A 38-year-old woman presents with hypertension, hypokalemia, metabolic alkalosis, and suppressed plasma renin. Adrenal CT shows a 1.5 cm left adrenal adenoma. Adrenal vein sampling shows lateralization to the left. The biochemical mechanism of hypertension in this condition is:

• A Excess cortisol activating mineralocorticoid receptors due to overwhelmed 11β-HSD2
• B Excess DHEA-S from adrenal zona reticularis converting to active androgens
• C Autonomous aldosterone excess independently activating MR, causing sodium retention, volume expansion, renin-independent hypertension, and potassium wasting ✓
• D Catecholamine excess from adrenal medullary hyperplasia causing sympathetic stimulation

Explanation

Primary hyperaldosteronism (Conn syndrome) results from autonomous aldosterone production by an adrenal adenoma (Conn adenoma), most commonly due to somatic mutations in KCNJ5 (potassium channel), CACNA1D (calcium channel), or ATP1A1/ATP2B3. Excess aldosterone acts on mineralocorticoid receptors (MR) in renal collecting ducts: (1) upregulates ENaC and Na/K-ATPase, causing sodium retention and volume expansion; (2) increases urinary K+ and H+ excretion causing hypokalemic metabolic alkalosis; (3) suppresses renin via volume-feedback. This is the most common secondary cause of hypertension (5-10% of hypertensives). Adrenal vein sampling is the gold standard for lateralization before surgery.

Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.