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LOCO 2 > Metabolic bone conditions > Flashcards

Metabolic bone conditions Flashcards

1
Q

Describe the blood serum results in osteoporosis

A

All normal

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2
Q

Describe the blood serum results in osteomalacia

A

Calcium low
Potassium low
Alkaline phosphatase high
PTH and vit D normal

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3
Q

Describe the blood serum results in Pagets

A

All normal except alkaline phosphatase

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4
Q

Describe the blood serum results in renal failure

A 
Calcium low
Potassium high
Alkaline phosphatase either normal or high
PTH high
Vit D low
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5
Q

Describe the blood serum results in primary hyperparathyroidism

A 
Calcium high
Phosphate low
Alkaline phosphatase either normal or high
PTH high
normal vit D
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6
Q

What is alkaline phosphatase produced from

A

Osteoblasts (bone) and the liver

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7
Q

At what rate is bone lost at the age of 40 onwards

A

0.7% a year

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8
Q

What speed is bone mass lost after menopause

A

2-9% a year

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9
Q

What 2 scores can bone mineral density expressed as

A

T or Z score

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10
Q

What is a T score

A

Number of standard deviations from the mean young (30y) same gender and ethnicity

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11
Q

What is a Z score

A

Number of standard deviations from mean aged, same gender and ethnicity

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12
Q

In terms of T score, when and how is a diagnosis of osteoporosis made

A

t score below 2.5

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13
Q

What does DEXA stand for

A

Dual energy X-ray absorptiometry

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14
Q

What is the prevalence of osteoporosis at

a) 50 and
b) 80

A

a) 2%

b) >25%

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15
Q

In terms of T score, when is a diagnosis of osteopenia made

A

between 1 and 2.4

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16
Q

What kind of bones are more susceptable to osteoporotic bone loss

A

High proportion of trabecular bone

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17
Q

Give 2 examples of bone susceptible to osteoporosis

A

Vertebral bodies

Femoral neck

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18
Q

Briefly describe/ define osteoporosis

A

Relative increase in resorption is not matched by formation. Bone is normally mineralised so there is less bone

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19
Q

Is loss evenly distributed in osteoporosis

A

No- trabeculae bone is more at risk

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20
Q

Why is trabeculae bone more at risk of osteoporosis

A

Because it has a greater surface area, and is in areas that respond to new stresses

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21
Q

How does osteoporotic bone differ to normal bone

A

Cortices and trabeculae are thinned

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22
Q

How would you treat an osteoporosis patient who is over 75 and has low trauma fracture

A

Bisphosphonate calcium and vit D

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23
Q

How would you treat an osteoporosis patient aged 50-75 and low trauma fracture

A

DEXA scan

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24
Q

Why are calcium supplements given to people with osteoporosis

A

Reduce negative calcium balance

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25
Q

Why are vitamin D supplements given to people with osteoporosis

A

Significant numbers of elderly are deficient

26
Q

Name 5 non supplemental treatments for osteoporosis

A 
HRT
Selective oestrogen receptor modulator 
Bisphosphonates
Teriparatide
Denosumab
27
Q

How does denosumab work

A

Monoclonal antibody that binds to RANKL

Inhibits osteoclast formation

28
Q

Name a selective oestrogen receptor modulator

A

Raloxifene

29
Q

Why are bisphosphonates given to treat osteoporosis

A

Potent inhibitors of bone resoprtion

Reduce fracture risk by 50%

30
Q

Name 3 complications of bisphosphonates

A

Giant osteoclasts
Osteonecrosis of the jaw
Atypical fractures

31
Q

Why is teriparatide used to treat osteoporosis

A

Intermittent exposure to PTH will activate osteoblasts more than osteoclasts

32
Q

How is denosumab administered

A

Subcutaneous injection every 6 months

33
Q

What is the colloquial name for ostemalacia

A

Rickets

34
Q

Briefly describe the underlying pathophysiology of osteomalacia

A
  • Insufficient calcium and phosphate to mineralise new bone osteoid
  • Bones softer and more liable to bend/ fracture
35
Q

What does osteomalacia usually result from

A

Vit D deficiency

36
Q

Is osteomalacia more or less deforming in adults than children and why

A

Less deforming because the epiphyseal growth plates are closed

37
Q

What can looser lines on an x-ray suggest

A

Pseudofractures

38
Q

What are pseudofractures

A

Areas of unmineralised bone which can progress to insufficiency fractures.

39
Q

Where do pseudofractures most commonly form

A

At areas of higher bone turnover

40
Q

What % of osteroid is unmineralised in normal bone

A

<20%

41
Q

Describe the bone biopsy of an osteomalcia patient

A

Wide seams of unmineralised osteroid
Mineralised bone green in severe cases
Up to 100% covered by unmineralised osteoid

42
Q

What must osteoid thickness be greater than

A

14um

43
Q

3 treatments for osteomalacia

A

Vit D supplements
Dietary- calcium
Sun or UV

44
Q

What foods may be recommended to increase calcium

A

Milk, bread, beans, pulses, dried fruit, green + leafy veg

45
Q

What % of the population have Pagets disease when aged

a) >50
b) >80

A

a) 3%

b) 10%

46
Q

State the 3 phases of Pagets disease

A

1) Initially increased rate of bone resorption
2) Compensatory phase/ proliferative
3) Burnt out phase/ sclerotic

47
Q

What happens in the first phase of Pagets

A

Large number of giant osteoclasts

48
Q

What happens in the second phase of Pagets

A

Increased bone formation

Accelerated deposition in disorganised manner

49
Q

What happens in the sclerotic phase of Pagets

A

Hypercellularity may diminish
Bone is dense
Hyper-vascular bone marrow

50
Q

How does the bone appear in the final stage of Pagets

A

Prominent cement lines

Bone marrow replaced by fibrovascular CT

51
Q

Name 5 bones commonly affected by pagets

A 
Pelvis
Femur
Vertebrae
Skull 
Tibia
52
Q

Name a rare, late complication of Pagets disease

A

Osteosarcoma

53
Q

In what % of paget cases does osteosarcoma occur

A

1|%

54
Q

What is osteosarcoma

A

Among the most malignant of cancers
Usually in a long bone, near the knee
Can spread rapidly usually to lungs

55
Q

5 treatment options for Pagets disease

A 
Bisphosphonates
Calcium and vit D supplements
Pain management
Surgery
Calcitonin
56
Q

How do bisphosphonates work to treat Pagets

A

Work directly on osteoclasts to slow bone resorption

57
Q

What is the duration of bisphosphonates for pagets

A
  • oral 2-6 months

- IV single infusion to 3 infusions

58
Q

What is the other name for sclerostosis

A

Van Buchem Syndrome

59
Q

Genetic inheritence of sclerostosis

A

Autosomal recessive

60
Q

Clinical signs of sclerostosis

A

Endosteal hyperotosis
Resistant to fracture
Excessive heigh

61
Q

What is sclerostin secreted by and what does it do

A

Osteocytes

Inhibits osteoblasts and thus bone formation

62
Q

How is sclerostosis treated

A

By an antibody to sclerostini (romosozumab)

LOCO 2 (25 decks)

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