Disorders of Bone Health Flashcards

1
Q

common fracture sites?

A

neck of femur
vertebral body
distal radius
humeral neck

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2
Q

what usually causes a colles fracture?

A

fall onto outstretched hand

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3
Q

why does osteoporosis cause a curvature of the spine (e.g thoracic kyphosis, loss of height)?

A

crumbing of vertebrae/wedge fractures in vertebrae

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4
Q

what is the most common osteoporotic fracture?

A

colles in younger

hip in elderly

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5
Q

how can bone density be assessed?

A

BMD (predicts fracture risk independently of other risk factors)
DEXA scan = most commonly used method of measuring BMD

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6
Q

how is DEXA scan used?

A

compares to other people of same age
= Z score
compares to young adult average
= Gives T score (<2.5 = osteoporosis)

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7
Q

what is a normal BMD?

A

within 1 standard deviation of the young adult reference average

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8
Q

osteopaenia BMD?

A

> 1 standard deviation below young adult mean but <2.5 SD below this value

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9
Q

osteoporosis BMD?

A

2.5 or more SD below young adult mean

severe osteoporosis = >2.5 below with a fragility fracture

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10
Q

which score is used if under 20?

A

only Z score

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11
Q

who should be refered for a DEXA scan?

A

patients over 50 with a low trauma fracture (often identified through fracture laison service)
patients at increased risk of fracture based on risk factors (calculated using risk assessment tool - FRAX or Qfracture - if >10% fracture risk over 1 years

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12
Q

SIGN objectives of osteoporosis management?

A

address risk factors for fracture (modifiable and non-modifiable)
assess fracture risk (use tools)

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13
Q

non modifiable fracture risk factors?

A
age
gender
ethnicity
previous fracture
family history
menopause <45
co-existing disease
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14
Q

modifiable risk factors for fracture?

A
BMD
alcohol
weight 
smoking
physical inactivity
pharmacological
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15
Q

what is the WHO fracture risk calculator?

A

calculates absolute risk by incorporating additional risk factors rather than just BMD
predicts 10 year fracture risk

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16
Q

who should be assessed with risk fracture assessment (Qfracture or WHO calculator)?

A

over 50 with risk factors

under 50 with very strong clinical risk factors (early menopause, glucocorticoids)

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17
Q

slide 41 algorithm

A

/…

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18
Q

what tests are done for osteoporosis?

A
history and examination
Us&amp;Es
LFTs
bone biochemistry
FBC
PV
TSH
consider
- Protein electrophoresis/Bence Jones proteins
Coeliac antibodies
Testosterone
25OH Vitamin D     PTH
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19
Q

name 4 secondary causes for osteoporosis

A

endocrine (hyperthyroid, hyperparathyroid, cushings)
GI (coeliac, IBD, chronic liver disease, chronic pancreatitis)
resp (CF, COPD)
chronic kidney disease

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20
Q

general lifestyle advice for osteoporosis?

A
High intensity strength training
Low-impact weight-bearing exercise (standing, one foot always on the floor) 
Avoidance of excess alcohol
Avoidance of smoking
Fall prevention
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21
Q

describe the osteoporotic diet?

A

RNI 700mg calcium (2-3 portions from milk and dairy foods group)
Postmenopausal women aim dietary intake 1000 mg calcium per day to reduce fracture risk (3-4 portion calcium rich foods)
Non-dairy sources include
bread and cereals (fortified)
fish with bones, nuts,
green vegetables, beans

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22
Q

what drug treatments are available for osteoporosis?

A
Calcium &amp; vitamin D supplementation
Bisphosphonates
Denosumab
Teriparatide
HRT
SERMS (Selective Estrogen Receptor Modulators)
Testosterone
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23
Q

when are calcium and vit D supplements used? (SIGN guidelines)

A

… slide 47

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24
Q

what are bisphosphonates and what do they do?

A

Anti-resorptive agents – alendronate and risedronate
Prevent bone loss at all sites vulnerable to osteoporosis and Reduce risk of hip and spine fracture
…..

