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eLCRS - 엔도 > Endo 13: Endocrine + Metabolic Bone disorders > Flashcards

Endo 13: Endocrine + Metabolic Bone disorders Flashcards

1
Q

What is the function of osteoclasts?

A
  • they release lysosomal enzymes –> which breaks down bone
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2
Q

What is the function of osteoblasts?

A
  • they synthesise osteoid

- -> and allow mineralization/calcification of osteoid

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3
Q

how does osteoclast differentiation occur?

A
  • RANKL = expressed on osteoblast surface
  • RANKL binds to RANK-R
  • -> to stimulate osteoclast formation + activity
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4
Q

What are the 2 main types of bone?

A
  • cortical bone - hard
  • trabecular bone - spongy / trabecular

note: both formed in a LAMELLAR pattern.

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5
Q

What is meant by a lamellar pattern?

A
  • collagen fibrils = laid in alternating orientations
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6
Q

What is the effect of Vit D deficiency on bone?

A
  • normal stress on abnormal bone –> causes insufficiency fractures (looser zones)
  • causes waddling gait

Children: Rickets
Adults: Osteomalacia

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7
Q

How does renal failure cause bone disease

A
  • decrease in renal function
  • leads to DECREASE in production of calcitriol
  • -> results in decrease in phosphate excretion
  • -> SO plasma phosphate level INCREASES
  • decrease in calcitriol production –> causes decrease in Ca2+ absorption in intestines
  • -> leads to hypocalcemia
  • -> which leads to PTH release
  • PTH breaks down bone matrix to try and restore blood Ca2+ level
  • -> leads to osteoporosis
  • hypocalcemia –> leads to decrease in bone mineralization
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8
Q

a combination of increased bone resorption + decreased bone mineralization leads to :

A

a combination of increased bone resorption + decreased bone mineralization leads to :

osteitis fibrosa cystica

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9
Q

how do you get extra skeletal calcification?

A

if you have imbalance between Ca2+ and phosphate

  • some of it form the main salts
  • -> which is deposited in the extra skeletal tissue
  • -> causing extra skeletal calcification
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10
Q

How do you treat osteitis fibrosa cystica

A
  • hyperphosphatemia
  • -> low phosphate diet
  • -> phosphate binders
  • alphacalcidol (active form of Vit D)
  • parathyroidectomy in tertiary hyperparathyroidism.
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11
Q

Define osteoporosis

A

loss of bony trabecular, reduced bone mass, weaker bone predisposed to fracture after minimal trauma

bone density more than 2.5 S.d below average value for healthy adults

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12
Q

how do you measure BMD?

A
  • dual energy x ray absorptiometry (DEXA)
  • mineral Ca2+ content of bone measured:
  • -> more mineral = greater bone density
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13
Q

What is the difference between osteoporosis + osteomalacia?

A

OSTEOMALACIA:

  • VIT D deficiency causing inadequately mineralized bone
  • abnormal serum biochemistry

OSTEOPOROSIS:

  • bone resorption exceeds formation
  • decreased bone mass
  • normal serum biochemistry
  • diagnosis: via DEXA scan
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14
Q

Why is postmenopausal estrogen deficiency a pre disposing condition for osteoporosis?

A
  • oestrogen deficiency –> causes loss of bone matrix

- -> which increases risk of fracture

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15
Q

What are other pre-disposing conditions for osteoporosis?

A
  • postmenopausal oestrogen deficiency
  • age related deficiency in bone homeostasis e.g osteoblast senescence
  • hyogonadism in young women/men
  • endocrine conditions
    e. g cushing’s, hyperthyroidism, primary hyperparathyroidism
  • iatrogenic
    e. g prolonged used of glucocorticoids, heparin
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16
Q

What are some treatment methods for osteoporosis?

A
  • bisphosphonates
  • denosumab
  • teriparatide
17
Q

How does Oestrogen HRT help with osteoporosis?

A
  • oestrogen has anti-resorptive effects on skeleton
  • which prevents bone loss

But prolonged use –> increases risk of breast cancer + venous thromboembolism

18
Q

How do bisphophonates help with osteoporosis?

A

bisphophonates = analogues of pyrophosphate

  • they bind to hydroxyapatite
  • and are ingested by osteoclast
  • -> which then impairs the ability of osteoclasts to resorb bone
  • it also decreases maturation of osteoclasts from their precursors
  • and promotes osteoclast apoptosis

NET RESULT = reduced bone turnover

19
Q

What are other uses of bisphosphonates?

A

treatment for:

  • osteoporosis
  • malignancy
  • paget’s disease (reduces bony pain)
  • severe hypercalcaemic emergency (IV)
20
Q

describe pharmacokinetics of bisphophonates.

