GC031 Back Pain In An Elderly Woman: Osteoporosis And Related Fractures
Osteoporosis is a systemic skeletal disorder characterized by low bone mineral density and microarchitectural deterioration, predisposing elderly women to fragility fractures, commonly vertebral compression fractures presenting as acute or chronic back pain.
Back Pain in an Elderly Woman: Osteoporosis and Related Fractures
Big idea: Osteoporosis is the most common metabolic bone disease, clinically silent until fractures occur, and carries devastating morbidity and mortality—especially from hip and vertebral fractures. The lecture walks through a 70-year-old woman with back pain as the index case, then systematically covers the definition, bone biology, pathophysiology, epidemiology, diagnosis (DXA, T-scores, FRAX), risk factors, clinical assessment, investigations, pharmacological and non-pharmacological management, fracture risk stratification, and management of specific osteoporotic fractures. [1]
Learning objectives (verbatim from slides): [1]
- Understand the common types of osteoporotic fractures and their clinical presentation
- Learn the epidemiology of osteoporotic fracture
- Understand the diagnosis of osteoporosis and measurement of bone density
- Recognize the risk factors for osteoporosis
- Understand the prevention and treatment of osteoporosis
- Learn the management of osteoporotic fractures
Clinical relevance: This is a bread-and-butter topic that spans endocrinology, geriatrics, orthopaedics, and primary care. It is heavily examined in both MCQ and SAQ/minicase formats, often through clinical vignettes of an elderly woman/man with a fracture or back pain.
Core Concepts and Mechanisms
"A systemic skeletal disease characterised by low bone mass and microarchitectural deterioration of bone tissue, with a consequent increase in bone fragility and susceptibility to fracture." [1]
Why this matters: The definition captures two inseparable elements—quantity (low bone mass) and quality (microarchitectural deterioration). Both contribute to bone fragility. A normal-density bone with disrupted microarchitecture can still fracture, and vice versa. This is why BMD alone doesn't perfectly predict fracture risk—hence the development of FRAX.
Osteoporosis vs Osteomalacia — A Common Exam Trap
Osteoporosis = normal mineral-to-osteoid ratio, but reduced total bone mass. ALP is normal. Osteomalacia = defective mineralization of newly formed osteoid (unmineralized osteoid on histology). ALP is elevated (from secondary hyperparathyroidism). Most common cause = vitamin D deficiency with very low serum 25(OH)D. [1] If the examiner gives you "elevated ALP + back pain + elderly," think osteomalacia or Paget's, NOT osteoporosis.
"In the adult skeleton, bone is constantly remodelled at multiple sites by the coordinated and sequential actions of bone-resorbing osteoclasts and bone-forming osteoblasts to repair microdamage and to adapt bone structure to the mechanical and metabolic needs." [1]
The cycle:
- Activation → Resorption (osteoclasts dig out old/damaged bone) → Reversal → Formation (osteoblasts lay down new osteoid, which mineralizes) → Quiescence
- This is "coupled": resorption and formation are linked so that bone removed ≈ bone replaced in health.
"Osteocytes represent > 95% of all bone cells, are embedded in the mineral, function as mechanosensors and fine-tune bone remodelling by osteoblasts and osteoclasts." [1]
Key players:
| Cell | Function | Relevant Drug Target |
|---|---|---|
| Osteoclasts | Bone resorption | Bisphosphonates, denosumab (anti-RANKL) |
| Osteoblasts | Bone formation | Teriparatide (PTH analogue), romosozumab (anti-sclerostin) |
| Osteocytes | Mechanosensing; produce sclerostin (inhibits Wnt → inhibits osteoblast activity) | Romosozumab |
RANK/RANKL/OPG axis (from lecture diagram): [1]
- Osteoblasts express RANKL on their surface
- RANKL binds RANK on osteoclast precursors → osteoclast differentiation & activation → bone resorption
- OPG (osteoprotegerin) is a decoy receptor produced by osteoblasts that binds RANKL and prevents it from activating RANK → inhibits resorption
- Denosumab is a monoclonal antibody that mimics OPG by binding RANKL
Sclerostin pathway:
- Osteocytes secrete sclerostin, which inhibits the Wnt signalling pathway in osteoblasts → suppresses bone formation
- Romosozumab blocks sclerostin → disinhibits Wnt → increases osteoblast activity (anabolic) AND decreases osteoclast activity (anti-resorptive) = dual effect [1]
"Increased rate of bone remodelling in both cancellous and cortical bone" + "Negative remodelling balance." [1]
Why does this happen?
