Primary Hyperparathyroidism: The Daily PANCE Blueprint

The answer is A. Primary hyperparathyroidism

A high calcium with a high — or even inappropriately normal — PTH is primary hyperparathyroidism until proven otherwise, and here the PTH is frankly elevated. That single pairing does almost all the diagnostic work, because in every other cause of hypercalcemia the parathyroid glands behave correctly and shut themselves off. Roughly 85% of cases are a single adenoma; the rest are four-gland hyperplasia or, rarely, carcinoma. The clinical picture is the old mnemonic and it holds up: stones, bones, abdominal groans, and psychiatric overtones — nephrolithiasis and nephrocalcinosis, bone pain and osteoporosis with a characteristic loss at the distal radius, constipation, nausea, peptic ulcer and pancreatitis, and the depression, fatigue, and cognitive fog that so often get blamed on stress or aging. The low phosphate is the fingerprint of PTH excess: PTH drives phosphate wasting at the proximal tubule while pulling calcium out of bone and reclaiming it distally, so calcium climbs as phosphate falls. The elevated 24-hour urine calcium is the deliberate discriminator in this stem — it is what separates this from familial hypocalciuric hypercalcemia. Work-up after the diagnosis is made: DEXA including the distal third of the radius, renal imaging for stones, and a sestamibi scan or neck ultrasound to localize the adenoma before surgery, never to make the diagnosis. Parathyroidectomy is the only cure, and it is indicated for symptomatic disease — hers qualifies on stones alone — or in asymptomatic patients under 50, with calcium more than 1 mg/dL above normal, a creatinine clearance under 60, or osteoporosis. Cinacalcet is a medical alternative for nonsurgical candidates. Now the distractors, each excluded by a specific number. Humoral hypercalcemia of malignancy is driven by PTH-related peptide, so the measured PTH is suppressed; it presents with higher calcium, faster onset, and a sick patient. Familial hypocalciuric hypercalcemia is the classic trap and the reason the urine calcium is in the stem: a calcium-sensing receptor mutation produces lifelong mild hypercalcemia with a normal or mildly high PTH, but a low urine calcium and a calcium-to-creatinine clearance ratio below 0.01 — and operating on these patients does nothing but harm. Vitamin D intoxication raises calcium and phosphate together while suppressing PTH. Secondary hyperparathyroidism from renal failure raises PTH but the calcium is low or normal and the phosphate is high; her creatinine is normal.