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Endo > Metabolic Bone Disease > Flashcards

Metabolic Bone Disease Flashcards

1
Q

What is the function of osteoblasts?

A

Synthesize organic components of bone

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2
Q

Mineralization is a _____ process

A

passive

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3
Q

Which cells account for 90% of bone tissue cells and are responsible for mechano-transduction in bone tissue?

A

Osteocytes

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4
Q

What is the function of osteoclasts?

A

Multi-nucleated giant cells that degrade bone matrix

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5
Q

Which type of bone (compact or trabecular) is more actively remodeled?

A

Trabecular

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6
Q

What type of remodeling is associated with each type of bone (Trabecular and Compact)

A

Trabecular: Cancellous remodeling

Compact: Cortical remodeling

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7
Q

What are the differences between cancellous and cortical remodeling?

A
  • Cancellous remodeling (Trabecular)
    • 12 BRUs/minute (25% turnover rate)
    • Higher surface to volume ratio
    • Complete remodeling takes 4-6 months
    • Osteoid laid down in discrete layers 3μm thick
    • Lamellae deposited in curved sheets that follow contour of the trabeculae
  • Cortical remodeling (Compact)
    • 3 BRUs/minute (2-3% turnover rate)
    • Accounts for 20% of turnover
    • Remodeling cycle takes 4-6 months
    • Osteoblasts plus blood vessels follow osteoclasts through hollowed out tunnel
    • Concentric lamellae laid down
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8
Q

How do PTH and 1,25(OH)D affect bone remodeling?

A

PTH and 1,25(OH)D are potent activators of osteoclast activity

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9
Q

How does the composition of bone contribute to its stability?

A

Bone is made up of a mixture of materials good at resisting tensile loads (protein) with materials good at resisting compression (mineral)

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10
Q

What is the primary protein component of the bone matrix?

A

Type I Collagen

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11
Q

What does the Mechanostat tell us about the properties of bone? How does this information contribute to our understanding of bone loss in the elderly?

A
  • Bone mass is stable within a narrow range of strain
  • Bone formation occurs in response to overloading and bone loss occurs in response to underloading

Decreased sensitivity to mechanical loading is a key mechanism by which bone is lost in older adults

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12
Q

Describe the hierarchical structure of bone from smallest components to largest

A

Collagen molecule → Collagen fibril → Collagen Fibers → Osteocyte lacuna (lamella) → Haversian canals (Osteons)

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13
Q

Why do bones have fairly high resistance to cracks?

A

The interfaces between lamellae and osteons (cement lines) can absorb/dissipate force

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14
Q

How are the functions of cortical and trabecular bone different?

A

Cortical: Fulfills mainly mechanical and protective function

Trabecular: Fulfills mainly metabolic function

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15
Q

What is the WHO definition of osteoporosis?

A
  • Compromised bone strength
  • Increased Risk of fracture
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16
Q

What is the gender preference in osteoporosis?

A

80% of cases are women - greater incidence than breast cancer

17
Q

Bone strength reflects the integration of ________ and _______

A

Bone density; Bone quality

18
Q

How are osteoporosis and BMD related?

Why is BMD necessary for osteoporosis diagnosis?

A

Low BMD density is a risk factor for fracture; A low trauma fracture partially due to low BMD is considered “established osteoporosis”

Most low trauma fractures occur in people who do not have osteoporosis

19
Q

What are differences of in vivo loading of long bones and vertebrae?

A

Long bones are slightly curved and loaded primarily by bending

Vertebrae are loaded primarily in compression and torsion

20
Q

What are some common risk factors for fracture of bone? Which is the most powerful predictor?

A
  • Past fracture (Most powerful predictor)
  • Sex (Females > Males)
  • Age
  • Glucocorticoid use (>7.5 mg/day)
  • BMD (more than 1 SD change)
21
Q

What are the differences between the FRAX and Garvan risk factor calculators?

A

FRAX: past fracture, glucocorticoids, hip function, rheumatoid arthritis, smoking, alcohol

Garvan: Past fracture (graded); Falls (graded)

22
Q

What causes the differences between men and women for risk of fracture?

A
  • Male bones grow larger than female bones
  • Women have a period of rapid bone loss peri-menopausally
  • In trabecular one, female loss tends to be patchier than males
23
Q

What is the most important differential diagnosis to osteoporosis? How is it different than osteoporosis?

