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LCRS Endocrinology > 13. Endocrine Bone Disorders > Flashcards

13. Endocrine Bone Disorders Flashcards

1
Q

Role and composition of bone

A

Provides a skeleton, but also acts as a resevoir for calcium and phosphate

Composed of calcium hydroxyapatide cyrstals and the organic osteoid formed from type 1 collagen

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2
Q

Osteoblast role

A

Synthesises osteoid and participates in mineralisation/ calcification of osteoid (formation)

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3
Q

Osteoclast role

A

Release lysosomal enzymes which break down bone

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4
Q

Control of osteoclast activity and formation

A

Controlled in part by osteoblasts (needed to become active)

RANKL is expressed on osteoblast surface

RANK-R expressed on the osteoclast precursor surface must bind to RANKL to allow activation.

Osteoblasts in turn express receptors for PTH and calcitriol which regulate the process.

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5
Q

Classification of bone types

A
  1. Cortical (hard bone)
  2. Trabecular (spongy)- meshwork of trabeculae
  3. Woven bone- disorganised collagen fibres, weaker

Cortical and trabecular bone is formed in a lamellar pattern- mechanically strong

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6
Q

Effects of 1,25 dihydroxycholecalciferol (calcitriol)

A

Principle effect: stimulates intestinal absorption of calcium and phosphate

Stimulates osteoclast formation (from prcursors)

Stimulates osteoblasts to produce osteoclast activity

Renal Effects - increased calcium reabsorption + decreased phosphate reabsorption via FGF23

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7
Q

How renal failure causes bone disease

A

Decreased renal function leads to a decrease in the production of calcitriol (since 1a hydroxylase is required)

Will also be a decrease in phosphate excretion so plasma phosphate increases

Decreased calcitriol production causes a decrease in calcium absorption leading to hypocalaemia:

Hypocalaemia causes increased PTH secretion: PTH will break down bone matrix leading to osteoperosis

Lack of calcium also decreases bone mineralisation

The combination leads to osteitis fibrosa cystica

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8
Q

Appearance of osteitis fibrosa cystica in x-rays

A

‘brown tumours’ radiolucent bone lesions- has a risk of fracture and is painful

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9
Q

Treatment of osteitis fibrosa cystica

A
  • Low phosphate diet ( to account for hyperphosphataemia)
  • Alphacidol- calcitriol analogues
  • Parathyroidectomy
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10
Q

Osteoperosis and BMD

A

A condition of reduced bone mass and a distortion of bone microarchitecture which predisposes to fracture after minimal trauma

BMD- Bone mineral density (2.5 standard deviations lower in osteoperosis)

BMD predicts fracture risk and is calculated using Dual X-ray Absorptiometry (DEXA) in the femoral head and lumbar spine

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11
Q

Osteoperosis vs Osteomalacia

A

Osteomalacia is caused by vitamin D deficiency causing inadequately mineralised bone- biochemistry abnormal (how you diagnose)

VS

In Osteoperosis the serum biochemistry is normal, bone reabsorption exceeds formation, diagnosied via DEXA scan

BOTH predispose fracture

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12
Q

Predisposing conditions of osteoperosis

A
  • Post-menopausal oestrogen deficiency
  • Age-related deficiency in bone homeostasis (osteoblast senescence)
  • Hypogonadism in young men and women
  • Endocrine conditions:
    • ​Cushing’s
    • Hyperthyroidism- increased bone turnover
    • Hyperparathyroidism
  • Latronergic- herparin, use of glucocorticoids
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13
Q

Osteoperosis treatment options

A
  • Oestrogen/Selective Oestrogen Receptor Modulators (see HRT lecture)
  • Bisphosphonates
  • Denusomab
  • Teriparatide
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14
Q

Action of bisphosphonates

A

Analogues of pyrophosphate

E.g alendronate, sodium etidronate

Binds to hydroxyapatite and is ingested by osteoclasts- impairs the ability of oestoclasts to resorb bones and decreases maturation, promotes apoptosis

NET RESULT= REDUCED BONE TURNOVER

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15
Q

Treatment of severe hpercalcaemic emergency

A

I.V saline used initially to REHYDRATE

Then use bisphosphates

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16
Q

How are bisphosphates taken

A
  • Orallt active but poorly absorbed
  • Must be taken on an empty stomach
  • Accumulates at the site of bone mineralisation and remains at the site until it is resorbed
  • LONG TERM EFFECTS OF ACCUMULATION UNCERTAIN
17
Q

Unwanted effects of bisphosphonates

A
  1. Oesphagitis- may require switch from oral to IV preparation
  2. Flu-like symptoms
  3. Osteonecrosis of the jaw- bone hardens and dies- risk in cancer patients
  4. Atypical fractures- over supression of bone remodelling
18
Q

Denusomab

A

A human monoclonal antibody which binds to RANKL and inhibits osteoclast formation and activity

Given subcutaneosly every 12 months as a second line treatment to bisphosphonates

19
Q

Teriparatide

A

Recombinant fraction of PTH which increases bone formation and bone resorption (formation outweighs)

Daily subcutaneous injection- very expensive- third line treatment

20
Q

Paget’s Disease characteristics

A

A very active, localised but disorganised bone metabolism- usually slowly progressive

  • Characterised by abnormal, large osteoclasts
  • Significant genetic component as well as evidence of viral origin
  • Men and women effecetd equally (though men may be more symptomatic)
  • Disease not apparent for 50-60 years
  • Get breakdown of bone and then bone being formed again in a disorganised manner- weakened
21
Q

Padget’s disease symptoms

A
  • Increased vascularity- warmth over affected bone
  • Increased osteoclast/blast activity- osteoclast followed by osteoblast so deformity then thickening of deformed bone
  • Increased fracture incidence
  • Bone pain (can get trapping of nerves)
  • Arthritis
  • Fracture
  • Deafness
22
Q

Diagnosis of Paget’s disease

A
  • Plasma Calcium = NORMAL
  • Plasma Alkaline Phosphatase (ALP) = usually HIGH- increases when there is increased bone activity

Radiology demonstrating variable features including:

  • Loss of trabecular (spongy/cancellous) bone
  • Increased density
  • Deformity

Radioisotope (Technetium) scanning can be performed to indicate the areas of involvement

23
Q

Treatment of Padget’s disease

A

Bisphosphonates- reduce bone pain and disease progression

Simple analgesia

LCRS Endocrinology (18 decks)

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