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Year 2 Pharmacology > NSAIDs and gout > Flashcards

NSAIDs and gout Flashcards

1
Q

what are the molecular inflammatory mediators?

A
  1. kinins, neuropeptides, vasoactive amines
  2. arachadonic metabolites
  3. cytokines, free radicals, proteases
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2
Q

what are the arachadonic acid metabolites?

A

PGs, thromboxanes, prostacyclin

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3
Q

what are the functional characteristics of NSAIDs?

A

analgesia
antipyretic
anti-inflammatory
primary target - PG production via COX1 and COX2

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4
Q

is acetaminophen an NSAID?

A

no

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5
Q

which COX enzyme is constitutively expressed?

A

COX1

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6
Q

what role do PGE2 and PGI2 play in inflammation?

A

edema and vascular permeability

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7
Q

what is the role of COX1?

A

homeostasis

PGs in stomach mucosa (protective)

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8
Q

what is the role of COX2?

A

production of inflammatory molecules

essential for normal kidney function

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9
Q

what are the nonselective NSAIDs?

A 
acetylsalicylic acid (aspirin) 
ibuprofen 
indomethacin
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10
Q

what is the selective NSAID? is it for COX1 or COX2?

A

celecoxib

COX2

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11
Q

once in the blood, aspirin is hydrolyzed to what?

A

salicylic acid

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12
Q

what is the MOA of salicylic acid?

A

reversible COX inhibitor

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13
Q

does aspirin have a potential for drug interactions? why or why not?

A

yes

80% bound to plasma proteins

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14
Q

what are the low dose effects of aspirin?

A

analgesic, antipyretic

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15
Q

what are the high dose effects of aspirin?

A

antiinflammatory

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16
Q

is the acetylation (an inhibition) of COX reversible or irreversible?

A

irreversible

17
Q

the antiinflammatory effects of aspirin come from inhibition of what COX enzyme?

A

COX2

18
Q

the analgesic effects of aspirin come from inhibition of what COX enzyme?

A

COX2

19
Q

what is the MOA of the antipyretic effects of aspirin?

A

blocks production of PGs in CNS to reset temperature control at hypothalamus

fall in temperature due to dilation of superficial blood vessels

20
Q

what is the effect of aspirin on bleeding time?

A

prolongs

21
Q

what are the adverse effects of aspirin?

A

GI tract upset
GI irritation
platelet inhibition

22
Q

GI tract upset from aspirin use is mediated by the inhibition of what COX enzyme?

A

COX1

23
Q

keterolac, naproxen, oxaprozin, piroxicam, and sulindac are what class of drug?

A

NSAID

24
Q

which NSAIDs have less GI adverse effects?

A

COX2 selective inhibitors

25
Q

what is the main adverse effect of the COX2 selective inhibitors?

A

CV thrombotic events

26
Q

what are the COX2 selective inhibitors?

A

celecoxib
etoricoxib
meloxicam

27
Q

which COX2 selective inhibitor is approved for rheumatoid arthritis?

A

celecoxib (celebrex)

28
Q

what are the actions of acetaminophen? does it have antiinflammatory properties?

A

analgesic and antipyretic

no

29
Q

what are the drug interactions for acetaminophen? why?

A

ethanol, isoniazid

metabolism by cyp450

30
Q

what is the MOA of capsaicin?

A

release of substance P leading to depletion and prevention of reaccumulation

31
Q

gout is characterized by accumulations of what type of crystals?

A

monosodium urate (uric acid)

32
Q

what is the primary NSAID used to treat severe gout?

A

indomethacin

33
Q

what is the role of colchicine? what is the MOA?

A

used to be primary gout agent

inhibits leukocyte migration and phagocytosis

34
Q

what are the xanthine oxidase inhibitors?

A

allopurinol

febuxostat

35
Q

what are the uricosuric agents?

A

probenecid

sulfinpyrazone

36
Q

allopurinol and febuxostat are what type of drug for gout?

A

xanthing oxidase inhibitors

37
Q

probenecid and sulfinpyrazone are what type of drug for gout?

A

uricosuric

Year 2 Pharmacology (70 decks)

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