Clinical meaning
Secondary hypertension accounts for 5-10% of all hypertension cases and is caused by an identifiable, often correctable underlying condition. The NP must suspect secondary hypertension when: hypertension presents before age 30 or after age 55 without risk factors, blood pressure is severely elevated or resistant to ≥3 antihypertensive agents at optimal doses including a diuretic (resistant hypertension), there is an acute rise in previously controlled blood pressure, or target organ damage is disproportionate to hypertension duration. Major causes include: (1) Renovascular hypertension (renal artery stenosis): atherosclerotic disease in elderly or fibromuscular dysplasia in young women — activation of RAAS from renal hypoperfusion; (2) Primary aldosteronism (Conn syndrome): autonomous aldosterone production causing sodium retention, potassium wasting, and volume expansion — most common endocrine cause; (3) Pheochromocytoma: catecholamine-secreting adrenal tumor causing episodic severe hypertension with headache, palpitations, and diaphoresis (classic triad); (4) Cushing syndrome: cortisol excess activating mineralocorticoid receptors; (5) Thyroid disorders: both hyper- and hypothyroidism can cause hypertension; (6) Coarctation of the aorta: congenital narrowing typically distal to left subclavian artery — upper extremity hypertension with diminished femoral pulses; (7) Obstructive sleep apnea: most common secondary cause in obese patients — intermittent hypoxia activates sympathetic nervous system; (8) Chronic kidney disease: volume overload and RAAS activation; (9) Drug-induced: NSAIDs, oral contraceptives, decongestants, stimulants, corticosteroids.