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1 - PBS2 > 96 - Drugs Affecting Bone > Flashcards

96 - Drugs Affecting Bone Flashcards

1
Q

Proportions of trabecular and cortical bone

A

Bones are 20% trabecular, 80% cortical

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2
Q

Effect of tetracycline on teeth

A

When consumed during tooth development, binds to calcium ions. Leads to yellow/brown discolouration of dentine.

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3
Q

Amount of bone remodelled each year in adults

A

25% of trabecular bone remodelled each year
3% of cortical bone remodelled each year
~10% of total bone remodelled each year

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4
Q

Five phases of bone remodelling

A 
– Activation
– Resorption
– Reversal
– Formation
– Quiescence
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5
Q

How can growth factors be released in bone remodelling?

A

Embedded in bone, released during bone resorption.

Recruit, activate osteoblasts to begin making new osteoid over resorbed bone.

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6
Q

Osteoclastogenesis

A

Upstream pro-resorptive cytokines promote stromal cell RANKL (membrane associated or soluble).
RANKL stimulates osteoclastic precursors (in conjunction with M-CSF) to differentiate into mature osteoclasts

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7
Q

Factors regulating bone remodelling

1-5

A

1) Parathyroid hormone
2) Oestrogen
3) Glucocorticoids
4) Sequestered cytokines in bone
5) Calcitonin

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8
Q

Parathyroid hormone role

A

Increased osteoblast activity, increased osteoclast activity

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9
Q

Oestrogen role, with respect to bone

A

Decreased osteoclast activity

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10
Q

Glucocorticoid effect on bones

A

Increased osteoclast activity

Decreased osteoblast activity

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11
Q

Calcitonin effect on bones

A

Decreased osteoclast activity

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12
Q

Effect of dexamethasone on bones

A

Increases RANKL and decreases OPG

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13
Q

Things regulating serum calcium concentration

1-3

A

Parathyroid hormone
Vitamin D
Calcitonin

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14
Q

How does PTH increase serum Ca2+?

A

Increased vitamin D synthesis
Mobilises Ca2+ from bone
Reduces renal Ca2+ excretion

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15
Q

How does calcitonin decrease serum Ca2+?

A

Decreases osteoclast activity and Ca2+ resorption from bone.

Inhibits Ca2+ resorption in the kidney

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16
Q

Where does calcitonin come from?

A

C cells of the thyroid gland

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17
Q

Vitamin D synthesis

A

Cholesterol metabolised in the skin, catalysed by UV exposure.
This results in liver producing calcifediol in the liver.
Calcifediol is metabolised to calcitriol in the kidney.
Calcitriol is the active part of vitamin D

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18
Q

Effect of calcitriol on plasma Ca2+

A

Increases plasma Ca2+.
Increased intestinal absorption
Decreased renal excretion
Increased osteoclast activity

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19
Q

Blood Ca2+ homeostasis

A

Thyroid gland detects high Ca2+, releases calcitonin.

Parathyroid glands detect low Ca2+, release PTH.

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20
Q

Disorders of bone

1-5

A 
Hypocalcaemia
Hypercalcaemia
Hypophosphataemia
Hyperphosphateaemia
Osteoporosis
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21
Q

What can cause hypocalcaemia?

A

Vitamin D deficiency

22
Q

What can cause hypercalcaemia?

A

Malignancies

23
Q

What can cause hypophosphataemia?

A

Nutritional deficiency

24
Q

What can cause hyperphosphataemia?

A

Renal failure

25
Q

Definition of osteoporosis

A

Reduction in bone mass more than 2.5 standard deviations below the normal for healthy 30 year old woman

26
Q

Definition of osteopaenia

A

Reduction in bone mass more than 1-2.5 standard deviations below the normal for healthy 30 year old woman

27
Q

When is peak bone density?

A

20s to 30s.

28
Q

When does bone density begin decreasing?

A

Age 35-40 (decrease about 0.5-1% per year)

29
Q

Effect of osteoporosis on bone

A

Loss of trabeculae and thinning leads to reduced cross-sectional area, so that loads on bone are relatively greater.

30
Q

Anti-resorptive agents for bone disorders

1-3

A

Bisphosphonates
Selective oestrogen receptor modulators (SERM)
RANK-L inhibitors

31
Q

Anabolic agents for bone disorders

1-4

A

PTH
Oral Ca2+
Oral vitamin D analogues
Calcitonin

32
Q

Bisphosphonate structure

A

Enzyme resistant analogues of pyrophosphate (pyrophosphate is essential for binding to bone mineral).

33
Q

Bisphosphonate mechanism of action

A

Inhibit binding of osteoclasts to bone surface, promote osteoclast apoptosis.
Inhibit osteoclast recruitment.
Promote osteoclast apoptosis
Inhibit osteoclast binding to bone.
Accumulate at sites of bone mineralisation, stay for long periods

34
Q

Bisphosphonate administration and side effects

A

Oral administration daily/weekly
IV administration
Poorly absorbed.
Adverse GIT effects (osteophagitis)

35
Q

How does oestrogen affect bones?

A

Decreases osteoclast proliferation, differentiation, activation
Promotes osteoclast apoptosis
Increases life span of osteoblasts and osteocytes
Doesn’t increase bone mass, but maintains mass, slows bone loss.

36
Q

Problem with oestrogen for slowing bone loss

A

A lost of side effects, can lead to cancers

37
Q

Drug replacement for oestrogen (for bones)

A

Selective oestrogen receptor modulators (SERMS)

38
Q

Selective oestrogen receptor modulators (SERMS) mechanism

A

Agonist at oestrogen receptors in bone and cardiovascular tissue
Antagonist at oestrogen receptors in mammary tissue and uterus (decreases cancer risk)

39
Q

Side effects of SERMS

A

Increased DVT risk, pulmonary embolism risk

40
Q

Human MAb that binds RANK-L

A

Denosumab

41
Q

Denosumab action

A

Human MAb that binds RANK-L
Inhibits RANKL activity
Reduces osteoclastic differentiation, survival , activity

42
Q

Antiresorptive and anabolic drug

A

Strontium ranelate

43
Q

Side effects of strontium ranelate

A

Increased incidence of MI.

For this reason, is a last line of treatment for severe osteoporosis.

44
Q

Drug based on PTH

A

Teriparatide

45
Q

Effect of PTH administration on bones

A

At low levels, is anabolic.

Long-term, high exposure to PTH leads to bone catabolism.

46
Q

Common adjunctive therapy for osteoporosis

A

Oral Ca2+

47
Q

What is vitamin D administered for?

A

Deficiency states, EG rickets, osteomalacia, endocrine dysfunction (hypoparathyroidism), chronic renal disease (where calcitriol can’t be produced by kidney)

48
Q

Effect of calcitonin on bones

A

Decreases osteoclastic resorption and mobilisation of Ca2+ from bone.

49
Q

How is calcitonin administered?

A

Synthetic salmon calcitonin (salcatonin) given as an injection.

50
Q

What is calcitonin used to treat?

A

Paget’s disease, hypercalcaemia associated with neoplasia

1 - PBS2 (96 decks)

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