Metabolic bone disease Flashcards

1
Q

What are the 3 main metabolic bone disorders?

A
  • osteoporosis
  • Paget disease
  • Rickets and osteomalacia
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2
Q

What is osteoporosis?

A
  • condition characterised by weakness of the bones, due to lower than normal bone density
  • results in fragility fractures
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3
Q

What is a T-score and what are the ranges for osteoporosis, osteopenia, and normal?

A
  • T-score = used to measure bone mineral density (BMD)
  • Osteoporosis = T-score < -2.5
  • Osteopenia = T-score between -1 and -2.5
  • Normal: T-score > -1
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4
Q

At what age does peak bone mass occur?

A
  • peak bone mass usually occurs at age 50 and declines thereafter
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5
Q

What is the pathology of osteoporosis?

A
  • bone loss is accelerated in osteoporosis by an imbalance between the rates of bone resorption and formation, which are governed by the activity of osteoclasts and osteoblasts respectively
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6
Q

What are some risk factors for osteoporosis?

A
  • Non-modifiable: elderly, female, early menopause, small size, family history, steroid use, diabetes
  • Modifiable: poor calcium and vitamin D intake, lack of exercise, smoking, alcohol excess
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7
Q

How does osteoporosis usually present/first diagnosed?

A
  • patients usually present with fragility fractures and are then screened for osteoporosis
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8
Q

What are the 3 typical fragility fractures?

A
  • Colles fracture of the wrist
  • Neck of femur fracture
  • Vertebral body fracture
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9
Q

How do vertebral compression (or wedge) fractures usually present and what is the management?

A
  • usually present with thoracic or lumbar back pain after a minor fall
  • often multiple wedge fractures and kyphotic deformity of the spine
  • these fractures are stable and treatment is aimed at controlling pain (analgesia)
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10
Q

What investigations should be done for suspected osteoporosis?

A
  • DEXA (dual-energy X-ray absorptiometry) scan: to measure BMD
  • x-rays: if suspected fractures
  • MRI spine: to look for vertebral fractures
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11
Q

What is the management for osteoporosis?

A
  • Lifestyle: stop smoking, control diabetes better, diet (vit D, calcium, protein), regular weight-bearing exercise
  • Medications: bisphosphonates, denosumab, teriparatide, Adcal-D3, raloxifene, calcitonin
  • Prevention of falls: OH, mobility aids etc.
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12
Q

What is Paget’s disease?

A
  • a disorder of bone metabolism characterised by focal increases in bone remodelling, resulting in abnormal bone production
  • this leads to mechanical weakness of the bone
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13
Q

What is the pathology of Paget’s disease?

A
  • increased bone resorption (increased osteoclast activity)
  • osteoblasts then respond by producing weak, disorganised bone
  • repeated cycles of this result in disorganised bone breakdown and formation
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14
Q

What are the clinical features of Paget’s disease?

A
  • often asymptomatic and picked up incidentally on x-ray or raised ALP blood test
  • symptoms: bone pain, deformity, fragility fractures
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15
Q

What are the investigations for Paget’s disease?

A
  • Bloods: raised ALP, normal Ca, normal phosphate
  • X-ray: shows areas of disorganised bone with areas of lysis and sclerosis (the cortex is usually thickened too), pathological fractures
  • Isotope bone scans: often show multiple areas of focal increased uptake (sensitive but not specific)
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16
Q

What is the management for Paget’s disease?

A
  • analgesia
  • bisphosphonates (eg. alendronic acid): inhibits osteoclast activity
  • note: monitor at regular 6 or 12 month intervals for recurrence
17
Q

What should be done for patients with Paget’s disease before they go into theatre for surgery if needed?

A
  • Ensure patients are cross-matched for blood in advance of planned surgery
  • Pagetic bone is highly vascular and bleeds a lot during surgery
18
Q

Normal vs osteoporotic bone diagram…

A
19
Q

What is Rickets and what is osteomalacia?

A
  • Both conditions are the result of failure of mineralisation of bone, increased osteoid in osteomalacia
  • Rickets: occurs in the growing skeleton
  • Osteomalacia (soft bones): occurs in adults
20
Q

What is the main cause of Rickets / osteomalacia?

A
  • vitamin D deficiency
21
Q

What are some causes of vitamin D deficiency?

A
  • poor diet
  • low sunlight exposure
  • malabsorption
22
Q

What are the clinical features of Rickets and osteomalacia?

A
  • hypocalcaemia symptoms can occur
  • Rickets: growth is impaired, older children develop bowing of long bones (varus/valgus deformities of the knee)
  • Osteomalacia: tends to present with vague bone pain (localised bone pain may be due to a fracture)
23
Q

What are the investigations for Rickets and osteomalacia?

A
  • Serum alkaline phosphatase (ALP): raised
  • Serum vitamin D: low
  • PTH: raised
  • Calcium and phosphate: low or normal
24
Q

What is the management for Rickets and osteomalacia?

A
  • vitamin D replacement
  • (underlying cause of vitamin D deficiency should be addressed)
25
Q

Osteoporosis drug therapies?

A
  • Bisphosphonates: attach to bone crystals and inhibit osteoclast activity, this maintains bone density and reduces risk of fracture
  • Adcal D3: calcium is a major mineral found in bone and is important for maintaining healthy bones, vitamin D needed to help body absorb calcium
  • Denosumab: monoclonal antibody that targets the RANK ligand
  • Teriparatide: form of PTH
26
Q

Why, in Paget’s disease, are both lytic and sclerotic lesions found on plain radiographs of the affected bone?

A
  • Osteoclasts more active, greater bone resorption, you get lytic areas on x-ray
  • Osteoblasts lay down bone more randomly, so you get sclerotic areas on x-ray