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Endocrine 2 > Osteoporosis Drugs - Fitz > Flashcards

Osteoporosis Drugs - Fitz Flashcards

1
Q

T-Score - what is it?

A

of SDs away from the average BMD of a middle age woman

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2
Q

T-Score - important ones

A

Above -1 = normal
-1 to -2.5 = osteopenia
Below -2.5 = osteoporosis

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3
Q

Each SD (T-score) correlates with what risk? BMD?

A

2x risk for vertebral fracture (10-20% BMD loss)

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4
Q

Preventing and treating osteoporosis requires what?

A

Adequate vitamin D and calcium

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5
Q

Calcium carbonate vs. Calcium citrate - Pros and Cons

A

Carbonate - Cheap, but needs stomach acid (meals)

Citrate - Expensive, but does not need stomach acid

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6
Q

Calcium absorption is only feasible with what else?

A

Adequate vitamin D3

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7
Q

Normal vitamin D requirement

When is it more? (6)

A

400-800 IU/day

Malabsorption, corticosteroids, anticonvulsants, loop diuretics, heparin, low sunlight exposure

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8
Q

Corticosteroids - which ones to worry about? (3)

Why is vitamin D requirement higher?

A

Prednisone, Methylprednisolone, Budesonide

Vitamin D is like a steroid, thus the steroid drugs compete for absorption and activation of vitamin D

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9
Q

A middle aged woman w/ COPD is being treated for increased severity w/ corticosteroids. What should be supplemented?

A

Vitamin D

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10
Q

Anticonvulsants - which ones to worry about? (2)

Why?

A

Carbamazepine, Phenytoin

Induces P450, thus increased metabolism of Vitamin D

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11
Q

A middle aged woman w/ epilepsy is being treated. What should be supplemented?

A

Vitamin D

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12
Q

Loop diuretics - why is the calcium requirement higher?

A

Causes calcium wasting

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13
Q

3 uses of bone density testing (1 important one here)

A
  • Diagnose osteoporosis
  • Predict fracture risk
  • Monitor therapy - INITIATION OF GLUCOCORTICOIDS
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14
Q

Vitamin D activation requires what 3 things?

A

Sunlight, liver, kidney

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15
Q

PTH vs. calcitonin

A 
PTH = increased bone resorption, increased Ca++ release
Calcitonin = decreased bone resorption
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16
Q

Secondary causes of osteoporosis (via Ca++ or Vitamin D) (6)

A

MM, HyperPT, Hypogonadism, Liver disease, Kidney disease, Malabsorption

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17
Q

2 main classes of osteoporosis drugs

A
  • Anti-resorption (osteoclast inhibitors)

- Anabolic (osteoblast activators)

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18
Q

Estrogen deficit leads to what?

Why?

A

Increased osteoclast activity

Estrogen normally causes apoptosis of osteoclasts to maintain the balance btwn blasts and clasts

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19
Q

A 55 y/o newly post-menopause female patient shows progressive bone weakening and is now below the fracture threshold. What should be suspected? Why?

A

Inadequate intake of Ca++ and Vitamin D (should not reach this level of bone weakness until old age)

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20
Q

Benefits to hormone (estradiol) replacement therapy for menopausal women?

A
  • Increased bone health

- Decreased menopause symptoms

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21
Q

Risks to HRT for menopausal women?

A
  • INCREASED RISK OF BREAST and UTERINE CANCERS

- Increased risk of heart attack, stroke, thrombosis

22
Q

Treatment decisions for osteoporosis should be based on what?

A

FRACTURE RISK, age, BMD, other risk factors

23
Q

A middle age woman recently started menopause, and her doctor suggests starting prophylactic therapy for osteoporosis. She chooses not to take HRT due to the cancer risks. What is the best alternative?

A

Raloxifene (selective estrogen-receptor modulators)

24
Q

HRT vs. SERMs – actions in bone

A

BOTH are AGONISTS at ER in osteoclasts - cause increased osteoclast apoptosis to maintain the balance

25
Q

HRT vs. SERMs – actions in breast

A

HRT - AGONIST at ER in breast [and uterus] (cancer risk)

SERMs – ANTAGONIST at ER in breast (BC prevention)

26
Q

Tamoxifen - what is it?

