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Physiology · Renal and acid–base: potassium in diabetic ketoacidosis
Sample itemA patient in diabetic ketoacidosis has a serum potassium of 5.6 mmol/L on arrival, though total body potassium is depleted from osmotic diuresis. After starting insulin infusion, the serum potassium falls sharply. What is the mechanism of this fall?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
A. Insulin drives potassium into cells through stimulation of the Na-K ATPase
Insulin deficiency and hyperosmolality shift potassium out of cells, so serum potassium appears normal or high despite depletion of body stores. Insulin therapy stimulates Na-K ATPase in muscle and fat, moving potassium back into cells and unmasking the deficit, so potassium must be monitored and replaced.
Option by option
A. Insulin drives potassium into cells through stimulation of the Na-K ATPase (correct)
Correct. Insulin promotes cellular uptake of potassium.
B. Insulin increases renal potassium secretion alone
Renal potassium secretion is not the main effect of insulin and would not explain a rapid fall.
C. Insulin lowers aldosterone secretion
Insulin does not lower aldosterone secretion.
D. Insulin inhibits potassium absorption in the gut
Insulin does not inhibit potassium absorption in the gut.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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