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Systems: MSK AB > Metabolic Bone Disease > Flashcards

Metabolic Bone Disease Flashcards

1
Q

What are the 2 main cells of bone remodelling?

A
  • Osteoblasts

- Osteoclasts

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2
Q

What type of cell do osteoblasts develop from?

A

Mesenchymal progenitor cell

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3
Q

What type of cell do osteoclasts develop from?

A

Myeloid progenitor cell

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4
Q

What is the role of osteoclasts?

A

Bone resorption

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5
Q

What is the role of osteoblasts?

A

Bone formation

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6
Q

How do osteoblasts control osteoclasts?

A
  • When stimulated they produce RANKL
  • RANKL binds to pre-osteoclasts
  • Activation of osteoclasts
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7
Q

What produces vitamin D?

A

UVB

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8
Q

Where is vitamin D stored?

A

Liver, fat and muscle

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9
Q

Where is vitamin D activated?

A

Kidney

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10
Q

In what form is vitamin D found in the skin?

A

7DHC

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11
Q

In what form is vitamin D found in the liver?

A

25(OH)vit D

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12
Q

In what form is vitamin D stored in the kidney?

A

1,25(OH)2 vit D

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13
Q

What happens to PTH when extracellular calcium is reduced?

A

Increases

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14
Q

What is Paget’s disease?

A
  • Localised disorder of bone turnover

- Increased bone resorption followed by increased bone formation

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15
Q

What does Paget’s disease lead to?

A

Disorganised bone: bigger, less compact, more vascular and mores susceptible to deformity and fracture

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16
Q

What is the aetiology of Paget’s disease?

A
  • Strong genetic component
  • 15-30% are familial
  • Loci of SQSTMI
  • Restricted geographic distribution: those of Anglo-Saxon origins
  • Environmental trigger: Possibility of chronic viral infection within Osteoclast
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17
Q

How does Paget’s disease present?

A
  • Patient>40 years
  • Bone pain
  • Bony deformity (occasional)
  • Excessive heat over Pagetic bone
  • Neurological complications (such as nerve deafness)
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18
Q

How is Paget’s investigated?

A

X-ray

  • Marked expansion of the bone
  • Dense and lucid areas

Bone scan
-Most useful definitive test

Isolated elevation of serum alkaline phosphotase

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19
Q

What can rarely develop from Paget’s?

A

Osteosarcoma in the affected bone

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20
Q

How is Paget’s disease treated?

A
  • No evidence to treat asymptomatic Paget’s unless in skull or in area requiring surgical intervention.
  • Do not treat based on a raised alkaline phosphatase alone
  • Intravenous Bisphosphonate therapy-One off zoledronic acid infusion
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21
Q

What is the difference between rickets and osteomalacia?

A
  • Rickets occurs in children before the epiphyseal plates fuse
  • Osteomalacia occurs in adults after the epiphyseal plates fuse
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22
Q

What causes rickets/osteomalacia?

A

Severe nutritional vitamin D or Calcium deficiency causes insufficient mineralisation and thus Rickets in a growing child and Osteomalacia in the adult when the epiphyseal lines are closed

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23
Q

What does vitamin D do?

A

Stimulates the absorption of calcium and phosphate from the gut and calcium and phosphate then become available for bone mineralisation

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24
Q

What effect doe low vitamin D have on muscle function?

A

Impaired function

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25
Q

How does Rickets present in infants?

A
  • Stunted growth
  • Bandy legs (once they start walking)
  • Splayed epiphyses
  • Large head (due to failure of fontanelles to close)
  • Nodules on sides of ribs
  • Failure to thrive
  • Fragile
26
Q

What are the symptoms of osteomalacia?

A
  • Bone pain
  • Muscle weakness
  • Increased falls risk
27
Q

What develops in osteomalacia?

A

Microfractures

28
Q

What is osteogenesis imperfecta?

A
  • Genetic disorder of connective tissue characterised by fragile bones from mild trauma and even acts of daily life
  • Other non bone clinical features
  • Broad clinical spectrum
29
Q

What is the cause of OI?

A

Defects in type I collagent (There are 8 types of OI in total with 1 to 4 being the most common)

30
Q

Describe types 1-4 of OI.

A
  • Type I: Milder form-when child starts to walk and can present in adults
  • Type II: Lethal by age 1
  • Type III: Progressive deforming with severe bone dysplasia and poor growth
  • Type IV : Similar to type 1 but more severe
31
Q

What non-skeletal features can OI present with?

A
  • Growth deficiency
  • Defective tooth formation (dentigenesis imperfecta)
  • Hearing loss
  • Blue sclera
  • Scoliosis / Barrel Chest
  • Ligamentous laxity
  • Easy bruising
32
Q

What scoring chart is used for hypermobility in OI?

A

Beighton score

33
Q

How is OI managed?

A
  • Surgical: to treat fractures
  • Medical: IV bisphosphonates to prevent fractures
  • Social: education and social adaptions
  • Genetic: genetic counselling for parents and next generation
34
Q

How do we define osteoporosis?

A

A metabolic bone disease characterised by low bone mass and micro architectural deterioration of bone tissue, leading to enhanced bone fragility and a consequent increase in fracture risk

35
Q

How is osteoporosis defined by DXA scan?

