Which best describes primary hyperaldosteronism?

Which best describes primary hyperaldosteronism?

• A. Autonomic adrenal response causing sodium loss and potassium gain
• B. Autonomous aldosterone secretion causing sodium retention, potassium wasting, metabolic alkalosis, and suppression of renin
• C. Aldosterone deficiency causing hyponatremia and hyperkalemia
• D. Aldosterone resistance causing hyponatremia and metabolic acidosis

Answer: (B)

Primary hyperaldosteronism is when the adrenal gland makes aldosterone autonomously, independent of the renin–angiotensin system. The excess aldosterone acts on the distal nephron to increase sodium reabsorption, which expands extracellular fluid and raises blood pressure, while it promotes potassium and hydrogen ion excretion, leading to hypokalemia and metabolic alkalosis. The increased volume also feeds back to suppress renin release, so renin levels are low. That’s why this description fits best: autonomous aldosterone secretion causing sodium retention, potassium wasting, metabolic alkalosis, and suppression of renin. The other options describe opposite effects (sodium loss, potassium gain; aldosterone deficiency; aldosterone resistance) that do not match the physiology of primary hyperaldosteronism.

Primary hyperaldosteronism is when the adrenal gland makes aldosterone autonomously, independent of the renin–angiotensin system. The excess aldosterone acts on the distal nephron to increase sodium reabsorption, which expands extracellular fluid and raises blood pressure, while it promotes potassium and hydrogen ion excretion, leading to hypokalemia and metabolic alkalosis. The increased volume also feeds back to suppress renin release, so renin levels are low.

That’s why this description fits best: autonomous aldosterone secretion causing sodium retention, potassium wasting, metabolic alkalosis, and suppression of renin. The other options describe opposite effects (sodium loss, potassium gain; aldosterone deficiency; aldosterone resistance) that do not match the physiology of primary hyperaldosteronism.