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Stage 2: Ageing > Osteoporosis and Metabolic Bone Disease > Flashcards

Osteoporosis and Metabolic Bone Disease Flashcards

1
Q

What is the difference between men and women in terms of changes in bone mass with age?

A

Men reach a higher peak bone mass which declines more gradually and less than women

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2
Q

What happens to bone in menopause?

A
  • Women lose hormones abruptly in menopause
  • Therefore in the immediate menopausal period women can lose up to 5% of their bone mass and then it stabilises to gradual decline
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3
Q

Why might someone never have been able to reach peak bone mass and what is the effect of this?

A
  • Illness, T1D, steroids
  • They don’t have enough bone in mid 30s and then have natural losses
  • Their loss tends to be more
  • Increased fracture risk
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4
Q

What determines peak bone mass?

A

Genes, nutrition, exercise

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5
Q

What causes the increase in bone mass?

A

Nutrition and vitamin D in the womb

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6
Q

What causes the decrease in bone mass?

A

1) Age related bone loss

2) Reduced physical activity

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7
Q

What is DEXA?

A
  • Dual energy X-ray absorptiometry
  • Bone density scan using densitometry X ray
  • Measures how much mineral is in an area/mineralisation of bone esp. in the spine (trabecular) and hip (cortical)
  • 2D image
  • Results are given as standard deviation - the number of units above or below average
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8
Q

What is osteoporosis?

A

Systemic skeletal disorder characterised by low bone mass and microarchitectural deterioration of bone tissue and an increased risk of fracture

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9
Q

What bone mineral density (BMD) value is described as osteoporosis?

A

< 2.5 SD of normal (really more than 2.5 SD, -2.5 SD or lower)

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10
Q

What bone mineral density (BMD) value is described as osteopenia?

A
  • BMD between 1 and 2.5 SD below the average
  • Not as bad as osteoporosis
  • Bone density between the low end of the normal range (between -1 and 1 SD of normal) and osteoporosis
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11
Q

What is a fragility fracture?

A
  • A fracture following a fall from standing height or less (where normally this fall would not have caused a fracture)
  • Vertebral fractures may occur spontaneously, or as a result of routine activities, without any trauma
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12
Q

What is important to remember about treatment for fractures?

A

Treatment can only prevent fragility fractures not high impact fractures

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13
Q

Why are women at a greater risk of osteoporosis?

A

Due to the decrease in oestrogen production at menopause, which accelerates bone loss

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14
Q

What is the prevalence of osteoporosis in 80 year olds and what is the impact of this on diagnosis?

A
  • Almost 50% (compared to 2% at 50)
  • Therefore questions need of DEXA scan to diagnose and treat if someone has a fragility fracture bc the probability that they have osteoporosis is so high in this age group
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15
Q

Describe vertebral fractures in osteoporosis

A
  • Often unrecognised and undiagnosed bc they don’t always result in neurological complications, sometimes just pain
  • Make someone at higher risk of having subsequent fractures
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16
Q

Why are hip fractures the worst?

A

Bc they almost always require surgical intervention and are associated with high mortality and morbidity and a lot of use of resources

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17
Q

What are modifiable determinants of low bone structure and function?

A

1) Low BMI < 18.5
2) Alcohol intake > 14 units/week
3) Smoking
4) Current or frequent use of steroids
5) Vitamin D and calcium homeostasis (deficiencies)

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18
Q

What are non-modifiable determinants of low bone structure and function?

A

1) Age
2) Gender
3) Ethnicity (caucasians and asians higher risk)
4) Previous fragility fracture
5) FH of hip fracture

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19
Q

What diseases are associated with low bone mass and fractures?

A

1) Diabetes
2) Inflammatory rheumatic diseases
3) Chronic liver disease
4) CKD

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20
Q

What other more specific diseases are associated with low bone mass and fractures bc of treatments used to treat them, chronic inflammation and immobility?

