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Year 2 Clinical > Bone Health and Osteoporosis > Flashcards

Bone Health and Osteoporosis Flashcards

1
Q

Definition of osteoporosis?

A

Progressive systemic skeletal disease characterised by low bone mass and micro-architectural bone tissue deterioration

There is a consequent increase in bone fragility and fracture susceptibility

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2
Q

Common fracture sites in the skeleton?

A
  • Neck of femur (incidence rises dramatically when >70)
  • Vertebral body
  • Distal radius (most frequent up to the age of 70)
  • Humeral neck
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3
Q

Morbidity and mortality assoc. with hip fractures?

A

1/2 of patients lose independence

1/5 die within a year of their fracture

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4
Q

Occurrence of osteoporotic fractures in women?

A

Majority of hip fractures occur in women >75 years

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5
Q

Reason for women suffering more osteoporotic fractures?

A

Women have lower peak bone mass

AND

Accelerated loss of bone during the menopause

AND

Increased longevity

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6
Q

Presentation of vertebral fractures?

A

Many present “silently” (with no symptoms)

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7
Q

Describe the domino fracture effect

A

A vertebral fracture increases the risk of kyphosis

Also, if a patient has had 1 fracture, they have an increased risk of another fracture

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8
Q

Describe the domino fracture effect

A

A vertebral fracture increases the risk of kyphosis

Also, if a patient has had 1 fracture, they have an increased risk of another fracture

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9
Q

Where does remodelling of bone occur?

A

Bone undergoes a continual remodelling cycle at distinct sites (BONE REMODELLING UNITS)

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10
Q

Purpose of bone remodelling?

A

10% of the adult skeleton is remodelled every year, which contributes to:
• Calcium homeostasis
• Skeletal repair

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11
Q

Process of bone remodelling?

A

Beginning of cycle:
• Osteoclasts appear on a previously inactive surface and begin to resorb bone

They are then replaced with osteoblasts that fill the cavity, by laying down OSTEOID; this is MINERALISED, to form new bone

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12
Q

Main problem with bone remodelling in osteoporosis?

A

There is a relative or absolute increase in resorption over formation; this leads to increased bone loss

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13
Q

Structure when osteoporotic bone loss occurs?

A

Osteoporotic bone has:
• Loss of bone
• Large spaces
• Breaks in the microscopic architecture (overall weakened bone that fractures easily)

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14
Q

Regulation factors of peak bone mass?

A
  • Genetics (most important factor)
  • Body weight (part. being underweight)
  • Sex hormones (oestrogen; post-menopause acceleration of bone loss)
  • Diet
  • Exercise
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15
Q

Regulating factors of bone loss?

A
  • Sex hormone deficiency
  • Body weight
  • Genetics
  • Diet
  • Immobility
  • Diseases
  • Drugs, e.g: steroids, aromatase inhibitors
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16
Q

Age at which peak bone mass is reached?

A

Bone mass increases in men and women until a peak is attained, at ~30 years

This is the consolidated and maintained until the patient reaches 40

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17
Q

Age at which bone mass starts to decrease?

A

In both sexes, slow rate of bone loss starts at 40 years; but, in post-menopausal women, there is accelerated bone loss

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18
Q

Which patients with are targeted with therapeutic intervention?

A

At those with high risk of low impact fracture

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19
Q

Non-modifiable clinical risk factors for fragility fracture?

A

Age, gender and ethnicity

Previous fracture

FH

Early menopause (≤ 45 years)

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20
Q

Modifiable clinical risk factors for fragility fracture?

A

BMD (bone mineral density)

Alcohol and smoking

Weight

Physical inactivity

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21
Q

Other clinical risk factors for fragility fracture?

A

Co-morbidities

Pharmacological risk factors

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22
Q

Use of the WHO fracture risk calculator (FRAX)?

A

Allows calculation of absolute risk, by incorporating additional risk factors (rather than just BMD)

It produces a prediction of the 10 year risk of major osteoporotic fracture or hip fracture

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23
Q

Advantages of FRAX?

A

Freely available (internet)

Calculates 10 year absolute risk of hip or major osteoporotic fracture

Can be used with or without BMD

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24
Q

Questions asked in FRAX)

A
  • Age
  • Gender
  • BMI
  • Previous fracture
  • Smoking
  • Alcohol ≥3 u/d
  • Steroids
  • RA, diabetes, OI, untreated hyperthyroidism, hypogonadism, premature menopause, malnutrition, malabsorption, chronic liver disease
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25
Q

Disadvantages of FRAX?

A

Underestimates vertebral fracture risk

Same level of risk assigned to all secondary causes

Dichotomised variables smoking/alcohol

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26
Q

Advantages of Qfracture?

