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*MSK-Rheum > Metabolic bone disease > Flashcards

Metabolic bone disease Flashcards

1
Q

What is osteoporosis?

A

Loss of:

  • bone density,
  • micro-architectural deterioration of bone tissue

with consequent increase in

  1. bone fragility
  2. & fracture susceptibility
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2
Q

What is Type 1 osteoporosis and its characteristics?

A

T1 = post menopausal

  1. decreased oestrogen & trabecular bone
  2. increased bone loss
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3
Q

What is type 2 osteoporosis and its characteristics?

A

T2 = senile

  • happens in M & F >70y/o
  1. nutrition and decrease Phys activity
  2. decreased cortical and trabecular bone
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4
Q

What are the causes of osteoporosis?

A

Causes:

Idiopathic (estrogen decline, ageing, etc)

Secondary Osteoporosis 

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5
Q

What are the causes of secondary osteoporosis?

A
  1. Malabsorption Disorders 
  2. Medications
  3. Rheumatology
  4. Organ - kidney (e.g. vit d and ca affect) and liver disease
  5. Endocrinology
  6. (blood/lymph) Malignancy: myeloma, lymphoma, leukemia  –> e.g. would affect bone
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6
Q

What medications cause osteoporosis?

A

Medications:

  • steroids,
  • phenytoin,
  • aromatase inhib,

NB: steroids, LT anticonvulsant and menopause (e.g. dc oestrogen) are all RF for osteoporosis

  • androgen deprivation 
  • heparin,

(NB; antacids are also an RF)

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7
Q

What are the rheum causes of osteoporosis?

A

Rheumatology:

  • RA,
    • is also a RF for osteoporosis
  • SLE,
  • ankylosing spondylitis 
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8
Q

What are the endocrine causes of 2ndry osteoporosis?

A

Endocrinology:

  • hyperparathyroidism,
  • hyperthyroidism,
    • NB: thyroid disese and replacement and liver disease are osteoporosis risk factors
  • premature menopause,
  • DM,
  • Cushing’s syndrome 
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9
Q

What are RF for osteoporosis?

A

Risk factors:

  • family history,
  • spinal cord injury,
  • poor lifestyle/physical activity/nutrition,
  • smoking & alcohol,

Also: thyroid replacement, thyroid/liver disease, corticosteroid use, antacids, LT anti-convulsant use, menopause, RA,

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10
Q

What bloods are checked in osteoporosis?

A

Bone bloods all normal

  • FBC, TFTs, U&Es, vit D, bone profile inc. calcium

NB: exclude MM with blood & urine electrophoresis

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11
Q

What tool score is used in osteoporisis and what are the subssequent management steps?

A

FRAX tool score

  • Low FRAX score = lifestyle changes + supplements  & follow up in 5 years
  • Medium FRAX Score = DEXA SCAN
  • High FRAX/ T Score: <2.5 / Fragility Fracture = pharmacological management 
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12
Q

What can be seen on XR?

A

XRay of acute #s

mean >30% bone loss

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13
Q

When is a DEXA scan indicated?

A

DEXA scan -

  • if low impact fracture,
  • X-ray findings,
  • steroid Rx,
  • early menopause,
  • FHx
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14
Q

What is a T-score?

A

T score –

SD the bone density is above or below the young normal mean bone mineral density from population of 20-30 years old Caucasian women (race and sex)

> -1.0 is normal

-1.0–> -2.5 = osteopenia

<-2.5 is osteoporosis

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15
Q

What is a Z score?

A

Z score – SD the measurement is above or below the age matched mineral bone density

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16
Q

What is the conservative management of OPorosis?

A
  • lifestyle,
  • weight bearing exercise,
  • avoid smoking & alcohol
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17
Q

What is the medical management of OPorosis?

A
  • oestrogen replacement,
  • Ca & vit D replacement
  • Anti-resorptive e.g. dc OC number and function
  • anabolic (increase OB)
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18
Q

What is the surgical management of OPorosis?

A

Surgical:

  • vertebroplasty,
  • kyphoplasty
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19
Q

What type of drugs are:

  • bisphosphonates?
  • RANKL inhibitors?
  • SERM?
A

They are all anti-resorptive drugs

they reduce OC number and function

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20
Q

What drugs are anti-resorptive e.g. reduce OC number and function?

A

Bisphosphonates e.g. alendronate

RANKL inhibitors e.g. Denosumab

SERM - selective oestrogen reuptake modulators e.g. Raloxifene

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21
Q

What type of drug is synthetic PTH and new coming soon denosumab?

A

An anabolic drug that increases osteoblast acitvity

denosumab is a new anabolic coming soon

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22
Q

What are the anabolic drugs for Oporosis tx?

A

synthetic PTH e.g. teriparatide

Denosumab

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23
Q

What type of drug is strontium ranelate (oporosis tx)?

A

a dual action agent e.g. both anti-resorptive (dc OC) and anabolic (ic OB)

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24
Q

How does alendronate work?

A

alendronate is 1st line bisphosphonate for Oporosis as

  • it inhibits farnseyl diphosphate synthase enzyme
  • therefore it stops OC activation
    *
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25
Q

How should alendronate be taken?