A

1) Cystic fibrosis
2) HIV
3) Epilepsy
4) MS
5) Stroke

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21
Q

Explain the link between diabetes and low bone mass and fractures

A
  • Women with T1D are 12x more likely to have a hip fracture and women with T2D are 1.7x more likely
  • This is due to low bone turnover, reduced anabolic effect of insulin and IGF-1 (deficient)
  • Therefore they reach a lower peak bone mass
  • Poor vision and neuropathy also increase fracture potential bc increased risk of fall
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22
Q

Explain the link between inflammatory rheumatic disease and low bone mass and fractures

A
  • Increased expression of RANKL and interleukins which activate osteoclasts
  • More likely to be on steroids
23
Q

Explain the link between gastrointestinal disease and low bone mass and fractures

A
  • Inflammation
  • Intestinal malabsorption e.g. coeliac disease
  • Bowel surgery
  • More likely to be on steroids
24
Q

Explain the link between chronic liver disease and low bone mass and fractures

A

Malnutrition, low BMI and cholestasis (and alcohol?) are risk factors

25
Explain the link between CKD and low bone mass and fractures
- Renal osteodystrophy (CKD associated renal bone disease) - Can be either due to a high bone turnover disease (osteitis fibrosa cystica due to secondary hyperparathyroidism) - OR low bone turnover disease (adynamic bone disease, osteomalacia) - Bone which doesn't turnover normally is at increased risk of fracture - Osteoporosis - Drug related
26
Why are vertebral fractures (prevalence 21%) difficult to treat in haemodialysis patients?
Many of the commonly used treatment mechanisms (bone sparing therapy) cannot be used in renal patients bc of renal impairment
27
Explain how you quantify fracture risk/diagnose osteoporosis
- FRAX calculates the 10 year absolute risk of major osteoporotic fracture and hip fracture - Gives guidelines about what to do - Has good risk factors but doesn't include e.g. HIV, medication other than steroids or if there is more than one fracture - Includes hip (femoral neck) BMD which predicts fracture risk more than spine - Bone markers in urine and serum are useful to monitor treatment but not for diagnosis
28
What investigations are done to investigate fractures/osteoporosis?
1) Bone profile 2) PTH 3) 25 OH vitamin D 4) U&Es, LFTs 5) Coeliac screen 6) TFTs 7) Gonadotrophins 8) DEXA scan 9) X rays/MRI if suspicion of fracture 10) Serum electrophoresis esp. in older people
29
What makes up a bone profile?
Corrected calcium, phosphate, magnesium and alkaline phosphate
30
Why do you do serum electrophoresis when investigating bone?
Checking for conditions that could masquerade as osteoporosis, low bone mass or fractures e.g. multiple myeloma - Also look for free light chains
31
What is DEXA used for?
Diagnosis and monitor treatment
32
How are exercise interventions used to manage osteoporosis?
Static and dynamic weight bearing exercises slow down the decline of hip and lumbar BMD (not always practical)
33
How is diet used to treat osteoporosis?
- Want to ensure diet before using treatments - Need adequate calcium in diet to meet the recommendation of 700-1000 mg/day - Vitamin D in diet
34
Describe use of vitamin D supplements to treat vitamin D deficiency and osteoporosis
- Bc of inadequate sunshine hours and diet low in vitamin D, at least 800 IU of vitamin D3 is recommended - Oral vitamin D3/cholecalciferol is the treatment of choice in vitamin D deficiency - Aim for serum 25OH vitamin D > 75 nmol/L in clinic
35
What is vitamin D and how is it made/used?
- Vitamin D is essential for musculoskeletal health - Vitamin D is largely made in the skin - Vitamin D obtained by skin or diet undergoes 25 hydroxylation in the liver and then is converted into activated vitamin D form (1,25 hydroxy vitamin D) in the kidney - Animal sources = cholecalciferol - Non animal sources = ergocalciferol - Vitamin D promotes calcium absorption from the gut, enables mineralisation of newly formed osteoid tissue bone (immature bone) and plays an important role in muscle function
36
What level of serum 25OHD is deficient?
< 30 nmol/L
37
What level of serum 25OHD is adequate and what level is sufficient for almost the whole population?
