Bit · Endo
Conn vs Cushing vs Pheochromocytoma
Three adrenal hypertensions. Each one is a different hormone running unchecked. The pivot is which lab pattern fits: aldosterone, cortisol, or catecholamines.
Mechanism
All three cause secondary hypertension via an adrenal-driven hormone excess:
- Conn syndrome (primary hyperaldosteronism) — adrenal adenoma (or bilateral hyperplasia) autonomously secretes aldosterone. Aldosterone drives renal Na⁺ reabsorption (HTN) and K⁺ excretion (hypokalemia). Plasma renin is suppressed. ALDO/RENIN ratio elevated.
- Cushing syndrome — cortisol excess. Most common cause overall is iatrogenic (exogenous steroids). Endogenous: Cushing disease = pituitary ACTH-secreting adenoma; ectopic ACTH (small-cell lung cancer, carcinoid); adrenal adenoma/carcinoma (ACTH-independent). HTN, hyperglycemia, central obesity, moon facies, buffalo hump, striae, easy bruising, proximal muscle weakness, osteoporosis.
- Pheochromocytoma — catecholamine-secreting tumour of adrenal medulla (chromaffin cells). 'Rule of 10s' historically: 10% extra-adrenal, 10% bilateral, 10% malignant, 10% familial, 10% in kids. Associated with MEN 2A/2B, von Hippel-Lindau, NF1. Paroxysmal HTN, palpitations, pounding headache, diaphoresis (the 5 P's). Diagnose with plasma free or 24-h urinary metanephrines.
Differentiator Table
| Conn (hyperaldosteronism) | Cushing | Pheochromocytoma | |
| Excess hormone | Aldosterone | Cortisol | Catecholamines (epi, norepi) |
| BP pattern | Sustained HTN | Sustained HTN | Paroxysmal HTN with surges |
| K⁺ | Low (hypokalemia) | Mildly low or normal | Normal |
| Glucose | Normal | Hyperglycemia | Hyperglycemia during attacks |
| Body habitus | Normal | Central obesity, moon face, buffalo hump, purple striae, thin skin | Often thin / weight loss |
| Best initial test | Plasma aldosterone : renin ratio (↑) | 24-hr urinary free cortisol, late-night salivary cortisol, low-dose dexamethasone suppression | Plasma free or 24-hr urinary metanephrines |
| Confirmation | Saline suppression test | High-dose dexamethasone (distinguishes pituitary from ectopic from adrenal) | Adrenal MRI/CT; MIBG scan |
| Triggers / clues | Resistant HTN + spontaneous hypokalemia + metabolic alkalosis | Steroid use, central obesity + striae + bruising + diabetes | Paroxysms with headache + palpitations + sweating; family history MEN2/VHL/NF1 |
| Treatment | Adenoma: adrenalectomy. Hyperplasia: spironolactone/eplerenone | Treat cause (taper steroids, resect adenoma, etc.) | α-blockade FIRST (phenoxybenzamine), then β-blockade, then surgical resection |
The Pivot
Three questions decide it:
- Hypokalemia + HTN + suppressed renin? → Conn.
- Central obesity + striae + diabetes + HTN? → Cushing.
- Paroxysmal HTN with headaches and sweating? → Pheo.
Pheo trap: never give a β-blocker first. Unopposed α-stimulation worsens the HTN. Always α-block before β-block.
NBME-Style Stem
A 41-year-old man presents with episodic headaches, palpitations, and diaphoresis. Blood pressure during an episode is 220/130 mm Hg, returning to 138/82 between episodes. He has a strong family history of medullary thyroid carcinoma and hyperparathyroidism. 24-hour urinary metanephrines are elevated. Which of the following is the most appropriate first step in management?
Concept Anchor
Conn = aldo (K⁺ down, BP up). Cushing = cortisol (sugar up, skin thin, fat central). Pheo = catecholamines (paroxysms, headaches, sweat). The hormone is always the pivot — its lab gives the diagnosis and tells you what to block.