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Endocrinology > Disorders of bone growth (incl osteoporosis) > Flashcards

Disorders of bone growth (incl osteoporosis) Flashcards

1
Q

What is Osteoporosis?

A

Progressive systemic skeletal disease characterised by low bone mass and microarchitectural deterioration of bone tissue, with a consequent increase in bone fragility and susceptibility to fracture.

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2
Q

Why are the number of hip fractures in the UK on the rise?

A

Due to an increase in the elderly population.

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3
Q

Approximately how many people in the UK suffer from osteoporosis?

A

Approx. 3 million

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4
Q

What are the symptoms of osteoporosis?

A

Fractures

without fractures, osteoporosis is asymptomatic

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5
Q

What are the common fracture sites due to osteoporosis?

A

Neck of femur
Vertebral body
Distal radius
Humeral neck

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6
Q

What percentage of the human skeleton is remodeled each year?

A

About 10%

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7
Q

Bone undergoes a ______ remodeling cycle at distinct sites called ___________________.
This contributes to calcium homeostasis and also to _______ ________.

A

Bone undergoes a continual remodeling cycle at distinct sites called bone remodeling units.
This contributes to calcium homeostasis and also to skeletal repair.

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8
Q

Which cells secrete the substance of bone?

A

Osteobalsts

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9
Q

Which substance, put down by osteoblasts, is mineralised to form new bone?

A

Osteoid

unmineralised organic compound of bone

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10
Q

What, in osteoporosis, leads to increased bone loss?

A

In osteoporosis, there is a relative or absolute increase in resorption over formation that leads to increased bone loss

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11
Q

Which regulating factors cause bone loss?

A

Sex hormone deficiency

Body weight

Genetics

Diet

Immobility

Diseases

Drugs (e.g. glucocorticosteroids, aromatase inhibitors)

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12
Q

What is the major determinant of bone loss in women after menopause?

A

Oestrogen deficiency

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13
Q

Who do we target therapeutic intervention for in patients with osteoporosis?

A

Those at high risk of low impact fractures

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14
Q

Name 6 NON-MODIFIABLE clinical risk factors for fragility fractures:

A 
Age
Gender
Ethnicity
Previous fracture
Family history
Early menopause (45 or younger)

(co-existing disease is also a risk factor)

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15
Q

Name 5 MODIFIABLE clinical risk factors for fragility fractures:

A 
BMD (bone mineral density)
Alcohol
Weight
Smoking
Physical inactivity

(there are also pharmacological risk factors)

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16
Q

What does the WHO fracture risk calculator do?

A

allows calculation of absolute risk by incorporating additional risk factors rather than just BMD (bone mineral density)

prediction of 10 year fracture risk of major osteoporotic fracture or hip fracture

(has some limitations)

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17
Q

What does “FRAX” underestimate?

A

Underestimated vertebral fracture risk

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18
Q

What is the negative side of using Qfracture?

A

Does not include BMD when available

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19
Q

What does a DEXA scan measure?

A

Bone mineral density (BMD)

predicts fracture risk

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20
Q

Who do you refer for DXA?

A

Anyone with a 10 year risk assessment for any OP fracture of at least 10%

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21
Q

What is osteopenia?

A

Low bone mass

BMD >1 SD below the yound adult mean but less hen >2,5 below this value

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22
Q

What is the BMD in osteoporosis?

A

> (or equal to) 2.5 SD below the young adult mean

worse than osteopenia

23
Q

What is severe osteoporosis?

A

BMD ≥2.5 SD below the young adult mean with fragility fracture

24
Q

Which investigations would you do for someone with ostorporosis presentation?

A 
U + Es
FBC
LFTs
PV
TSH
Bone biochemistry
25
Q

Name 4 secondary causes of osteoporosis:

A

Endocrine eg hyperthyroidism, hyperparathyroidism, Cushing’s disease

Gastrointestinal eg coeliac disease, IBD, chronic liver disease, chronic pancreatitis

Respiratory eg CF, COPD

Chronic kidney disease

26
Q

What lifestyle advice for management of osteoporosis would you give?

A

High intensity strength training

Low impact weight bearing exercise (standing, one foot always on the floor)

Avoidance of excess alcohol

Avoidance of smoking

Fall prevention

Diet:
RNI 700mg calcium (2-3 portions from milk and dairy foods group)
Postmenopausal women aim dietary intake 1,000mg calcium per day to reduce fracture risk (3-4 portion calcium rich foods)
Non-dairy sources include
bread and cereals (fortified),
fish with bones, nuts,
green vegetables, beans

27
Q

Which drug treatments are available to treat osteoporosis?

A

Calcium & vitamin D supplementation

Bisphosphonate

Denosumab

Teriparatide

Strontium Ranelate

HRT

SERMS (Selective Estrogen Receptor Modulators)

Testosterone

28
Q

What does the SIGN guidelines say about taking calcium supplements and bisphosphonates?

