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LOCO 2 > Metabolic Bone Conditions and Ageing > Flashcards

Metabolic Bone Conditions and Ageing Flashcards

1
Q 
What can be seen in the serum blood results in osteomalacia?
Calcium
Phosphate
Alkaline phosphatase
PTH
1,25 (OH)2 vitamin D
A 
Decreased
Decreased
Increased
Increased
Decreased
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2
Q 
What can be seen in the serum blood results in Paget's?
Calcium
Phosphate
Alkaline phosphatase
PTH
1,25 (OH)2 vitamin D
A

All normal apart from alkaline phosphatase which is VERY high.

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3
Q 
What can be seen in the serum blood results in renal failure?
Calcium
Phosphate
Alkaline phosphatase
PTH
1,25 (OH)2 vitamin D
A 
Decreased
Increased
Normal to high
Increased
Decreased
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4
Q 
What can be seen in the serum blood results in primary hyperparathyroidism?
Calcium
Phosphate
Alkaline phosphatase
PTH
1,25 (OH)2 vitamin D
A 
Ca increased
PO4 decreased
Normal to increased
PTH Increased
Normal
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5
Q 
What can be seen in the serum blood results in osteoporosis?
Calcium
Phosphate
Alkaline phosphatase
PTH
1,25 (OH)2 vitamin D
A

All normal

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6
Q

Where is alkaline phosphatase produced? (2)

A

Bone (osteoblasts)

Liver

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7
Q

Compare the matrix to mineral ratio in osteoporosis and osteomalacia.

A

Normal in osteoporosis but the whole box is smaller, but in osteomalacia there is more matrix so it is almost 50-50.

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8
Q

Both men and women lose bone mass from age of 40 onwards - at what rate?

A

0.7% a year

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9
Q

In women bone loss speeds up after menopause from 0.7% a year to…?

A

2-9% a year

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10
Q

Why are women more prone to osteoporosis?

A

Men start with more bone to begin with

Menopause speeds bone loss up

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11
Q

How is bone mineral density expressed?

A

T or Z score

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12
Q

What is the T-score?

A

Number of standard deviations from the young (30 yr) same sex and ethnicity mean

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13
Q

What is the Z-score?

A

Number of standard deviations from aged, sex and ethnicity matched mean

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14
Q

At what age do we have peak bone mass?

A

About 40

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15
Q

What does a T-score of greater than -1 mean?

A

Normal

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16
Q

What does a T-score of less than or equal to -2.5 mean?

A

Osteoporosis

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17
Q

What does a T-score of less than -1 and greater than -2.5 mean?

A

Osteopenia

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18
Q

What bones are more susceptible to osteoporotic bone loss? Give two examples.

A

Bones that have high proportion of trabecular bone

Vertebral bodies and femoral neck

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19
Q

What is the prevalence of osteoporosis at 50 years?

A

2%

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20
Q

What is the prevalence of osteoporosis at 80 years?

A

Greater than 25%

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21
Q

How is osteoporosis diagnosed? (2)

A 
A fracture from low force (this is a red flag)
DEXA scan (dual energy X-ray absorptiometry)
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22
Q

Why is trabecular bone particularly at risk? (2)

A

Greater surface area (10x more)

In locations that has to respond to new stresses

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23
Q

Fundamentally, what is osteoporosis?

A

Relative increase in resorption not matched by formation. The bone is normally mineralised, but there is simply less bone.

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24
Q

Describe the cortices and trabeculae in osteoporosis in osteoporosis. What about the osteoid?

A

Cortices and trabeculae thinned

Osteoid seems normal (approx 20% un-mineralised osteoid)

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25
Q

What is the lifetime risk of vertebral fracture in women over 50?

A

1:3

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26
Q

What is the lifetime risk of a neck of femur fracture in women over 50?

A

1 in 5

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27
Q

How many post-menopausal women are there in England and Wales?

A

2 million

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28
Q

How many fractures a year in post-menopausal women?

Name the three most common places.

A

180,000

Hip, wrist, then vertebral

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29
Q

In the osteoporosis treatment path, what is the non-pharmacological treatment? (3)

A

1500mg calcium supplements a day
800 IU vitamin D a day
Physical activity 3x a week for at least 30 mins

30
Q

What else can be given for osteopororis? (6)

A 
Alendronate
Resedronate
Raloxifene
Calcitonin
Etidronate
HRT
31
Q

What is excluded if there are vasomotor symptoms (and no fragility fractures)?

A

Etidronate

32
Q

Who is HRT given to? How long for?

A

Oestrogen replacement 1st choice in peri-menopausal women. Treatment for at least 5 years.

33
Q

What is raloxifene?

A

Selective oestrogen receptor modulator

34
Q

What is denosumab? How is it given? How does it work?

A

Monoclonal antibody (binds to RANKL)
Subcutaneous injection every 6 months
Inhibits osteoclasts formation, activity and survival by binding to the RANKL

35
Q

What is teriparatide? Why does this help with osteoporosis treatment?

A

Recombinant form of PTH
Intermittent exposure to PTH will activate osteoblasts more than osteoclasts (but chronically it will cause osteoclast proliferation).

36
Q

What are bisphosphonates?

How many % do they reduce fracture risk by?

