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Year 2- ENDO mine > Endrocrine and metabolic bone disorders > Flashcards

Endrocrine and metabolic bone disorders Flashcards

1
Q

what 2 components make up bone?

A

It is composed of 2 components – the inorganic component formed predominantly by hydroxyapatite crystals and the organic osteoid formed predominantly from type 1 collagen fibres

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2
Q

what is the purpose of bone?

A

As well as providing a skeleton, bone is a reservoir for calcium and phosphorus

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3
Q

what do osteoblasts do?

A

synthesise osteoid and participate
in mineralisation/calcification
of osteoid

-bone formation

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4
Q

what do osteoclasts do?

A

release lysosomal enzymes
which break down bone

-bone resorption

Osteoblasts express receptors for PTH & calcitriol (1,25 (OH)2 vit D) – regulate balance between bone formation & resorption

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5
Q

how do osteoclasts become activated?

A

osteoclasts are switched on by osteoblasts

RANKL expressed on osteoblast surface

RANKL binds to RANK-R (on osteoclast) to stimulate osteoclast formation and activity

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6
Q

define the following:
Cortical :
Trabecular:
Woven bone:

A

Cortical (hard) bone
Trabecular (spongy or trabecular) bone
Both formed in a lamellar pattern = collagen fibrils laid down in alternating orientations, mechanically strong
Woven bone – disorganised collagen fibrils, weaker

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7
Q

what is the effect on bone of vit D deficiency?

what is it called in children and adults

A

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

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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8
Q

what are the three types of hyperparathyroidism and what happens in them?

A
  1. adenoma (primary hyperparathyroidism)
    - high PTH
    - high Cal
    - neg feedback does not occur, parathyroid gland does its own thing
    - normal kidney function
  2. low plasma Cal eg renal failure, vit deficiency (secondary hyperparathyroidism)
    - high PTH
    - low Cal (cannot get higher)
  3. chronic low plasma cal (tertiary hyperparathyroidism)
    - high PTH
    - high Cal
    - parathyroid glands get really big and cannot be switched off so there is no neg feedback . difference between this and the first one is that this is accompanied with chronic kidney failure
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9
Q

what condition can arise due to renal failure and bone disease?

A

vascular calcification

and osteitis fibrosa cystica

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10
Q

what is osteitis fibrosa cystica

A

see slide

Osteitis fibrosa cystica (hyperparathyroid bone disease) – rare
= XS osteoclastic bone resorption 2o to high PTH
due to decreased bone mineralisation and caused by a surplus of parathyroid hormone (PTH) from overactive parathyroid gland(s)
side note:‘Brown tumours’ = radiolucent bone lesions

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11
Q

what is the treatment for osteitis fibrosa cystica (hyperparathyroid bone disease)?

A

Hyperphosphataemia
Low phosphate diet
Phosphate binders – reduce GI phosphate absorption

Alphacalcidol – ie calcitriol analogues

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

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12
Q

what is osteoporosis?

A

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

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)

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13
Q

what does BMD do?

A

BMD predicts future fracture risk

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14
Q

how do you measure BMD?

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)

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15
Q

what are the differences between osteomalacia ad osteoporosis?

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- hence cannot be diagnosed using a blood test 
Diagnosis via DEXA scan
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16
Q

predisposing conditions for osteoporosis

A

Postmenopausal oestrogen deficiency: Oestrogen deficiency leads to a loss of bone matrix and Subsequent increased risk of fracture

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

Hypogonadism in young women and in men

Endocrine conditions: Cushing’s syndrome, Hyperthyroidism, Primary hyperparathyroidism

Iatrogenic
Prolonged use of glucocorticoids and Heparin

17
Q

treatment options for osteoporosis

A

Oestrogen/Selective Oestrogen Receptor Modulators
Bisphosphonates
Denosumab
Teriparatide

18
Q

how does oestrogen help with osteoporosis?

-what are the risks and precautions that need to be taken?

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

19
Q

how do bisphosphonates work?

A

Bind avidly to hydroxyapatite and ingested by osteoclasts – impair ability of osteoclasts to reabsorb bone
Decrease osteoclast progenitor development and recruitment
Promote osteoclast apoptosis (programmed cell death)
Net result = reduced bone turnover.

20
Q

what are the uses of bisphosponates?

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)
21
Q

what are the pharmacokinetics of bisphosphonates?

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

22
Q

what are the unwanted actions of bisphosphonates?

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

23
Q

what is 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

24
Q

what s 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
£££

25
Q

what is paget’s disease (of bone)?

A

Accelerated, localised but disorganised bone remodelling
Excessive bone resorption (osteoclastic overactivity) followed by a compensatory increase in bone formation (osteoblasts)
New bone formed = WOVEN bone
structurally disorganised
mechanically weaker than normal adult lamellar bone
BONE FRAILTY
BONE HYPERTROPHY & DEFORMITY

26
Q

what is paget’s disease characterised by histologically?

A

Characterised by abnormal, large osteoclasts – excessive in number

27
Q

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
28
Q

how is paget’s disease diagnosed?

A

Plasma [Ca2+] normal
*Plasma [alkaline phosphatase] usually increased (this is a bone enzyme)
Plain x rays = Lytic lesions (early), thickened, enlarged, deformed bones (later)
Radionuclide bone scan demonstrates extent of skeletal involvement

29
Q

suggest a treatment option for paget’s disease?

A

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

Year 2- ENDO mine (19 decks)

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