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Pharm II > Osteoporosis Drugs > Flashcards

Osteoporosis Drugs Flashcards

1
Q

Osteocytes signal what 2 types of cells?

A

Osteoblasts and osteoclasts

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2
Q

What type of cells break down and resorb bone?

A

Osteoclasts

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3
Q

What type of cells form and deposit bone?

A

Osteoblasts

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4
Q

What is the primary regulator of osteoclasts?

A

Osteoblasts

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5
Q

Is bone remodeling resorption or formation dominant?

A

Resorption dominant (clasts > blasts) (3 weeks to dig pit, 3-4 months for new bone formation)

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6
Q

What is the key for osteoporosis treatment and fracture prevention?

A

Decreasing bone resorption

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7
Q

What is the progression of a monocyte in bone remodeling? (4 steps)

A

Monocyte → preosteoclast → osteoclast → bone resorption

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8
Q

What is the progression of stem cells in bone remodeling? (4 steps)

A

Stem cells → preosteoblasts → osteoblasts → release RANKL and OPG

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9
Q

What has a positive feedback mechanism with osteoclast formation?

A

RANKL

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10
Q

What inhibits RANKL?

A

OPG

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11
Q

What 4 things regulate bone remodeling?

A

PTH, vit D, calcitonin, estrogen

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12
Q

When is PTH release stimulated?

A

Low serum blood calcium (via calcium sensing receptor, CaSR)

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13
Q

How does PTH increase circulating calcium?

A

↑ osteoclast activity and # via RANKL

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14
Q

How does vitamin D increase circulating calcium? (2)

A

↑ intestinal absorption and ↓ renal excretion, stimulates osteoclast activity through RANKL (in combo w/ PTH)

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15
Q

How does calcitonin decrease circulating calcium?

A

Inhibits osteoclasts to ↓ resorption (also ↓ renal reabsorption)

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16
Q

What stimulates calcitonin release?

A

High circulating calcium

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17
Q

When does calcitonin contribute to bone maintenance?

A

Pregnancy and lactation

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18
Q

What does estrogen increase? Decrease?

A

↓ IL-6 (pro-osteoclast) ↑ OPG (inhibitor of RANKL)

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19
Q

What condition is described as the following: Bone mass is decreased Structural integrity of trabecular bone is impaired Cortical bone becomes more porous and thinner Makes bones weaker/ more likely to fracture

A

Osteoporosis

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20
Q

How many standard deviations from N is defined as osteoporosis?

A

2.5

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21
Q

How many standard deviations from N is defined as osteopenia?

A

1

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22
Q

What leads to a 14% death rate from osteoporosis?

A

Hip fractures leading to subsequent consequences (another common complication = spinal compression fractures (often unknown to pt))

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23
Q

What is the greatest RF for osteoporosis?

A

Postmenopausal women

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24
Q

Besides postmenopausal women, what are other less prominent RF’s for osteoporosis? (4)

A

Long-term glucocorticoid use Thyrotoxicosis Alcoholism Malabsorption syndrome

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25
Q

What is the DOC for osteoporosis? (drug class)

A

Bisphosphonates

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26
Q

What are other treatment options for osteoporosis besides bisphosphonates (DOC)? (general)

A

Calcium and vit D (not always enough on their own), HRT- estrogen, SERMs, calcium regulating hormones

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27
Q

What is the MOA for calcium and vit D?

A

Increase circulating calcium

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28
Q

What is the use for calcium and vit D?

A

Use in combo for osteoporosis (cannot prevent/ treat osteoporosis alone/ adequate calcium intake needed for any other treatment to work/ vit D must be adequate for optimal absorption of calcium)

29
Q

What is the preferred route of administration for calcium?

A

Chewable (not all preparations absorbed equally)

30
Q

Calcitonin drug class?

A

Hormone drugs (also includes estrogen and raloxifene)

31
Q

What is the MAO for calcitonin? (2)

A

Decrease bone resorption of calcium, antagonizes PTH hormone

32
Q

What is the use of calcitonin? (2)

A

Osteoporosis (not 1st line), Paget’s disease

33
Q

What are the 2 possible routes of administration for calcitonin?