30-50 nmol/L is adequate | > 50 nmol/L is sufficient for almost the whole population (aim for >75 in clinic)
38
What is the main bone sparing pharmacological therapy used to prevent vertebral, non-vertebral and hip fractures in men and women?
Bisphosphonates
39
Describe how you treat with bisphosphonates and long term risks
- Available as weekly/monthly tablets or yearly infusions - Keeps bone turnover low (keeps bone quiet) - Treat for 3-5 years and then assess fracture risk unless on steroids, > 75 or previous fracture - Long term risk of osteonecrosis of the jaw (rare by serious) and atypical fracture
40
Why do you treat with bisphosphonates for 3-5 years and then assess fracture risk?
- Bc it might make the bone adynamic/suppressed or have such a low bone turnover that it is excessively mineralised so that it loses its metabolic activity but is not able to protect itself - Over-treated bone is also associated with atypical fractures on its own
41
What are other pharmacological treatments used to treat osteoporosis?
1) HRT (younger post-menopausal women) 2) Selective oestrogen receptor modulators (SORM) e.g. raloxifene (hormone preparation) 3) Testosterone replacement in some hypogonadal men (improves bone mass) 4) Denosumab - targeted towards the molecular mechanisms in bone 5) Teriparatide
42
What is teriparatide, what does it do and when is it used?
- Only anabolic/bone forming treatment which is recombinant PTH - Given only as a one off for a period of 18-24 months - PTH given for a short period of time brings about increased formation, creates an anabolic window and increases bone mass greatly - Sometimes used in patients with v high fracture risk
43
Describe Paget's disease of the bone
- Localised disorder of bone remodelling - Disorganised chaotic mosaic of new bone formation resulting in less compact and more vascular bone susceptible to deformity and fracture - Causes pain - Higher incidence of osteosarcoma - Driven by genetic and environmental factors - More common in Europeans and men - Rare in people < 55
44
How does Paget's disease of the bone present/is diagnosed?
- Present with bone pain, deformities, fractures or isolated increase in bone alkaline phosphate (BALP) - Sometimes is asymptomatic and picked up by incidental consistent elevated BALP finding
45
How is Paget's disease of the bone treated?
Bisphosphonates at much higher strength than for osteoporosis
46
What do you have to be careful not to miss when assessing fracture risk?
Cancer (bone metastases) compared to osteoporosis
47
When does bone metastasis occur?
- 80% of patients with advanced breast or prostate cancer - 15-30% of thyroid, lung or renal cancers - Metastatic cells flourish within the bone microenvironment bc bones are very vascular
48
How does bone metastasis present?
1) Severe pain 2) Pathological/atypical fractures 3) Abnormalities in calcium
49
How does cancer treatment lead to bone loss?
- Accelerated bone loss occurs following therapy for breast cancer (blocks oestrogen) or prostate cancer (androgen deprivation) - so patients need to be actively protected for bone loss which they will eventually develop from treatment - Steroids and/or immunomodulant used for treatment during bone marrow transplant result in bone loss
50
What enzyme deficiencies lead to bone problems (rare)?
1) Hypophosphatasia 2) Mucopolysaccharidosis 3) Homocysteinurea 4) Alkaptonuria
51
Describe hypophosphatasia
- Heritable rickets - Sub-normal BALP activity - Depending on severity can present in infants, children or adults with fractures
52
Describe mucopolysaccharidosis
- Inherited metabolic condition - Diminished activity of lysosomal enzymes that degrade glycosaminoglycans - Accumulation of compels carbohydrates within the bone marrow - Associated with low bone mass and high fracture risk
53
Describe homocysteinurea
- Autosomal recessive disorder - Cystathione beta deficiency - Marfanoid habitus - Thromboembolism and osteoporosis e.g. could present with vertebral compressions secondary to back pain
54
Describe alkaptonuria
- Autosomal recessive disorder - Homogentisic acid oxidase deficiency - Accumulation of homogentisic acid - Discolouration of urine and connective tissue

Stage 2: Ageing (10 decks)

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