Primary hyperaldosteronism (Conn syndrome)

Cushing syndrome is the clinical state of chronic glucocorticoid excess from any cause, most often exogenous glucocorticoid use, diagnosed by demonstrating loss of normal cortisol suppression or diurnal rhythm with at least two of three screening tests. Treatment targets the underlying source: withdrawal or tapering of exogenous steroid, transsphenoidal surgery for a pituitary cause, or adrenalectomy for an adrenal or ectopic tumor, with steroidogenesis inhibitors reserved for persistent or unresectable disease.

Pheochromocytoma and paraganglioma are catecholamine-secreting tumors of adrenal medullary chromaffin cells and extra-adrenal sympathetic ganglia, causing sustained or paroxysmal hypertension with headache, sweating, and palpitations, diagnosed by plasma free or 24-hour urine fractionated metanephrines before any imaging is obtained. First-line treatment is surgical resection preceded by alpha blockade with phenoxybenzamine (or off-label doxazosin) for 10 to 14 days, with a beta blocker added only after alpha blockade is established.

An adrenal incidentaloma is an adrenal mass 1 cm or larger discovered on imaging obtained for an unrelated reason, most often a benign nonfunctioning adenoma but requiring evaluation for hormone hypersecretion and malignancy in every patient. Management is surgical excision for functioning tumors, masses 4-6 cm or larger, or those with malignant imaging features, and periodic monitoring for smaller nonfunctioning lesions with benign imaging characteristics.

Adrenal cortical carcinoma is a rare, aggressive adrenal tumor that frequently secretes cortisol, androgens, or both, presenting with rapid-onset Cushing syndrome, virilization, or an incidentally discovered large adrenal mass. First-line therapy for localized disease is open resection, with adjuvant mitotane to reduce recurrence, and combination chemotherapy (etoposide, doxorubicin, cisplatin) plus mitotane for advanced or metastatic disease; mitotane-induced adrenal insufficiency requires lifelong glucocorticoid, and often mineralocorticoid, replacement.

Hypokalemia is a serum potassium level below 3.5 mEq/L, most often caused by gastrointestinal or renal potassium losses, and it produces weakness, ileus, and arrhythmia risk through altered membrane excitability. Diagnosis rests on the urine potassium-creatinine ratio to separate renal from extrarenal causes, and treatment is intravenous or oral potassium chloride, with concurrent magnesium repletion, dosed to severity and symptoms.

Renal artery stenosis causes renovascular hypertension through renal hypoperfusion and renin-angiotensin activation, most often from atherosclerosis in older patients or fibromuscular dysplasia in young women. Most patients are managed with optimal medical therapy (an ACE inhibitor or ARB plus risk-factor control), reserving revascularization for medically refractory hypertension, recurrent flash pulmonary edema, or progressive kidney impairment from bilateral or solitary-kidney disease.

Resistant hypertension is blood pressure that remains above target despite three optimally dosed antihypertensives including a diuretic, or that requires four or more drugs. Evaluation excludes pseudoresistance and secondary causes, and treatment optimizes the regimen, emphasizes a mineralocorticoid antagonist, and addresses lifestyle and adherence.

Secondary hypertension is high blood pressure from an identifiable, often correctable cause, such as primary aldosteronism, renal or renovascular disease, obstructive sleep apnea, or endocrine tumors. It should be suspected with resistant, early-onset, or abrupt hypertension, and identifying the cause can cure or greatly improve control.