Metabolic Bone Disease Flashcards

1
Q

Osteoclasts?

A

Breaks down bone and leaves a pit

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2
Q

Osteoblasts

A

Come and fill the pit with new bone- remodelling

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3
Q

How often is there complete remodelling of the skeleton?

A

Every 13 years

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4
Q

What is the main external factor which stimulates bone?

A

Vitamin D

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5
Q

Sources of vitamin D?

A

Sun, oily fish and egg yolk

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6
Q

Form of vitamin D absorbed into skin?

A

7DHC

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7
Q

How does skin melanin affect vitamin D absorption?

A

The more melanin, the harder to absorb adequate vitamin D

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8
Q

What happens to 7DHC when it goes to the liver?

A

Hydrolysed into 25(OH)vit D

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9
Q

What is the storage form of vitamin D?

A

25(OH) Vit D

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10
Q

Where is vitamin D?

A

Fat and muscle of liver

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11
Q

What happens when we need to vitamin D physiologically?

A

Vitamin D hydrolysed by kidney into 1,25 (OH)2 Vit D (active form)

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12
Q

Function of calcium?

A

Maintain extracellular calcium within tight limits

->allows for heart to pump and nerves to conduct

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13
Q

How are phosphate and
calcium absorbed with the help of vitamin D?

A

If enough in the diet, absorbed from the gut.
If not enough, calcium and phosphate are absorbed from the bone

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14
Q

Which hormone helps to get calcium from bone?

A

Parathyroid hormone

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15
Q

Paget’s disease?

A

Increased bone resorption followed by increased bone formation

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16
Q

What result does Paget’s disease have on bone?

A

Disorganised bone; bigger, less compact, more vascular and more susceptible to deformity and fracture

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17
Q

Predisposition to Paget’s disease?

A

Strong genetic component but with an environmental trigger e.g. possible chronic viral infection

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18
Q

Paget’s disease only occurs over the age of?

A

40

->will not be diagnosed in someone younger

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19
Q

Symptoms of Paget’s disease?

A

Bone pain
Excessive heat over Paget bone
Nerve associated deafness

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20
Q

Investigation for diagnosis?

A

Isotope bone scan

->does not usually need to go on to a bone biopsy

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21
Q

What is important to note about Paget’s disease and joints?

A

Does not cross joints

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22
Q

What will be seen in bloods in someone with Paget’s?

A

Raised ALP

->do not treat based on raised ALP along, need symptoms too unless in skull

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23
Q

Treatment of Paget’s disease?

A

Only if symptomatic or affecting skull

IV bisphophonate therapy- one off
IV zoledronic acid

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24
Q

What causes rickets and osteomalacia?

A

Severe vitamin D or calcium deficiency causing soft bone
Can be due to diet deficiency or malabsorption

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25
Q

What is the difference between rickets and osteomalacia?

A

Rickets- occurs before growth plates fuse
Osteomalacia- occurs after growth plates fuse

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26
Q

As well as bone, what is affected by low vitamin D?

A

Muscle function

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27
Q

Bloods tests in rickets and osteomalacia?

A

Low calcium
Raised ALP
Raised PTH- trying to get calcium out of bone
Very low vitamin D

28
Q

Abnormalities seen in a patient with rickets?

A

Fontanelles do not close
Lumps on rib cage
Barrel chest
Wide joints at wrist and elbow

29
Q

Treatment for rickets?

A

Calcium and vitamin D supplements

-Ricket’s is very rare in the UK and can be a sign of severe child abuse

30
Q

Who tends to get osteomalacia?

A

Elderly
Living in care home with little sun
Middle aged Asian women, more likely to stay at home or cover their skin

31
Q

Symptoms of osetomalacia?

A

Bone pain
Muscle aches

32
Q

What is commonest genetic disorder affecting bone?

A

Osteogenesis Imperfecta

33
Q

Osteogenesis Imperfecta?

A

Genetic disorder of CT characterised by fragile bones from mild trauma or even acts of daily life e.g. picking up school bag

34
Q

Signs and symptoms of Osteogenesis Imperfecta?

A

Growth deficiency
Defective tooth formation
Hearing loss
Blue sclera
Scoliosis
Barrel chest
Ligamentous laxity
Easy bruising

35
Q

When is the only other time you might see blue sclera?

A

Marfans’ syndrome

36
Q

Describe the management of osteogenesis imperfecta.

