Drugs for Bone & Joint Disorders Flashcards

1
Q

Three drug classes used in the management of RA

A

NSAIDs
glucocorticoids
DMARDs

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2
Q

Which of the drug classes used in the management of RA does NOT slow disease progression?

A

NSAIDs

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3
Q

List the three types of DMARDs

A

conventional (traditional)
biologic
targeted

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4
Q

What does DMARD stand for

A

disease modifying antirheumatic drugs

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5
Q

What are the differences between the types of DMARDs used for RA?

A

conventional = nonspecific

biologic = targets one specific component of immune system

targeted = targets one specific component of RA immune response

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6
Q

Drug classes that are biologic DMARDs

A

TNF antagonists
B lymphocyte depleting agent
T cell activation inhibitor

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7
Q

Drug classes that are targeted DMARDs

A

IL-6 receptor antagonists
IL-1 receptor antagonist
JAK inhibitors

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8
Q

mechanism of action of methotrexate

A

folate antagonism

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9
Q

adverse effects of methotrexate

A

hepatic fibrosis
bone marrow suppression
GI ulceration
pneumonitis

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10
Q

all DMARDs result in:

A

immunosuppression (risk for infection)

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11
Q

cautions with DMARDs and vaccinations?

A

live vaccinations are contraindicated

inactivated vaccinations may not be as effective

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12
Q

Adverse effects of TNF antagonists

A

infection/neutropenia (black box warning)
injection site reactions
infusion reactions
skin reactions

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13
Q

Drugs used for the management of gout flare up

A

NSAIDs
glucocorticoids
colchicine

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14
Q

Potential mechanism of action of colchicine?

A

inhibition of WBC infiltration via disruption of cellular microtubules

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15
Q

adverse effects of colchicine

A

toxicity to rapidly proliferating cell groups:

  • GI ulcers/perforation
  • myelosuppression
  • myopathy
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16
Q

Drugs used in long term preventative therapy of gout

A

xanthine oxidase inhibitors
probenecid
pegloticase & rasburicase

17
Q

Goal of long term gout preventative therapy?

A

decrease uric acid concentrations

18
Q

methods to decrease uric acid concentrations in the plasma?

A
  1. inhibit formation
  2. accelerate excretion
  3. convert to metabolite
19
Q

List a xanthine oxidase inhibitor

A

allopurinol
febuxostat

20
Q

mechanism of action of xanthine oxidase inhibitors

A

inhibit xanthine oxidase (which is required for uric acid formation)

21
Q

adverse effects of xanthine oxidase inhibitors

A

GI reactions
drowsiness
headaches

initial therapy can induce a gout attack

22
Q

treatment options for hypocalcemia

A

PO or IV calcium

23
Q

treatment options for hypercalcemia

A

mild = drugs that inhibit calcium absorption (see future flashcard)

severe = IV saline + loop diuretic

24
Q

two types of IV calcium

A

calcium chloride
calcium gluconate

25
what is cinacalcet used for
hyperparathyroidism
26
mechanism of action of cinacalcet
mimics calcium at PTH receptor = negative feedback & prevention of further PTH secretion
27
adverse effects of cinacalcet
N/V diarrhea hypocalcemia
28
how does exogenous vitamin D increase blood levels of calcium?
increased intestinal absorption increased bone resorption decreased renal excretion
29
mechanism of action of calcitonin
inhibition of osteoclasts (inhibits bone resorption) inhibition of tubular calcium resorption (increases excretion)
30
What are bisphosphonates
structural analog of pyrophosphate, which is a normal constituent of bone
31
mechanism of action of bisphosphonates
incorporate into bone & remain active for years (decreases osteoclast activity, decreases bone resorption)
32
adverse effect of bisphosphonates
esophagitis! (drink with full glass of water & remain upright)
33
List some bisphosphonates
alendronate risedronate ibandronate zoledronate
34
Both IV bisphosphonates can cause:
renal damage
35
administration of exogenous estrogen decreases bone resorption via what mechanism?
inhibits the increase in osteoclast number
36
Why may a SERM be preferred to exogenous estrogen in the treatment of bone demineralization?
increases bone density with less risks