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OR7.1 | Metabolic Bone Disorders — Graded Quiz
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A 70-year-old woman with a DXA T-score of -3.0 at the femoral neck and a prior fragility fracture of the wrist is started on alendronate 70 mg weekly. Six weeks later she is readmitted with severe epigastric pain and odynophagia. Endoscopy reveals oesophageal ulceration. What is the most appropriate next management step?
Correct. Oesophageal ulceration is an absolute indication to stop oral bisphosphonates. IV zoledronic acid (5 mg once yearly) is the appropriate alternative with equivalent fracture-prevention efficacy.
Oral bisphosphonate-related oesophageal ulceration requires discontinuation of the oral agent. Injectable zoledronic acid (5 mg IV annually) is the most appropriate alternative bisphosphonate — it bypasses the GI tract entirely and has robust anti-fracture efficacy.
Oral bisphosphonates should be stopped when oesophageal complications occur. IV zoledronic acid bypasses the GI route entirely.
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A 40-year-old woman with chronic kidney disease (eGFR 18 mL/min) presents with bone pain and muscle weakness. Biochemistry: Ca 1.95 mmol/L (↓), PO4 2.1 mmol/L (↑), ALP 280 IU/L (↑), PTH 320 pg/mL (markedly ↑), 25-OH vitamin D 12 ng/mL (↓). X-ray shows subperiosteal erosions at the radial aspect of the middle phalanges of the index fingers. What is the primary mechanism causing her bone disease?
Correct. In CKD, the kidney cannot convert 25-OH vitamin D to active calcitriol (1-alpha-hydroxylation fails), causing hypocalcaemia and compensatory secondary hyperparathyroidism with high PTH and phosphate retention.
Renal osteodystrophy in CKD results from failure of renal 1-alpha-hydroxylation (so 25-OH VitD cannot be converted to active calcitriol), phosphate retention, and secondary hyperparathyroidism. Subperiosteal erosions at the radial aspect of the middle phalanges are the classic radiological sign of secondary hyperparathyroidism (osteitis fibrosa cystica).
The key defect in CKD-related bone disease is reduced renal 1-alpha-hydroxylase activity, impairing calcitriol synthesis and triggering secondary hyperparathyroidism.
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A 4-year-old boy presents with bilateral genu varum (bow-legs). X-ray shows fraying and cupping of the metaphyses of the distal femur and proximal tibia. Serum calcium is 1.8 mmol/L (↓), phosphate is 0.8 mmol/L (↓), ALP is markedly elevated, and 25-OH vitamin D is 9 ng/mL. The boy has been exclusively breastfed with no sun exposure. After 6 months of vitamin D and calcium therapy, the bow-legs persist. What is the next appropriate management step?
Correct. In a 4-year-old with nutritional rickets and persistent bow-legs after 6 months of treatment, continued medical treatment with reassessment is appropriate — significant remodelling potential remains. Surgery (osteotomy) is deferred until near skeletal maturity or if deformity is functionally severe.
Deformities in young children with nutritional rickets often correct spontaneously with adequate vitamin D + calcium therapy. However, if significant deformity persists after medical treatment and the child approaches skeletal maturity, corrective osteotomy (valgus tibial osteotomy for genu varum) is indicated. Decisions for surgery are based on the age of the child, severity, and remodelling potential.
Surgical correction of rickets-related deformities should be deferred until near-skeletal maturity or until all medical treatment has failed, due to the high remodelling potential in young children.
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A 78-year-old man with extensive Paget's disease of the skull and femur develops progressive high-frequency hearing loss bilaterally. On examination, his femur is bowed anterolaterally with skin warmth. ALP is 740 IU/L. What is the most likely mechanism of his deafness?
Correct. Hearing loss in Paget's disease is predominantly sensorineural and due to compression of the vestibulocochlear nerve (CN VIII) by pagetic overgrowth in the petrous temporal bone.
Hearing loss in Paget's disease most commonly results from compression/entrapment of the 8th (vestibulocochlear) cranial nerve by pagetic skull bone involving the temporal bone (specifically, bony overgrowth of the internal auditory canal). Sensorineural hearing loss is more common than conductive loss.
The deafness in Paget's disease is caused by direct bony compression of the 8th cranial nerve as pagetic bone enlarges in the skull base and temporal bone.
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A 52-year-old woman presents with bone pain, muscle weakness, and a serum 25-OH vitamin D of 9 ng/mL. Her biochemistry shows: Ca 2.05 mmol/L, PO4 0.6 mmol/L (↓), ALP 390 IU/L (↑), PTH 160 pg/mL (↑). She has no malabsorption history and gets some sun exposure. Urine calcium excretion is markedly low. X-ray shows a faint transverse band at the medial femoral neck. Which is the most likely single underlying aetiology?
Correct. The full biochemical picture — low 25-OH VitD, low phosphate from secondary hyperparathyroidism, markedly elevated ALP, high PTH, low urinary calcium — combined with Looser's zones confirms osteomalacia due to vitamin D deficiency.
The combination of low vitamin D, low phosphate (secondary hyperparathyroidism causes phosphaturia), elevated PTH, very low urinary calcium (due to maximal renal calcium conservation), and Looser's zone confirms osteomalacia. Despite some sun exposure, her vitamin D level is severely deficient, making dietary/lifestyle insufficiency the most likely cause in the absence of malabsorption.
