Ageing and Metabolic Bone Conditions Flashcards

(38 cards)

1
Q

How would osteoporosis appear on a blood test?

A

Normal calcium, normal phosphates, normal alkaline phosphatase, normal PTH, normal 1,25 vitamin D

ALL NORMAL VALUES

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2
Q

How would osteomalacia appear on a blood test?

A

Reduced calcium, phosphates and 1,25 dihydroxyvitamin D and increased PTH and alkaline phosphatase

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3
Q

How would Paget’s disease appear on a blood test?

A

Normal calcium, phosphates, PTH and vitamin D but VERY HIGH levels of alkaline phosphatase

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4
Q

How would renal failure appear on a blood test?

A

Reduced calcium and vitamin D with increased phosphates, alkaline phosphatase (or normal) and PTH.

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5
Q

How would primary hyperparathyroidism appear on a blood test?

A

Normal vitamin D, normal/increased alkaline phosphatase, increased PTH and calcium with decreased phosphates.

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6
Q

From what age do we begin to lose bone mass?

A

30

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7
Q

What is a T score in relation to bone mineral density?

A

A comparison against a 30 year old’s bone density matched for the same sex and ethnicity

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8
Q

What is a Z score in relation to bone mineral density?

A

A comparison against a normal individual’s bone density matched for age, sex and ethnicity

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9
Q

What is a normal bone mineral density?

A

> -1 SD from mean (T score)

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10
Q

What values indicate osteopenia on DEXA scans?

A

Between -1 to -2.5 SD from mean (T score)

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11
Q

What values indicate osteoporosis on a DEXA scan?

A

Less than -2.5 SD from mean (T score)

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12
Q

What type of bone is most susceptible to osteoporosis?

A

Trabecular bone as it has a higher turnover rate and a larger surface area

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13
Q

Which bones are most susceptible to osteoporosis?

A

Vertebral bodies, femoral neck and wrist

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14
Q

How may osteoporosis be treated conservatively?

A

With calcium and vitamin D supplements and more weight-bearing exercise

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15
Q

What treatments are used in osteoporosis?

A

HRT, SERMs (raloxifine), bisphosphonates, teriparatide and denosumab

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16
Q

How may osteoporosis be treated with HRT?

A

This is the first choice in premature menopause for women as oestrogen inhibits osteoclasts

17
Q

How may osteoporosis be treated with raloxifene?

A

This is a selective oestrogen receptor modulator which may be used to prevent osteoporosis in post-menopausal women

18
Q

How may osteoporosis be treated with bisphosphonates?

A

Directly inhibits osteoclasts by acting on enzyme in them which work to breakdown bone

19
Q

How may osteoporosis be treated with teriparitide?

A

This is a PTH analogue which works to activate osteoblasts more than osteoclasts when given in particular doses

20
Q

How may osteoporosis be treated with denosumab?

A

Monoclonal antibody which binds to RANKL to prevent it from activating osteoclast differentiation (by RANK receptor activation)

21
Q

What are the potential complications of bisphosphonate use?

A

Can lead to giant osteoclasts, osteonecrosis of the jaw and atypical fractures (subtrochanteric and femoral shaft – and old osteocytes signal for remodelling but there are fewer good osteoclasts to facilitate this)

22
Q

What is osteomalacia?

A

Where there is insufficient calcium and phosphate to mineralise new osteoid –> bones soften

23
Q

What is the most common cause of osteomalacia?

A

Vitamin D deficiency

24
Q

How does disease severity differ between osteomalacia and rickets?

A

Rickets is the form of osteomalacia that occurs in children, and therefore the epiphyseal growth plate is still open which means that more long-term deformity can result from the condition

25
What are the most important lab results seen to diagnose osteomalacia?
Low serum calcium and phosphate with a high alkaline phosphatase
26
What are the dietary sources of calcium?
Milk, bread, beans, plies, dried fruit and green leafy vegetables
27
What is Paget's disease?
The excessive breakdown and formation of bone, followed by disorganized bone remodelling
28
What are the three phases of Paget's disease?
Increased rate of bone resorption - large numbers of giant osteoclasts Compensatory phase - accelerated deposition of bone in disorganised manner (woven bone) Burnt out phase - hyper-cellularity of bone diminishes leading to Pagetic bone with hyper-vascular bone marrow
29
Which bones are most commonly affected by Paget's disease?
Pelvis, femur, skull, vertebra and tibia.
30
Which cancer may occur as a result of Paget's disease?
Osteosarcoma - there are giant cells and is one of the most malignant of cancers, metastasising rapidly to the lungs
31
Where does osteosarcoma often metastasise to?
Lungs
32
How is Paget's disease treated?
Bisphosphonates, calcium and vitamin D supplements, pain management and surgery
33
How does the 'burnt out phase' of Paget's disease appear histologically?
There is irregular, thickened trabecular bone with prominent cement lines with bone marrow replaced by fibre-vascular connective tissue
34
How do you diagnose osteosarcoma from a histological specimen?
Giant cells confirm the diagnosis of osteosarcoma arising out of Paget's disease
35
What is sclerotosis (Van Buchem syndrome)?
An autosomal recessive disorder where there is absent or reduced production of sclerostin (usually inhibits osteoblasts). Therefore results in endosteal hyperostosis --> fracture resistance and excessive height
36
What is sclerostin?
Compound secreted by osteocytes to inhibit osteoblasts
37
What is the mode of inheritance of Van Buchem syndrome (sclerotosis)?
Autosomal recessive disorder
38
What is the consequence of Van Buchem syndrome?
Endosteal hyperostosis --> fracture resistance and excessive height