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Pharmacology 2 > NSAIDs & Immunosuppressants > Flashcards

NSAIDs & Immunosuppressants Flashcards

10 questions

1
Q

NSAIDs have eicosanoid-depressing action. what are eicosanoids?

A

PGs and interleukins

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2
Q

what catalyzes the formation of PGs and thromboxane from arachidonic acid?

A

COX enzymes

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3
Q

MOA of NSAIDs?

A

non-selective inhibitors of COX-1 and COX-2 enzymes

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4
Q

all NSAIDs, except _____ irreversibly inhibit COX-1 and COX-2 by acetylation of the enzymatic active site

A

aspirin

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5
Q

what is leukotrienes usually accompanied by?

A

release of histamine

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6
Q

housekeeping enzyme that is found in the stomach

A

COX-1

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7
Q

what hormone is a major product of COX-1? what does it do?

A

thromboxane
platelet aggregation

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8
Q

why is aspirin effective at reducing cardiac events?

A

because it inhibits platelet COX-1

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9
Q

enzyme that induces the inflammatory response

A

COX-2

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10
Q

where does COX-2 work? (3)

A

kidney
lungs
inflammatory cells

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11
Q

what 2 drug types inhibit COX-2 gene expression?

A

NSAIDs
glucocorticoids

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12
Q

why can the use of NSAIDs not eliminate leukotriene synthesis?

A

NSAIDs do not inhibit lipoxygenases

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13
Q

what is required for NSAIDs to be an antiinflammatory?

A

large doses 600-800mg

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14
Q

how does pyresis occur?

A

pyrogens stimulate interleukin-1 release = stimulates PG in hypothalamus = increases thermo set point

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15
Q

what is the DOC for pyresis? what should be avoided when taking it?

A

acetaminophen

avoid ethanol

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16
Q

how does pain occur?

A

PGs sensitize pain fibers to stimuli

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17
Q

what makes acetaminophen different?

A

only works in the CNS

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18
Q

what NSAID is used to inhibit premature labor?

A

indomethacin

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19
Q

what kind of inflammation can NSAIDs work well for? (3)

A

osteoarthritis
RA
ankylosing spondylitis

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20
Q

how is aspirin converted to salicylate?

A

by first pass hepatic metabolism

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21
Q

what does it mean when large doses of aspirin exhibit non-linear kinetics?

A

it has an increased half life

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22
Q

what is a sign that aspirin dose is too high?

A

tinnitus

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23
Q

what NSAID can interfere with the antiplatelet effect of aspirin by preventing acetylation of acetylsalicylic acid?

A

ibuprofen

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24
Q

what kind of NSAIDs have little effect on platelets, thus little risk of bleeding?

A

nonacetylated salicylates

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25
Q

what’s important about nonsalicylate NSAIDs?

A

less GI toxicity

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26
Q

what are the 4 nonsalicylate NSAIDs?

A

diclofenac
etodolac
ibuprofen
indomethacin

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27
Q

which 2 nonsalicylate NSAID are relatively COX-2 selective?

A

diclofenac
etodolac

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28
Q

which 2 nonsalicylate NSAIDs have some inhibitory action against lipoxygenase? (decrease leukotriene)

A

diclofenac
indomethacin

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29
Q

ADR of diclofenac?

A

increased risk of MI

30
Q

ADR of indomethacin? (2)

A

CNS (esp in elderly)
increased risk of GI ulcers

31
Q

which nonsalicylate NSAID is only used for acute moderately severe pain?

A

indomethacin

32
Q

-coxib

A

COX-2 inhibitors

33
Q

what is the half life of celecoxib?

A

10 hours

34
Q

what is celecoxib used for? (3)

A

arthritis
dysmenorrhea
post-surgical pain

35
Q

ADR of celecoxib? (2)

A

increased risk of MI
increased risk of stroke

36
Q

why do NSAIDs have a small Vd?

A

highly bound to plasma albumin

37
Q

how are NSAIDs mostly excreted?