The Looser's zone (pathognomonic of osteomalacia), combined with low vitamin D, elevated PTH, low phosphate, and low urinary calcium all point to osteomalacia from vitamin D insufficiency.
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A 65-year-old postmenopausal woman presents for DXA screening. Her T-score is -1.8 at the hip. She has a family history of hip fracture, smokes 15 cigarettes/day, has a BMI of 18.5 kg/m2, and takes no medications. FRAX 10-year major osteoporotic fracture risk is calculated at 24%. What is the most appropriate next management step?
Correct. A FRAX 10-year risk of 24% for major osteoporotic fracture exceeds treatment thresholds in most guidelines regardless of whether T-score reaches -2.5. Bisphosphonate plus calcium/vitamin D is appropriate first-line pharmacotherapy.
In patients with osteopenia (T-score -1.0 to -2.5) but high FRAX-estimated fracture risk (≥20% for major osteoporotic fracture or ≥3% for hip fracture in the US/UK guidelines), pharmacological treatment with bisphosphonates is recommended in addition to lifestyle modifications and calcium/vitamin D supplementation. Risk factors like smoking, low BMI, and family history significantly increase FRAX score beyond the BMD alone.
FRAX risk assessment integrates clinical risk factors beyond BMD alone. A FRAX of 24% warrants pharmacological treatment even with a T-score that is only osteopenic.
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A 75-year-old man with Paget's disease is treated with a single infusion of intravenous zoledronic acid 5 mg. Three months later, serum ALP has fallen from 920 IU/L to 185 IU/L and the patient reports marked improvement in bone pain. He is now asymptomatic. When should zoledronic acid be re-administered?
Correct. Zoledronic acid for Paget's disease produces durable remission. Re-treatment is guided by clinical and biochemical relapse (symptom recurrence or ALP elevation), not a fixed interval.
Intravenous zoledronic acid (5 mg single infusion) is the treatment of choice for Paget's disease and typically achieves remission (ALP normalisation or near-normalisation) lasting up to 5 years or more. Re-treatment is indicated when symptoms recur or when ALP rises above the upper limit of normal or above a defined threshold on monitoring.
Zoledronic acid single infusion achieves durable remission in most patients. Annual infusion is not required; monitoring ALP and re-treating on relapse is the evidence-based approach.
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A 32-year-old woman presents with diffuse bone pain and weakness. Investigations reveal: Ca 2.05 mmol/L, PO4 0.55 mmol/L (↓), ALP 350 IU/L (↑), PTH 145 pg/mL (↑), 25-OH vitamin D 35 ng/mL (normal). Urinary phosphate is markedly elevated. CT abdomen/pelvis incidentally reveals a 1.5 cm soft tissue mass in the right thigh. What is the most likely diagnosis?
Correct. Tumour-induced osteomalacia presents with adult-onset hypophosphataemia (renal phosphate wasting), elevated ALP, secondary hyperparathyroidism, osteomalacia symptoms, normal 25-OH vitamin D, and an occult FGF-23-secreting mesenchymal tumour. Resection is curative.
Tumour-induced osteomalacia (oncogenic osteomalacia) is caused by FGF-23-secreting mesenchymal tumours. FGF-23 inhibits renal phosphate reabsorption and suppresses 1-alpha-hydroxylase, causing profound hypophosphataemia and low/inappropriately normal 1,25-OH2 vitamin D despite normal 25-OH vitamin D. Treatment is complete surgical resection of the culprit tumour.
The key clue is adult-onset isolated hypophosphataemia with renal phosphate wasting, normal 25-OH vitamin D (distinguishing it from nutritional deficiency), and a soft tissue mass. This is oncogenic osteomalacia.
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An 18-month-old child presents with nutritional rickets. After 3 months of standard vitamin D (cholecalciferol) and calcium treatment, clinical improvement is seen. Which of the following is the FIRST radiological sign of healing rickets on plain X-ray of the wrist?
Correct. The first radiological sign of healing rickets is the zone of provisional calcification (ZPC) appearing as a dense white transverse line at the metaphysis within 2-4 weeks of treatment.
The first radiological sign of healing rickets is the appearance of a zone of provisional calcification (ZPC) — a dense transverse white line at the metaphysis that represents the re-mineralisation front. This typically appears within 2-4 weeks of commencing treatment, before clinical deformity improvement becomes apparent.
The ZPC at the metaphysis is the earliest radiological healing sign in rickets, appearing before clinical deformity resolution or cortical normalisation.
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A 67-year-old woman on teriparatide (recombinant PTH 1-34) for severe osteoporosis completes 24 months of treatment. Her endocrinologist advises sequential antiresorptive therapy. Which is the most appropriate next treatment?
Correct. After completing teriparatide, a bisphosphonate (alendronate, risedronate, or zoledronic acid) must be initiated immediately to preserve the anabolic-phase bone density gains.
Teriparatide (anabolic agent) significantly increases bone mass during the 18-24 month treatment course. However, the gains in BMD are rapidly lost if no treatment is given after stopping. Sequential therapy with a bisphosphonate (typically alendronate or zoledronic acid) is required immediately after completing teriparatide to consolidate the bone mass gains.
Without antiresorptive follow-up after teriparatide, BMD gains are reversed within 12-18 months. Sequential bisphosphonate therapy is mandatory.
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