- Peak bone mass is reached around age 20–40 [3]
- After ~40, gradual bone loss occurs (~1% per year) [3]
- In postmenopausal women: oestrogen deficiency → increased RANKL, decreased OPG → accelerated osteoclast activity → resorption >> formation → rapid bone loss in first 5–10 years post-menopause
- In age-related (Type 2) osteoporosis: decreased calcium/vitamin D intake and absorption, decreased renal 1α-hydroxylase activity, secondary hyperparathyroidism → increased bone turnover [3]
Pathophysiology of glucocorticoid-induced osteoporosis [1]
Glucocorticoids cause osteoporosis through multiple mechanisms:
- Decrease osteoblast differentiation, function, and lifespan (apoptosis of osteoblasts and osteocytes)
- Increase osteoclast lifespan
- Decrease intestinal calcium absorption and increase renal calcium excretion → secondary hyperparathyroidism
- Decrease sex hormones (suppress GnRH)
- Myopathy → increased fall risk
- Fracture risk increases rapidly, even before significant BMD decline (because of bone quality deterioration)
Past Paper Alert — GIOP
2024 MCQ Q31: A 50-year-old man with weight gain, osteopenia, and L3 wedge fracture after receiving frequent injections for knee OA for > 1 year. Answer: D. Iatrogenic due to exogenous steroid (intra-articular steroid injections). [7]
Clinical Presentation
"Clinically silent until fractures occur." [1]
"Lifetime fracture risk could be as high as 40%." [1]
Common sites: Wrist, Vertebra, Hip [1]
| Fracture | Typical Mechanism | Clinical Features | Key Points |
|---|---|---|---|
| Distal radius (Colles') | Fall on outstretched hand (FOOSH) | "Dinner fork" deformity | Often the earliest osteoporotic fracture (younger post-menopausal women ~55–65y) |
| Vertebral | Lifting, bending, or spontaneous | Acute/chronic back pain, height loss, kyphosis ("dowager's hump") | Many are subclinical (only ~1/3 come to clinical attention) |
| Hip (femoral neck / intertrochanteric) | Fall from standing height | Shortened, externally rotated limb; inability to weight-bear | Most devastating; carries highest mortality |
Hip fractures: [1]
"One-year mortality rate: 20–30%" "40–60% of survivors cannot regain pre-fracture level of mobility within one year" "20–60% of previously independent patients require assistance with at least one ADL"
Vertebral fractures: [1]
"20% excess mortality 5-year post-fracture" "Acute and chronic back pain, deformity and height loss, diminished quality of life"
"The most common metabolic bone disease." [1]
"Osteoporotic fractures in lifetime: 1 in 3 postmenopausal women, 1 in 5 men aged ≥ 50 years." [1]
"1 osteoporotic fracture occurs every 3 seconds." [1]
"Hip and vertebral fractures as the hallmark complications." [1]
Key epidemiological features:
- Exponential increase with age
- Female predominance (W:M ratio for hip fractures in HK ≈ 2.2) [1]
- HK age-standardised hip fracture incidence: Men 149, Women 324, Total 230 per 100,000 person-years [1]
Diagnosis
WHO Diagnostic Categories: [1]
| Category | T-Score | Definition |
|---|---|---|
| Normal | ≥ −1.0 | BMD within 1 SD of young adult mean |
| Osteopenia | −1.0 to −2.5 | BMD 1–2.5 SD below young adult mean |
| Osteoporosis | ≤ −2.5 | BMD ≥ 2.5 SD below young adult mean |
| Severe (established) osteoporosis | ≤ −2.5 + ≥ 1 fragility fracture | BMD criteria + fracture history |
"Low-trauma / low-energy fracture in a postmenopausal woman or elderly — defined as a fracture that occurs from a fall from standing height or lower." [1]
This means that even if you haven't done a DXA, a fragility fracture in the appropriate demographic is sufficient for a clinical diagnosis of osteoporosis and warrants treatment.
