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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
Q

Explain the link between CKD and low bone mass and fractures

A
  • 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
Q

Why are vertebral fractures (prevalence 21%) difficult to treat in haemodialysis patients?

A

Many of the commonly used treatment mechanisms (bone sparing therapy) cannot be used in renal patients bc of renal impairment

27
Q

Explain how you quantify fracture risk/diagnose osteoporosis

A
  • 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
Q

What investigations are done to investigate fractures/osteoporosis?

A

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
Q

What makes up a bone profile?

A

Corrected calcium, phosphate, magnesium and alkaline phosphate

30
Q

Why do you do serum electrophoresis when investigating bone?

A

Checking for conditions that could masquerade as osteoporosis, low bone mass or fractures e.g. multiple myeloma
- Also look for free light chains

31
Q

What is DEXA used for?

A

Diagnosis and monitor treatment

32
Q

How are exercise interventions used to manage osteoporosis?

A

Static and dynamic weight bearing exercises slow down the decline of hip and lumbar BMD (not always practical)

33
Q

How is diet used to treat osteoporosis?

A
  • 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
Q

Describe use of vitamin D supplements to treat vitamin D deficiency and osteoporosis

A
  • 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
Q

What is vitamin D and how is it made/used?

A
  • 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
Q

What level of serum 25OHD is deficient?

A

< 30 nmol/L

37
Q

What level of serum 25OHD is adequate and what level is sufficient for almost the whole population?

A

30-50 nmol/L is adequate

> 50 nmol/L is sufficient for almost the whole population (aim for >75 in clinic)

38
Q

What is the main bone sparing pharmacological therapy used to prevent vertebral, non-vertebral and hip fractures in men and women?

A

Bisphosphonates

39
Q

Describe how you treat with bisphosphonates and long term risks

A
  • 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
Q

Why do you treat with bisphosphonates for 3-5 years and then assess fracture risk?

A
  • 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
Q

What are other pharmacological treatments used to treat osteoporosis?

A

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
Q

What is teriparatide, what does it do and when is it used?

A
  • 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
Q

Describe Paget’s disease of the bone

A
  • 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
Q

How does Paget’s disease of the bone present/is diagnosed?

A
  • 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
Q

How is Paget’s disease of the bone treated?

A

Bisphosphonates at much higher strength than for osteoporosis

46
Q

What do you have to be careful not to miss when assessing fracture risk?

A

Cancer (bone metastases) compared to osteoporosis

47
Q

When does bone metastasis occur?

A
  • 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
Q

How does bone metastasis present?

A

1) Severe pain
2) Pathological/atypical fractures
3) Abnormalities in calcium

49
Q

How does cancer treatment lead to bone loss?

A
  • 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
Q

What enzyme deficiencies lead to bone problems (rare)?

A

1) Hypophosphatasia
2) Mucopolysaccharidosis
3) Homocysteinurea
4) Alkaptonuria

51
Q

Describe hypophosphatasia

A
  • Heritable rickets
  • Sub-normal BALP activity
  • Depending on severity can present in infants, children or adults with fractures
52
Q

Describe mucopolysaccharidosis

A
  • 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
Q

Describe homocysteinurea

A
  • Autosomal recessive disorder
  • Cystathione beta deficiency
  • Marfanoid habitus
  • Thromboembolism and osteoporosis e.g. could present with vertebral compressions secondary to back pain
54
Q

Describe alkaptonuria

A
  • 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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