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MSK > Metabolic Bone Disease > Flashcards

Metabolic Bone Disease Flashcards

1
Q

What are factors which stimulate osteoclast expression of RANK ligand?

A

PTH, glucocorticoids, vitamin D, IL-11…
Osteoblast produces small molecule - RANK ligand which activates osteoclast to be multinucleated and remove bone

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2
Q

How is Vitamin D absorbed?

A

Skin as 7DHC
Then in liver 25(OH)Vit D (not active)
Then metabolised in kidney 1,25(OH)2 Vit D

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3
Q

What is Paget’s disease of bone?

A

Localised disorder of bone turnover
Increased bone resorption followed by increased bone formation
Leads to disorganised bone - bigger, less compact, more vascular and more easily deformed or fractured

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4
Q

Describe the genetic component of Paget’s disease?

A

15-30% are familial
Loci of SQSTMI
Restricted geographical distribution
Environmental trigger - possibly chronic viral infection within osteoclast

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5
Q

What are the symptoms of Paget’s disease?

A

Presents in a patient over 40 years old with bone pain
Occasionally with bone deformity
Excessive heat over the Pagetic bone or neuro complications (nerve deafness)

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6
Q

What is the presentation of Paget’s disease?

A

Isolated elevation serum alkaline phosphatase
Bone pain and local heat
Bone deformity and fracture
Hearing loss
Rare development of osteosarcoma

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7
Q

What investigations are done for Paget’s disease?

A

X-ray and isotope bone scan
Paget’s disease does not cross a joint

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8
Q

What is the treatment of Paget’s disease?

A

Don’t treat asymptomatic unless in skull or in area of surgical intervention
Do not treat on raised alkaline phosphatase alone
IV Bisphosphonate therapy - one off IV zoledronic acid

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9
Q

What is the cause of Rickets and osteomalacia?

A

Severe nutritional vitamin D or calcium deficiency causes insufficient mineralisation
Muscle function also impaired in low vitamin D
Lack of vitamin D means less absorption of calcium and phosphate from gut so less available for bone mineralisation

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10
Q

What is the difference between Rickets and Osteomalacia?

A

Rickets is before the epiphyseal plate has fused
While osteomalacia is after - adult version

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11
Q

What is the blood results of Rickets and osteomalacia?

A

Low calcium, raised alkaline phosphatase, raised PTH and very low Vitamin D

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12
Q

What is the presentation of Rickets?

A

Small, fontanelles don’t close, skull looks bigger than it should, rickety rosery (lumps on ribs), lumps on epiphysis and bent legs

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13
Q

What is the presentation of osteomalacia?

A

Waddle gait
Muscle affected
Difficulty getting out of chair
Non-specific aching of bones
Can have micro-fractures on edges of bone - looser zones

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14
Q

How is rickets and osteomalacia treated?

A

Replace calcium and vitamin D - have to give lots
Sometimes if child has bowed legs then surgical intervention

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15
Q

What is osteogenesis imperfecta?

A

Genetic disorder of connective tissue characterised by fragile bones from mild trauma and even acts of daily life
Broad clinical range

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16
Q

What is the collagen defect in osteogenesis imperfecta?

A

Defects in type 1 collagen
Twenty eight different types genetically - first 4 are most common

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17
Q

What are signs and symptoms of osteogenesis imperfecta?

A

Growth deficiency, defective teeth formation, hearing loss, blue sclera, scoliosis, barrel chest, ligamentous laxity and easy bruising
Biggest problem is easy bone fractures

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18
Q

What is the management of OI?

A

Surgical to treat fractures
Medical to prevent fractures - IV bisphosphonates
Social - education and social
Genetic - genetic counselling

19
Q

What is the definition of osteoporosis?

A

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

20
Q

How is osteoporosis diagnosed?

A

Result on DXA bone scanning <2.5
Thin bones

21
Q

How is risk of osteoporosis measured?

A

FRAX - fracture risk assessment tool
Age, sex, BMI, fracture before, smoker, steroids, RA, alcohol and secondary osteoporosis
If more than 10% then refer to bone density assessment

22
Q

What is Q fracture calculator?

