Osteoporosis - Diagnosis and Treatment Flashcards

1
Q

Clinical risk factors of osteoporosis

A
  • Advancing age
  • Previous fracture
  • Glucocorticoid therapy (GIO)
  • Family history of Hip fracture
  • Low body weight (BMI <20 kg/m2)
  • Current cigarette Smoking and excessive alcohol consumption (>3.5 unit/day)
  • Rheumatoid arthritis
  • Secondary Osteoporosis (hypogonadism, premature menopause, malabsorption, chronic liver disease)
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2
Q

Clinical/public health impact of osteoporosis

A
  • 3 million people have osteoporosis in the UK.
  • 80 000 hip / 50 000 wrist / 120 000 vertebra
  • £1.7 billion per annum.
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3
Q

What is the WHO definition of osteoporosis? (DXA)

A
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4
Q

What can you use to assess someone’s fracture risk assessment?

A
  • FRAX
    • Risk will be underestimated if high dose/multiple fractures
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5
Q

How to use FRAX?

A

National Osteoporosis Guideline Group- NOGG

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6
Q

What are the limitations of FRAX?

A
  • Does not accommodate all known risk factors
    • Falls, biochemical markers
  • Lacks detail on some risk factors-Dose response effects of glucocorticoids, smoking, prior fracture
  • Depends on adequacy of epidemiological information
  • Model relevant only for untreated patients
  • Not well validated in younger population
  • Only accounts for Hip/NOF BMD
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7
Q

Explain Qfracture risk score

A

Qfracture- online fracture-risk scoring tool, developed in the UK, which can be used to predict the absolute risk of hip fracture and of major osteoporotic fractures (spine, wrist, hip or shoulder) over timeframes of one to ten years.

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8
Q

What are current medical treatment options in osteoporosis?

A
  • Calcium and Vitamin D
    • Dietary calcium intake should be 700mg/day
  • Bisphosphonates
    • Reduce bone turnover
    • Increase bone density
      • Remodelling space
      • Secondary mineralisation
    • Preserve bone structure
    • Bone is stronger

Increase bone density

  • Remodelling space
  • Secondary mineralisation

Preserve bone

structure

Bone is

stronger

Increase bone density

  • Remodelling space
  • Secondary mineralisation

Preserve bone

structure

Bone is

s

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9
Q

Are all bisphonsphonates the same?

A

Nitrogen containing bisphos= more potent

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10
Q

How to give IV Zoledronate? & when advised

A

5mg annually

  • Nephrotoxicity signal
  • Avoid if eGFR <35
  • Ensure vitamin D replete
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11
Q

Explain alendronic acid

A
  • Alendronic acid
  • First line treatment-COST+NICE
  • Generic
  • Used forover 20 yrs
  • Reduces risk of vert, non-vert and hip fractures
  • Very limited data in those > 80 y/o
  • BUT up to 60 % of patients will stop treatment at 6 months
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12
Q

Explain risedronate

A
  • Lower bone affinity and loss potent than alendronic acid
  • May enable greater access to osteocytes
  • Possibly explains similar efficacy to more potent antiresorptives
  • Fewer gI side effects
  • Preferred treatment for GIOP
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13
Q

Explain Ibandronate

A
  • Monthly 150 mg oral
    • Convenience and tolerability (GI_
    • Non-inferiority head to head with alendroic acid (BMD)
  • IV every 3 months
    • No renal toxicity
  • Second line oral biphosphonate
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14
Q

What can happen if someone takes IV bisphosphonate for a long period of time

A

Atypical fractures

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15
Q

Duration of treatment with bisphophonates

A
  • There is clear benefit for 5 years (then stop if NO vertebral fractures)
  • Use for 10 years for people with vertebral fractures
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16
Q

Explain Denosumab & how it works

A
  • Highlypotent & rapidly acting antiresoprtive
  • Human monoclonal antibody against RANK ligand
  • Biggest decrease in individuals with vertebral fractures
17
Q

Explain the drug safety of denosumab

A
  • Can cause severe hypocalcaemia (DO NOT USE in patient’s with hypocalcaemia)
  • Patients with severe renal impairment or dialysis should have monitored calcium levels
  • Causes rare cases of ATYPICAL (femoral fractures)
18
Q

What are the indications for teriparatide?

A
  • Use restricted by cost
  • In severe osteoporosis
    • When multiple vertebral fractures
  • Use in women over age 55
  • Duration of treatment now 24 months
19
Q

Explain romosozumab-anabolic agent

A
  • Monoclonal anti-sclerostin antibody
  • Osteocytes produce sclerostin, which inhibits bone formation
  • Inhibition of sclerostin, enhances osteoblast function, improves bone mass and reduces fracture
  • 210 mg s/c monthly for 12 months
  • Restricted license for use in Scotland, not endorsed by NICE
20
Q

What are some emergency therapies in osteoporosis?

A
  • Abolaparatide – Parathyroid hormone related protein analogue
  • Odanacatib - Cathepsin K inhibitor- initial promising results, but discontinued due to small increase in strokes