Cushing's Syndrome

A patient gains 30 pounds in two months, bruises from a blood pressure cuff, and has a blood glucose of 248 — but they don't have diabetes. Cortisol is running the show.

Cushing's syndrome results from prolonged exposure to excess cortisol — most commonly from exogenous corticosteroid therapy (prednisone, dexamethasone), not from an adrenal tumor. Endogenous causes include pituitary adenomas (Cushing's disease) and ectopic ACTH-secreting tumors. Excess cortisol mimics a state of chronic stress: it mobilizes glucose (hyperglycemia), retains sodium and water (hypertension, edema, hypokalemia), breaks down protein (muscle wasting, thin skin, striae, poor wound healing), and redistributes fat centrally (moon face, buffalo hump, truncal obesity with thin extremities). Immune suppression is significant — the patient is infection-prone, yet classic inflammatory signs may be blunted, masking serious infection. Diagnosis involves 24-hour urine free cortisol, late-night salivary cortisol, and the dexamethasone suppression test. A key nursing priority is monitoring for hyperglycemia, hypertension, hypokalemia, and subtle signs of infection. Skin integrity is fragile; even routine blood pressure cuffs or tape removal can cause bruising or tears.

Key Distinctions

Don't confuse Cushing's (excess cortisol → hyperglycemia, hypertension, hypokalemia, weight gain) with Addison's (cortisol deficit → hypoglycemia, hypotension, hyperkalemia, weight loss) — they are metabolic mirror images. Students mistake iatrogenic Cushing's from long-term steroid use as rare, but it is actually the most common cause. Moon face and buffalo hump are fat redistribution, not generalized obesity — extremities remain thin.

Clinical Pearl

Think of cortisol as the 'too much of everything bad' hormone: too much sugar, too much sodium, too much fat, too little potassium, too little immune defense.