In primary hyperaldosteronism (Conn syndrome), potassium concentration is typically:

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Multiple Choice

In primary hyperaldosteronism (Conn syndrome), potassium concentration is typically:

Explanation:
Excess aldosterone in Conn syndrome drives the collecting ducts to reabsorb sodium while increasing potassium (and hydrogen) ion secretion. Aldosterone upregulates ENaC channels and Na+/K+ ATPase activity in principal cells, creating a lumen-negative potential that promotes potassium—and hydrogen ion—secretion into the urine. The result is potassium wasting and a fall in serum potassium, i.e., hypokalemia. While potassium can be normal in some individuals depending on intake and other factors, the characteristic and most common finding is decreased potassium.

Excess aldosterone in Conn syndrome drives the collecting ducts to reabsorb sodium while increasing potassium (and hydrogen) ion secretion. Aldosterone upregulates ENaC channels and Na+/K+ ATPase activity in principal cells, creating a lumen-negative potential that promotes potassium—and hydrogen ion—secretion into the urine. The result is potassium wasting and a fall in serum potassium, i.e., hypokalemia. While potassium can be normal in some individuals depending on intake and other factors, the characteristic and most common finding is decreased potassium.

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