Excess PTH causes cortical bone loss via RANKL-mediated osteoclast activation; classic radiology: subperiosteal resorption, salt‑and‑pepper skull, brown tumors. Primary (adenoma), secondary (CKD/vit D deficiency), tertiary (autonomous) forms dictate biochemistry and treatment. DEXA: cortical loss at one‑third radius; labs—↑PTH, ↑ALP; Ca high in primary/tertiary, low‑normal in secondary; phosphate low in primary, high in CKD. Orthopaedic issues: fragility fractures, brown tumors, tendon ruptures; treat endocrine cause first, then stabilize fractures as per principles. Parathyroidectomy is definitive for symptomatic primary disease; watch for hungry bone syndrome post‑op.
What is the most characteristic radiological finding in hyperparathyroidism?
Which of the following laboratory findings is typically associated with primary hyperparathyroidism?
What is the definitive treatment for symptomatic primary hyperparathyroidism?
Which condition represents the severe skeletal form of hyperparathyroidism characterized by cystic bone lesions?
In secondary hyperparathyroidism due to chronic kidney disease, which of the following is typically observed?
What is the 'hungry bone syndrome' that can occur post-parathyroidectomy?
What is the common biochemical profile in a patient with primary hyperparathyroidism?
Which of the following is a common orthopedic complication of hyperparathyroidism?
What is the typical radiographic appearance of the skull in hyperparathyroidism?
Which of the following is NOT a skeletal manifestation of hyperparathyroidism?
