Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

pharmacology > Drugs affecting bone metabolism > Flashcards

Drugs affecting bone metabolism Flashcards

1
Q

Describe calcium homeostasis

A

1 for PTH release from parathyroid glands in response to low plasma Ca2+ levels
3 for 3 effects of circulating PTH (bone - promote osteoclast activity), intestine and kidney absorb Ca2+)
1 for negative feedback (calcitonin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How do PTH and osteoclast precursors interact?

A

PTH stimulates recruitment of osteoclast precursors, and differentiation into osteoclasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How might cytokines such as ILs interact with osteoclast precursors?

A

Stimulate recruitment of osteoclast precursors, and differentiation into osteoclasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How might a cytokine such as IGF-1 interact with osteoblast precursors?

A

Promotes differentiation into osteoblasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Where might IGF-1 be found?

A

Circulating in the bloodstream or stored in osteoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is RANKL? Describe how it can change blood Ca2+ levels?

A

RANKL is an activating factor that stimulates transcription, pushing osteoblasts to osteoclasts. RANKL interacts with RANK receptors on osteoclast precursors. These then form multinucleated osteoclasts that resorb bone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Provide 3 examples that stimulate RANKL pathway and 1 example that inhibits RANKL pathway

A

Calcitriol, PTH and ILs stimulate, osteoprotogerin inhibits by being a decoy for RANKL - by not allowing interaction with RANK receptors, it inhibits osteoclast activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

3 diseases bisphosphonates are used for?

A

Osteoporosis, Paget’s disease, hypercalcaemia (due to malignancies)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are bisphosphonates?

A

Analogues of pyrophosphate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What do bisphosphonates do and how? (3)

A

Inhibit bone breakdown and resorption
Taken up by osteoclasts in matrix - inhibit recruitment and promote apoptosis
Indirectly stimulate osteoblasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

2 examples of bisphosphonates?

A

alendronate and risedronate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Can bisphosphonates be taken orally?

A

Poorly absorbed orally, can be taken with lots of water to prevent gastro-oesophageal irritation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Common adverse effects of bisphosphonates?

A

GI upset, musculoskeletal pain, headache

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Rare adverse effects to bisphosphonates?

A

Osteonecrosis of the mandible; risk increased by recent dental work or jaw trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

When are SERMS used?

A

selective oestrogen receptor modulators used in post-menopausal osteoporosis; a decline in oestrogen leads to a loss in bone-protective effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Agonist and antagonistic properties of SERMS?

A

agonist: bone and cardiovascular system (tibolone - vagina, and prosteogenic effect on breasts, common ADRs are headache, dizziness and vaginal bleeding)
antagonist: breast and uterus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Side effects of SERMS?

A

hot flushes, thromboembolism, dizziness, GI upset, leg cramps

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

When is Vitamin D used?

A

treatment in deficiency states, rickets and osteomalacia, hypocalcaemia due to hypoparathyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the common clinical form of Vitamin D3 used in treatment?

A

calcitriol/ 1,25-dihydroxycholecalciferol - most biologically active form of Vitamin D

20
Q

How might vitamin D be administered?

A

oral preparations and injectable calciferol

21
Q

What is Vitamin D’s distribution?

A

Lipid soluble - can be transported to fat stores and remain there for months

22
Q

A common ADR of vitamin D

A

hypercalcaemia

23
Q

Examples of calcium salts and routes of administration

A

oral: gluconate, carbonate or lactate salts
intravenous: gluconate preferred or chloride

24
Q

Disadvantage of carbonates?

A

poorly absorbed and binds to phosphates

25
Q

Routes of administration of calcium salts to avoid

A

SC or IM injections are severely irritant

26
Q

When to use calcium salts?

A

deficiency states, hypocalcaemia in hypoparathyroidism, prevention and treatment of osteoporosis

27
Q

Common ADRs of calcium salts

A

GI disturbances, especially in oral form

28
Q

What is teriparatide and significance of its structure?

A

peptide with human parathyroid hormone sequence

  • given SC intermittently, stimulates osteoblasts
  • given in postmenopausal women in terms of fracture rates and bone density
29
Q

Side effects of teriparatide

A

nausea, dizziness, injection site reactions, joint pain

- risk of osteosarcoma limits duration of therapy

30
Q

In what diseases is it good to use calcitonin?

A

Paget’s disease and osteoporosis

31
Q

What does calcitonin do?

A

stimulates calcium uptake into bone and inhibits bone resorption

32
Q

Duration of effect of calcitonin (relative)?

A

Rapid, short acting

33
Q

Types of calcitonin

A

Porcine (pig) calcitonin or synthetic (salmon) form

34
Q

How is calcitonin administered?

A

Injected subcutaneously because it is a peptide

35
Q

What is cincalcet?

A

calcium mimetic agent

36
Q

When is cincalcet used?

A

in PTH-induced hypercalcaemia, to decrease PTH secretion, lower Ca2+ plasma levels
(works in same way as having high Ca2+ levels)

37
Q

mechanism of cincalcet?

A

increase sensitivity of calcium ion sensing receptor on PTH cells

38
Q

common ADRs of cincalcet?

A
  • nausea and vomiting
  • also need to monitor for hypocalcaemia, and calcium and phosphate levels
  • drug interactions
39
Q

What is denosumab, what is it directed at?

A

a monoclonal antibody

directed to RANKL and its receptor RANK

40
Q

mechanism of action of denosumab?

A

decreases osteoclast activity, and consequently bone resorption

41
Q

common ADRs of denosumab?

A

hypocalcaemia, hypercholesterolaemia, eczema, osteonecrosis rarely

42
Q

How is denosumab administered?

A

SC

43
Q

What else needs to be taken with denosumab?

A

concomitant vitamin D and calcium supplementation

44
Q

What is the significance of bisphosphonates being taken up into the bone?

A

bisphosphonates can be incorporated into the bone matrix, taken up by osteoclasts causing apoptosis

45
Q

Effect of glucocorticoids on osteoblasts and osteoclasts?

A
  • inhibit differentiation pathway to form osteoblasts
  • can inhibit osteoclasts and IGF
  • tend to lose Ca2+ from the bone when using potent anti-inflammatory agents

pharmacology (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions