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Year 2- Anatomy > Metabolic Bone Disease > Flashcards

Metabolic Bone Disease Flashcards

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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
What is the difference between rickets and osteomalacia?
Rickets- occurs before growth plates fuse Osteomalacia- occurs after growth plates fuse
26
As well as bone, what is affected by low vitamin D?
Muscle function
27
Bloods tests in rickets and osteomalacia?
Low calcium Raised ALP Raised PTH- trying to get calcium out of bone Very low vitamin D
28
Abnormalities seen in a patient with rickets?
Fontanelles do not close Lumps on rib cage Barrel chest Wide joints at wrist and elbow
29
Treatment for rickets?
Calcium and vitamin D supplements -Ricket's is very rare in the UK and can be a sign of severe child abuse
30
Who tends to get osteomalacia?
Elderly Living in care home with little sun Middle aged Asian women, more likely to stay at home or cover their skin
31
Symptoms of osetomalacia?
Bone pain Muscle aches
32
What is commonest genetic disorder affecting bone?
Osteogenesis Imperfecta
33
Osteogenesis Imperfecta?
Genetic disorder of CT characterised by fragile bones from mild trauma or even acts of daily life e.g. picking up school bag
34
Signs and symptoms of Osteogenesis Imperfecta?
Growth deficiency Defective tooth formation Hearing loss Blue sclera Scoliosis Barrel chest Ligamentous laxity Easy bruising
35
When is the only other time you might see blue sclera?
Marfans' syndrome
36
Describe the management of osteogenesis imperfecta.
Surgical- to treat fractures Medical- to prevent fracture e.g. IV bisphoshonates Social- eduction adaptations Genetic- genetic counselling for parents and next generation
37
What is osteoporosis?
Metabolic bone disease characterised by low bone mass
38
What does osteoporosis increase risks of?
Fractures
39
How can osteoporosis be diagnosed?
Bone density scans Bone biopsy- all bone features thinner
40
When do people reach peak bone mass?
Age of 25
41
In women, when is there accelerated loss of bone density?
Menopause ->this is why osteoporosis is more common in women than men
42
What is used to assess who is at risk of fractures?
FRAX assessment tool Q fracture ->used in clinical practice
43
If risks of fractures in the next ten years, what scan is done?
DXA scan ->measures level of bone mineral density
44
Who is at risk of osteoporosis?
>50yrs (women specifically) Women>men Previous fractures increase risks of another
45
Endocrine causes of osetoporisis?
Thyrotoxicosis Hyper and hypoparathyroidism Cushings Hyperprolactinaemia Hypopituitarism Early menopause
46
Rheumatic causes of osteoporosis?
Rheumatoid arthritis Ankylosing spondylitis Polymyalgia rheumatica
47
GI casuses of osteoporosis?
IBD Liver disease Malabsorption e.g. chronic pancreatitis, coeliac disease, ischaemic bowel
48
Medications which can cause osteoporosis?
Oral steroids PPI Enzyme inducing anti-epileptic meds Aromatase inhibitors- used to breast cancer GnRH inhibitors- used in prostate cancer Warfarin
49
Management of osteoporosis?
Minimise risk factors Ensure good calcium and vitamin D Fall prevention strategies Medications- previous management options more important for meds to work
50
Hehe lecturer said chocolate is a good source of calcium
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
How should you manage patients on long-term steroids to reduce risks of osteoporosis?
Early bone density scan If >65, DXA scan not necessary, just treat for osteoporosis
52
What are the two categories of bone meds?
Antiresorptive therapies- reduce bone breakdown Anabolic therapies- those that rebuild bone
53
Give some examples of antiresorptive therapies which help to reduce the breakdown of bone.
HRT SERMs Bisphophonates Denosumab
54
Give some examples of anabolic therapies which help to build bone up.
Teriparatide Romosuzumab
55
Pros and cons of HRT?
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
Side effects of SERMS?
Hot flushes Increased risk of blood clots Lack of protection at hip site
57
SERMS reduces risks of fracture rates EXCPET for?
Vertebral fratures
58
What is generally the first line osteoporosis medication after non-medical management?
Oral bisphosphonates ->reduce fracture risks without cancer risks
59
Side effects of bisphosphonates?
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
How is Denosumab taken?
Subcutaneous injection every 6 months
61
Which med can be given for osteoporosis in those with renal disease?
Denosumab
62
Side effects of denosumab?
Symptomatic hypocalcaemia if given when vitamin D depleet ONJ- osteonecrosis of jaw Atypical femoral shaft fractures
63
Teriparatide is an anabolic therapy. Pros ad cons?
Very effective- greatly reduces fracture risks Expensive so only given to severe cases
64
Side effects of Teriparatide?
Injection site irritation Hypercalcaemia- rarely
65
Romosozumab is another anabolic therapy. Pros and cons?
Monthly injection compared to daily of teriparatide Higher risk of allergy
66

Year 2- Anatomy (14 decks)

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