A

Nasal spray or injection

34
Q

What are the SEs of calcitonin? (3)

A

Allergy, rhinitis/ sinusitis (nasal spray), N/V (injection) (salmon calcitonin = more active but cannot use if allergy)

35
Q

What is the MOA of teriparatide and abaloparatide?

A

PTH receptor type 1- RG agonist

36
Q

What is the use for teriparatide and abaloparatide?

A

Osteoporosis (more osteoblast activity) and formation of new bone (only anabolic drugs for osteoporosis)

37
Q

What route of adminitration allows Teriparatide to have intermittent effects?

A

S.C. injection, short t1/2 = peaks in 30 min, gone in 3 hours

38
Q

What are the SEs of both Teriparatide and Abaloparatide?

A

Hypercalcemia and hypercalciuria

39
Q

Teriparatide and Abaloparatide can both cause hypercalcemia and hypercalciuria. What is an additional SE of just Abaloparatide?

A

Hyperuricemia

40
Q

Teriparatide and Abaloparatide are contraindicated in what situation?

A

Osteosarcoma (black label)

41
Q

What is the MOA for rhPTH?

A

PTH receptor type 1- R0 agonist

42
Q

What is the use for rhPTH?

A

Hypoparathyroidism (more osteoclast activity)

43
Q

Teriparatide drug class?

A

PTH drugs

44
Q

Abaloparatide drug class?

A

PTH drugs

45
Q

rhPTH drug class?

A

PTH drugs

46
Q

Denosumab drug class?

A

Rank-ligand inhibitor

47
Q

What is the MOA for Denosumab? (2)

A

Inhibits bone resorption, Ab against RANKL = inhibits RANKL

(necessary for formation of mature osteoclasts)

48
Q

Denosumab is used for the treatment of osteoporosis in what populations?

A

Men and postmenopausal women with high fracture risk

49
Q

One of the benefits/ uses of Denosumab is the increase of what?

A

Bone mass and strength in cortical and trabecular bone

50
Q

What is the route of admintration for Denosumab?

A

SC injection q 6 months

51
Q

What are the contraindications for Denosumab? (3)

A

Hypocalcemia and pregnancy > IMC

52
Q

Alendronate drug class?

A

Bisphosphates

53
Q

Ibandronate drug class?

A

Bisphosphates

54
Q

Risedronate drug class?

A

Bisphosphates

55
Q

Zoledronic acid drug class?

A

Bisphosphates

56
Q

Route of administration for Alendronate?

A

Oral

57
Q

Route of administration for Ibandronate?

A

Oral/ IV

58
Q

Route of administration for Risedronate?

A

Oral

59
Q

Route of administration for Zoledronic acid?

A

IV

60
Q

What is the primary MOA for bisphosphonates?

A

Substitutes for PO4 in Ca binding (incorporated into bone)

61
Q

Although not the primary MOA, what drug class involves P-C-P bond analogs of pyrophosphate and inhibition of osteoclast activity and bone resorption?

A

Bisphosphates

62
Q

What is the DOC for post-menopausal osteoporosis?

A

Bisphosphates

63
Q

When must oral bisphosphates be taken due to very poor absorption?

A

Taken on empty stomach and seated upright for 30 min after taking (taken daily)

64
Q

What is the SE for Bisphosphates (all routes of administration)?

A

Osteonecrosis of the jaw

(will limit bone turnover with each dose = dense bones (non-flexible) = brittle bone)

65
Q

What is the SE for oral Bisphosphates? (2)

A

GI sxs/ discomfort, esophageal ulceration

66
Q

What are the SEs for IV Bisphosphates? (2)

A

Renal toxicity (if given too fast), N/V

67
Q

What are the contraindications for oral Bisphosphates? (2)

A

Inability to stand/ sit upright or esophageal disease

68
Q

What is the contraindication for IV Bisphosphates?

A

Renal disease

Pharm II (13 decks)

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