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Block 4: Pathophysiology and pharmacology > Bone abnormalities > Flashcards

Bone abnormalities Flashcards

1
Q

What is osteoporosis?

A

Weak or fragile bones caused by loss in density

Increases likelihood of fracture

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2
Q

What is Osteopetrosis?

A

Increased density of bones

Very rare

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3
Q

What can cause fractures?

A

Normal bone + Excessive force

Weak bone + Normal force

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4
Q

What conditions are characterised by defective mineralisation in bones?

A

Rickets (Osteomalacia)

Hyperparathyroidism

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5
Q

What conditions are characterised by changes in bone structure?

A

Osteogenesis Imperfecta (type I collagen defect causing brittle bones)
Paget’s Disease (overactive osteoclasts causing poor quality woven bone)
Tumours

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6
Q

What blood tests can be used to assess bone?

A

Alkaline Phosphatase, Albumin (routine)

Calcium, Phosphate, Vitamin D, Parathyroid hormone (additional tests)

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7
Q

What imaging can be used to assess bone?

A

Plain X-Ray
Radionuclide scans (radioactive material injected into body - can be aimed at osteoblasts or osteoclasts)
CT/ MRI/ Ultrasound

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8
Q

When would you do a bone biopsy?

A

Query malignancy

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9
Q

How is bone density assessed?

A

DEXA Scan

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10
Q

What bones are commonly fractured due to osteoporosis?

A

Neck of femur
Vertebral bodies
Wrist

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11
Q

What are the wider complications of osteoporosis?

A 
Increased risk of fractures
Quality of life - loss of confidence, less exercise, loss of independence 
Pain 
Long term admission
High mortality (e.g. due to #NOF) 
Cost to health service
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12
Q

What are some risk factors for osteoporosis?

A 
Old age 
Sex (females esp. post-menopause) 
Ethnicity (Caucasian + Asian populations) 
Low BMI
Family history 
Smoking/ alcohol 
Immobility 
Vit D or Calcium deficiencies 
Long term steroids
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13
Q

How does ageing influence osteoporosis?

A

Reduced physical activity
Decreased osteoprogenitor cells means decreased osteoblasts (+ decreased activity of osteoblasts) so new bone not being formed
Increased RANKL (in post-menopausal women) stimulates osteoclasts to resorb bone causes net loss and lower bone density

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14
Q

How can osteoporosis be prevented?

A 
Secondary prevention (e.g. mobility aids, additional care) 
FRAX tool (assesses risk factors for fractures - used by GPs to guide management) 
DEXA Scan (to assess bone density to guide management)
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15
Q

How does a DEXA scan work?

A

2 X-ray beams of different energy levels aimed at patient

Soft tissue subtracted to determine bone density

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16
Q

What scores are used to analyse DEXA scans?

A

T-score:
Normal <1 SD
Osteopenia -1 to -2.5 SD
Osteoporosis >-2.5 SD

17
Q

How is osteoporosis managed?

A 
Diet 
Exercise 
Supplements (e.g. Vit D and calcium)
Fall prevention (e.g. mobility aids)
Medication (1st line = bisphosphonates, 2nd line = SERMs, PTH, Denosumab)
18
Q

What bisphosphonates are used to manage osteoporosis?

A 
Alendronic Acid (Alendronate) - taken orally OD or OW 
Risedronate 
Zoledronic acid (not on drugs list)
19
Q

How do bisphosphonates work?

A

Slow rate of bone remodelling
Alendronic acid = binds to hydroxyapatite crystals so osteoclasts take up bisphosphonate which prevents osteoclasts making seal with bone (so osteoclasts cannot form seal and resorb bone)
Some bisphosphonates work by inducing apoptosis of osteoclasts

20
Q

What are the problems with taking alendronic acid?

A

Must be taken on empty stomach and sit upright for half hour as bisphosphonates are irritants to oesophageal mucosa

21
Q

What conditions are bisphosphonates used to treat?

A

Osteoporosis
Paget’s Disease
Hypercalcaemia of malignancy

22
Q

What are the side effects of bisphosphonates?

A

Asymptomatic hypocalcaemia
GI disturbance/ Oesophageal reactions
Osteonecrosis - need to be aware of pts dental hygiene

23
Q

What are selective estrogen receptor modulators?

A

Raloxifene
Tissue specific - mixed agonist/ antagonist
Agonist in bones to stimulate bone formation
Antagonist in breast and uterine tissue so no increased risk of cancer as with HRT

24
Q

How does parathyroid hormone work as treatment for osteoporosis?

A

Promotes bone production
Subcutaneous injection OD
SEs: hypercalcaemia, muscle cramp, nausea/ vomiting, can cause bone loss if given continuously

25
Q

What is Denosumab?

A

Monoclonal antibody used to treat osteoporosis by inhibiting osteoclast formation, function and survival (by mopping up RANKL)
Administered by SC injection

26
Q

What is the difference between Rickets and Osteomalacia?

A

Both characterised by defective mineralisation (usually due to vitamin D deficiency resulting in low calcium and phosphate)
Rickets = defective mineralisation at growth plates causing growth retardation and joint deformity (affects children)
Osteomalacia = defective mineralisation of osteoid (affects children and adults)

27
Q

What features of Rickets can be seen in imaging?

A

Widening of the epiphyseal growth plates

28
Q

What are the symptoms of osteomalacia?

A

Can be asymptomatic
Proximal muscle weakness
Bone pain
Fractures

29
Q

What blood tests results would you expect to see in a patient with Rickets or Osteomalacia?

A 
Calcium Phosphates (Low) 
Alkaline Phosphatase (High) 
Vitamin D (Low)
30
Q

How is Rickets/ Osteomalacia typically managed?

A

Education - diet

Vitamin D supplements

31
Q

What is Paget’s Disease of the bone?

A

Imbalance in bone remodelling causing increased bone turnover (overactive osteoclasts leads to overactive osteoblasts)
Leads to weak woven bone due to speed at which is being remodelled
Lytic and sclerotic lesions
Can be focal (affecting one bone) or multifocal
Results in overgrowth, bowing, pain, fracture, deformity
More susceptible to malignancies

32
Q

What blood test results would you expect to see in a patient with Paget’s Disease of the bone?

A 
Alk P (high) 
Serum Ca (normal)
PTH (normal)
33
Q

How can Paget’s Disease of the bone be managed?

A 
Mobility aids 
Analgesia 
Supplements
Bisphosphonates (osteoclast apoptosis, decreased depth of resorption site) 
Surgery
34
Q

What is osteogenesis imperfecta?

A

Group of disorders characterised by defective production of type I collagen through genetic mutation of collagen genes (hereditary)
Systemic - causes brittle bones, blue/ grey tinted sclera,, brownish teeth, growth retardation, hearing loss, fractures
Type I and Type II (type II more severe and can cause scoliosis, respiratory depression etc. - high fatality at birth)
Can be confused with child abuse in ED

Block 4: Pathophysiology and pharmacology (10 decks)

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