A

Calcium supplements should not be taken within 2 hours of oral Bisphosphonates

29
Q

What are bisphosphonates and what do they do?

A

Bisphosphonates and antiresorptive agents
Prevent bone loss at all sites vulnerable to osteoporosis
Reduce risk of hip and spine fracture
Bisphosphonates and analogues of pyrophosphate that adsorb onto bone within the matrix
Bisphosphonates are ingested by osteoclasts leading to cell death thereby inhibiting bone resorption
Increases BMD

e.g. Alendronate and Risedronate

30
Q

How long is it ok to be on bisphosphonate therapy?

A

Good data for benefir for 5 years
(10 years if vertebral fracture)

Long term concerns:
Osteonecrosis of the jaw
Oesophageal Ca
Atypical fractures

31
Q

How is Zolendronic Acid administered?

A

IV infusion (once yearly for 3 years)

5mg in 100mls NaCl over 15 minutes

32
Q

What is the risk of acute phase reaction with first infusion of Zoledronic Acid?

A

1 in 3 acute phase reaction with 1st infusion –-> paracetamol

33
Q

What effect of fracture risk does Zoledronic Acid treatment have?

A

Approximately 70% reduction in vertebral fracture

40% reduction in hip fracture

34
Q

What is Denosumab and how does it work?

A 
Antibody
Binds to RANKL (high affinity)
Inhibits RANK
Inhibits osteoclast activity
Decreases bone resorption
Increases bone density
35
Q

How is Denosumab administered?

A

Subcutaneous injection 6 monthly

36
Q

What does Denosumab do?

A

Increases bone density by binding to RANKL, inhibiting RANK and therefore, inhibiting osteoclast activity, causeing increased bone density.

Reduces risk of vertebral fracture by approx. 68%
Reduces risk of hip fracture by 40%
And reduces risk of non-vertebral fracture by approx. 20%

37
Q

What is Strontium Ranelate

A

An Antoresorptive agent

3rd line agent

(fracture risk reduction lightly less than bisphosphonate)

(contraindications:)
Contraindicated if history of thromboembolic disease, IHD, peripheral arterial disease, uncontrolled hypertension

Not recommended if there is an alternative osteoporosis treatment available

38
Q

What type of agent is strontium ranelate?

A

Antiresorptive agent

39
Q

What type of agent is Denosumab?

A

Fully Human Monoclonal Antibody

40
Q

What is Teriparatide?

A

Recombinant parathyroid hormone (1-34)

Stimulates bone growth rather than reducing bone loss – anabolic agent

41
Q

What effects do corticosteroids have one bone?

A

Direct:
Reduction of osteoblast activity and lifespan
Suppression of replication of osteoblast precursors
Reduction in calcium absorption

Indirect:
Inhibition of gonadal and adrenal steroid production

42
Q

What is the aim of osteoporosis therapy?

A

To provide sustained efficacy to reduce the long-term risk of fractures

43
Q

What is Paget’s disease of bone?

A

Abnormal osteoclastic activity followed by increased osteoblastic activity

–> Abnormal bone structure with reduced strength and increased fracture risk

may be single site - monostotic or multiple sites - polyostotic

44
Q

Paget’s disease of bone may be single site or multiple sites, what are the names for these?

A

Monostotic - single site

Polystotic - multiple sites

45
Q

Which bones are predominantly affected by Paget’s?

A

Long bones, pelvis, lumbar spine and skull.

46
Q

Does incidence of Paget’s disease of bone increase or decrease with age?

A

Increases with age

rare < 40 y

47
Q

What is the typical presentation of Paget’s?

A

Presents with bone pain, deformity, deafness or compression neuropathies

(osteosarcoma - rare complicaion)

(may be incidental finding on XR or isolated raised alkaline phosphate)

48
Q

What would test results likely show in patient with Paget’s?

A

Diagnose on XR
Isotope bone scan shows distribution
Raised alkaline phosphotase with NORMAL LFTs

49
Q

How is Paget’s treated if pain not responding to analgesia

A

Treat with bisphosphonates if pain not responding to analgesia

50
Q

What is Osteogenesis Imperfecta?

A

Rare group of genetic disorders mainly affecting bone

(most secondary to mutations of type 1 collagen genes (COL1A1, COL1A2))

(most autosomal dominant inheritance)

51
Q 
There are at least 8 types of Osteogenesis Imperfecta, of varying severity. Which types are:
Mild (1)
Very severe (2)
Neonatal lethal (1)
A

Mild – type 1

Very severe - types III and IV

Neonatal lethal – type II

52
Q

What other presentations may osteogenesis imperfecta be associated with?

A

Blue sclerae

Dentinogenesis Imperfecta

53
Q

Is there a cure for Osteogenesis Imperfecta?

A

No

fracture fixation, surgery to correct deformities, bisphosphonates

54
Q

When does Osteogenesis Imperfecta present?

A

More severe forms - present with fractures in childhood

Mild forms - may not present til adult life

Endocrinology (10 decks)

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