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Endocrine W4 > Disorders Of Bone Health (otesoporosis) > Flashcards

Disorders Of Bone Health (otesoporosis) Flashcards

1
Q

Osteoporosis

A

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

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2
Q

Osteoporosis risk factors

A

Prevalence in the UK – osteoporosis affects
~ 2% of women at the age of 50y

~ almost 50% of women at 80 y

It is considered a “silent disease” as it is asymptomatic unless a fracture has occurred. Consider assessing high risk individuals.

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3
Q

Bone physiology

A

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

~10% of the adult skeleton is remodelled each year

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4
Q

Three cell types contribute to bone homeostasis

A

-osteoblasts

-oestoclasts

-osteocytes

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5
Q

osteoblasts

A

bone forming cells

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6
Q

Osteoclasts

A

responsible for bone breakdown/resorption

increasing age, there is increased osteocalst activity

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7
Q

Osteocytes

A

mature bone cells within the bone matrix, help to maintain bone and act as mechanosensors

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8
Q

Regulating Factors- peak bone mass (5)

A

Genetics (70-80 %)

Body Weight

Sex hormones

Diet

Exercise

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9
Q

Regulating factors- bone loss (7)

A

Sex hormone deficiency

Body weight

Genetics

Diet

Immobility

Diseases ( eg rheumatoid arthritis)

Drugs especially glucocorticoids, aromatase inhibitors

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10
Q

Osteoporosis- clinical outcomes (3)

A

Osteoporotic fractures: major cause of pain, disability, death.

~50% of hip fracture patients cannot live independently.

~20% of hip fracture patients die within a year of their fracture.

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11
Q

Osteoporosis- common fracture sites (4)

A

Neck of femur

Vertebral body

Distal radius

Humeral neck

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12
Q

Osteoporosis- Who to assess? (4)

A

Anyone >age 50 years with risk factors

Anyone under 50 years with very strong clinical risk factors eg
~Early menopause
~Glucocorticoids

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13
Q

Osteoporosis- when to refer to DXA scan?

A

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

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14
Q

Clinical Risk Factors for Fragility Fracture- non modifiable (7)

A

Age

Gender

Ethnicity

Previous fracture

Family history

Menopause ≤ 45 years

Co-existing diseases

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15
Q

Clinical Risk Factors for Fragility Fracture- modifiable (6)

A

BMD

Alcohol

Weight

Smoking

Physical inactivity

Pharmacological risk factors

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16
Q

Fracture Risk Calculators (3)

A

Allow calculation of absolute risk by incorporating additional risk factors rather than just BMD.

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

Some limitations

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17
Q

Fracture Risk Calculators (3)

A

Allow calculation of absolute risk by incorporating additional risk factors rather than just BMD.

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

Some limitations

18
Q

Osteoporosis- who to refer to DEXA scan (4)

A

Patients over 50 y with low trauma fracture – often identified through
Fracture Liaison Service (FLS) – “Stop at One”

Patients at increased risk of fracture based on risk factors
– calculated use risk assessment tool FRAX or Qfracture > 10% risk fracture over 10 years

19
Q

Bone density measurements (5)

A

Normal : BMD within 1 SD of the young adult reference mean

Osteopenia (low bone mass) :BMD >1 SD below the young adult mean but <2.5 SD below this value

Osteoporosis : BMD ≥ 2.5 SD below the young adult mean

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

If younger than 20 y, only Z score reported

20
Q

Bone density measurements (5)

A

Normal : BMD within 1 SD of the young adult reference mean

Osteopenia (low bone mass) :BMD >1 SD below the young adult mean but <2.5 SD below this value

Osteoporosis : BMD ≥ 2.5 SD below the young adult mean

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

If younger than 20 y, only Z score reported

21
Q

Assessment osteoporosis

A

History and examination

U+Es LFTs Bone biochemistry
FBC PV TSH

Consider:
Protein electrophoresis/Bence Jones proteins
Coeliac antibodies
Testosterone

25OH Vitamin D PTH

22
Q

Lifestyle advice for management of osteoporosis (5)

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

23
Q

Diet- management osteoporosis (6)

A

RNI 700mg calcium (2-3 portions from milk and dairy foods group)

Postmenopausal women aim dietary intake 1000 mg 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

24
Q

Drugs- management osteoporosis (7)

A

Calcium & vitamin D supplementation

Bisphosphonates

Denosumab

Teriparatide

Romosozumab

HRT

Testosterone

25
Q

Calcium and Vitamin D (6)

A

reduce risk of non-vertebral fractures in patients who are at risk of deficiency due to insufficient dietary intake or limited sunlight exposure.