"Gold standard: the only means for diagnostic classification according to WHO diagnostic criteria." [1]
"Central DXA at hip and spine are the recommended sites." [1]
"BMD measurements at these regions of interest are the best predictor of fracture risk for the corresponding sites." [1]
"For every reduction of 1 SD, fracture risk increases by 1.5–2 times overall." [1]
T-score vs Z-score:
- T-score = number of SDs from peak bone mass of young healthy adult of same sex and ethnicity → used in postmenopausal women and men ≥ 50 [1][3]
- Z-score = compared to age-matched population → used in premenopausal women and men < 50; Z-score ≤ −2.0 suggests secondary cause [3]
High Yield — T-score Interpretation
2022 MCQ Q17: 90-year-old man, fell, hip fracture → what would most likely be present? Answer: C. T-score of −3 on DEXA scan (i.e., osteoporosis). [8] This tests whether you know that hip fractures in the elderly are almost always associated with osteoporosis.
"Simple ethnic-specific web-based tool that integrates clinical information to predict a 10-year probability of major osteoporotic fracture and hip fracture." [1]
"Applies only to postmenopausal women or men aged ≥ 50 years who have NOT been treated." [1]
"Does NOT apply to pre-menopausal women or younger adults." [1]
Why FRAX? BMD alone has poor sensitivity for predicting fractures. FRAX incorporates clinical risk factors (age, sex, BMI, prior fracture, parent hip fracture, glucocorticoid use, smoking, alcohol, rheumatoid arthritis, secondary osteoporosis) ± BMD to give a more clinically useful 10-year fracture probability.
Risk Factors for Osteoporosis
Risk factors:
- Female sex
- Increasing age
- Low body weight ( < 45 kg)
- Family history of osteoporosis or fragility fracture
- Premature menopause (age < 40) or early menopause (age 40–45)
- Low calcium intake
- Lack of exercise or sedentary lifestyle
- Smoking
- Excessive alcohol intake ( > 3 standard drinks per day)
- Lack of sun exposure
- Prolonged immobilization
| Category | Examples |
|---|---|
| Endocrine | Cushing's, hyperthyroidism, hyperparathyroidism, hypogonadism, type 1 DM, prolactinoma |
| GI | Malabsorption (coeliac, Crohn's, gastrectomy), PBC |
| Rheumatological | Rheumatoid arthritis, ankylosing spondylitis |
| Renal | CKD (renal osteodystrophy) |
| Haematological | Multiple myeloma |
| Drugs | Glucocorticoids, PPI, anticonvulsants, thiazolidinediones [1] |
| Other | Prolonged immobilisation, anorexia nervosa |
Drugs That Increase Osteoporosis Risk — Lecture Slide
The lecture specifically lists: glucocorticoid, PPI, anticonvulsants, thiazolidinediones as drugs increasing osteoporosis risk, and hypnotics, diuretics as drugs increasing fall risk. [1] Do not confuse these two categories.
Clinical Assessment
Detailed history of clinical risk factors for osteoporosis and/or fractures:
- Smoking and alcohol
- Personal / parental history of fracture(s)
- Fall risk
- Estimate daily dietary calcium intake
- Past health: prolonged sex hormone deficiency (age of menopause, use of HRT), type 1 diabetes, anorexia nervosa, rheumatological diseases, GI disease / malabsorption syndrome (gastrectomy, intestinal bypass, Crohn's disease, coeliac disease)
- Drug history: glucocorticoid, PPI, anticonvulsants, thiazolidinediones (osteoporosis risk); hypnotics, diuretics (fall risk)
| System | Finding | Potential Clinical Implication |
|---|---|---|
| General | Loss of height / kyphosis | Vertebral fracture |
| General | Weight gain / central obesity | Cushing's syndrome |
| General | Weight loss | Malabsorption |
| General | Goitre / eye signs | Thyrotoxicosis |
| General | Joint disease | Rheumatoid arthritis |
| General | Eunuchoid | Hypogonadism |
| Teeth | Poor dentition | Increased risk of osteonecrosis of jaw (important before starting bisphosphonates/denosumab) |
| CNS | Muscle weakness | Vitamin D deficiency |
| CNS | Gait and balance | High fall risk |
| Test | What It Detects/Excludes |
|---|---|
| CBC | Anaemia (myeloma / coeliac disease) |
| Renal and liver function tests | Renal or liver failure, alcohol abuse |
| Calcium, phosphate, PTH | Primary hyperparathyroidism, myeloma |
| ALP | Osteomalacia, Paget's disease |
| 25(OH)D | Vitamin D deficiency, osteomalacia |
| TSH ± fT4 | Hyperthyroidism |
| Testosterone (in men) | Male hypogonadism |
| Fasting glucose, HbA1c | Diabetes mellitus |
| 24hr urine calcium | Hypercalciuria |
| Selected: BTMs, SPEP, cortisol, prolactin, anti-tTG | Myeloma, Cushing's, coeliac disease |
Why Check These Labs?
