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OR7.1 | Metabolic Bone Disorders — Practice Quiz
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A 68-year-old postmenopausal woman presents with acute-onset severe mid-thoracic back pain following a minor fall. DXA scan reports a T-score of -2.8 at the lumbar spine. X-ray shows a wedge compression fracture of T8. Which single finding best defines her diagnosis of osteoporosis?
Correct. A DXA T-score ≤ -2.5 is the WHO diagnostic criterion for osteoporosis. This patient's score of -2.8 meets the threshold.
Osteoporosis is defined by WHO as a DXA T-score ≤ -2.5 at the lumbar spine, femoral neck, or total hip. A T-score between -1.0 and -2.5 is osteopenia. The presence of a fragility fracture with T-score ≤-2.5 confirms severe osteoporosis.
Recall that osteoporosis is defined by DXA T-score ≤ -2.5. While fragility fractures and back pain support the diagnosis, the T-score is the definitive diagnostic criterion.
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A 45-year-old woman with no sun exposure and malabsorption secondary to coeliac disease presents with diffuse bone pain, proximal muscle weakness, and waddling gait. Serum calcium is mildly low, phosphate is low, ALP is elevated, and 25-OH vitamin D is 8 ng/mL (reference 30–100). X-ray of the femoral neck shows transverse radiolucent bands perpendicular to the cortex. What is the most likely diagnosis?
Correct. Looser's zones (pseudofractures) are pathognomonic of osteomalacia, caused by deficient vitamin D mineralisation of osteoid.
Looser's zones (pseudofractures) are pathognomonic of osteomalacia — transverse, ribbon-like radiolucencies perpendicular to the bone cortex, most commonly at the femoral neck, pubic rami, scapular border, and ribs. They represent accumulated unmineralised osteoid at sites of stress.
The combination of low vitamin D, low Ca and PO4, elevated ALP, proximal myopathy, and Looser's zones on X-ray is the classic presentation of osteomalacia.
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A 3-year-old child presents with bow-legs, wrist widening (rachitic rosary), frontal bossing, and delayed closure of the anterior fontanelle. Serum calcium is borderline low, phosphate is low, ALP is markedly elevated, and X-ray shows cupping and fraying of the metaphyses of the distal radius and ulna. Urine shows phosphaturia. What is the most appropriate first-line treatment?
Correct. Nutritional rickets is treated with vitamin D and calcium supplementation. Deformities in young children usually correct spontaneously with adequate vitamin D therapy.
Nutritional rickets is treated with vitamin D supplementation (cholecalciferol) and adequate dietary calcium. Bony deformities such as genu varum (bow-legs) in young children often correct spontaneously with medical treatment; surgical correction (osteotomy) is reserved for persistent deformity after skeletal maturity.
Surgical correction of rickets deformities is deferred until after skeletal maturity unless deformity persists and is functionally significant; the primary treatment is vitamin D and calcium.
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An 82-year-old man presents with headaches, progressive deafness, and a bowed right tibia with a warm, erythematous overlying skin. Serum ALP is 850 IU/L (reference 30–120), while calcium and phosphate are normal. Technetium-99m bone scan shows intense focal uptake in the right tibia and skull. What is the most likely diagnosis?
Correct. Paget's disease presents with focal bony hypertrophy, markedly raised ALP with normal Ca/PO4, bowing deformity, deafness, and intense focal bone scan uptake.
Paget's disease of bone is characterised by markedly elevated ALP (often the only biochemical abnormality) with normal serum calcium and phosphate. It presents with bone pain, deformity (bowed tibia, enlarged skull), deafness (8th nerve compression), high-output cardiac failure, and increased fracture risk. Bone scan shows intense localised uptake.
The combination of markedly elevated ALP, normal calcium/phosphate, focal bony hypertrophy, bowed tibia, and deafness is classic for Paget's disease of bone.
