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Endo > Osteoporosis, Osteomalacia and Paget's Disease > Flashcards

Osteoporosis, Osteomalacia and Paget's Disease Flashcards

1
Q

What is the main function of cortical bone?

A

Mechanical and protective function

Always on outside and surrounds trabecular bone

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2
Q

What is the main function of trabecular bone?

A

Metabolic function

~20% of bone

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3
Q

What type of bone is more actively remodeled?

A

Trabecular bone

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4
Q

What is the temporal different in bone resorption versus bone formation?

A

Bone resorption is relatively rapid (requires about 2 weeks)

Bone formation is slow, requiring 4-6 months

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5
Q

What kind of bone has a higher turnover rate?

A

Trabecular or cancellous – higher surface to volume ratio

Cortical or compact bone has a lower turnover rate, less vascularity

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6
Q

What gives bone its compressive strength? What about its tensile strength?

A

Compressive - mineral

Tensile-protein

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7
Q

What is the primary protein of bone’s extracellular matrix?

A

Type 1 collagen

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8
Q

What types of cracks are less able to propagate?

A

Transverse cracks to cement lines

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9
Q

What is the dual physiology of bone?

A

Mechanical physiology - loading and unloading

Mineral physiology - Ca balance, phosphate balance

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10
Q

What is thought to play a role in decreased bone density in older adults?

A

Decreased sensitivity to mechanical loading

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11
Q

How should we look at osteoporosis?

A

Instead of thinking of it as patients suffering from low bone mineral density (BMD), consider osteoporosis as a risk factor for fractures

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12
Q

How does WHO define osteoporosis?

A

Skeletal disorder categorized by compromised bone strength predisposing to an increased risk of fracture

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13
Q

What two main features reflect the integration of bone strength?

A 
Bone density (easily measured) 
Bone quality (not as easily measured)
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14
Q

How is osteoporosis established on a DEXA scan?

A

T-score >-2.5 in a postmenopausal women or man over 50

*but not all >-2.5 should be diagnosed with osteoporosis

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15
Q

How are long bones loaded?

A

By bending - tension on one side and compression on the other

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16
Q

How are vertebrae loaded?

A

Primarily in compression and torsion

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17
Q

What does BMD correlated with?

A

Compressive strength but doesn’t give any information about tensile strength

18
Q

What is the single most powerful predictor of future fractures?

A

Past fractures

19
Q

How does sex contribute to risk?

A

Lifetime fracture risk for women is 50%

For men it is 25-30%

20
Q

What is responsible for this differences in the sexes of fracture percentage?

A

Male bones grow larger
Female bones go through rapid bone loss peirimenopausally
Female loss in trabecular bone tens to be patchier than in males – impact on strength

21
Q

What are some other risk factors for increased hip fractures?

A

Age

Use of glucocorticoids at doses >7.5 mg

22
Q

What are the two best fracture risk calculators?

A

FRAX

Garvan

23
Q

What is another differential when thinking about osteoporosis?

A

Osteomalacia

24
Q

What leads to osteomalacia?

A

If the mineral components of bone matrix are not present in sufficient quantity then the matrix will be under mineralized and weak.

25
Q

What test shows if osteomalacia is present?

A

Dynamic histomorphometry
Use tetracycline
Normal bone – have 2 sharp lines that mark the mineralization front
Osteomalacia – have a smudge and increased ostend volume

26
Q

What are some common lab findings in osteomalacia?

A

Elevated PTH (secondary)
Elevated Alk phos
Elevated P1NP

27
Q

Is it possible for a person to have both osteomalacia and osteoporosis?

A

Yes

28
Q

Drugs that work by limiting the initiation of new bone remodeling units

A

Antiresorptives - bone formation takes longer than bone resorption, inhibiting the process of remodeling allows the remodeling space to be filled –> reduction in fracture risk and increase in BMD

29
Q

What percent of CaCO3 is elemental calcium?

A

40%

30
Q

What percent of Ca citrate is elemental calcium?

A

21%

31
Q

Estrogens and selective estrogen receptor modulators

A

Tamoxifen
Raloxifene
Prevent increased remodeling that occurs after menopause

32
Q

Bisphosphonates

A

Oral - Alendronate, Risedronate

IV - Pamidronate, Zoledronic acid

33
Q

Mechanism of bisphosphonates

A

Resemble pyrophosphate but oxygen replaced by carbon

Inhibit conversion of mevalonate to farnesyl, interfere with protein modification in osteoclasts, leading to apoptosis

34
Q

Injected decoy for RANKL
Binds to RANKL, making it unable to bind endogenous receptor RANK and interrupts RANKL-RANK signaling preventing osteoclast differentiation

A

Denosumab

35
Q

Synthetic produced fragment of PTH

When given episodically exerts an anabolic effect and increases bone mass

A

Teriparatide

36
Q

What is the storage form of vitamin D?

A

25-OH vitamin D - 25-hydroxylated in the liver

37
Q

What is the active form of vitamin D?

A

1, 25-OH vitamin D
1-hydroxylated in the kidney
Has direct effects on the intestinal epithelium to increase Ca and phosphate absorption and on bone to increase remodeling

38
Q

What are some things that may cause secondary hyperparathyroidism?

A

Nutritional deficiency
Renal disease leading to impaired vitamin D activation
GI disease leading to malabsorption
Use of medications that accelerate vitamin D clearance (anti-epileptic drugs)

39
Q

What is the role of FGF23?

A

Key regulator of phosphate homeostasis, acting as a phosphaturic hormone
Inhibits the expression of 1-hydroxylase, reducing vitamin D activation

40
Q

What are some examples of hypophosphatemic disorders?

A

Tumor induced osteomalacia
Autosomal dominant hypophosphatemic rickets
Autosomal recessive hypophosphatemic rickets
X-linked hypophosphatemic rickets
All include elevated levels of FGF23, hypophosphatemia and osteomalacia

41
Q

How does osteomalacia present during growth?

A

Rickets

42
Q

What is Paget’s Disease?

A

Foci of exerverant, unregulated bone turnover

  1. Woven bone
  2. Increased vascularity
  3. Bone deformity - bowing, osteitis deforming

Endo (11 decks)

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