Osteoporosis Drug Treatment Flashcards

1
Q

Osteoporosis drug classes:

A
PTH
Vitamin D analogs
Calcium
Bisphosphonates
Calcitonin
Selective estrogen receptor modulators
Thiazide diuretics
RANK-L inhibitors
Calcimimetics
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2
Q

Osteoprotegerin affect?

A

Decreased osteoclastic activity

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3
Q

What is a parathyroid hormone drug?

A

Teriparatide

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4
Q

What does teriparatide do?

A

Makes structurally-normal new bone by binding PTH receptor

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5
Q

Administration of teriparatide:

A

Sub Q once daily for up to two years to prevent bone fractures

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6
Q

What are the fat soluble forms of vitamin D?

A

D2: Ergocalciferol
D3: Cholecalciferol

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7
Q

Affect of PTH on vitamin D?

A

Stimulated 1,25-OH vitamin D3 formation

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8
Q

Affect of FGF 23 on vitamin D?

A

Inhibits 1,25-OH vitamin D3 formation and increase renal phosphate excretion

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9
Q

Vitamin D preparations:

A

Cholecalciferol (D3)
Ergocalciferol (D2)
Calcitriol (1,25-OH vitamin D3)
Paricalcitol (1,25-OH vitamin D2)

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10
Q

When is the active for of vitamin D preparations (calcitriol and paricalcitol) needed?

A

When renal pathology is present

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11
Q

Calcium preparations:

A

Calcium carbonate

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12
Q

What is the treatment for osteoporosis?

A

Calcium + Vitamin D3 supplementation (each has mixed results when used alone)

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13
Q

Bisphosphonates:

A

Alendronate

Etidronate

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14
Q

Mechanism of bisphosphonates?

A

Non-hydrolysable analogs of pyrophosphates normally present in bone; reduce osteoclastic dissolution of hydroxyapatite in bone; no affect on osteoblasts

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15
Q

Risk factors for bisphosphonates:

A

Osteonecrosis of jaw with dental procedures
Sickle cell disease
Radiation/chemotherapy
Local ischemia

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16
Q

Mechanism of action for selective estrogen receptor modulators?

A

Binds both alpha and beta receptors in bone

17
Q

Where are alpha estrogen receptors (ERalpha) in bone found?

A

Cortical bone

18
Q

Where are beta estrogen receptors (ERbeta) in bone found?

A

Trabecular bone

19
Q

What specifically does estrogen cause in bones?

A

Decreased response of RANK-L receptor to RANK-L
Reduction of IL-6, TNF-alpha, and M-CSF
Stimulation of osteoprotegerin

20
Q

Net effect of estrogen:

A

Decreased osteoclast activation

Osteoblasts left unopposed

21
Q

What is a selective estrogen receptor agonist?

A

Raloxifene

22
Q

Raloxifene affect on estrogen receptors?

A

ERalpha: partial agonist
ERbeta: antagonist

23
Q

What does short-term administration of calcitonin cause?

A

Inhibits osteoclastic bone activity

24
Q

What does long-term administration of calcitonin cause?

A

Inhibits both osteoblastic and osteoclastic activity (rarely used)

25
Q

What do thiazide diuretics lead to?

A

Decrease in calcium excretion in the urine

26
Q

What channel do thiazide diuretics affect?

A

Inhibit NCC leading to decreased Na+ reabsorption

27
Q

What does inhibition of NCC lead to?

A

Decreased Na+ concentration in epithelial cells leading to increased basolateral Ca/Na antiporter leading to decreased Ca intracellularly driving the Ca reabsorption via apical membrane TRPV5

28
Q

What is a RANK-L inhibitor?

A

Denosumab

29
Q

What does binding to RANK cause?

A

Activation of nuclear factor kappa-B

30
Q

What is osteoprotegrin?

A

A soluble receptor for RANK-L released to bind and inactivate RANK-L

31
Q

What is Denosumab?

A

A monoclonal antibody against RANK-L

32
Q

How does Denosumab work?

A

Binds RANK-L to inactivate it therefore inhibiting osteoclastic activity

33
Q

Risks of Denosumab?

A
  1. ) Mandibular necrosis with dental work

2. ) Hip fractures

34
Q

What drug is a Calcimimetic?

A

Cinacalcet

35
Q

How does Cinacalcet work?

A

Allosteric activator of calcium sensing receptor (in PT gland)

36
Q

What does Cinacalcet cause?

A

PTH secretion inhibition

37
Q

What is Cinacalcet used for?

A

Hyperparathyroidism resulting from:

  1. ) Chronic kidney disease
  2. ) Parathyroid carcinoma
38
Q

What are the side effects of Cinacalcet?

A

Cardiac arrhythmia

Heart failure