A

Bisphosphonates should be taken

  • 1x weekly
  • sitting upright 30m before breakfast w/ large glass of water
    • sit uprights for ~20 mins (oesophageal problems)
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26
Q

what are the SE’s of bisphosphonates?

A

Jaw osteonecrosis

peptic ulcer disease (PUD)

in long term use

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27
Q

How does denosumab work?

A

denosumab is a RANKL inhibitor and therefore it stops osteoclasts asorbing bone (as RANKL is on OC)

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28
Q

What are the side effects of RANKL / denosumab?

A
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29
Q

What type of drug is Raloxifene?

A

Raloxifine is a SERM - a selective oestrogen reuptake modulator

it stimulates osteoblasts and inhibits OC’s

30
Q

What are the side effects of SERM/raloxifene?

A

the SE of selective oestrogen reuptake modulators =

Systemic:

  • hot flushes
  • flu like syx

Lower limb:

  • leg cramps,
  • ankle oedema,
31
Q

How does teriparatide work?

A

teriparatide is a synthetic PTH that works by stimulating OB’s to deposit bone

(While the parathyroid hormone (PTH) is classically considered to be a bone catabolic agent, when delivered intermittently at low doses PTH potently stimulates cortical and trabecular bone growth in animals humans.)

32
Q

What are the side effects of teriparatide?

A

the SE of synthetic PTH =

  • dizziness
  • joint pain
  • rare = osteosarcoma
33
Q

What is osteomalacia?

A

Loss of bone mineralisation - the quality of the bone

(while osteoporosis is loss of bone densisty e.g. micoarchitectual)

34
Q

What causes osteomalacia?

A

its loss of bone mineralisation is related to

  • vitamin D deficiency –>
  • inadequate deposits of calcium & phosporus in bone matrix ==> bone softening
  • = mineralisation defect
35
Q

what are the changes to

  • bone amount
  • mineralisation
  • bone turnover
  • bone strength

in osteoporosis vs osteomalacia?

A
  • Bone Amount
    • is NORMAL in osteomalacia but REDUCED in osteoPOROSIS
  • Bone Mineralisation
  • is REDUCED in osteomalacia and NORMAL in osteoPOROSIS
  • Bone turnover
  • is INCREASED in BOTH
  • Bone strength
  • is REDUCED in both
36
Q

How can vitamin D deficiency occur (e.g. Vitamin D deficiency causes osteomalacia)

A

Decreased intake

Decreased absorption

Excess loss

Metabolism defect

37
Q

how do you get decreased intake of vitamin D?

A

less sunlight

less diet

38
Q

how do you get decreased absorption of vitamin D?

A

GI disease

39
Q

How do you get excess loss of vitamin D?

A

nephrotic syndrome

40
Q

what metabolism defects cause vitamin D deficiency?

A
  • hereditary rickets (hypophosphatemia)
  • CKD (e.g. vit D not activated)
  • Fanconi syndrome (kidney tubule defect)
  • Defective 25-OH
    • (liver disease/anticonvulsants, cannot activate 1st step of vit D)
  • defective 1-a
    • (renal osteodystrophy e..g in CKD)
  • type 2 resistance: bone resistance to vitamin D -
    • resistance to vitamin D action
    • increased vitamin D metabolism (anti-convulsants)
41
Q

What else can cause osteomalacia apart from vit D deficiency?

A
    • Calcium deficiency (dietary)
    • phosphate deficiency
      • in TPN
      • chronic phosphate binder therapy (used in CKD to lower serum phosphate in those with CKD to stop the phos dc Ca - e.g. CKD mineral and bone disorder)
42
Q

How does osteomalacia present?

A

’s

skeletal pain

bony tenderness

waddling gait

hypotonia

43
Q

osteomalacia presents similarly to rickets, which symptoms and similar and which differ?

A

both osteomalacia and rickets present with skeletal pain, bony tenderness and #s

osteomalacia - waddling gait, hypotonia

Rickets -

  • Poor Growth
  • Ricketic Rosary (enlarged costochondral junction on CXR), knobby deformities
  • Harrisons groove (weakened ribs pulled by the muscles ==> flaring over the diaphragm & sternum maybe pectus excavatum)
44
Q

what would Ca, Phos, VIt D and PTH levels show in osteomalacia?

A
  • Ca = Low
  • Phos = Low
  • Vit D = Low
  • PTH = HIGH
45
Q

What is the sign of rickets you would see on bone scan/x ray?

A

Epiphyseal plate widening

46
Q

What signs of osteomalacia would you would see on bone scan/x ray?

A

osteopenia (loss of bone density but not as severe as OPorosis)

Looser’s zones - psuedofractures e.g. transverse lucencies parthway through a bone usually at right angle to the involved cortex

fissures

stress #

47
Q

What is the treatment of osteomalacia?

A

Treat cause - e.g. coeliac, hypophosphataemia and vit D supplements

48
Q

How do you treat severe deficiency causing osteomalacia?

A

High dose

oral

vit D

e.g. 60,000U weekly x 5 weeks = 300,000U total

THEN do a maintenance tx of alfacalcidiol D3 2x daily

49
Q

What are the ways to replace vitamin D?