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A 55-year-old woman with osteoporosis (T-score -3.1) and a recent wrist fragility fracture is started on bisphosphonate therapy. Which mechanism best explains how bisphosphonates reduce fracture risk?
Correct. Bisphosphonates inhibit osteoclast activity (via inhibition of farnesyl pyrophosphate synthase), reducing bone resorption and increasing bone mineral density.
Bisphosphonates inhibit osteoclast-mediated bone resorption by inhibiting farnesyl pyrophosphate synthase in the mevalonate pathway, reducing osteoclast activity and lifespan. This tips the balance in favour of bone formation, increasing bone mineral density and reducing fracture risk.
Bisphosphonates work by inhibiting osteoclasts. Vitamin D analogues increase intestinal calcium absorption; teriparatide directly stimulates osteoblasts; bisphosphonates do not suppress PTH.
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A 6-year-old boy presents with bilateral genu valgum (knock-knees) and X-ray shows flaring and fraying of the metaphyses. Serum phosphate is very low (0.5 mmol/L), calcium is normal, ALP is markedly elevated, and 1,25-OH2 vitamin D is low despite normal dietary vitamin D intake. Urine phosphate is elevated. Which diagnosis best fits?
Correct. Isolated hypophosphataemia with renal phosphate wasting, normal calcium, low/normal 1,25-OH2 vitamin D, and rickets unresponsive to standard vitamin D doses points to X-linked hypophosphataemic rickets.
X-linked hypophosphataemic rickets (XLH, vitamin D-resistant rickets) is characterised by isolated hypophosphataemia due to renal phosphate wasting, normal or low 1,25-OH2 vitamin D, normal serum calcium, and rickets deformities unresponsive to standard vitamin D doses. Treatment requires phosphate supplementation plus calcitriol.
Nutritional rickets shows low calcium and responds to standard vitamin D doses. The isolated hypophosphataemia with renal phosphate wasting here suggests hypophosphataemic (vitamin D-resistant) rickets.
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A 72-year-old man with known Paget's disease of the pelvis reports sudden onset of severe pelvic pain. Plain X-ray shows a lytic lesion replacing the previously sclerotic Paget's bone with soft tissue extension. Serum ALP, which was 600 IU/L one year ago, is now 3200 IU/L. What is the most important complication to exclude?
Correct. A sudden dramatic rise in ALP, new lytic destruction, and soft tissue extension in a Paget's lesion should immediately raise concern for sarcomatous transformation (osteosarcoma) — a rare but lethal complication.
Sarcomatous transformation (osteosarcoma) occurs in less than 1% of Paget's disease cases but carries a very poor prognosis. It should be suspected when there is a sudden marked rise in ALP beyond baseline, new lytic destruction, soft tissue extension, or severe worsening pain in a previously stable Pagetic lesion.
A sudden surge in ALP with new lytic change and soft tissue extension in Paget's disease should always prompt urgent evaluation for sarcomatous transformation.
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A 60-year-old woman on long-term corticosteroid therapy for rheumatoid arthritis sustains a vertebral compression fracture. Serum calcium, phosphate, and ALP are all normal. DXA shows T-score of -2.6. Her PTH is mildly elevated and vitamin D level is 15 ng/mL. What pattern of bone disease is most expected in chronic glucocorticoid use?
Correct. Glucocorticoids suppress osteoblasts (reducing bone formation) and increase osteoclast activity (increasing resorption), causing rapid bone loss especially in trabecular bone.
Glucocorticoid-induced osteoporosis results from direct suppression of osteoblast function and increased osteoclast activity, combined with impaired intestinal calcium absorption and secondary hyperparathyroidism. All patients on long-term corticosteroids should receive calcium, vitamin D, and bisphosphonate prophylaxis.
Glucocorticoids cause osteoporosis primarily through osteoblast suppression and increased osteoclast-mediated bone resorption, leading to rapid trabecular bone loss.
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