A

Potent inhibitors of bone resorption

Approx 50%

37
Q

How do bisphosphonates work?

A

They are released locally during bone resorption and so are concentrated under the osteoclasts. They inhibit osteoclast activity and promote osteoclast apoptosis. They also may modulate signalling from osteoblasts to osteoclasts, causing increased OPG production and decreased RANKL expression.

38
Q

What are the complications of bisphosphonates? (3)

A

Giant osteoclasts
Osteonecrosis of the jaw
Atypical fractures

39
Q

Give two examples of atypical fractures.

Why does this occur with bisphosphonate treatment?

A

Subtrochanteric and femoral shaft

Old osteocytes signal for remodelling but fewer good osteoclasts.

40
Q

What is the current osteoporosis treatment paradigm?

A
  1. Inhibitors of bone resorption (to slow the loss of bone mass, 3-6 years)
  2. Bone anabolic substances (to increased bone mass, but can’t recover lost microarchitecture, up to 2 years)
41
Q

What is the future osteoporosis treatment paradigm?

A
  1. Bone anabolic substances (1 year)

2. Inhibitors of bone resorption (up to 6 years or even longer)

42
Q

What is osteomalacia also known as?

A

Rickets

43
Q

What is osteomalacia usually the result of?

A

Vitamin D deficiency either in diet or production

44
Q

Is rickets more deforming in children or adults? Why?

A

Children

The epiphyseal growth plate is still open

45
Q

What happens as a consequence of rickets?

A

Insufficient calcium and phosphate to mineralise new bone osteoid. Bones become softer and more liable to bend or fracture.

46
Q

What are the lab results like for osteomalacia?

Calcium, Phosphorus and Alkaline phosphatase

A

Low serum calcium and phosphorus

High alkaline phosphatase

47
Q

What type of fracture is common in osteomalacia? What can this progress to?

A

Pseudofractures (areas of unmineralised bone)

Can progress to insufficiency fractures

48
Q

Where do pseudofractures form?

A

Areas of higher bone turnover

49
Q

How many % is normal bone unmineralised osteoid?

How does this differ in osteomalacia?

A

<20%

There are wide seams of unmineralised osteoid. In severe cases up to 100% of bone covered by unmineralised osteoid.

50
Q

With tetracycline labelling, what can be seen in rickets? (3)

A

Diffuse label (suggestive of altered mineralisation)
Single label
No label

51
Q

Osteoid thickness must be greater than…?

A

14μm

52
Q

What is the treatment for osteomalacia? (3)

A

Vitamin D supplements – may need to take for rest of life
Increase dietary calcium (milk, bread, beans, pulses, dried fruit, green leafy veg)
Sun/UV exposure (15 mins on hands and face 2-3x a week)

53
Q

The liver converts cholecalciferol to…?

A

25-dihydroxyvitamin D3

54
Q

The kidney converts 25-dihydroxyvitamin D3 to…?

A

1,25-dihydroxyvitamin D3

55
Q

What is Paget’s disease also known as?

A

Osteitis deformans

56
Q

What is the prevalence of Paget’s in population <40?
>50?
>80?

A

Rare
3%
10%

57
Q

What are the 3 phases of Paget’s disease?

A

Initial phase
Compensatory/proliferative phase (mixed)
Burnt out/sclerotic phase

58
Q

What is seen in the initial phase? (2)

A

Increased rate of bone resorption

Large number of giant osteoclasts

59
Q

What is seen in the compensatory phase? (2)

A

Increased bone formation

Accelerated deposition in disorganised manner

60
Q

What is seen in the burnt out phase? (5)

A

Bone hyper-cellularity may diminish leaving dense, “Pagetic bone”
Hyper-vascular bone marrow
Irregular thickened trabeculae
Prominent cement lines
Bone marrow replaced by fibrovascular connective tissue

61
Q

What bones are commonly affected in Paget’s? (5)

A 
pelvis
femur
vertebrae
skull
tibia
62
Q

What is a rare complication of Paget’s disease?

A

Osteosarcoma

63
Q

Where do osteosarcomas usually occur?

A

In long bones, often near the knee

64
Q

Osteosarcoma is among the most malignant of cancers and it can spread rapidly, usually to lungs. To prevent spread, what can be done?

A

Removal of part of the affected bone, or limb amputation.

65
Q

How is Paget’s treated? (5)

A

Bisphosphonates (work directly on osteoclasts to slow bone resorption) - oral 2-6 months, single to 3 IV infusion(s)

Calcium and vitamin D supplements

Pain management

Surgery

Calcitonin (used less than bisphosphonates)

66
Q

Sclerostosis is also known as…?

How is it inherited?

A

Van Buchem syndrome

Autosomal recessive

67
Q

What is Van Buchem syndrome associated with?

A

Associated with absence or reduced production of sclerostin

68
Q

What cells secrete sclerostin? What does it do?

A

Osteocytes

Inhibits osteoblasts so stops bone formation

69
Q

What happens in Van Buchem syndrome? (3)

A

Endosteal hyperostosis
Resistance to fracture
Excessive height

70
Q

What is romosozumab?

By how much does it increase bone mass density and how does this compare to aldrenronate and teriparatide?

A

Sclerostin antibody

11.3% (compared to 4% and 7%)

LOCO 2 (28 decks)

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