A
  • orally active but poorly absorbed
  • -> so take on empty stomach
  • accumulates at site of bone mineralization
  • -> and remains part of bone until it is resorbed
21
Q

What are some unwanted actions of bisphosphonates?

A
  • esophagitis
    (need to switch from oral to IV administration)
  • osteonecrosis of the jaw
    (esp in cancer patients)
  • atypical fractures
    (over suppression of bone remodeling in prolonged bisphosphoate use –> rest bisphosphonate use after 5 years)
22
Q

How do Denosumab work?

A
  • Denosumab = human monoclonal antibody
  • it binds to RANKL –> inhibits osteoclast formation + activity
  • hence inhibits bone resorption

note: given subcutaneously every 6months/ 12 months

23
Q

How do Teriparatide work?

A
  • they are recombinant fragments of PTH
  • consisting of 34 a.acids
  • it increases bone formation + bone resorption
  • but formation outweighs resorption

note: daily subcutaneous injection - expensive

24
Q

What is the 1st/2nd/3rd line of treatment for osteoporosis?

A

1st: Bisphosphonates
2nd: Denosumab
3rd: Teriparatide

25
Q

What is Paget’s disease?

A

Paget’s disease = acerbated/ localized but disorganized bone remodeling

  • -> results in excessive bone resorption –> followed by compensatory increase in bone formation
  • -> new (compensatory) bone formed = woven bone

woven bone = structurally disorganized
–> mechanically weaker than lamellar bone

26
Q

Why does paget’s disease cause bone frailty, hypertrophy, and deformity?

A
  • because new (compensatory) bone formed = woven bone
  • woven bone = structurally disorganized
  • -> mechanically weaker than lamellar bone
  • excessive bone resorption –> followed by compensatory increase in bone formation
27
Q

What is paget’s disease characterized by?

A
  • characterized by abnormal/ large osteoclasts

–> excessive in number

28
Q

What are clinical features of paget’s disease?

A

commonly affected: skull, thoracolumbar spine, pelvis, femur, tibia

  • arthritis
  • fracture
  • pain
  • bone deformity
  • deafness
  • increased vascularity
  • radiculopathy
29
Q

How would you diagnose paget’s disease?

A
  • Plasma [Ca2+] = normal
  • plasma [alkaline phosphatase] = increased
  • plain xray = lytic lesions (in early stage)
  • thick, enlarged/ deformed bones (in later stage)
  • radionuclide bone scan
30
Q

How would you treat Paget’s disease?

A
  • give bisphosphonates

- give simple analgesia

31
Q

Vit D deficiency treatment in patients with:

a) normal renal function
b) impaired renal function

A
  • normal renal function:
  • give 25 hydroxyvitamin D
  • abnormal renal function: (the
  • give alfacalcidol
32
Q

Vit D excess (intoxication) can lead to:

A
  • hypercalcaemia
  • hypercalciuria
  • -> due to increased intestinal absorption of calcium
33
Q

Hyperparathyroidism:

what are the 3 types of hyperparathyroidism?

A
  1. primary hyperparathyroidism
  2. Secondary Hyperparathyroidism
  3. Tertiary Hyperparathyroidism
34
Q

What the difference between osteoporosis + Osteomalacia?

A

Osteomalacia
- Vit D deficiency in adults –> causing inadequately mineralized bone
- serum biochemistry = abnormal
(low vit D, low [Ca], high PTH)

Osteoporosis 
- bone resorption exceeds formation 
- decreased bone mass 
- serum biochemistry = normal 
diagnosis via DEXA scene
35
Q

what is the effect of primary hyperparathyroidism on

a) [Ca2+] levels?
b) [PTH] levels?

what is the causes of primary hyperparathyroidism ?

A
  1. primary hyperparathyroidism
    = adenoma (no neg feedback)
    –> autonomouss PTH secretion –> increases [Ca2+]
36
Q

what is the effect of secondary hyperparathyroidism on

a) [Ca2+] levels?
b) [PTH] levels?

what is the causes of secondary hyperparathyroidism ?

A
  1. Secondary Hyperparathyroidism
    = Low Plasma [Ca] e.g renal failure, Vit D def
    –> increase in PTH –> low or almost same [Ca]
37
Q

what is the effect of tertiary hyperparathyroidism on

a) [Ca2+] levels?
b) [PTH] levels?

what is the causes of tertiary hyperparathyroidism ?

A
  1. Tertiary Hyperparathyroidism
    = Chronic low plasma [Ca]
    –> parathyroids act autonomously–> increase in PTH –> increase in [Ca]

eLCRS - 엔도 (20 decks)

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