A

Application for those aged 30-85, men and women
Contains variable including CV risks, falls and TCA

23
Q

What is an DEXA?

A

Dual energy X-ray absorptiometry
Pictures of spine and hip, also lateral view
Computer generates bone mass
Less radiation than CT
Calculates T score (<2.5 is osteoporosis)

24
Q

Who is at risk of osteoporosis?

A

1 in 2 women over 50 will have osteoporotic fracture
1 in 5 men over 50
50 year old women has 17% risk of hip fracture
If you suffer a vertebral fracture then more likely to have another

25
Q

What are the endocrine cause of osteoporosis?

A

Thyrotoxicosis, hyper or hypoparathyroidism, cushing’s, hyperprolactinaemia, hypopituitarism and early menopause

26
Q

What are rheumatic causes of osteoporosis?

A

RA, ankylosing spondylitis and polymyalgia rheumatica

27
Q

What are gastroenterological causes of osteoporosis?

A

Inflammatory disease - UC and chrons
Liver disease - PBC, CAH, alcoholic cirrhosis and viral cirrhosis
Malabsorption - chronic pancreatitis, coeliac, whipples disease and short gut syndromes

28
Q

What are medications which cause osteoporosis?

A

Steroids, PPI, enzyme inducting antiepileptic medications, aromatase inhibitors, GnRH inhibitors and warfarin

29
Q

How do we prevent osteoporosis fractures?

A

Minimise risk factors
Ensure good calcium and vitamin D
Falls prevention strategies
Medications

30
Q

What is the SIGN guidelines of osteoporosis treatment?

A

New emphasis on fracture risk assessment and fracture reduction
Treatment decisions after DXA scanning and individual report - if fracture score is 15% then would be at treatment threshold

31
Q

What is the steroid guidance for osteoporosis?

A

If under age of 50 and on steroids - should have DXA scan
50-65 years - start oral bisphosphonate and DXA scan
Over 65 - oral bisphosphonate

32
Q

What medications will help osteoporosis?

A

Antiresorptive therapies- HRT, SERMs, bisphosphonates and Denosumab
Anabolic therapies - Teriparatide and Romosuzumab

33
Q

What is the side effects of HRT therapy?

A

Increased risks of blood clots
Increased risk of breast cancer with extended use into late 50/60s
Increased risk of heart disease and stroke if used after large gap from menopause

34
Q

What are SERM medication?

A

Selective oestrogen receptor modulator
Reduces risk of vertebral fractures and no effect on non-vertebral fractures

35
Q

Describe bisphosphonates

A

Generally fist line of treatment
Adequate renal function requires and calcium + vitamin D status
Good dental health and hygiene advised

35
Q

What are the negative effects of SERMS?

A

Hot flushes if taken close to menopause
Increased clotting risk
Lack of protection at hip site

36
Q

What is the mechanism of action of bisphosphonates?

A

Nitrogen containing inhibit osteoclasts
Interfere with mevalonic acid pathways - cholesterol metabolism
Reduce risk of vertebral and hip fractures

37
Q

What are the side effects of bisphosphonates?

A

Oesophagitis
Iritis/ uveitis
Atypical femoral shaft fractures - rare
Drug holiday for 1-2 years
Osteonecrosis of jaw

38
Q

Describe Denosumab

A

Monoclonal antibody against RANKL
Reduces osteoclastic bone resorption
Subcutaneous injection every 6 months
Safer in patients with significant renal impairment than bisphosphonates

39
Q

What are the side effects of denosumab?

A

Allergy/ rash
Symptomatic hypocalcaemia if given when vitamin D deplete
Osteonecrosis of jaw and AFF

40
Q

What is teriparatide?

A

PTH analogue
Single daily injection - stimulates bone to make bone given for 2 years

41
Q

What are the side effects of Teriparatide?

A

Injection site irritation
Rarely hypercalcaemia
Allergy
Cost

42
Q

What is Romosozumab?

A

Humanised monoclonal antibody inhibiting sclerostin
Increases bone formation and decreases bone reabsorption
Given by monthly sc injections

43
Q

What are the side effects of Romo?

A

Allergy or serve skin reaction
If you have history of CVD then can cause heart attack or stroke

MSK (39 decks)

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