A

Surgical- to treat fractures
Medical- to prevent fracture e.g. IV bisphoshonates
Social- eduction adaptations
Genetic- genetic counselling for parents and next generation

37
Q

What is osteoporosis?

A

Metabolic bone disease characterised by low bone mass

38
Q

What does osteoporosis increase risks of?

A

Fractures

39
Q

How can osteoporosis be diagnosed?

A

Bone density scans
Bone biopsy- all bone features thinner

40
Q

When do people reach peak bone mass?

A

Age of 25

41
Q

In women, when is there accelerated loss of bone density?

A

Menopause

->this is why osteoporosis is more common in women than men

42
Q

What is used to assess who is at risk of fractures?

A

FRAX assessment tool
Q fracture

->used in clinical practice

43
Q

If risks of fractures in the next ten years, what scan is done?

A

DXA scan

->measures level of bone mineral density

44
Q

Who is at risk of osteoporosis?

A

> 50yrs (women specifically)
Women>men
Previous fractures increase risks of another

45
Q

Endocrine causes of osetoporisis?

A

Thyrotoxicosis
Hyper and hypoparathyroidism
Cushings
Hyperprolactinaemia
Hypopituitarism
Early menopause

46
Q

Rheumatic causes of osteoporosis?

A

Rheumatoid arthritis
Ankylosing spondylitis
Polymyalgia rheumatica

47
Q

GI casuses of osteoporosis?

A

IBD
Liver disease
Malabsorption e.g. chronic pancreatitis, coeliac disease, ischaemic bowel

48
Q

Medications which can cause osteoporosis?

A

Oral steroids
PPI
Enzyme inducing anti-epileptic meds
Aromatase inhibitors- used to breast cancer
GnRH inhibitors- used in prostate cancer
Warfarin

49
Q

Management of osteoporosis?

A

Minimise risk factors
Ensure good calcium and vitamin D
Fall prevention strategies
Medications- previous management options more important for meds to work

50
Q

Hehe lecturer said chocolate is a good source of calcium

A

And that you don’t need to be healthy to get good calcium intake

->and I am a women so need to reduce my risks as much as possible hehe

51
Q

How should you manage patients on long-term steroids to reduce risks of osteoporosis?

A

Early bone density scan
If >65, DXA scan not necessary, just treat for osteoporosis

52
Q

What are the two categories of bone meds?

A

Antiresorptive therapies- reduce bone breakdown
Anabolic therapies- those that rebuild bone

53
Q

Give some examples of antiresorptive therapies which help to reduce the breakdown of bone.

A

HRT
SERMs
Bisphophonates
Denosumab

54
Q

Give some examples of anabolic therapies which help to build bone up.

A

Teriparatide
Romosuzumab

55
Q

Pros and cons of HRT?

A

Reduces risks of all fractures
Increased risks of blood clots
Increased risk of breast cancer with extended use into late 50s/early 60s
Increased risks of heart disease if used after a large gap after menopause

56
Q

Side effects of SERMS?

A

Hot flushes
Increased risk of blood clots
Lack of protection at hip site

57
Q

SERMS reduces risks of fracture rates EXCPET for?

A

Vertebral fratures

58
Q

What is generally the first line osteoporosis medication after non-medical management?

A

Oral bisphosphonates

->reduce fracture risks without cancer risks

59
Q

Side effects of bisphosphonates?

A

Oesophagitis
Uveitis/iritis
Atypical femoral shaft fracture*
ONJ (osteonecrosis of jaw)*

->those on bisphosphonates need to has a break for 1-2 years after being on for ten years to reduce the risks of the tow conditions with *

60
Q

How is Denosumab taken?

A

Subcutaneous injection every 6 months

61
Q

Which med can be given for osteoporosis in those with renal disease?

A

Denosumab

62
Q

Side effects of denosumab?

A

Symptomatic hypocalcaemia if given when vitamin D depleet
ONJ- osteonecrosis of jaw
Atypical femoral shaft fractures

63
Q

Teriparatide is an anabolic therapy.
Pros ad cons?

A

Very effective- greatly reduces fracture risks
Expensive so only given to severe cases

64
Q

Side effects of Teriparatide?

A

Injection site irritation
Hypercalcaemia- rarely

65
Q

Romosozumab is another anabolic therapy.
Pros and cons?

A

Monthly injection compared to daily of teriparatide
Higher risk of allergy

66
Q
A