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25
Q

bisphosphonates

A

……

26
Q

bisphosphonates

A

………

27
Q

bisphosphonates

A

……..

28
Q

how is zoledronic acid used?

A

Once yearly IV infusion for 3 years
5 mg in 100 ml NaCl over 15 mins
1 in 3 acute phase reaction with first infusion – paracetamol
~ 70% reduction in vertebral fracture, 40% reduction in hip fracture

29
Q

what is denosumab and what does it do?

A

Denosumab – fully human monoclonal antibody that targets and binds with high affinity and specificity to RANKL (receptor activator of nuclear factor-kB ligand)
This prevents activation of its receptor, RANK, inhibiting development and activity of osteoclasts, decreasing bone resorption and increasing bone density.

30
Q

how is denosumab given?

A

Subcutaneous injection 6 monthly

31
Q

what are the side effects of denosumab?

A

hypocalcaemia
eczema
cellulitis
(no impact on renal impairment)

32
Q

what is teriparatide and what does it do?

A

Recombinant parathyroid hormone (1-34)

Stimulates bone growth rather than reducing bone loss – anabolic agent

33
Q

when is teriparatide used?

A

> 65y with T score < -4 or below
T score of – 3.5 plus > 2 fractures
Aged 55-64y with T score -4 or below plus more than 2 fractures ( plus intolerant/unsatisfactory response to oral agents)

34
Q

when is osteoporosis treated?

A

antiresorptive treatment when T score = -2.5
If ongoing steroid requirement >/=7.5mg prednisolone for 3 months or more or if there is a prevalent vertebral fracture, consider treatment with T score < -1.5

35
Q

what are the direct effects of corticosteroids on bone?

A

Reduction of osteoblast activity and lifespan
Suppression of replication of osteoblast precursors
Reduction in calcium absorption

36
Q

what are the indirect effects of corticosteroids on bone?

A

Inhibition of gonadal and adrenal steroid production

37
Q

what 4 systems can glucocorticoids effect?

A

…..slide 59

38
Q

how does steroid dose relate to fracture risk?

A

individual variability to glucocorticoids
dose dependant fracture but no safe dose
rapid loss of BMD (30% in first 6 months)
- partially reversible on cessation of treatment
different fracture threshold so different treatment threshold

39
Q

why are osteoporotic fractures dangerous?

A

with every fracture, the risk of further fractures is increased
neck of femur fractures have high morbidity and mortality

40
Q

what is pagets disease of bone?

A

abnormal osteoclastic activity followed by increased osteoblastic activity resulting in abnormal bone structure with reduced strength and increased fracture risk
can be monostotic or polyostotic (single or multiple sites)

41
Q

what can trigger pagets disease?

A

viral
environmental
biomechanical
in genetically predisposed individual

42
Q

where does pagets mostly affect?

A

long bones
pelvis
lumbar spine
spine

43
Q

how does pagets present?

A
bone pain
deformity
deafness
compression neuropathy
osteosarcoma is a rare complication
44
Q

how is pagets diagnosed?

A

incidental finding on X ray or isolated high Alk Phos
diagnosis = X ray
isotope bone scan shows distribution of disease
biochem shows raised alk phos with normal LFTs

45
Q

how is pagets managed?

A

bisphosphonates if pain not responding to analgesia

46
Q

what is osteogenesis imperfecta?

A

rare group of genetic disorders mainly affecting bone

47
Q

what causes osteogenesis imperfecta?

A

most are secondary to mutations of type 1 collagen genes

most are autosomal dominant

48
Q

what are the types of osteogenesis imperfecta?

A

at least 8 types

  • type 1 = mild
  • type 2 = neonatal (lethal)
  • types 3 and 4 = very severe
49
Q

how does osteogenesis imperfecta?

A

most severe forms = fractures in childhood
mild = may not present until adulthood
blue sclera
dentinogenesis imperfecta

50
Q

how is osteogenesis imperfecta managed?

A

no cure
only fracture fixation, surgery to correct deformity
bisphosphonates

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