A

kidneys

38
Q

what are 3 ADR specific for aspirin/salicylates? what causes them?

A

hypersensitivity -
rhino conjunctivitis
angioedema
urticaria

increased leukotriene synthesis

39
Q

a patient presents with rhino conjunctivitis, angioedema, and urticaria after taking aspirin/salicylate. about when did the patient take it?

A

within the last 3 hours

40
Q

why do NSAIDs cause increased BP?

A

allow full vasoconstriction caused by NE

41
Q

how do NSAIDs cause salt/water retention? what can it lead to? (3)

A

decrease renal blood flow and GFR
hyperkalemia
interstitial nephritis
reversible acute kidney failure

42
Q

the nephrotoxicity of celecoxib is = to _____ NSAIDs

A

non-selective

43
Q

how do NSAIDs cause GI ulceration and bleeding?

A

inhibit PG who are produced by the stomach to maintain the mucosal integrity

44
Q

what can be given to geriatric patients with prior history of NSAID-induced GI ulceration?

A

misoprostol

45
Q

stable analogue of PGE1 used to treat gastric erosions and ulcerations caused by NSAIDs

A

misoprostol

46
Q

what 2 products can be used together to prevent NSAID-induce GI ulcers but can predispose patients to C. diff?

A

NSAID + H2 receptor antagonist (famotidine)

OR

NSAID + proton pump inhibitor (omeprazole)

47
Q

what do many physicians Rx to treat arthritis in elderly patients?

A

NSAID + PPI (omeprazole)

48
Q

what CNS reactions can NSAIDs cause?

A

headache
rebound headache
dizziness

49
Q

why are NSAIDs CI in pregnancy?

A

can cause fatal pulmonary hypertension in fetus

50
Q

what is safe to use in pregnancy to treat pain?

A

acetaminophen

51
Q

ADR of acetaminophen?

A

hepatotoxicity

52
Q

when does toxicity from acetaminophen occur?

A

when glutathione is depleted

(glutathione pushes the toxic metabolite out of the system)

53
Q

what is the treatment for acetaminophen overdose?

A

gastric lavage + IV N-acetylcysteine

54
Q

how does ethanol increase the risk of acetaminophen hepatic toxicity?

A

ethanol increases CYP450

55
Q

class of drugs that increase gene expression of lipocortin which inhibits phospholipase A2 and inhibits inflammation

A

corticosteroids

prednisone
prednisolone

56
Q

drug class that suppresses interleukin-2 production in T lymphocytes

A

calcineurin inhibitors

57
Q

what are the 2 calcineurin inhibitors?

A

cyclosporine
tacrolimus

58
Q

which calcineurin inhibitor is used to prevent graft-vs-host disease?

A

cyclosporine

59
Q

which calcineurin inhibitor is used to reduce risk of organ rejection?

A

tacrolimus

60
Q

ADR of cyclosporine?

A

swelling gums

61
Q

how are corticosteroids metabolized?

A

liver

62
Q

suppress intracellular signaling pathway important for cell growth and proliferation of T lymphocytes

A

mTOR inhibitors

63
Q

what are the 2 mTOR inhibitors?

A

Sirolimus
Everolimus

64
Q

what is sirolimus used for?

A

reduce risk of organ rejection by coating coronary stents

65
Q

what is everolimus used for? (2)

A

reduce risk of organ rejection
HER-2 negative breast cancer

66
Q

blocks DNA synthesis and expansion of lymphocyte populations

A

IMDH inhibitors

67
Q

what are the 3 IMDH inhibitors?

A

azathioprine
mycophenolate
leflunomide

68
Q

what are the 3 uses for azathioprine and mycophenolate?

A

RA
Crohn’s disease
transplants

69
Q

what are the 2 uses for leflunomide?

A

RA
HER-2 negative breast cancer

70
Q

which 2 immunosuppressants can be used for HER-2 negative breast cancer?

A

everolimus
leflunomide

Pharmacology 2 (22 decks)

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