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Hormones > Endo 14: Endocrine and metaboic bone disorders > Flashcards

Endo 14: Endocrine and metaboic bone disorders Flashcards

1
Q

Outline component of bone

A

Organic components
(osteoid – unmineralised bone)
(35% bone mass)

Inorganic mineral component
(65% bone mass)

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2
Q

Outline composition of organic and inorganic component of bone

A

Organic: Type 1 collagen fibres (95%)

Inorganic: Calcium hydroxyapatite crystals
fill the space between collagen fibrils

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3
Q

Function of osteoblast

A

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

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4
Q

Function of osteoclast

A

Osteoclasts

release lysosomal enzymes
which break down bone
bone resorption

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5
Q

How do you activate an osteoclast

A

The osteoclast must recognise RANKL expressed on osteoblast/stromal cell by its RANK receptor

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6
Q

T/f Osteoclasts contain RANKL

A

False, osteoblasts do

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7
Q

How do osteoblasts regulate balance between been formation and resorption

A

Osteoblasts express receptors for PTH & calcitriol (1,25 (OH)2 vit D) in response to which RANKL expression can be altered

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8
Q

Differentiate type of bone

A

Cortical (hard) bone… around side

Trabecular (spongy or trabecular) bone

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9
Q

Outline formation of normal bone

A

collagen fibrils laid down in alternating orientations, mechanically strong and then mineralisation occurs

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10
Q

What is woven bone

A

Woven bone – disorganised collagen fibrils, weaker

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11
Q

Effect of vitamin D deficiency on bone… in

Children
Adults

A

Inadequate mineralisation of newly formed bone matrix (osteoid)

Children: RICKETS:

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

Adults: OSTEOMALACIA

  • after epiphyseal closure, affects bone
  • skeletal pain, increased fracture risk, prox myopathy
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12
Q

What is a looser zone and where does this occur

A

Normal stresses on abnormal bone cause insufficiency fractures…..

femur and pelvis

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13
Q

What is a symptom of vitamin D deficiency on bone

A

Waddling gait - typical

Looser zones

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14
Q

Differentiate 1o, 2o and 3o hyperparathyroidism

A

1o- lack of -ve feedback

2o- vit D defic or renal failure

3o- parathyroids revved up due to kidney failure for example (because not enough vit D) and stay revved up even after kidney failure cured

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15
Q

Effect of renal failure on bone disease

A

Can’t make calcitriol, not enough Ca2+ reabsorption, hypocalcaemia, less bone mineralisation

If kideys aren’t working, you can’t excrete phosphate, so increased phosphate (which binds calcium and reduces free calcium in blood) so hypocalcaemia, so high PTH so bone resoprtion of Ca2+ (active osteoclasts).

These 2 combined= OSTEITIS FIBROSA CYSTICA

Increased plasma PO43- leads to VASCULAR CALCIFICATION (bad for heart)

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16
Q

What is Osteitis fibrosa cystica what is it caused by and what is seen radiologically

A

Due to hyperparathyroid bone disease

XS osteoclastic bone resorption secondary to high PTH- Peppered skull

‘Brown tumours’ = radiolucent bone lesions

17
Q

How is osteitis fibrosa cystica treated

A

Hyperphosphataemia

  • Low phosphate diet
  • Phosphate binders – reduce GI phosphate absorption

Alphacalcidol – ie calcitriol analogues

Parathyroidectomy in 3o hyperparathyroidism
-Indicated for hypercalcaemia and/or hyperparathyroid bone disease

18
Q

What is osteoporosis

A

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

19
Q

How is osteoporosis classified

A

Bone mineral density (BMD) > 2.5 standard deviations below the average value for young healthy adults (usually referred to as a T-score of -2.5 or lower)

20
Q

What does bone mineral density predict

A

Fracture risk

21
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)

22
Q

Differentiate osteomalacia and osteoporosis biochemistry

A

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
23
Q

What predisposes you to osteoporosis

A

Postmenopausal oestrogen deficiency

  • Oestrogen deficiency leads to a loss of bone matrix
  • Subsequent increased risk of fracture
24
Q

Other pre-disposig conditions for osteoporosis

A

Postmenopausal oestrogen deficiency

Age-related deficiency in bone homeostasis (men and women) due to osteoblast senescence

Hypogonadism in young women and in men

Endocrine conditions

  • Cushing’s syndrome
  • Hyperthyroidism
  • Primary hyperparathyroidism

Iatrogenic

  • Prolonged use of glucocorticoids (i.e. not for replacement, for high GC dose for immunosupression i.e. rheumatoid)
  • Heparin
25
Q

Treatment for osteoporosis

A

Oestrogen/Selective Estrogen Receptor Modulators (SERMs….. also used for contraceptive)

Bisphosphonates

Denosumab

Teriparatide

26
Q

Outline treatment of oestrogen for osteoporosis

A

Treatment of post-menopausal women with pharmacological doses of oestrogen

  • Anti-resorptive effects on the skeleton
  • Prevents bone loss

Women with an intact uterus need additional progestogen to prevent endometrial hyperplasia/cancer

Use limited largely due to concerns re:

  • Increased risk of breast cancer
  • Venous thromboembolism
27
Q

Outline treatment of osteoporosis with bisphosphonates

A

Bind avidly to hydroxyapatite and ingested by osteoclasts – impair ability of osteoclasts to resorb bone

Decrease osteoclast progenitor development and recruitment

Promote osteoclast apoptosis (programmed cell death)

Net result = reduced bone turnover.

28
Q

Use 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

Pharmacokinetics of bisphosphnates

A

Orally active but poorly absorbed; take on an empty stomach (food, especially milk, reduces drug absorption generally)

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

Oral (or IV if oesophagitis)

30
Q

Unwanted action of bisphonates

A

Oesophagitis
- may require switch from oral to iv preparation

Osteonecrosis of the jaw
- greatest risk in cancer patients receiving iv bisphosphonates to try to reduce their calcium

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

31
Q

How does denosumab work

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

What is 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
£££

33
Q

What is pagets disease of bone

A

Accelerated, localised but disorganised bone remodelling

Excessive bone resorption (osteoclastic overactivity) followed by a compensatory increase in bone formation (osteoblasts) ….

but the new bone is woven bone

34
Q

Outline woven bone in paget’s disease

A

structurally disorganised

mechanically weaker than normal adult lamellar bone

35
Q

Effects of paget’s disease on bone

A

BONE FRAILTY

BONE HYPERTROPHY & DEFORMITY (areas of resorbed bone next to areas of new, disorganised bone)

36
Q

What causes paget’s

A

Maybe genetic…..

men and women equally affected

Most asymptomatic…

characteriesed by absormal, large osteoclasts, excessive in number

37
Q

Clinical features of paget’s disease of bone

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

38
Q

Diagnosis of paget’s disease

A

Plasma [Ca2+] normal (as the bone resorption is only in certain areas)

*Plasma [alkaline phosphatase] usually increased (from bone not liver, different isoenzyme)

Plain x rays =
-Lytic lesions (early), thickened, enlarged, deformed bones (later)

Radionuclide bone scan demonstrates extent of skeletal involvement

39
Q

Treatment of paget’s

A
  • Bisphosphonates – very helpful for reducing bony pain and disease activity
  • Simple analgesia

Hormones (23 decks)

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