Unique adverse effect

A

Other SERM

Uterine/endometrial BLEEDING, CANCER (or hyperplasia)

27
Q

Common adverse effect of HRT and SERMs

A

Venous thromboembolic events (DVTs, PEs, etc.)

28
Q

Bisphosphonates - MoA (2)

A
  • Pyrophosphate analogs that incorporate into bone matrix, bind hydroxyapatite crystals (bone Ca++) and inhibit osteoclastic resorption.
  • Accumulates in osteoclasts, inhibits FPP SYNTHASE, decreases prenylated G proteins, and causes apoptosis
29
Q

Bisphosphonates - drugs

A

(“-ronate”)

“PAIRZ of Bi’s” - Pamidronate, Alendronate, Ibandronate, Risedronate, Zoledronate

30
Q

Bisphosphonates - contraindication

A

Hypocalcemia

31
Q

Bisphosphonates - adverse effects (oral)

A

Esophagitis, esophageal ulcers

32
Q

Describe bi-phasic half-life of bisphosphonates

A

Rapid clearance from blood, but LONG residence w/in bone

33
Q

Ways to cope w/ Bisphosphonate adverse effects (oral)

A
  • Take w/ water
  • Don’t eat or drink anything for 30 min after
  • Don’t lie down for 30 min after
34
Q

Patient is taking oral Bisphosphonate and is either non-compliant or still struggling w/ esophagitis issues. Alternative?

A

Zoledronate (IV bisphosphonate)

35
Q

Adverse effect of IV bisphosphonates

A

Osteonecrosis of the jaw

36
Q

A patient is diagnosed w/ osteonecrosis of the jaw. She denies taking any IV bisphosphonates. Other potential causes?

A

MM, breast cancer, prostate cancer, dental trauma/surgery

37
Q

A patient is getting Bisphosphonate therapy for over 5 years. Potential risk? Why?

What is recommended? Why?

A

Risk of increased fractures - osteoclast activity may stay low for years after discontinuing therapy (abnormal blast-clast balance)

Re-evaluation of need for continued therapy

38
Q

Which osteoporosis drugs can be used for PREVENTION of osteoporosis?

A

SERMs, Bisphosphonates

39
Q

Which osteoporosis drugs can be used for TREATMENT ONLY?

A

Calcitonin, Denosumab, Teraparatide

40
Q

A post-menopausal woman is showing signs of low BMD and high risk for fractures. She starts bisphosphonates but cannot seem to comply with their strict regulations. What is an alternative drug?

A

Denosumab

41
Q

Denosumab - MoA

A

Monoclonal antibody against RANKL ligand on osteoblasts –> prevents maturation of osteoCLASTS (requires RANK-RANKL binding between a blast and an immature clast)

42
Q

A patient w/ osteoporosis has a compression fracture of a vertebra and is experiencing significant pain. Normal analgesics are working some, but the doctor wants to prevent further bone weakening. Good potential drug?

A

Calcitonin

43
Q

Which drug is an ANABOLIC drug for bones rather than an ANTI-CATABOLISM drug?

A

Teriparatide

44
Q

Teriparatide - MoA

A

PTH fragment that stimulates osteoblast activity, thereby increasing BMD and decreasing fractures

45
Q

Teriparatide - use

A

HIGH RISK patients ONLY

46
Q

Teriparatide - adverse effect

A

Risk of osteosarcoma

47
Q

PTH causes increased bone destruction, but Teriparatide (a PTH fragment) causes increased bone density. Why?

A

PTH is constantly expressed when it’s needed, whereas Teriparatide is administered INTERMITTENTLY. This dosing regimen somehow makes the difference

48
Q

An osteoporosis patient needs a drug that will most-effectively increase BMD. What to give?

A

Teriparatide

49
Q

2 reasons for natural osteoporosis in elderly

A
  • Senescense of osteoblasts

- Persistent PTH increase due to decreased renal and intestinal function (decreased Ca++)

50
Q

Cinacalcet - MoA

Uses? (2)

A

Increases sensitivity of CaSR –> lowers PTH level

Secondary hyperparathyroidism (CKD) or parathyroid cancer-induced Ca++ level increase

Endocrine 2 (12 decks)

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