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Pharmacology III > NSAIDs > Flashcards

NSAIDs Flashcards

1
Q

______ are inflammatory mediators that can cause bronchospasm.

A

Leukotrienes, PGs, TXA

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2
Q

______ is a potent vasodilator and platelet inhibitor generated mostly by COX-2

A

prostacyclin

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3
Q

_______ is a potent vasoconstrictor and platelet aggregator generated mostly by COX-1

A

TXA2

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4
Q

This drug is a nonselective, irreversible COX1 and COX2 inhibitor

A

ASA

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5
Q

describe the kinetics of ASA at high doses above 600mg…

A

zero order

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6
Q

________ of urine promotes excretion of ASA

A

Alkalinization

acids ionize in basic soln., ionized cannot cross membranes

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7
Q

4 effects of ASA

A

analgesic
antipyretic
anti-inflammatory
anti-platelet

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8
Q

how long does ASA last? why?

A

8-10 days… until new platelets

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9
Q

Long term use of ASA decreases risk of…

A

CRC

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10
Q

Progression of ASA metabolic adverse effects…

A

low dose respiratory alkalosis

THEN

high dose metabolic/resp acidosis

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11
Q

A single dose of ASA ______ bleeding time

A

doubles

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12
Q

ASA should be stopped _______ before elective surgery

A

1 week

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13
Q

______ doses of ASA decrease uric acid excretion, _______ doses increase uric acid excretion

A

Low ASA = decreased

High ASA = increased

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14
Q

ASA competes with uric acid at the ______ receptor

A

OAT-2

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15
Q

ASA asthma occurs due to…

A

increased leukotrienes (COX inhibition –> 5-LOX activity)

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16
Q

Is ASA teratorgenic?

A

no

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17
Q

Which NSAID should be avoided with these conditions?

•
gastric ulcer
•
severe hepatic damage
•
hypoprothrombinemia
•
Vitamin K deficiency
•
hemophilia
A

ASA

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18
Q

Fatal dose of ASA is…

A

20g

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19
Q

This is a salicylic acid derivative that is NOT metabolized to salicylic acid…

A

diflunisal

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20
Q

does diflunisal have CNS action and therefore antipyretic action?

A

no

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21
Q

Reverse COX-2 inhibitor with less gastropathy/GI risk

A

Celecoxib

22
Q

What increases the risk fo cardiovascular disease with celecoxib?

A

increased TXA2 = platelet aggregation

COX-2 Inhibition shifts to favor TXA2 production from COX-1

23
Q

the below are contraindications for which drug?

GI disease, asthma, breast feeding,
pregnancy, renal failure,

A

celecoxib

24
Q

Nonspecific, reversible inhibitor of COX-1 and COX 2 w. lowest SE profile

A

ibuprofen

25
Q

ibuprofen has metabolites that produce free radicals… what severe SE can occur due to this?

A

agranylocytosis, aplastic anemia

26
Q

This NSAID reduces PMN migration via PLA inhibition

A

indomethacin

27
Q

This NSAID has very potent anti-inflammatory effects but has high incidence of SEs-

A

indomethacin

28
Q

which NSAID is used for PDA?

A

indomethacin

29
Q

This is a potent COX inhibitor that decreases AA bioavailability

A

diclofenac

30
Q

what can be combined with NSAIDs to limit GI toxicity?

A

misoprostol

31
Q

This is an NSAID that is used as an analgesic in post-op pain, and may be combined with opiates to reduce opiate burden

A

ketorolac

32
Q

combining _____ with ASA reduces effects on platelets

A

ibuprofen

33
Q

What is the mean half-life of naproxen?

A

13 hours

34
Q

does naproxen cross the placental barrier?

A

yes

35
Q

what NSAID is bound to plasma proteins, where displacement can cause drug interactions? (particularly warfarin)

A

naproxen

36
Q

These two NSAIDs inhibit PMN migration and lymphocyte function. They also decrease ROS production

A

“-oxicams”

piroxicam, meloxicam

37
Q

This is an NSAID not on the market in the US, it has serious SEs but is very potent

A

phenylbutazone

38
Q

3 side effects of acetaminophen…

A

skin rash
ASA cross-sensitivity
neutropenia

39
Q

major serious SE of acetamiophen

A

hepatic necrosis

40
Q

What is the dose of acetaminophen that can cause hepatotoxicity?

A

10-15g

41
Q

what dose of acetaminophen can be fatal?

A

25g

42
Q

2 labs that can show acetaminophen toxicity

A

serum transaminase

lactic acid dehydrogenase

43
Q

acetaminophen toxicity can progress to what three things?

A

encephalopathy, coma, death

44
Q

______ is responsible for acetaminophen’s liver damage

A

intermediate metabolite

45
Q

When does toxicity occur biochemically in acetaminophen administration?

A

when metabolites exceed reduced glutathione

46
Q

specific antidote for acetaminophen poisoning and timeline

A

N-acetylcysteine w/in 10 hours

47
Q

Which NSAID?

Hx of PUD, but not active

A

celecoxib

NSAIDs + misoprostol or prazols

48
Q

Which Analgesic?

active PUD

A

acetaminophen or opioids

49
Q

COX1 or COX2?

produces G protective PG production

promotes platelet aggregation and vasoconstriction

A

COX-1

50
Q

COX1 or COX2?

Promotes inflammation

inhibits platelet aggregation

promotes vasodilation

A

COX-2

Pharmacology III (15 decks)

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