Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology Exam 5 > Osteoporosis Drugs > Flashcards

Osteoporosis Drugs Flashcards

1
Q

What is osteoporosis?

A

a condition of skeletal fragility characterized by reduced bone mass and microarchitectual deterioration

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

What are the disease-related causes (3)?

A

hypogonadism (menopause, aging), hyperparathyroidism, hyperthyroidism

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

What are the drug-induced causes (4)?

A

1) glucocorticoids (3rd leading cause overall)
2) thryroid replacements
3) GnRH agonist/antagonist suppression of gonadal steroid synthesis (prostate cancer, uterine cancer, endometriosis, breast cancer)
4) aromatase inhibitors (breast cancer)

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

What mediates resorption?

A

osteoclasts

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

What mediates reformation?

A

osteoblasts (secrete new matrix)

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

Once the new matrix is formed, what happens?

A

calcification of matrix

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

Osteoblast precursor + stress/circulating hormones = ____

A

RANKL

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

RANKL-> ____ -> _____

A

RANK, osteoclast precursor

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

An osteoblast precursor can become which two things?

A

a mature osteoclast (via RANKL) OR mature osteoblast

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

What can also mediate the formation of an osteoblast from an osteoblast precursor (and not an osteoclast)?

A

secreted factors from mature osteoclasts

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

What are the characteristics of osteoporosis (3) and what is the net result?

A

reduced bone mass and degraded bone architecture:
1) increased osteoclast number and activation
2) decreased osteoclast apoptosis
3) increased osteoblast apoptosis
Net result: deeper, larger resorption cavities in bone

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

What are the anti-resorptive agents (5)?

A

bisphosphonates, calcitonin, denosumab, estrogen, reloxifene

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

What is the selective estrogen receptor modulator?

A

raloxifene

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

What is the bone forming agent?

A

teriparatide

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

What does Vitamin D (calcitrol) supplementation cause?

A

increased calcium absorption from small intestine = increased bone mineralization

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

What is the active metabolite of Vitamin D?

A

Calcitrol

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

What happens with large doses of vitamin D?

A

increased bone resorption (increased osteoclast recruitment to bone sites)

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

Bisphosphonates, aka…

A

pyrophosphate analogs

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

What are the three bisphosphonates and how are the taken?

A

Alendronate - oral (daily, weekly)
Ibandronate - oral (daily, monthly), i.v. (3 months)
Zoledronate - i.v. (yearly)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the properties of bisphosphonates (2)?

A

1) high affinity for bone, Ca chelator, incorporates stabilized structure
2) inhibits bone resorption: decreased osteoclast function and increased apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the indications/uses for bisphosphonates (3)?

A

osteoporosis due to aging, postmenopausal women, steroids

22
Q

How are bisphosphonates administered?

A

oral, <10% absorbed, water only, upright position to prevent heartburn, esophageal irritation

23
Q

Why might high doses of bisphosphonates be used and what is the risk with high doses?

A

cancer treatment- risk for osteonecrosis of jaw

24
Q

What is the main risk of Zoledronate?

A

potential for renal toxicity

25
Q

What is Calcitonin?

A

thyroid gland hypocalcemic hormone

26
Q

How does Calcitonin work?

A

decreases bone resorption: calcitonin receptor on osteoclasts: decreased resorption border surface area (physical effect)

27
Q

What are the uses of calcitonin?

A

osteoporosis (PMW, steroids), low efficacy (fracture prevention?)

28
Q

How is Calcitonin administered?

A

human, salmon calcitonin (daily injection, nasal spray). less immune response to salmon calcitonin

29
Q

What is Denosumab?

A

human monoclonal antibody

30
Q

How does Denosumab work (2)?

A

1) binds to RANKL = decreased activation of RANK

2) decreased osteoclast formation/activation = decreased resorption, increased bone mineral density (prevents fractures)

31
Q

How is Denosumab administered?

A

s.c. injection every 6 months

32
Q

What is the adverse effect of Denosumab?

A

increased infection risk?

33
Q

What is estrogen?

A

Hormone replacement therapy

34
Q

How does estrogen work?

A

decreases bone resorption: decreased RANKL and cytokines = decreased osteoclast proliferation and activation, decreased osteoblast apoptosis

35
Q

What are the long-term risks of estrogen use in PMW (4)?

A

breast cancer, thromboembolism, stroke, CV risk

36
Q

What is the limited use of estrogen?

A

non-responders with normal CV

37
Q

What is Raloxifene?

A

selective estrogen receptor modulator

38
Q

How does Raloxifene work on estrogen receptors?

A

estrogen receptor agonist in bone, antagonist in breast and endometrium

39
Q

How does Raloxifene work?

A

decreases osteoclast formation and activation = decreased resorption, increased bone mineral density, decreased fractures in PMW.

40
Q

What is the use of Raloxifene?

A

osteoporosis in PMW with breast cancer or family history

41
Q

How is Raloxifene administered?

A

oral, daily

42
Q

What are the adverse effects of Raloxifene (2)?

A

risk for venous thrombosis, pulmonary embolism

43
Q

What is Teriparatide?

A

bone forming agent, active peptide of PTH

44
Q

What does hyperparathyroidism cause and when can Teriparatide cause this?

A

bone resorption, decreased bone mineral density. can happen with high continuous doses

45
Q

How does Teriparatide work with low, intermittent doses (2)?

A

1) low, intermittent PTH = increased bone growth

2) increases osteoblast number and activation, increased survival = bone formation

46
Q

What is the use of Teriparatide?

A

severe osteoporosis with high fracture risk

47
Q

How is Teriparatide administered?

A

daily s.c. injection, up to 2 years

48
Q

What is the adverse effect of Teriparatide?

A

may increase risk for osteosarcoma (rats)?

49
Q

What are the drugs to know (9)?

A

Alendronate, Ibandronate, Zoledronate, Calcitonin, Densumab, Raloxifene, Estrogen, Vitamin D, Teriparatide

50
Q

Should you go look at the review questions in the lecture?

A

Uh, JAHH!

51
Q

What did one ocean say to the other ocean?

A

Nothing, they just waved.

Pharmacology Exam 5 (9 decks)

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