A

Freely available (internet)

More variables included, e.g: dementia, PD, medications

Hx of falls or resident in nursing homes

Smoking and alcohol can be given in quantities

Can use variable time for absolute risk

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27
Q

Advantages of Qfracture?

A

Does not inc. BMD, when available

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28
Q

Who should have risk factor assessment?

A

Anyone >age 50 with risk factors

Anyone <50 years with very strong clinical risk factors:
• Early menopause
• Glucocorticoids

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29
Q

When should a patient be referred for a DEXA scan?

A

Any patient with a 10 year risk assessment of at least 10%, for any osteoporotic fracture

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30
Q

How is bone density assessed?

A

Bone mineral density predicts fracture risk INDEPENDENT of any other risk factors

DEXA scan are usually used to measure BMD

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31
Q

Interpreting DEXA scan results?

A

Normal:
• BMD within 1 SD of the young adult reference mean

Osteopenia (low bone mass)
• BMD >1 SD below the young adult mean but <2.5 SD below this value

Osteoporosis:
• BMD ≥ 2.5 SD below the young adult mean

Severe osteoporosis:
• BMD ≥2.5 SD below the young adult mean with fragility fracture

32
Q

If the patient is <20 years old, how is the DEXA scan result reported?

A

Only the Z score is reported

33
Q

Relationship between BMD and fracture risk?

A

As BMD decreases, verterbal fracture risk increases

34
Q

Ix for osteoporosis?

A

U&Es, LFTs, FBC, PV and TSH

Bone biochemistry

Consider doing:
• Protein electrophoresis
• Urinary Bence Jones proteins (indicate multiple myeloma, a bone marrow malignancy, which can cause osteoporosis)
• Coeliac antibodies
• Testosterone
• 24-OH vitamin D
• PTH
35
Q

Secondary causes of osteoporosis?

A

Endocrine:
• Hyperthyroidism
• Hyperparathyroidism
• Cushing’s disease

GI:
• Coeliac disease
• IBD
• Chronic liver disease
• Chronic pancreatitis

Respiratory:
• CF
• COPD

Renal:
• Chronic kidney disease

36
Q

Lifestyle advice for Mx of osteoporosis?

A

High intensity strength-training and low-impact weight bearing exercise (standing with one foot always on the floor)

Avoid smoking and excess alcohol

Prevent falling

37
Q

Calcium in the diet for Mx of osteoporosis?

A

700 mg of Ca2+ is required in most patients; post-menopausal women should aim their dietary intake at 1000 mg of Ca2+ per day

38
Q

Portions of foot required for osteoporosis?

A

For 700 mg, 2-3 portions form milk and dairy)

For 100mg, 3-4 portions of calcium-rich foods

Non-dairy sources:
• Bread and cereals (fortified)
• Fish with bones
• Nits
• Green vegetables
• Beans
39
Q

Pharmacological treatment of osteoporosis?

A

Calcium & vitamin D supplementation

Bisphosphonate

Denosumab

Teriparatide

Strontium Ranelate

HRT

SERMS (selective oestrogen receptor modulators)

Testosterone

40
Q

When is calcium and vitamin D replacement used for osteoporosis?

A

R-calcium and vitamin D supplementation can be used to reduce risk of non-vertebral fractures in patients at high risk of deficiency due to insufficient diet or limited sunlight exposure

If dietary calcium is adequate (>700 mg daily), Vitamin D only may be preferred as the osteoporosis treatment adjunct

41
Q

Cautions with calcium supplementation?

A

Should not be taken within 2 hours of oral bisphosphonates

42
Q

When is a patient automatically considered to be at risk of vitamin D deficiency?

A

If low exposure to sun (cultural or housebound)

43
Q

Examples of bisphonphonates?

A

Alendronate

Risedronate

Zoledronic acid

44
Q

Uses of bisphosphonates?

A

Prevent bone loss at sites vulnerable to osteoporosis

Reduce risk of hip and spinal fracture; reduce risk of fragility fracture by ~50% in patients with post-menopausal osteoporosis

45
Q

Mechanism of action of bisphosphonates?

A

Anti-resorptive agent that are
analogues of pyrophosphate

They adsorb onto bone within the matrix and are ingested by osteoclasts, leading to cell death (so bone resorption is inhibited)

Filling of resorption sites with new bone increases BMD

46
Q

Duration of bisphosphonate therapy?

A

For 5 years (if a vertebral fracture, 10 years)

After stopping, drugs stay in bone and the effect remains for 2-3 more years

47
Q

Potential side effects of bisphosphonate therapy?

A

Osteonecrosis of the jaw

Oesophageal carcinoma

Atypical fractures

48
Q

Administration of Zoledronic acid?

A

Once yearly IV infusion for 3 years:

• 5mg in 100ml of NaCl is given over 15 minutes

49
Q

Potential side effect of Zoledronic acid and treatment?

