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Y2 Endocrinology > Endocrine and metabolic bone disorders > Flashcards

Endocrine and metabolic bone disorders Flashcards

1
Q

What proportion of the body’s calcium is stored in the bone

A

> 95%

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2
Q

What components is bone made of

A 
Organic compound (35%) - osteoid, unmineralised bone 
Type 1 collagen - 95%

Inorganic compound (65%) -Calcium hydroxyapatite crystals fill the space between collagen fibrils

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3
Q

Which cells are found in the bone

A

Osteoblasts - synthesise osteoid and participate in mineralisation/calcification of osteoid (bone formation)

Osteoclasts - release lysosomal enzymes which break down bone (resorption)

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4
Q

What is bone remodelling

A

Osteoblasts -> osteoblasts

Dynamic process

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5
Q

Describe the process of osteoclast differentiation

A
  1. RANKL expressed on osteoblast surface
  2. RANKL binds to RANK-R to situlate osteoclast formation and activity
  3. Osteoblasts express PTH and calcitriol receptors to regulate between formation and resorption
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6
Q

What are the types of bone

A

Cortical - hard

Trabecular - spongy or trabecular

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7
Q

In which pattern is cortical and trabecular formed

A

Lamellar pattern - collagen fibrils laid down in alternating orientations
Mechanically strong

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8
Q

Describe woven bone

A

Disorganised collagen fibrils

Weaker

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9
Q

What are the effects of vit D deficiency on bone

A

Inadequate mineralisation of newly formed bone matrix (osteoid)
Normal stresses on abnormal bone cause insufficiency fractures - Looser zones
Waddling gait - typical

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10
Q

What are the effects of vit D deficiency on bone in children

A

Rickets
affects cartilage of epiphysial growth plates and bone
skeletal abnormalities and pain, growth retardation, increased fracture risk

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11
Q

What are the effects of vit D deficiency on bone in adults

A

Osteomalacia
after epiphyseal closure, affects bone
skeletal pain, increased fracture risk, prox myopathy

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12
Q

What could cause the types of hyperparathyroidism

A

Primary - Adenoma

Secondary - Renal failure, vit D deficiency (low Ca)

Tertiary - autonomous parathyroids (chronic low plasma Ca)

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13
Q

Draw a diagram to show how renal failure can cause bone disease

A
  1. Reduce phosphate excretion leads to greater plasma levels -> Vascular calcification
  2. Reduced calcitriol and Ca absorption
  3. Hypocalcaemia
  4. Increased PTH and reduced bone mineralisation
  5. Bone resorption increase from PTH
  6. osteitis fibrosa cystica
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14
Q

Describe osteitis fibrosa cystica

A

Hyperparathyroid bone disease
Rare
XS osteoclastic bone resorption secondary to high PTH
Characteristic = brown tumours

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15
Q

What is treatment for osteitis fibrosa cystica

A

Hyperphosphataemia
Low phosphate diet
Phosphate binders – reduce GI phosphate absorption

Alphacalcidol – ie calcitriol analogues

Parathyroidectomy in 3 hyperparathyroidism
Indicated for hypercalcaemia or hyperparathyroid bone disease

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16
Q

Describe osteoporosis

A

Loss of bony trabeculae, reduced bone mass, weaker bone predisposed to fracture after minimal trauma

17
Q

What is the significance of BMD in osteoporosis

A

Bone mineral density (BMD) > 2.5 standard deviations below the average value for young healthy adults (T-score < -2.5)
BMD predicts future fracture risk

18
Q

How is BMD measured

A

Dual Energy X-ray Absorptiometry (DEXA) - femoral neck and lumbar spine
Mineral (calcium) content of bone measured, the more mineral, the greater the bone density (bone mass)

19
Q

Compare osteoporosis to osteomalacia

A

Both predispose to fracture

OSTEOMALACIA
Vitamin D deficiency (adults) causing inadequately mineralised bone
Serum biochemistry abnormal (low 25(OH) vit D, low/low N Ca2+, high PTH (2o hyperparathyroidism)

OSTEOPOROSIS
Bone reabsorption exceeds formation
Decreased bone MASS
Serum biochemistry normal
Diagnosis via DEXA scan
20
Q

