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Multiple Choice

Heparin therapy is commonly associated with which electrolyte disturbance?

The key idea here is that heparin can cause hyperkalemia by suppressing aldosterone production. Heparin can reduce renin release and inhibit aldosterone synthesis in the adrenal cortex, leading to hypoaldosteronism. With less aldosterone, the kidneys excrete less potassium, so potassium levels tend to rise, especially in patients with kidney disease or other risk factors. This often manifests days after starting heparin and may accompany a mild metabolic acidosis (type 4 RTA) from reduced aldosterone activity. That’s why hyperkalemia is the electrolyte disturbance most commonly linked to heparin therapy. The other electrolyte disturbances listed don’t fit as reliably with heparin use. Hypokalemia would imply excessive potassium loss or shift, which isn’t the typical effect of heparin. Hyponatremia and hypomagnesemia aren’t characteristic consequences of starting heparin.

The key idea here is that heparin can cause hyperkalemia by suppressing aldosterone production. Heparin can reduce renin release and inhibit aldosterone synthesis in the adrenal cortex, leading to hypoaldosteronism. With less aldosterone, the kidneys excrete less potassium, so potassium levels tend to rise, especially in patients with kidney disease or other risk factors. This often manifests days after starting heparin and may accompany a mild metabolic acidosis (type 4 RTA) from reduced aldosterone activity. That’s why hyperkalemia is the electrolyte disturbance most commonly linked to heparin therapy.

The other electrolyte disturbances listed don’t fit as reliably with heparin use. Hypokalemia would imply excessive potassium loss or shift, which isn’t the typical effect of heparin. Hyponatremia and hypomagnesemia aren’t characteristic consequences of starting heparin.