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Conn Syndrome, also known as Primary Hyperaldosteronism, is characterized by excessive secretion of aldosterone from the adrenal cortex, independent of renin regulation. The most common causes include aldosterone-producing adrenal adenoma and bilateral adrenal hyperplasia.
Excess aldosterone leads to increased sodium and water reabsorption, resulting in hypertension, while promoting potassium excretion causing hypokalemia. This electrolyte imbalance contributes to symptoms such as muscle weakness, fatigue, cramps, and in severe cases, cardiac arrhythmias.
A key diagnostic feature of Conn Syndrome is low plasma renin activity with high aldosterone levels, resulting in an elevated aldosterone-to-renin ratio (ARR). Metabolic alkalosis is also commonly observed due to increased hydrogen ion loss.
Patients typically present with resistant hypertension that does not respond well to standard antihypertensive therapy. Unlike secondary hyperaldosteronism, edema is usually absent due to the “aldosterone escape” phenomenon.
Diagnosis involves screening with ARR, followed by confirmatory suppression tests and imaging such as CT scan of the adrenal glands. Management depends on the underlying cause, including surgical removal of adenoma or medical therapy with aldosterone antagonists like spironolactone.
This conceptual diagram provides a quick visual summary of causes, pathophysiology, symptoms, and lab findings, making it ideal for rapid revision before exams.
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