A

Osteomalacia - Quantity of bone is insufficient and architecture is impaired (matrix is under-mineralized and weak)

24
Q

How is osteomalacia seen on imaging?

A
  • In normal bone, 2 sharp lines mark mineralization front (seen with tetracycline labeling)
    • Separation between the lines is a measure of how quickly new bone mineralizes
    • In osteomalacia, lines are smudged and there is increased osteoid volume (seen by staining)
25
Q

What becomes elevated in osteomalacia? Why?

A

PTH - mineral deficiency drives hyperparathyroidism

Bone isoform of alkaline phosphatase - associated with osteoblast hyperactivity

P1NP - Pro-peptide of type 1 collagen

26
Q

What two classes of drugs are used to reduce the risk of low trauma fracture? How does each work?

A
  • Antiresorptives: work by limiting initiation of new BMUs (bone modeling units)
    • Since bone formation takes longer than bone resoprtion, inhibiting rate of process allows remodeling space to be filled
  • Anabolics (Teriparatide) = synthetic PTH analog
    • When given as a daily subcutaneous injection, action on osteoblasts is greater than action on osteoclasts
27
Q

What minerals in the diet can improve risk for fracture?

A

Vitamin D, Calcium, Phosphate

28
Q

What is the difference in calcium supplements of calcium carbonate vs. calcium citrate?

A

Calcium Carbonate is 40% elemental calcium wherease Calcium Citrate is only 21% elemental calcium - this affects how much should be taken

29
Q

How does estrogen serve as a treatment for osteoporosis?

A

Selective estrogen receptor modulators (SERMS): Synthetic estrogen with altered properties to enhance therapeutic benefit

30
Q

How are bisphosphonates (Aledronate, Risedronate) useful in preventing fracture? What do new forms do that overcome the problem of poor absorption?

A

Bisphosphonates inhibit the conversion of mevalonate to farnesyl → inhibition of protein farnesylation → leads to osteoclast apoptosis

Old bisphosphonates were given orally and absorbed poorly; Newer forms are adminstered parenterally (Zoledronic acid)

31
Q

What is the function of Denosumab?

What is a side effect?

A

Denosumab serves as a decoy receptor for RANKL

  • When RANKL binds the drug, it is unable to bind the endogenous receptor (RANK) → interruption of this interaction prevents osteoclast differentiation
  • Side Effect: Atypical femoral fractures
32
Q

What is the role of vitamin D in maintenance of stable calcium levels? How is it inactivated?

A

Vitamin D facilitates calcium absorption in the intestine, renal resorption of calcium, and increases bone remodeling

Vitamin D is inactivated by 24-hydroxylation

33
Q

Describe the interaction between PTH and Vitamin D

A
  1. When CaSR senses low calcium PTH is released
  2. PTH stimulates the kidney to activate vitamin D (25 → 1,25)
  3. Skeleton increases bone turnover
34
Q

What regulates phosphate excretion?

A

PTH and fibroblast growth factor 23 (FGF23)

35
Q

How does FGF23 reduce vitamin D?

A

FGF23 inhibits expression of 1-hydroxylase which reduces vitamin D activation

FGF23 increases activity of 24-hydroxylase (increases vitamin D clearance)

36
Q

How does FGF23 reduce PTH and Phosphate?

A

FGF23 lowers phosphate through the urine

Decreasing phosphate levels in the urine leads to decreased PTH secretion

37
Q

How is FGF23 associated with hypophosphatemic disorders? What are different ways this can occur?

A

Hypophosphatemic disorders occur due to accumulation of FGF23

  • Tumor induced osteomalacia (tumors secrete FGF23)
  • Autosomal dominant hypophosphatemic rickets (FGF23 mutation)
  • Autosomal recessive hypophosphatemic rickets (FGF23 degredation is impaired)
  • X-linked hypophosphatemic rickets
38
Q

How can Osteomalacia lead to rickets?

A

Rickets is the consequence of osteomalacia before closure of the growth plates

39
Q

What is the mechanism of dysfunction in Paget’s disease of bone?

How does it present?

A

Unregulated bone turnover

  • Impaired biomechanical performance (woven bone)
  • Increased vascularity
  • Bone deformity (abnormal modeling and dysregulated remodeling)

Endo (18 decks)

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