an anabolic state, such as during aggressive refeeding. Insulin drives phosphate, along with glucose and amino acids, into cells to support new tissue synthesis, which can reveal or worsen existing phosphate depletion. Diabetic ketoacidosis is tied to this risk because treating DKA with insulin accelerates the same intracellular shift of phosphate. Patients often arrive with depleted total body phosphate due to osmotic diuresis and reduced intake, so the insulin-driven push into cells can precipitate or worsen hypophosphatemia, making monitoring and possible supplementation important during and after starting therapy. Vitamin D deficiency can lower phosphate absorption, but it doesn’t typically create the acute intracellular shift seen with refeeding or insulin therapy. Acute kidney injury tends to raise serum phosphate (due to reduced excretion) rather than lower it. Tumor lysis syndrome releases phosphate into the bloodstream from lysed cells, which also tends to cause hyperphosphatemia rather than hypophosphatemia.

Phosphate moves into cells when the body shifts from a catabolic to an anabolic state, such as during aggressive refeeding. Insulin drives phosphate, along with glucose and amino acids, into cells to support new tissue synthesis, which can reveal or worsen existing phosphate depletion.

Diabetic ketoacidosis is tied to this risk because treating DKA with insulin accelerates the same intracellular shift of phosphate. Patients often arrive with depleted total body phosphate due to osmotic diuresis and reduced intake, so the insulin-driven push into cells can precipitate or worsen hypophosphatemia, making monitoring and possible supplementation important during and after starting therapy.

Vitamin D deficiency can lower phosphate absorption, but it doesn’t typically create the acute intracellular shift seen with refeeding or insulin therapy. Acute kidney injury tends to raise serum phosphate (due to reduced excretion) rather than lower it. Tumor lysis syndrome releases phosphate into the bloodstream from lysed cells, which also tends to cause hyperphosphatemia rather than hypophosphatemia.

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