A

Acute phase reaction (fever, flu-like, night sweats, rigors, diffuse MSK pain, GI effects, and eye inflammation)

Treat with paracetamol

50
Q

What is Denosumab?

A

Fully human monoclonal Ab

51
Q

Mechanism of action of Denosumab?

A

Targets and binds, with high affinity and specificity, to RANKL (receptor activator of nuclear factor-kB ligand)

Prevents receptor activation (RANK), which:
• Inhibits development and activity of osteoclasts
• Decrease bone resorption
• Increase bone density

52
Q

Administration of Denosumab?

A

S/C injection every 6 months

53
Q

Potential side effects of Denosumab?

A

Hypocalcaemia

Eczema

Cellulitis

There are no contraindication in severe renal impairment

54
Q

What is Strontium Ranelate?

A

Anti-resorptive agent that is 3rd line for fracture risk reduction

It is not recommended when there is an alternative osteoporosis treatment available

55
Q

Contraindications with strontium ranelate?

A 
Hx of:
• Thromboembolic disease
• IHD
• Peripheral arterial disease
• Uncontrolled hypertension
56
Q

What is Teriparatide?

A

Recombinant PTH that stimulates bone growth (rather than reducing bone loss), i.e: it is an anabolic agent

57
Q

When is Teriparatide used?

A

> 65 years with T score < -4

T score of – 3.5 with >2 fractures

Aged 55-64 years with a T score of -4 or below with >2 fractures (plus intolerant/unsatisfactory response to oral agents)

58
Q

When to pharmacologically treat a patient with osteoporosis?

A

In most patients, consider treatment with anti-resorptive therapy when:
• T-score ≤ -2.5

If ongoing steroid requirement of ≥ 7.5mg prednisolone for 3 months/more OR if there is a prevalent vertebral fracture:
• Consider treatment with T-score < -1.5

59
Q

Direct effects of corticosteroids on bone?

A
  • Reduction of osteoblast activity and lifespan
  • Suppression of replication of osteoblast precursors
  • Reduction in calcium absorption
60
Q

Indirect effect of corticosteroids on bone?

A

Inhibition of gonadal and adrenal steroid production

61
Q

Effects of glucocorticoids on calcium metabolism?

A

Kidney

Gut (reduced Ca2+ absorption)

Bone (decreased matrix synthesis resorption)

Pituitary

62
Q

Fracture risk with steroids?

A

Is dose-dependent; there is a rapid loss of BMD in the 1st 6 months (partially reversible)

63
Q

What is Paget’s disease of bone?

A

Excessive breakdown and formation of bone, followed by disorganized bone remodeling, i.e: there is abnormal osteoclastic activity that is then followed by increased osteoblastic activity

64
Q

Aetiology of Paget’s disease of bone?

A

Uncertain but may be a viral, environmental or biochemical trigger in a genetically susceptible individual

65
Q

Consequences of Paget’s disease of bone?

A

Abnormal bone structure with reduced strength, so increased fracture risk

66
Q

Sites inv. with Paget’s disease of bone?

A

Monostotic (single site) or polyostotic (multiple sites)

Predominantly affects long bones, pelvis, lumbar spine and skull; does not affect fingers and toes (SPARING)

67
Q

Occurrence of Paget’s disease of bone?

A

Rare <40 years and incidence increases with age

68
Q

Presentation of Paget’s disease of bone?

A

Bone pain, deformity, deafness or compression neuropathies

69
Q

Complication of Paget’s disease of bone?

A

Osteosarcoma (rare)

70
Q

Ix and diagnosis of Paget’s disease of bone?

A

May be incidental finding on X-ray or isolated raised Alk Phos

Diagnose with:
• X-ray
• Isotope bone scan shows distribution
• Raised alkaline phosphatase with normal LFT

71
Q

Treatment of Paget’s disease of bone?

A

With bisphosphonates, if pain not responding to analgesia

72
Q

What is osteogenesis imperfecta?

A

Rare group of genetic disorders mainly affecting bone, with at least 8 types of varying severity

Most are secondary to mutations in type 1 collagen genes (COL1A1, COL1A2); also, most show autosomal dominant inheritance

73
Q

Types of osteogenesis imperfecta and presentation?

A

Type I (mild) - may not present till adulthood

Types III and IV (very severe)

Type II (neonatal lethal - they have fractures in utero)

More severe forms present with childhood fractures

74
Q

Causes of childhood fractures?

A

Most common is trauma

If “no Hx of trauma”, consider NAI

Rare cause is osteogenesis imperfect

75
Q

Treatment of osteogenesis imperfecta?

A

No cure but can use:
• Fracture fixation
• Surgery to correct deformities
• Bisphosphonates

Year 2 Clinical (119 decks)

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