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Q1: Definition and recognition (2 min)
Examiner: Define primary aldosteronism. How common is it, and how would you recognise it clinically?
Expected answer:
- Primary aldosteronism is autonomous aldosterone excess that is independent of the renin-angiotensin system, so the hallmark is HIGH aldosterone with SUPPRESSED (low) renin. Conn syndrome refers specifically to a unilateral aldosterone-producing adenoma.
- It is the commonest specifically-treatable cause of secondary hypertension: about 5 to 10% of all hypertension and over 20% of resistant hypertension — far more common than once thought.
- Recognition hinges on resistant hypertension (above target on three agents including a diuretic), spontaneous or diuretic-induced hypokalaemia with metabolic alkalosis, an adrenal incidentaloma, or early-onset hypertension or stroke under 40 (or a family history).
- Crucially, most patients are normokalaemic, so a normal potassium does not exclude it — screen on the blood-pressure pattern.
Q2: Investigations (3 min)
Examiner: Walk me through the diagnostic pathway.
Expected answer:
- The discipline is screen, confirm, localise.
- Screen: aldosterone-to-renin ratio (ARR) — the single best case-finding test. Correct interfering drugs first: stop the mineralocorticoid antagonist and potassium-wasting diuretics at least 4 to 6 weeks prior; interpret ACEi/ARB and beta-blockers with care.
- Confirm autonomy: a suppression test — oral salt loading, saline infusion, fludrocortisone suppression, or a captopril challenge — in which aldosterone fails to suppress.
- Localise: CT adrenal for anatomy, then adrenal venous sampling (AVS) — the gold standard to prove unilateral versus bilateral disease before surgery. CT alone is unreliable; a nodule may be a non-functioning incidentaloma.
- In young patients (under 40) or with a family history, test for familial hyperaldosteronism type I (the CYP11B1/CYP11B2 chimeric gene).
Q3: Management (3 min)
Examiner: How do you treat it?
Expected answer:
- Unilateral disease (adenoma or unilateral hyperplasia, proven by AVS): laparoscopic adrenalectomy — potentially curative; give a mineralocorticoid receptor antagonist first to control blood pressure and potassium.
- Bilateral adrenal hyperplasia (the commonest cause) or a patient unfit/unwilling for surgery: medical therapy with a mineralocorticoid receptor antagonist — spironolactone first-line; switch to eplerenone if gynaecomastia, impotence or menstrual irregularity are intolerable. Add ACEi/ARB or a calcium-channel blocker and sodium restriction.
- Familial hyperaldosteronism type I: low-dose glucocorticoid (dexamethasone) suppresses ACTH-driven aldosterone synthase.
- Treat severe hypokalaemia with potassium repletion and avoid potassium-wasting diuretics.
Q4: A discriminator and prognosis (2 min)
Examiner: A young man has hypertension, hypokalaemia and alkalosis, but both renin AND aldosterone are low. What is that, and what is the overall prognosis of primary aldosteronism?
Expected answer:
- Low renin AND low aldosterone with hypertension, hypokalaemia and alkalosis is a pseudoaldosteronism — classically Liddle syndrome, an autosomal dominant gain-of-function of the epithelial sodium channel (ENaC). Treat with amiloride or triamterene; spironolactone is ineffective.
- Prognosis: adrenalectomy cures hypertension in 30 to 60% of unilateral disease and improves it in most of the rest; bilateral disease is well controlled medically (cure uncommon, but potassium and cardiovascular risk normalise).
- Untreated, aldosterone confers cardiovascular damage disproportionate to blood pressure (atrial fibrillation, heart failure, LVH, stroke), so targeted treatment reduces cardiovascular morbidity more than standard antihypertensives.