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Musculoskeletal + Rheumatology > Metabolic Bone Disease > Flashcards

Metabolic Bone Disease Flashcards

1
Q

What is osteomalacia?

A

Severe nutritional Vitamin D or calcium deficiency, causing insufficient mineralisation and ‘soft’ bones

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2
Q

What is vitamin D’s role in bone mineralisation?

A

Vitamin D stimulates the absorption of calcium and phosphate from the gut, calcium and phosphate then become available for bone mineralisation

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3
Q

What group is osteomalacia/Ricket’s most common in?

A

Children and elderly

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4
Q

When is the condition known as Rickett’s as opposed to Osteomalacia?

A

Rickets in a growing child and osteomalacia in the adult when the epiphyseal lines are closed

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5
Q

What causes osteomalacia?

A

Vitamin D deficiency

  • Malabsorption
  • Diet
  • Lack of sunlight

Chronic pancreatitis

Chronic renal failure, as unable to hydroxylate vitamin D

Liver disease

Drug induced/anti-convulsants

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6
Q

How does Ricket’s present?

A

Growth retardation

Apathy/Irritability

Hypotonia

Deformities

  • Wide joints
  • Odd shaped ribs
  • Persistent fontanelles/Large forehead
  • Oddly curved spine
  • Bow legged
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7
Q

How does osteomalacia present?

A

Bone pain/tenderness

Muscle weakness and aches

Proximal myopathy/waddling gait

Pathological fractures

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8
Q

What investigations are used in osteomalacia diagnosis?

A

Decreased serum 25-hydroxyvitamin D

Decreased Ca2+

Decreased phosphate

Increased PTH

Increased ALKP

Bone Biopsy

Xray

  • Looser zones
  • Osteopenia/radioluscent bone

DEXA scan, shows low bone mineral density

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9
Q

What are looser zones?

A

Thin band representing pseudo-fracture/fragility fractures

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10
Q

How is osteomalacia managed?

A

Vitamin D supplementation/colecalciferol

  • 50,000 IU once weekly for 6 weeks
  • 20,000 IU twice weekly for 7 weeks
  • 4000 IU daily for 10 weeks
  • Maintenance supplementary dose 800 IU or more per day should be continued for life after the initial treatment
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11
Q

What is Paget’s disease?

A

Chronic condition characterised by increased and disordered localised bone turnover

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12
Q

Describe the pathophysiology of Paget’s

A

Increased bone resorption (bone break down) followed by increased bone formation

Leads to structurally disorganised weaker bone

  • Bigger
  • Less compact
  • More vascular
  • More susceptible to deformity and fracture
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13
Q

What sex is more likely to be affected by Paget’s?

A

M>F

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14
Q

What age group is more likely to be affected by Paget’s?

A

>70s

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15
Q

Give risk factors for Paget’s

A

FH

Male

>Age

Northern latitude

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16
Q

How does Paget’s present?

A

Asymptomatic in 70% of cases, so most common finding is elevated ALKP

Bone deformity or fracture

  • Large skull and bowing of legs

Excessive heat

Deep boring bone pain or due to impingement on nerves

Neurological complications

  • Hearing loss due to compression of vestibulocochlear nerve

Rare development of osteosarcoma in affected bone

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17
Q

Which bones are most commonly affected by Paget’s?

A

Pelvis

Lumbar spine

Femur/long bones of the extremities

Skull

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18
Q

What investigations are used in diagnosis of Paget’s?

A

Isolated elevated ALKP

  • Marker of osteoblastic activity

Normal Ca+ and Phosphate (PO4)

Xray

Bone biopsy, to exclude other conditions

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19
Q

What Paget’s signs are seen on X-Ray?

A

Thickened bone/dense areas

Lytic lesions/destruction of area of bone

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20
Q

How is Paget’s managed?

A

If asymptomatic, do not treat unless in skull or area requiring surgical intervention

Analgesia if pain

IV Bisphosphonate therapy, slows down bone lysis so move on to this if analgesia is not sufficient

One off IV zoledronic acid

Surgery

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21
Q

What surgical methods can be used in Paget’s management?

A

Correct bone deformities

Decompress impinged nerve

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22
Q

Give complications of Paget’s

A

Osteoarthritis if developing at a joint

Osteosarcoma

High output cardiac failure

Hypercalcaemia

Secondary immobility

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23
Q

What is Osteogenesis Imperfecta?

A

Genetic disorder of absent/defective type 1 collagen characterised by fragile bones and fractures

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24
Q

How many types of OI are there?

A

28

25
Q

Describe type 1 osteogenesis imperfecta

A

Milder form, when child starts to walk and can present in adults

26
Q

Describe type 2 OI

A

Lethal by age 1

27
Q

Describe type 3 OI

A

Progressive deforming with severe bone dysplasia and poor growth

28
Q

Describe type 4 OI

A

Similar to type 1 but more severe

29
Q

How does OI present?

