Primаry Aldоsterоnism (Cоnn Syndrome) (Study Outline) For study only—this is not medicаl аdvice or a substitute for professional care. 1. Background Definition:Primary aldosteronism is excessive, autonomous secretion of aldosterone from the adrenal cortex (zona glomerulosa), independent of renin.This leads to sodium retention, potassium loss, and metabolic alkalosis. Pathophysiology: Aldosterone excess → ↑ Na⁺ and water reabsorption → volume expansion and hypertension. Increased K⁺ and H⁺ secretion → hypokalemia and metabolic alkalosis. Suppressed renin due to feedback inhibition from increased volume. Major Causes: Aldosterone-producing adenoma (Conn syndrome) — most common. Bilateral adrenal hyperplasia. Rare: unilateral adrenal carcinoma, familial hyperaldosteronism (genetic). Epidemiology: Accounts for 5–10% of hypertension cases. More common in middle-aged adults; slight female predominance. 2. History Symptoms (often subtle): Hypertension — may be resistant to standard therapy. Muscle weakness, fatigue, cramps, paresthesias (due to hypokalemia). Polyuria and polydipsia (from renal K⁺ wasting). Headaches, palpitations, nocturia possible. Usually no peripheral edema (due to “aldosterone escape” — natriuresis balancing fluid retention). Historical Clues: Early-onset hypertension or family history of endocrine hypertension. Severe or refractory hypertension in a relatively young patient. Hypokalemia not explained by diuretics. 3. Exam Findings Vital Signs: Persistent or resistant hypertension (often moderate to severe). Cardiovascular: Possible left ventricular hypertrophy or secondary changes from chronic hypertension. Neuromuscular: Muscle weakness or arrhythmias (if severe hypokalemia). Volume Status: Usually euvolemic (no significant edema). Physical Exam: Often otherwise unremarkable. 4. Making the Diagnosis Step 1 – Screening: Plasma Aldosterone-to-Renin Ratio (ARR): Elevated aldosterone with suppressed renin = suggestive. High ARR (>20:1) strongly supports diagnosis. Step 2 – Confirmatory Testing: Oral sodium loading test, saline infusion test, or fludrocortisone suppression test: Failure of aldosterone suppression confirms autonomous secretion. Step 3 – Determine Etiology (Localization): Adrenal CT scan: evaluates for adenoma, carcinoma, or bilateral hyperplasia. Adrenal venous sampling (AVS): Gold standard for lateralization (differentiates unilateral adenoma from bilateral hyperplasia). Performed prior to surgery to confirm source of excess aldosterone. Step 4 – Additional Labs: Electrolytes: Hypokalemia, metabolic alkalosis. Renin: Suppressed (low plasma renin activity). Aldosterone: Elevated (>15 ng/dL in most cases). Gold Standard: Confirmatory suppression testing demonstrating autonomous aldosterone production with low renin activity. 5. Management (Exam Concepts) (Conceptual overview only—no dosing or treatment regimens.) Unilateral Aldosterone-Producing Adenoma: Laparoscopic adrenalectomy is definitive. Medical therapy (if not surgical candidate): mineralocorticoid receptor antagonists (spironolactone, eplerenone). Bilateral Adrenal Hyperplasia: Medical management preferred (mineralocorticoid antagonists). Monitor electrolytes, BP, and renal function. General Care: Control hypertension. Normalize potassium and acid–base status. Screen for secondary cardiovascular and renal complications. Exam Tips: Hypertension + hypokalemia = suspect primary aldosteronism. Low renin, high aldosterone. Distinguish from secondary aldosteronism (both renin and aldosterone elevated — e.g., renal artery stenosis). Adrenal venous sampling differentiates unilateral from bilateral disease before surgery. NBME-Style Practice Question A 40-year-old woman presents with fatigue, muscle cramps, and difficult-to-control hypertension. Her blood pressure is 165/100 mm Hg. Laboratory results show Na⁺ 148 mEq/L, K⁺ 3.0 mEq/L, and metabolic alkalosis. Plasma renin activity is suppressed, and plasma aldosterone concentration is markedly elevated. Which of the following is the most appropriate next diagnostic step? A. High-dose dexamethasone suppression testB. Oral sodium loading testC. 24-hour urinary free cortisol testD. Plasma metanephrine level
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