A

Alfacalcidol and calcitrol are both already in 1a-25 form

TF they are good for renal disease

ergocalciferol = 25 form

TF is good for general poeple, malabsorption and liver disease

50
Q

what is pagets disease of the bone (osteitis deformans)?

A

excessive breakdown and formation of bone; disorganised remodelling of bone

(unknown aetiology: multiple theories e.g. viral, genetic)

51
Q

what ages is pagets disease of the bone highest?

A

incidence increases with age

>50s mostly seen in >80s

52
Q

what inheritance pattern is oesitis deformans/pagets disease of the bone?

A

autosomal dominant

(SQSTM1)

53
Q

what is the bone like in pagets disease of the bone (osteitis deformans)?

A

the bone is softer

but thickened

& liable to pathological fractures

(excessive breakdown and formation of bones)

54
Q

What are the phases of osteitis deformans?

A
  • lytic e.g. OC resorption
  • mixed e.g. resorption and formation
  • sclerotic e.g. OB formation
55
Q

where are the common sites for pagets disease of the bone / osteitis deformans?

A
  • spine
  • skull
  • pelvis
  • femur
  • tibia
56
Q

what are the tibial signs of pagets disease of the bone?

A
  • progressive bowing of the legs
  • weakness and fracture
57
Q

what are the spinal signs of pagets disease of the bone?

A

kyphosis

58
Q

what are the skull signs of pagets disease of the bone?

A
  • osteoporosis circumscripta - focal lytic lesion of skull bone seen on x-ray in pts with pagets bone disease
  • characteristic frontal bossing of the skull,
    • characteristic radiological appearance of thickening on skull X-ray
  • changes in shape of maxilla and mandible –> loose teeth
59
Q

what are the general presentation signs of pagets disease of the bone / osteitis deformans?

A

mostly asymptomatic

but

  • bone pain AT REST (unusual)
  • deformity
  • OA (secondary)
  • pathological fracture (lysis around # on xray, low impact etc)
    *
60
Q

what are the neurological presentation signs of pagets disease of the bone / osteitis deformans?

A

BOTH sensorineural and confuctive deafness

–> bony deformation in ear causes damage to cranial nerves

61
Q

what are the cardiac presenting signs of pagets disease of the bone / osteitis deformans?

A

hight output cardiac failure due to increased vascularity of pagets bones

bone acts as an AV fistula

62
Q

what is leontiasis ossea (a syx in pagets disease of bone)?

A

facial bone thickening

(is rare)

NB: you do get maxilla and mandible thickening = losening of teeth

63
Q

how may paraplegia occur in pagets disease of the bone?

A

it is rare but paraplegia may happen due to vertebral involvement

64
Q

do you get hyper or hypo calcaemia assoc with pagets disease of bone?

A

hypercalcaemia

bone is thicker but softer and liable to pathological # from the excessive/disorganised bone remodelling e.g. breakdown and formation of bone

65
Q

1% of of people experience osteosarcoma transformation with pagets disease of the bone.

What are 3 signs of this occuring?

A
  1. jaw pain
  2. lytic lesion
  3. sudden high ALP
66
Q

What investigations should be done if pagets disese of the bone is suspected?

A

Bedside

  • urine sample –> high excretion of hydroxyproline (shows inc bone turnover)
  • urinalysis – exclude MM (light chains e.g. BJP/abnormal antibody)

Bloods

  • ALP = raised*
  • Ca = normal/high
  • phosphate normal

Scans

  • +ve nuclear medicine bone scan*
    • bone isotope scans show hot areas
  • XR = lytic black aread and white sclerotic
    • also on XR = bony expansion, blurred appearance, osteoporosis, fractures

Invasive

  • bone biopsy

*= shows active disease

67
Q

How do you manage active pagets disease of the bone?

A

Medical:

if the ALP is 3x normal = with a short course of bisphosphonates

  • 8 x weeks
  • high dose risedronate (not alendronate thats for oporosis)
  • OR IV zoledronate - one dose!

These often induce sustained remission = bone pain resolves and ALP = normal

Surgical:

management of #’s

68
Q

How to you manage the maintenence of pagets disease of the bone?

A
  • pain management
  • physiotherapy
  • Ca and Vit D supplements to avoid hyperPTH (e.g. prevent it kicking in and breaking down bone further)
69
Q

What is the name for the condition associated with increased bone density, there is hardening of the bones; increased sclerosis and obliteraiton of the medullary canal?

A

Osteopetrosis

a.k.a. marble bone disease

70
Q

What is the pathophysiology of osteopetrosis?

A

decreased OC function

failure of bone resorption

71
Q

How is osteopetrosis treated?

A

bone marrow transplantation

calcitriol - need to turn the hormone off (e.g.calcitriol builds bone,) by giving it

72
Q

What is the condition called where islands of deep cortical bone appear within the medullary cavity and cancellous bone of long bones?

A

osteopoikilosis – is a disorder of increased bone density+

e.g. spotted bone disease

it is asymptomatic

*MSK-Rheum (6 decks)

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