What are the pre-disposing conditions for osteoporosis

A 
Postmenopausal oestrogen deficiency
Age-related deficiency in bone homeostasis (eg osteoblast senescence)
Hypogonadism in young women and in men
Endocrine conditions
Iatrogenic
21
Q

How does postmenopausal oestrogen deficiency lead to osteoporosis

A

Oestrogen deficiency leads to a loss of bone matrix

Subsequent increased risk of fracture

22
Q

Which endocrine disorders can lead to osteoporosis

A

Cushing’s syndrome
Hyperthyroidism
Primary hyperparathyroidism

23
Q

What are the latrogenic pre-disposing conditions for osteoporosis

A

Prolonged use of glucocorticoids

Heparin

24
Q

What are the treatment options for osteoporosis

A

Oestrogen/Selective Oestrogen Receptor Modulators
Bisphosphonates
Denosumab
Teriparatide

25
Q

What is the treatment in post-menopausal women for osteoporosis and what is required for women with an intact uterus

A

Oestrogen doses
Anti-resorptive effects on the skeleton
Prevents bone loss

Intact uterus - additional progestogen to prevent endometrial hyperplasia/cancer

26
Q

Why is oestrogen use limited

A

Increased risk of breast cancer

Venous thromboembolism

27
Q

What is the mechanism of action for bisphosphonates

A

Binds avidly to hydroxyapatite and ingested by osteoclasts - impairs ability of osteoclasts to reabsorb bone
Decrease osteoclast progenitor development and recruitment
Promote osteoclast apoptosis
Net result = reduced bone turnover.

28
Q

What are the uses of bisphosphonates

A

Osteoporosis – first line treatment

Malignancy - Associated hypercalcaemia, reduce bone pain from metastases

Paget’s disease – reduce bony pain

Severe hypercalcaemic emergency – i.v. initially (+++ re-hydration first)

29
Q

Describe the pharmacokinetics of bisphosphonates

A

Orally active but poorly absorbed - take on an empty stomach

Accumulates at site of bone mineralisation and remains part of bone until it is resorbed - months, years

30
Q

What are the unwanted actions of bisphosphoantes

A

Oesophagitis - may require switch from oral to iv preparation

Osteonecrosis of the jaw - greatest risk in cancer patients receiving iv bisphosphonates

Atypical fractures - may reflect over-suppression of bone remodelling in prolonged bisphosphonate use

31
Q

Describe denosumab

A

Human monoclonal antibody
Binds RANKL, inhibiting osteoclast formation and activity
Hence inhibits osteoclast-mediated bone resorption
SC injection 6/12ly
2nd line to bisphosphonates

32
Q

Describe teriparatide

A

Recombinant PTH fragment - amino-terminal 34 amino acids of native PTH
Increases bone formation and bone resorption, but formation outweighs resorption
3rd line treatment for osteoporosis
Daily s.c. injection
Expensive

33
Q

What is Paget’s disease

A

Accelerated, localised but disorganised bone remodelling
Excessive bone resorption (osteoclastic overactivity) followed by a compensatory increase in bone formation (osteoblasts)
New bone = woven which is disorganised and weaker
Leads to bone hypertrophy, deformity and frailty
Characterised by abnormal, large osteoclasts

34
Q

Describe the epidemics of Paget’s disease

A 
Often family history positive 
Viral origin 
Highest in UK, N. America, Australia and NZ
Lowest in Asian and Scandinavia 
Disease not apparent under 50
Asymptomatic
35
Q

What are the clinical features of Paget’s disease

A 
Skull, thoracolumbar spine, pelvis, femur and tibia most commonly affected
Arthritis
Fracture
Pain
Bone deformity
Increased vascularity  (warmth over affected bone) 
Deafness – cochlear involvement
Radiculopathy – due to nerve compression
36
Q

How is Paget’s disease diagnosed

A

Normal plasma Ca
Plasma alkaline phosphatase increased
Plain X-rays = lytic lesions (early) -> thickened enlarged deformed bones
Radionucleotide bone scan demonstrates extend of skeletal movement

37
Q

What are the treatment options of Paget’s disease

A

Bisphosphonates – very helpful for reducing bony pain and disease activity

Simple analgesia

Y2 Endocrinology (19 decks)

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