The labs are NOT to diagnose osteoporosis (that's DXA's job). They are to exclude secondary causes and detect osteomalacia. The most important discriminators: ALP (elevated in osteomalacia/Paget's, normal in osteoporosis) and 25(OH)D (very low in osteomalacia). [1]
Management of Osteoporosis
"The objective of treating osteoporosis is to reduce the likelihood of fragility fractures by strengthening the skeleton or decreasing fall frequency, or both." [1]
Indications for therapy in postmenopausal women and men age ≥ 50: [1]
- Prior hip or vertebral fracture
- BMD T-score ≤ −2.5 at spine or proximal femur
- BMD T-score between −1 and −2.5 (low bone mass) AND:
- 10-year risk of major fracture ≥ 20% (FRAX)
- 10-year risk of hip fracture ≥ 3% (FRAX)
- Healthy balanced diet rich in calcium and vitamin D
- Regular weight-bearing and muscle-strengthening exercises
- Avoidance of smoking and excessive alcohol intake
- Adequate sunlight exposure
Calcium: [1]
- Target: 800–1200 mg/day, ideally through dairy products
- Supplements if dietary intake < 800 mg/day (calcium carbonate or calcium citrate)
- Taken with food (gastric acidity promotes calcium absorption)
- Side effects: dyspepsia, constipation
Vitamin D: [1]
- Promotes calcium absorption in gut, maintains serum Ca/PO4 for mineralization, important for neuromuscular function
- Major source: skin synthesis of cholecalciferol (D3) under UV light (~10–15 minutes daily)
- Requirement: 800–1000 IU/day (up to 2000 IU/day in obese, limited sun, malabsorption)
- Major circulating form: 25(OH)D
- Desired target: 25(OH)D ≥ 75 nmol/L (30 ng/mL)
Exercise: [1]
- Weight-bearing exercises (brisk walking, jogging, Tai Chi, dancing, stair-climbing)
- Benefits: retards bone loss, increases muscle mass/strength, improves balance and reduces falls, improves QoL
Pharmacological Management
| Category | Drugs |
|---|---|
| Anti-resorptives | HRT, Raloxifene, Bisphosphonates, Denosumab |
| Anabolic agents | Teriparatide, Abaloparatide, Romosozumab |
Two targets for pharmacological intervention: (1) Inhibition of bone resorption (osteoclast), (2) Stimulation of bone formation (osteoblast). [1]
| Drug | 2y Spine BMD ↑ | 2y Hip BMD ↑ | RRR Vertebral # | RRR Non-vertebral # |
|---|---|---|---|---|
| PO Raloxifene | 2–3% | 1% | 50% | — |
| PO Bisphosphonates | 3–5% | 2–3% | 40–53% | 0–20% |
| IV Zoledronic acid | 5–6% | 3–4% | 70% | 25% |
| SC Denosumab | 6–8% | 3–4% | 68% | 20% |
| SC Teriparatide | 8–10% | 1.5–2% | 65–70% | 35% |
| SC Abaloparatide | 10% | 2–3% | 70–80% | 40% |
| SC Romosozumab | 11% (1y) | 4% (1y) | 48% (vs alendronate) | 20% (vs alendronate) |
Hormonal Replacement Therapy (HRT) [1]
- Mechanism: inhibits bone resorption, ↓ urinary Ca excretion, ↓ stromal cell cytokines
- Advantages: ↓ menopausal symptoms, improves CVD risk factors (but NOT outcome events)
- Disadvantages: endometrial cancer (must add progestogens if uterus intact), slight ↑ breast cancer risk, VTE
- Mainly for young postmenopausal women with climacteric symptoms — NOT indicated for osteoporosis alone [3]
Raloxifene (SERM) [1]
- Oestrogen-agonistic on bone → 40% ↓ vertebral fracture, but NOT non-vertebral fractures
- Oestrogen-antagonistic on endometrium and breast → ↓ incidence of invasive ER+ breast cancer
- Side effects: VTE, hot flushes, leg cramps
- Must discontinue during prolonged immobilization (VTE risk)
- Preferable in young postmenopausal women when hip fracture risk is not particularly high
Bisphosphonates [1]
"Mainstay of pharmacotherapy. Potent anti-resorptives."
