## Distinguishing Pheochromocytoma from Primary Aldosteronism ### Clinical Presentation Differences **Key Point:** Episodic (paroxysmal) hypertension with acute catecholamine surges is the hallmark discriminator of pheochromocytoma and is absent in primary aldosteronism, which causes sustained hypertension. ### Comparison Table | Feature | Pheochromocytoma | Primary Aldosteronism | | --- | --- | --- | | **Blood Pressure Pattern** | Episodic/paroxysmal spikes | Sustained, mild-to-moderate | | **Symptoms** | Headache, sweating, palpitations, anxiety (acute episodes) | Asymptomatic or fatigue | | **Serum Potassium** | Normal or high | Low (hypokalemia) | | **Plasma Renin** | Normal or elevated | Suppressed | | **Plasma Aldosterone** | Normal or low | Elevated | | **Urinary Metanephrines** | Elevated | Normal | | **24-h Urine Potassium** | Normal | Often elevated | ### High-Yield Clinical Pearl **High-Yield:** The **triad of episodic headache + profuse diaphoresis + palpitations** during acute hypertensive surges is virtually pathognomonic for pheochromocytoma. Primary aldosteronism patients do not experience these acute catecholamine-mediated symptoms because aldosterone causes chronic, steady sodium retention and potassium loss, not episodic hormone release. ### Biochemical Basis 1. **Pheochromocytoma:** Catecholamine (epinephrine, norepinephrine) secretion is episodic and unpredictable → acute α- and β-adrenergic effects → paroxysmal hypertension, tachycardia, sweating. 2. **Primary Aldosteronism:** Aldosterone secretion is relatively constant → chronic sodium reabsorption and potassium wasting → sustained hypertension, hypokalemia, metabolic alkalosis. ### Mnemonic **PHEO = Paroxysmal Hypertension, Episodic Outbursts** — remember the episodic nature as the key discriminator. **Aldosterone = Asymptomatic, Alkalosis, Adrenal adenoma** — sustained, silent, electrolyte-driven. [cite:Harrison 21e Ch 405]
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