Ageing and Metabolic Bone Conditions Flashcards Preview

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Flashcards in Ageing and Metabolic Bone Conditions Deck (38)
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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

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

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

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.

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.

6
Q

From what age do we begin to lose bone mass?

A

30

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

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

9
Q

What is a normal bone mineral density?

A

> -1 SD from mean (T score)

10
Q

What values indicate osteopenia on DEXA scans?

A

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

11
Q

What values indicate osteoporosis on a DEXA scan?

A

Less than -2.5 SD from mean (T score)

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

13
Q

Which bones are most susceptible to osteoporosis?

A

Vertebral bodies, femoral neck and wrist

14
Q

How may osteoporosis be treated conservatively?

A

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

15
Q

What treatments are used in osteoporosis?

A

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

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
Q

What are the most important lab results seen to diagnose osteomalacia?

A

Low serum calcium and phosphate with a high alkaline phosphatase

26
Q

What are the dietary sources of calcium?

A

Milk, bread, beans, plies, dried fruit and green leafy vegetables

27
Q

What is Paget’s disease?

A

The excessive breakdown and formation of bone, followed by disorganized bone remodelling

28
Q

What are the three phases of Paget’s disease?

A

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
Q

Which bones are most commonly affected by Paget’s disease?

A

Pelvis, femur, skull, vertebra and tibia.

30
Q

Which cancer may occur as a result of Paget’s disease?

A

Osteosarcoma - there are giant cells and is one of the most malignant of cancers, metastasising rapidly to the lungs

31
Q

Where does osteosarcoma often metastasise to?

A

Lungs

32
Q

How is Paget’s disease treated?

A

Bisphosphonates, calcium and vitamin D supplements, pain management and surgery

33
Q

How does the ‘burnt out phase’ of Paget’s disease appear histologically?

A

There is irregular, thickened trabecular bone with prominent cement lines with bone marrow replaced by fibre-vascular connective tissue

34
Q

How do you diagnose osteosarcoma from a histological specimen?

A

Giant cells confirm the diagnosis of osteosarcoma arising out of Paget’s disease

35
Q

What is sclerotosis (Van Buchem syndrome)?

A

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
Q

What is sclerostin?

A

Compound secreted by osteocytes to inhibit osteoblasts

37
Q

What is the mode of inheritance of Van Buchem syndrome (sclerotosis)?

A

Autosomal recessive disorder

38
Q

What is the consequence of Van Buchem syndrome?

A

Endosteal hyperostosis –> fracture resistance and excessive height