- Mechanism: pyrophosphate derivatives → bind to bone surface → taken up by osteoclasts → inhibit farnesyl pyrophosphate synthase (FPPS) in mevalonate pathway → osteoclast apoptosis
- Renal excretion: contraindicated when eGFR < 30 mL/min
- Poor intestinal absorption (must take on empty stomach with plain water, remain upright 30 min)
- Forms: Oral (alendronate, risedronate, ibandronate) and IV (zoledronic acid)
Side effects: [1]
- Upper GI irritation (oral bisphosphonates) — oesophagitis, ulceration
- Acute phase reaction (IV bisphosphonates, especially first dose) — flu-like symptoms
- Disabling muscle/bone pain — occasional
- Rare but serious:
- Osteonecrosis of the jaw (ONJ): 1–10 in 100,000
- Atypical femoral fracture (AFF): 20–50 in 100,000
Denosumab [1]
- Human monoclonal antibody to RANKL
- Very potent anti-resorptive
- SC injection every 6 months
- Can be used in CKD down to stage 4 (eGFR > 15 mL/min)
- Side effects: rash. Rare: hypocalcaemia, ONJ, AFF
- Critical point: Discontinuation of denosumab leads to rapid rebound bone loss and increased vertebral fracture risk → must be followed by another anti-resorptive (e.g. bisphosphonate) if stopped
Teriparatide [1]
- 1–34 amino-terminal fragment of PTH
- Key concept: High-level continuous PTH → bone resorption (cortical > trabecular). Low-dose intermittent PTH → anabolic action.
- SC injection 20 μg daily; limited to 2 years (concern with osteosarcoma in animal studies)
- Side effects: mild leg cramps, injection site reactions, hypercalcaemia
- Contraindications: skeletal malignancies/metastases, radiation therapy involving skeleton, hyperparathyroidism
Past Paper — Teriparatide Side Effects
2023 MCQ Q29: 75-year-old woman starting teriparatide. Which is a known side effect? Answer: not AFF (that's bisphosphonates), not GI reflux (that's oral bisphosphonates). The correct answer to look for would involve hypercalcaemia or injection site reactions. Note: the question listed options A (AFF), B (dizziness), C (GORD), D (hypocalcaemia). The intended answer in the context of teriparatide side effects is likely B (dizziness) — teriparatide can cause orthostatic hypotension/dizziness. Hypercalcaemia is the classically tested side effect of teriparatide. [9]
Abaloparatide [1]
- Synthetic analogue of PTH-related protein (PTHrP)
- Similar to teriparatide: daily SC, limited to 2 years
- Hypercalcaemia less common than teriparatide (3.4% vs 6.4%)
- FDA-approved 2017; NOT available in Hong Kong
Romosozumab [1]
"Humanised monoclonal antibody that binds and inhibits sclerostin... DUAL EFFECT: increases bone formation (↑ P1NP) and decreases bone resorption (↓ sCTX)."
- SC injection monthly for 1 year
- Side effects: injection site reactions, small risk of hypocalcaemia, ONJ/AFF ( < 0.1%)
- Caution in patients with high cardiovascular risk
- Contraindications: history of MI or stroke
Fracture Risk Stratification:
| Risk Category | Criteria | Treatment |
|---|---|---|
| Low Risk | Age < 65, T-score < −2.5, no prior fracture | Raloxifene (female) |
| High Risk | Age ≥ 65 + T-score < −2.5, OR FRAX MOF ≥ 20%/HF ≥ 3%, OR prior fracture > 24 months | Potent anti-resorptive (bisphosphonate / denosumab) |
| Very High Risk | Multiple fractures, recent MOF ≤ 24 months, T-score < −3.0, fracture on anti-resorptive therapy | Anabolic agents (teriparatide, romosozumab) |
Atypical Femoral Fractures (AFFs) and Osteonecrosis of Jaw (ONJ)
"Occur in the subtrochanteric region or diaphysis of the femur with unique radiological features: predominantly transverse fracture line, periosteal callus formation, minimal comminution."
"More common with long-term bisphosphonate therapy ( > 7–8 years): 113 per 100,000 person-years."
"Also reported with denosumab, with even lower incidence."