A

A result on DXA bone scanning <2.5 SDs below the young adult mean in a post-menopausal women (T score)

36
Q

What is fracture in osteoporosis related to?

A
  • Age
  • BMD
  • Falls
  • Bone turnover
37
Q

How can we assess risk of osteoporotic fracture?

A

Q fracture score

38
Q

What is Q fracture?

A

-Fracture risk score
-Applicable to those aged 30-85 (men and women)
-Contains multiple variables including CV risks, falls and TCAs
-Cannot add BMD
Some of the variable risks can not be altered by osteoporotic medications

39
Q

What does a DXA scan of the spine look at?

A
  • L2-L4

- Thickening means secondary degenerative change has occurred

40
Q

What does a DXA T score compare you to?

A

Young adult

41
Q

What does a DXA Z score compare you o?

A

Peer of the same age

42
Q

What should happen if someone’s fracture risk from osteoporosis is deemed significant?

A

If the risk is consider significant ( normally defined as a >10% risk of osteoporotic fracture over 10 years) the individual should be referred for a DXA scan ( Dual energy X-ray Absorptiometry)

43
Q

What should happen if someone is on oral steroids or has a low trauma fracture?

A

Should be referred for a DXA bone scan regardless of their fracture risk percentage

44
Q

How common is osteoporosis?

A
  • I in 2 women over 50 will have an osteoporotic fracture before they die
  • I in 5 men over 50 will suffer and osteoporotic fracture
  • A 50 year old woman has a lifetime risk of 17% of a hip fracture
  • If you suffer 1 vertebral fracture you are 5 times more likely to have another and twice as likely to have hip fracture than if you had no vertebral fractures.
45
Q

What endocrine causes of osteoporosis are there?

A
  • Thyrotoxicosis
  • Hyper and Hypoparathyroidim
  • Cushings
  • Hyperprolactinaemia
  • Hypopituitarism
  • Low sex hormone levels
46
Q

What rheumatic causes of osteoporosis are there?

A
  • Rheumatoid arthritis
  • Ankylosing Spondylitis
  • Polymyalgia Rheumatica
47
Q

What GI causes of osteoporosis are there?

A
  • Inflammatory diseases: UC and crohns
  • Liver diseases: PBC, CAH, Alcoholic cirrhosis, Viral cirrhosis (Hep C)
  • Malabsorption: Cystic Fibrosis, chronic pancreatitis, coeliac disease, whipples disease, short gut syndromes and ischaemic bowel
48
Q

What medications can cause osteoporosis?

A
  • Steroids
  • PPI
  • Enzyme inducting antiepileptic medications
  • Aromatase inhibitors (anti-oestrogens used in breast cancer)
  • GnRH inhibitors
  • Warfarin
49
Q

How does our bone mass change with time?

A
  • 0-20: increasing bone size
  • About 25: peak bone mass
  • Gradual decrease in bone mass
  • Accelerated bone loss when menopause begins
  • Gradual bone loss in the elderly
50
Q

How do we prevent osteoporotic fractures?

A
  • Minimise risk factors
  • Ensure good calcium and vitamin D status
  • Falls prevention strategies
  • Medications
51
Q

What medication helps to prevent osteoporotic fractures?

A
  • HRT: Oestrogen and testosterone
  • Selective oestrogen receptor modulator (raloxifene) SERM
  • Bisphosphonates
52
Q

What are the side effects of HRT?

A
  • Increased risks of blood clots
  • Increased risk of breast cancer with extended use into late 50s/early 60s
  • Increased risk of Heart disease and stroke if used after large gap from menopause (more than 3 year gap)
53
Q

What are the negative effects of SERM?

A
  • Hot flushes if taken close to menopause
  • Increased clotting risks
  • Lack of protection at hip site
54
Q

What is the first line pharmacotherapy for fracture prevention in osteoporosis?

A

Oral bisphosphonates

55
Q

What must be ensured before commencing oral bisphosphonates?

A
  • Adequate renal function
  • Adequate calcium and vitamin D status
  • Good dental health and hygiene advised
56
Q

What are the possible side effects of bisphosphonates?

A
  • Oesophagitis
  • Iritis/uveitis
  • Not safe when eGFR<30 mls/min
  • Osteonecrosis of the jaw
  • Atypical femoral shaft fractures

Drug holiday of 1-2 years after 10 years of use

57
Q

What is Denosumab?

A

A monoclonal antibody against RANKL

58
Q

How is denosumab used?

A
  • SC injection every 6 months

- Safer in patients with significant renal impairment then bisphosphonates

59
Q

What does denosumab do?

A

Reduces osteoclatic bone resportion

60
Q

What are the possible side effects of denosumab?

A
  • Allergy/rash
  • Symptomatic hypocalcaemia if given when vitamin D deplete
  • ?ONJ
  • ? Atypical femoral shaft fractures
61
Q

What is teriparatide?

A

Part of PTH that purely stimulates osteoblasts

62
Q

What are the side effects/disadvantages of teriparatide?

A
  • Injection site irritation
  • Rarely hypercalcaemia
  • Allergy
  • COST

Systems: MSK AB (43 decks)

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