If low exposure to sun or house-bound:
-consider at risk of Vitamin D deficiency

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

If dietary calcium is adequate, >700 mg daily

Vitamin D only may be preferred as the osteoporosis treatment adjunct

26
Q

Biphosphonates - what are they? (3)

A

analogues of pyrophosphate that adsorb onto bone within the matrix

ingested by osteoclasts leading to cell death thereby inhibiting bone resorption

Anti-resorptive agents – alendronate and risedronate

27
Q

Biphosphonates- how do they help? (4)

A

increases BMD by 5-8%

Prevent bone loss at all sites vulnerable to osteoporosis

Reduce risk of hip and spine fracture

reduce the risk of fragility fracture by ~50% in patients with post-menopausal osteoporosis

28
Q

Bisphosphonates- duration? (3)

A

Good data for benefit for 5 years (10 y if vertebral fracture)

Long-term concerns re: osteonecrosis of the jaw, atypical fractures

Consider “bone holiday” – though no robust evidence base

29
Q

Bone remodelling (5)

A

Bone undergoes a cycle of remodelling in a programmed sequence at discrete foci called bone remodelling units

1.osteoclasts appear on a previously inactive surface and begin to resorb the bone

2.Osteoclasts are then replaced by osteoblasts that fill the cavity by putting down osteoid that is mineralised to form new bone

3.After a normal bone remodelling cycle the resorption cavity is completely refilled with new bone

4.However, in osteoporosis, there is a relative or absolute increase in resorption over formation that leads to increased bone loss
__________

30
Q

Zoledronic Acid (4)

A

Once yearly IV infusion for 3 years

1 in 3 acute phase reaction with first infusion – paracetamol

~ 70% reduction in vertebral fracture, 40% reduction in hip fracture

Consider if intolerant of oral bisphosphonates or unable to comply with dosing regime

31
Q

Denosumab- mech action (2)

A

fully human monoclonal antibody that targets and binds with high affinity and specificity to RANKL (receptor activator of nuclear factor-kB ligand)

prevents activation of its receptor, RANK, inhibiting development and activity of osteoclasts, decreasing bone resorption and increasing bone density.

32
Q

Denosumab- dose + side effects (4)

A

Subcutaneous injection 6 monthly

Compared to placebo, reduces risk of vertebral fracture by ~68%, hip fracture by 40% and non-vertebral fracture by ~20%.

Adverse effects: Hypocalcaemia, eczema, cellulitis

No contraindication in severe renal impairment

33
Q

When to treat osteoporosis (2)

A

consider treatment with antiresorptive therapy when T score </= - 2.5

If ongoing steroid requirement >/=7.5mg prednisolone for 3 months or more or if there is a prevalent vertebral fracture, consider treatment with T score < -1.5 as fracture risk increased

34
Q

Paget’s disease of bone- aetiology + risk factors (4)

A

may be a viral/environmental/biomechanical trigger in genetically predisposed individual

Rare < 40 y; incidence increases with age:
> 55y: 3% of UK population
>85y: ~ 10%

35
Q

Paget’s disease of bone - bones it affects (4)

A

long bones

pelvis

lumbar spine

skull predominantly

36
Q

Paget’s disease of bone - presentation (7)

A

Presents with=
-bone pain
-deformity
-deafness
-compression neuropathies

Osteosarcoma is a rare complication

incidental finding on
- X-ray (XR)
-isolated high alkaline phosphatase

37
Q

Paget’s disease of bone- diagnosis (3)

A

Diagnose on XR;
-isotope bone scan shows the distribution of disease

-biochemistry shows raised alkaline phosphatase with otherwise normal LFTs

38
Q

Paget’s disease of bone
- treatment

A

Treat with bisphosphonates if pain not responding to analgesia

39
Q

Osteogenesis Imperfecta (3)

A

Rare group of genetic disorders mainly affecting bone

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

Most are autosomal dominant inheritance

At least 8 types, of varying severity
Type 1: mild
Type 2: neonatal (lethal)
Types 3 and 4: very severe

40
Q

Osteogenesis Imperfecta- presentation (5)

A

May be associated=
-blue sclerae
-dentinogenesis imperfecta

more severe forms present with fractures in childhood

mild form may not present until adulthood

Important differential diagnosis for suspected non-accidental injury

41
Q

Osteogenesis Imperfecta- treatment (4)

A

There is no cure only =
-fracture fixation

-surgery to correct deformities

-bisphosphonates

42
Q
A

Endocrine W4 (11 decks)

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