Why? Prolonged suppression of bone remodelling → accumulation of microdamage → stress fracture in cortical bone of the femoral shaft. Patients often have prodromal thigh pain before complete fracture.
Criteria: Exposed bone in the maxillofacial region that does not heal within 8 weeks, current/previous treatment with antiresorptive or antiangiogenic agents, no history of radiation to jaws or metastatic disease to jaws.
Incidence: 1:10,000 to 1:100,000
Risk factors: Age > 65, periodontitis, bisphosphonate use > 2 years, smoking, denture wearing, diabetes mellitus, invasive dental procedures (e.g. extractions).
Clinical implication: Always perform a dental examination before starting bisphosphonates/denosumab. Elective invasive dental procedures should be completed beforehand.
Management of Osteoporotic Fractures [1]
- Conservative management: symptoms usually improve in 6–8 weeks
- Vertebral body augmentation procedures (vertebroplasty/kyphoplasty) for intractable pain
- Open surgical intervention for:
- Significant neurological deficits
- Progressive and severe kyphotic deformity
- Intractable pain
- Usually non-operative: manipulation and cast application for 4–6 weeks
- Operative management in selected patients (e.g. intra-articular, unstable)
- Treat the underlying osteoporosis (pharmacological + non-pharmacological)
- Fall prevention measures [4]
- Secondary fracture prevention: Fracture Liaison Service model
"Equivalent to rickets in children. Abnormal histology: unmineralized osteoid. Most common cause: vitamin D deficiency with very low serum 25(OH)D."
"ALP high in osteomalacia (from secondary hyperparathyroidism), normal in osteoporosis."
| Feature | Osteoporosis | Osteomalacia |
|---|---|---|
| Bone mass | ↓ | ↓ |
| Mineral:osteoid ratio | Normal | ↓ (unmineralized osteoid) |
| ALP | Normal | ↑ |
| Calcium | Usually normal | ↓ or normal |
| Phosphate | Normal | ↓ |
| 25(OH)D | Variable | Very low |
| PTH | Normal or slightly ↑ | ↑ (secondary hyperPTH) |
| Histology | Thin trabeculae, normal mineralization | Wide osteoid seams, defective mineralization |
Exam Intelligence
- MCQ: An elderly woman with back pain and height loss. X-ray shows wedge compression fracture. What is the diagnosis? → Osteoporotic vertebral compression fracture
- MCQ: What is the gold standard investigation for diagnosing osteoporosis? → DXA
- MCQ: T-score of −2.8 — what category? → Osteoporosis
- SAQ: List 4 risk factors for osteoporosis → Female sex, increasing age, low body weight, premature menopause, glucocorticoid use, smoking, alcohol, family history, low calcium, sedentary lifestyle
- MCQ: Which drug is contraindicated in CKD with eGFR < 30? → Bisphosphonates (use denosumab instead)
- MCQ: Side effect of teriparatide → Hypercalcaemia
- MCQ: Mechanism of denosumab → Anti-RANKL monoclonal antibody
- SAQ/Minicase: Management of osteoporotic vertebral fracture → Conservative (analgesia, 6–8 weeks), vertebral augmentation for intractable pain, surgery for neuro deficits
- MCQ: Romosozumab contraindication → History of MI or stroke
- MCQ: ALP is elevated with back pain in elderly → Think osteomalacia or Paget's, NOT osteoporosis
| Trap | Correct Approach |
|---|---|
| Confusing osteoporosis and osteomalacia | ALP normal in osteoporosis, elevated in osteomalacia |
| Thinking FRAX applies to premenopausal women | FRAX only for postmenopausal women and men ≥ 50 |
| Forgetting bisphosphonate renal contraindication | eGFR < 30 → contraindicated |
| Thinking raloxifene prevents hip fracture | Only prevents vertebral fractures, NOT non-vertebral |
| Thinking HRT is first-line for osteoporosis in elderly | Only for young postmenopausal women with vasomotor symptoms |
| Assuming denosumab can be stopped freely | Rebound bone loss and fracture risk after discontinuation |
| Not checking dental status before anti-resorptive | ONJ risk |
| Past Paper | Question | Key Concept |
|---|---|---|
| 2020 MCQ Q4 [6] | Glucocorticoid-induced osteoporosis Tx in RA | Answer: Alendronate |
| 2022 MCQ Q17 [8] | 90yo, hip fracture, what finding? | T-score −3 on DEXA |
| 2023 MCQ Q29 [9] | Teriparatide side effects | Know hypercalcaemia, NOT AFF/GORD |
| 2024 MCQ Q31 [7] | Man with steroid injections → wedge fracture | Iatrogenic steroid-induced OP |
| 2023 Minicase Case 3 [10] | Red flags for back pain | Fever, neuro deficits, weight loss, age, trauma, steroid use |
| 2025 MCQ Q61 [11] | Metastatic vertebral collapse with cord compression | High-dose steroids + urgent decompressive surgery |
Q1: A 70-year-old woman presents with acute low back pain. XR lumbar spine shows a wedge compression fracture of L1. ALP and calcium are normal. What is the most likely diagnosis, and what investigation would you order to confirm? Model answer: Osteoporotic vertebral compression fracture. Order DXA scan to confirm osteoporosis (T-score ≤ −2.5).
