Hyperparathyroidism and Bone
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;...
Practised by MCQ
10What is the most characteristic radiological finding in hyperparathyroidism?
mcqWhich of the following laboratory findings is typically associated with primary hyperparathyroidism?
mcqWhat is the definitive treatment for symptomatic primary hyperparathyroidism?
mcqWhich condition represents the severe skeletal form of hyperparathyroidism characterized by cystic bone lesion...
mcqIn secondary hyperparathyroidism due to chronic kidney disease, which of the following is typically observed?
mcqWhat is the 'hungry bone syndrome' that can occur post-parathyroidectomy?
mcqWhat is the common biochemical profile in a patient with primary hyperparathyroidism?
mcqWhich of the following is a common orthopedic complication of hyperparathyroidism?
mcqWhat is the typical radiographic appearance of the skull in hyperparathyroidism?
mcqWhich of the following is NOT a skeletal manifestation of hyperparathyroidism?