A

Easy fracture, Main symptom

Growth deficiency

Defective tooth formation/Dentigenesis imperfecta

Hearing loss

Blue sclera

  • Vitreous humour is blue, sclera is see through

Scoliosis

Barrel chest

Ligamentous laxity

  • Chronic body pain due to loose ligaments resulting in hyper-flexibility

Easy bruising

Normal Ca, PTH, PO4, ALP

30
Q

What score assesses the degree of ligamentous laxity?

A

The Beighton Score

31
Q

How is OI managed?

A

Surgical, treats fractures

IV Bisphosphonates, to prevent fracture

Social and educational adaptations

Genetic counselling for parents and next generation

32
Q

What is osteoporosis?

A

Metabolic bone disease characterised by reduction in bone density leading to enhanced fragility and a consequent increase in fracture risk

33
Q

Describe the pathophysiology of osteoporosis

A

Breakdown of bone > Formation of bone = Porous bones (decreased bone density)

34
Q

What is the function of osteoclasts?

A

Break down/reabsorb bone

35
Q

What is the function of osteoblasts?

A

Produce new bone

36
Q

What is the function of Ca2+ and phosphate?

A

Used to build bone

37
Q

What is the function of PTH?

A

Tells body to break down bone to produce Ca2+ and phosphate

38
Q

What is the function of vitamin D?

A

Absorbs Ca2+ from gut, more Ca2+ to build bone

39
Q

What is the function of calcitonin?

A

Tells body to stop breaking down bone

40
Q

Give risk factors for osteoporosis

A

Post-menopausal women

Reduced mobility and activity

Low BMI

RA

Alcohol and smoking

Medications

  • Corticosteroids
  • SSRIs
  • PPIs
  • Anti-epileptics
  • Anti-oestrogens
41
Q

Give causes of non primary osteoporosis

A

Endocrine

  • Thyrotoxicosis
  • Hyper and hypoparathyroidism
  • Cushings
  • Hyperprolactinaemia
  • Hypopotituraism

Rheumatology

  • Rheumatoid arthritis
  • Ankylosing spondylitis
  • Polymyalgia rheumatica

GI

  • IBD
  • PBC
  • Hepatitis
  • Cirrhosis
  • Chronic pancreatitis
  • Coeliac
  • Malabsorption
42
Q

How does osteoporosis present?

A

Asymptomatic

Pathological fractures

43
Q

What investigations are used in osteoporosis diagnosis?

A

Normal Ca, ALKP, PO4 and PTH

FRAX tool to assess fracture risk over next 10 years

DEXA Bone Scanning, compares individual’s bone density to a healthy adult

X-ray spine, first line for suspected osteoporotic vertebral fracture

  • De-mineralisation
44
Q

What factors does FRAX take into account?

A

Age

Gender, higher in women

Bone Mineral Density, higher in low BMD

Glucocorticoid use

FH

Previous Fracture

Smoking

RA

Country specific

45
Q

When is a patient referred for a DEXA scan?

A

Referral for DEXA bone scanning based on FRAX score of >10% fracture risk at any site over next 10 years

46
Q

What does DEXA give?

A

T score

47
Q

What is a normal T score?

A

>-1

48
Q

What T score is suggestive of osteopenia?

A

-1.5 to -2.5

49
Q

What T score is diagnostic of osteoporosis?

A

<-2.5

50
Q

What lifestyle measures are used in osteoporosis management?

A

Activity and exercise

Maintain a healthy weight

Adequate calcium intake

Adequate vitamin D

Avoiding falls

Stop smoking

Reduce alcohol consumption

51
Q

What are the most commonly affected vertebrae in osteoporosis?

A

T7-T8 and T12-L1

52
Q

What is the management of osteoporosis?

A

Biphosphonates

HRT

Risedronate

Denosumab/monoclonal antibody, use if unable to tolerate biphosphonates

Raloxifene/SERM

53
Q

What are the requirements for bisphosphonates?

A

Adequate renal function required

Adequate calcium and vitamin D status required

Good dental health and hygiene advised

If over 75 and fragility fracture or long term steroid use, initiate without DEXA scan results

54
Q

What is the mode of action of bisphosphonates?

A

Inhibits osteoclasts

55
Q

Give examples of bisphosphonates

A

Alendronate

Risedronate

Etidronate

56
Q

Give side effects of bisphosphonates

A

GORD/GI upset, switch to risedronate

Atypical stress fractures of femoral shaft

Osteonecrosis of the jaw

Hypocalcaemia

Requires drug holiday 1-2 years after 10 years on oral bisphosphonates

57
Q

What is the follow up management of osteoporosis?

A

Low-risk patients not being put on treatment should be given lifestyle advice and followed up within 5 years for a repeat assessment

Patients on bisphosphonates should have a repeat FRAX and DEXA scan after 3-5 years

Treatment holiday should be considered if their BMD has improved and they have not suffered any fragility fractures. This involves a break from treatment of 18 months to 3 years before repeating the assessment.

58
Q

How should biphosphonates be given?

A

Take at least 30 minutes before breakfast with water and sit upright for 30 minutes following

Musculoskeletal + Rheumatology (16 decks)

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