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Osteoporosis & metabolic bone flashcards

18 high-yield MRCP Part 1 cards from the Intellect Medicos Rheumatology course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.

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  1. In postmenopausal osteoporosis, what are the serum calcium, phosphate, ALP and PTH?

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    All normal.

    Why? Osteoporosis is reduced bone mass with normal mineralisation; abnormal bone biochemistry suggests another cause (e.g. osteomalacia or hyperparathyroidism).

  2. What is the typical biochemical pattern in osteomalacia due to vitamin D deficiency?

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    Low or normal calcium, low phosphate, raised ALP and raised PTH (low 25-OH vitamin D).

    Why? Low vitamin D reduces calcium absorption, causing secondary hyperparathyroidism, which wastes phosphate in the urine.

  3. What is the characteristic X-ray finding in osteomalacia?

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    Looser's zones (pseudofractures) — transverse lucent bands.

    Why? Unmineralised osteoid accumulates, causing bone pain, proximal myopathy and a waddling gait.

  4. How is osteomalacia treated in CKD, compared with simple vitamin D deficiency?

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    CKD: an activated vitamin D such as alfacalcidol or calcitriol. Simple deficiency: cholecalciferol.

    Why? Diseased kidneys cannot perform 1-alpha-hydroxylation, so the active form is needed.

  5. A 74-year-old man has aching in his right tibia, which looks bowed. Calcium and phosphate are normal; ALP is 520 U/L. X-ray shows mixed lytic and sclerotic change with coarse trabeculae. What is the treatment for his bone pain?

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    A bisphosphonate (e.g. IV zoledronate or oral risedronate) — Paget's disease of bone.

    Why? Bisphosphonates suppress the excessive osteoclast activity driving Paget's disease.

  6. Name three complications of Paget's disease of bone.

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    Any three: hearing loss, high-output heart failure, osteosarcoma, pathological fractures, nerve compression.

    Why? Skull involvement affects the ossicles, cochlea or eighth nerve, causing hearing loss; highly vascular bone raises cardiac output.

  7. Osteogenesis imperfecta is usually autosomal dominant, caused by mutations in ______ (type I collagen), and presents with fractures, blue sclerae and hearing loss.

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    COL1A1/COL1A2

    Why? Type I collagen is a major component of bone, sclera, skin and tendons; bisphosphonates reduce fractures.

  8. Osteogenesis imperfecta is usually autosomal dominant, caused by mutations in COL1A1/COL1A2 (type I collagen), and presents with fractures, ______ and hearing loss.

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    blue sclerae

    Why? Type I collagen is a major component of bone, sclera, skin and tendons; bisphosphonates reduce fractures.

  9. What is the underlying defect in osteopetrosis?

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    Osteoclast dysfunction (failure of bone resorption).

    Why? Bone is dense but brittle; marrow space is lost (anaemia, extramedullary haematopoiesis) and foramina narrow (cranial nerve palsies). X-ray shows "bone within a bone".

  10. What DEXA T-score defines osteoporosis?

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    −2.5 or lower.

    Why? The T-score compares bone density with a young adult reference; −1.0 to −2.5 is osteopenia. The Z-score compares with age-, sex- and ethnicity-matched people.

  11. What dose and duration of oral glucocorticoid significantly raises osteoporosis risk?

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    Prednisolone 7.5 mg daily (or equivalent) for 3 months or more.

    Why? NOGG 2024: when starting this dose for 3 months or more, start bone protection at the same time — do not wait for a DXA scan, which can follow later.

  12. What is the first-line drug treatment for osteoporosis?

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    An oral bisphosphonate — alendronate (alternative risedronate).

    Why? Bisphosphonates bind hydroxyapatite and inhibit osteoclasts. IV zoledronate is used if oral is not tolerated.

  13. Name two serious long-term adverse effects of bisphosphonates.

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    Osteonecrosis of the jaw and atypical femoral fractures.

    Why? Dental review before starting reduces jaw osteonecrosis risk; new thigh or groin pain needs femoral imaging.

  14. What is the mechanism of denosumab, and what happens if it is stopped abruptly?

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    A monoclonal antibody against RANKL (given SC every 6 months); stopping causes rebound bone loss and multiple vertebral fractures.

    Why? If it must be stopped, follow with a bisphosphonate to prevent rebound.

  15. In very-high-risk osteoporosis (e.g. a vertebral fracture in the last 2 years, or T-score −3.5 or lower), which drug type may be used first-line?

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    An anabolic agent — teriparatide (PTH analogue), abaloparatide or romosozumab (anti-sclerostin antibody).

    Why? Building bone first, then following with an antiresorptive, gives greater fracture reduction; NOGG advises specialist referral and first-line anabolic treatment for some very-high-risk patients.

  16. Name one benefit and one important risk of raloxifene in postmenopausal osteoporosis.

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    Benefit: reduces vertebral fractures and breast cancer risk. Risk: venous thromboembolism (it can also worsen hot flushes).

    Why? Raloxifene is a selective oestrogen receptor modulator — oestrogen-like in bone, anti-oestrogen in breast.

  17. Osteosarcoma shows a "sunburst" pattern and ______ on X-ray, whereas Ewing sarcoma (translocation t(11;22)) shows "onion-skin" periosteal reaction.

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    Codman's triangle

    Why? Osteosarcoma is the commonest primary malignant bone tumour (metaphysis, near the knee); Ewing is a small round blue cell tumour of the diaphysis.

  18. Osteosarcoma shows a "sunburst" pattern and Codman's triangle on X-ray, whereas Ewing sarcoma (translocation ______) shows "onion-skin" periosteal reaction.

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    t(11;22)

    Why? Osteosarcoma is the commonest primary malignant bone tumour (metaphysis, near the knee); Ewing is a small round blue cell tumour of the diaphysis.

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