Q2: List four non-pharmacological measures for osteoporosis management. Model answer: (1) Adequate calcium intake 800–1200 mg/day, (2) Vitamin D 800–1000 IU/day / adequate sunlight, (3) Regular weight-bearing exercise, (4) Smoking cessation and avoidance of excessive alcohol.
Q3: Name three indications for starting pharmacotherapy for osteoporosis in a postmenopausal woman. Model answer: (1) Prior hip or vertebral fracture, (2) T-score ≤ −2.5, (3) T-score −1 to −2.5 with FRAX 10-year MOF ≥ 20% or hip fracture ≥ 3%.
Q4: A patient on long-term oral bisphosphonate develops prodromal thigh pain. What complication should you suspect and what are its X-ray features? Model answer: Atypical femoral fracture. XR: transverse fracture line in subtrochanteric/diaphyseal region, periosteal callus formation, minimal comminution.
Q5: Why is romosozumab contraindicated in patients with history of MI? Model answer: Clinical trial data (ARCH) showed a small increase in cardiovascular events with romosozumab versus alendronate. Sclerostin is also expressed in the vasculature, and its inhibition may have adverse cardiovascular effects.
High Yield Summary
Osteoporosis is a systemic skeletal disease of low bone mass + microarchitectural deterioration → fragility fractures (wrist, spine, hip). It is clinically silent until fractures occur. Diagnosed by DXA (T-score ≤ −2.5) or clinically by a low-trauma fracture. FRAX estimates 10-year fracture risk. Key risk factors include female sex, age, low body weight, smoking, alcohol, glucocorticoids, and premature menopause. Management combines non-pharmacological (calcium 800–1200 mg/d, vitamin D 800–1000 IU/d, weight-bearing exercise, smoking/alcohol cessation) with pharmacological therapy. Anti-resorptives (bisphosphonates = mainstay, denosumab) reduce fracture risk by inhibiting osteoclasts; anabolic agents (teriparatide, romosozumab) stimulate osteoblasts and are reserved for very high-risk patients. Bisphosphonates are contraindicated if eGFR < 30; denosumab can be used down to eGFR > 15. Rare but important side effects: ONJ and AFF with long-term anti-resorptives. Differentiate from osteomalacia (elevated ALP, low 25(OH)D, unmineralized osteoid). Hip fractures carry 20–30% one-year mortality. Vertebral fractures are mostly managed conservatively (6–8 weeks); surgery for neurological deficits.
Active Recall - Lecture Notes
[1] Lecture slides: GC 031. Back pain in an elderly woman_osteoporosis and related fractures.pdf (all pages) [2] Lecture slides: GC 235. Osteoporotic Related Fractures.pdf [3] Senior notes: Ryan Ho Endocrine.pdf (p48–51) [4] Senior notes: Maksim Surgery Notes.pdf (p215, p223, p252) [5] Senior notes: Maksim Medicine Notes.pdf (p109) [6] Past papers: 2020 Fourth Summative Assessment MCQ paper.pdf (Q1–Q5, Section B) [7] Past papers: 2024 Fourth Summative MCQ.pdf (Q31) [8] Past papers: 2022 Fourth Summative MCQ.pdf (Q17) [9] Past papers: 2023 Fourth Summative MCQ.pdf (Q29) [10] Past papers: 2023 Fourth Summative Minicase.pdf (Case 3, Section 1) [11] Past papers: 2025 Fourth Summative MCQ.pdf (Q61) [12] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (p1656–1658) [13] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf (p1026) [14] Lecture slides: Injuries to bone and joint WCS.pdf (p7, p10)
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