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metabolic bone disease Flashcards

1
Q

What controls the bone turnover

A

Osteoblasts

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2
Q

How do osteoblasts stimulate osteoclasts

A

Release RANK ligand which binds to the osteoclasts causing the intake of nuclei into the osteoclast and then the osteoclast divide which allows for more bone resorption

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3
Q

What stimulates osteoblasts

A

vitamin D

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4
Q

Where do we get vitamin D from

A

Sun
Oily fish and egg yolks

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5
Q

Describe the production of Vitamin D

A

UVB change 7DHC on the skin into the preform of vitamin D

the liver then changes this into 25(OH) vit D - which is the storage form

The kidney then changes the storage form into 1,25(OH)Vit D which is the active form for use

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6
Q

What Vitamin D is checked when doing tests

A

the storage vitamin D - 25(OH)vit D

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7
Q

What is the function of Vitamin D

A

Maintaining extracellular fluid calcium levels

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8
Q

What is Paget’s disease of bone

A

Increased bone resorption followed by increased bone formation which leads to a disorganised bone

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9
Q

What are the features of a bone after Paget’s disease

A

Bigger, less compact, more vascular and more susceptible to deformity and fracture

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10
Q

What genes are correlated with Paget’s disease

A

Loci of SQSTM1

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11
Q

What environmental triggers are thought to cause pagets disease

A

Chronic viral infection within osteoclasts

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12
Q

What are the symptoms of Paget’s disease

A

Over 40 years old patient presents with bone pain

Occasional deformity

Heat over the Pagetic bone due to the increased vascularity

Neurological complications - nerve deafness

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13
Q

What age is paget’s commonly in

A

Has to be over 40 at least but commonly around 60

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14
Q

What is the main way of diagnosing Paget’s disease

A

Bone scan

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15
Q

What is the common presentation of Paget’s -including bloods

A

Increased ALP

Bone pain and local heat

bone deformity or fracture

hearing loss

rare development of osteosarcoma in the affected bone

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16
Q

What is the treatment of Paget’s disease

A

IV bisphosphonate therapy - one off - first line - IV zoledronic acid

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17
Q

Should you treat someone with asymptomatic Paget’s disease

A

No unless the Paget’s is in their skull which would cause them nerve deafness

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18
Q

What causes rickets and osteomalacia

A

severe vit D or calcium deficiency

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19
Q

What is the difference between rickets and osteomalacia

A

Rickets occurs in children before the epiphyseal plates fuse while osteomalacia occurs in adults after the epiphyseal plate fuses

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20
Q

How do rickets and osteomalacia look on blood tests

A

Low calcium
raised alp
Raised PTH
very low vitamin D

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21
Q

How does rickets present

A

The fontanelles haven’t closed
Large forehead
odd shaped ribs and breast bone
odd curve to spine
Their epiphysis widen so there are more prominent parts on the bone

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22
Q

What is the treatment for Rickets and osteomalacia

A

Calcium and vitamin D supplements

23
Q

On Xray what is a common finding in osteomalacia

A

Micro - fractures

24
Q

What is osteogenesis imperfecta

A

Genetic disorder of connective tissue that is characterised by fragile bones which can fracture from mild trauma and normal daily acts

25
Q

What causes osteogenesis imperfecta

A

Defects in type one collagen

26
Q

What are the signs and symptoms of osteogenesis imperfecta

A

growth deficiency
defective tooth formation
hearing loss
blue sclera
scoliosis
barrel chest
ligamentous laxity
easily bruised

27
Q

What scoring system measures hypermobility

A

The beighton score

28
Q

What is the management of osteogenesis imperfecta

A

Surgical - to treat fractures

IV bisphosphonates to prevent the fractures

29
Q

What is osteoporosis

A

Metabolic bone disease characterised by low bone mass and micro-architectural deterioration of bone tissue which leads to bone fragility and increase in fracture risk

30
Q

What is the definition of osteoporosis on a bone density scan (DXA bone scan)

A

If you are more than 2.5 standard deviations below the young adult mean

31
Q

Why is osteoporosis in women over 50 common

A

There is an accelerated loss of bone when menopause begins

32
Q

Which gender most commonly gets osteoporosis

A

women but it is common in men

33
Q

Which age group is osteoporosis more common in

A

Older age

34
Q

How common is it to break fracture in men and women over 50

A

50% of women over 50

20% of men over 50

35
Q

What are endocrine causes of osteoporosis

A

Thyrotoxicosis - hyper thyroidism
hyper and hypoparathyroidism
cushings
hyperprolactinaemia
hypopituitarism
early menopause

36
Q

What are the rheumatic causes of osteoporosis

A

Inflammatory conditions:
Rheumatoid arthritis
ankylosing spondylitis
polymyalgia rheumatica

37
Q

What are GI causes of osteoporosis

A

UC and crohns

Liver disease - Primary biliary cirrhosis, chronic alcoholic hepatitis, alcoholic cirrhosis and viral cirrhosis (HEP C)

Malabsorption - chronic pancreatitis , coeliac disease, whipples, short gut and ischaemic bowel

38
Q

What medications cause osteoporosis

A

Steroids
PPI
Enzyme inducing anti epileptic medications
Aromatase
GnRH inhibitors
Warfarin

39
Q

What is the management of osteoporosis

A

Minimise risk factors of fractures

Ensure good intake of calcium and vitamin D

medications

40
Q

What medications are given in osteoporosis

A

Bisphosphonates are first line

Antiresorptive therapy - prevent breakdown of bone - HRT - hormone replacement therapy , SERMs - selective oestrogen receptor modulators , Biphosphonates and denosumab

Anabolic therapies - teriparatide - PTH analogue and romosuzumab - antiscerostin agent

41
Q

What are the side effects of HRT

A

Increased risk of blood clots

Increased risk of breast cancer if used into late 50s

Increased risk of heart disease and stroke if used after long time after menopause (more than 3 years usually)

42
Q

What are the negative effects of SERMs - selective oestrogen receptor modulators

A

Hot flushes if taken too close to menopause

Increased clotting risk

Lack of protection at the hip

43
Q

What is required for biphosphonates to be prescribed

A

adequate renal function and intake of calcium and vitamin D

44
Q

What are the side effects of biphosphonates

A

Oral bisphosphonates can cause heart burn and indigestion
Iritis /Uveitis
osteonecrosis of the jaw
atypical femoral shaft fractures
Drug holidays are given in between long spells of bisphosphonate treatments

45
Q

What is denosumab

A

Monoclonal antibody against RANK ligand which reduces osteoclastic bone resorption

46
Q

How often is denosumab given

A

injection every 6 months

47
Q

What is used in patients with significant renal impairment as treatment for osteoporosis

A

denosumab - safer than biphosphonates in patients with renal impairment

48
Q

What are the side effects of denosumab

A

Allergy/rash

symptomatic hypoglycaemia if given to someone who has low Vitamin D

Osteonecrosis of the jaw

Atypical femoral shaft fractures

49
Q

What is teriparatide

A

Anabolic therapy which is a PTH analogue - reduces refracture rates

50
Q

What are the side effects of teriparatide

A

Injection site irritation

Hypercalcaemia - rare

Allergy

Very expensive

51
Q

What is romosozumab

A

Monoclonal antibody which inhibits sclerotin

It increases bone formation and decreases resorption

52
Q

How often is romosozumab given

A

Monthly injections

53
Q

What are the side effects of romosozumab

A

High risk of allergy - difficulty breathing, swelling, burning eyes, red/purple rash

Severe symptoms - heart attack, stroke, chest pain and shortness of breath

MSK (36 decks)

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