NSAIDs

Question 1

______ are inflammatory mediators that can cause bronchospasm.

Answer 1

Leukotrienes, PGs, TXA

Question 2

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

Answer 2

prostacyclin

Question 3

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

Answer 3

TXA2

Question 4

This drug is a nonselective, irreversible COX1 and COX2 inhibitor

Answer 4

ASA

Question 5

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

Answer 5

zero order

Question 6

________ of urine promotes excretion of ASA

Answer 6

Alkalinization

acids ionize in basic soln., ionized cannot cross membranes

Question 7

4 effects of ASA

Answer 7

analgesic
antipyretic
anti-inflammatory
anti-platelet

Question 8

how long does ASA last? why?

Answer 8

8-10 days… until new platelets

Question 9

Long term use of ASA decreases risk of…

Answer 9

CRC

Question 10

Progression of ASA metabolic adverse effects…

Answer 10

low dose respiratory alkalosis

THEN

high dose metabolic/resp acidosis

Question 11

A single dose of ASA ______ bleeding time

Answer 11

doubles

Question 12

ASA should be stopped _______ before elective surgery

Answer 12

1 week

Question 13

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

Answer 13

Low ASA = decreased

High ASA = increased

Question 14

ASA competes with uric acid at the ______ receptor

Answer 14

OAT-2

Question 15

ASA asthma occurs due to…

Answer 15

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

Question 16

Is ASA teratorgenic?

Answer 16

no

Question 17

Which NSAID should be avoided with these conditions?

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

Answer 17

ASA

Question 18

Fatal dose of ASA is…

Answer 18

20g

Question 19

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

Answer 19

diflunisal

Question 20

does diflunisal have CNS action and therefore antipyretic action?

Answer 20

no

Question 21

Reverse COX-2 inhibitor with less gastropathy/GI risk

Answer 21

Celecoxib

Question 22

What increases the risk fo cardiovascular disease with celecoxib?

Answer 22

increased TXA2 = platelet aggregation

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

Question 23

the below are contraindications for which drug?

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

Answer 23

celecoxib

Question 24

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

Answer 24

ibuprofen

Question 25

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

Answer 25

agranylocytosis, aplastic anemia

Question 26

This NSAID reduces PMN migration via PLA inhibition

Answer 26

indomethacin

Question 27

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

Answer 27

indomethacin

Question 28

which NSAID is used for PDA?

Answer 28

indomethacin

Question 29

This is a potent COX inhibitor that decreases AA bioavailability

Answer 29

diclofenac

Question 30

what can be combined with NSAIDs to limit GI toxicity?

Answer 30

misoprostol

Question 31

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

Answer 31

ketorolac

Question 32

combining _____ with ASA reduces effects on platelets

Answer 32

ibuprofen

Question 33

What is the mean half-life of naproxen?

Answer 33

13 hours

Question 34

does naproxen cross the placental barrier?

Answer 34

yes

Question 35

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

Answer 35

naproxen

Question 36

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

Answer 36

"-oxicams" | piroxicam, meloxicam

Question 37

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

Answer 37

phenylbutazone

Question 38

3 side effects of acetaminophen...

Answer 38

skin rash ASA cross-sensitivity neutropenia

Question 39

major serious SE of acetamiophen

Answer 39

hepatic necrosis

Question 40

What is the dose of acetaminophen that can cause hepatotoxicity?

Answer 40

10-15g

Question 41

what dose of acetaminophen can be fatal?

Answer 41

25g

Question 42

2 labs that can show acetaminophen toxicity

Answer 42

serum transaminase lactic acid dehydrogenase

Question 43

acetaminophen toxicity can progress to what three things?

Answer 43

encephalopathy, coma, death

Question 44

______ is responsible for acetaminophen's liver damage

Answer 44

intermediate metabolite

Question 45

When does toxicity occur biochemically in acetaminophen administration?

Answer 45

when metabolites exceed reduced glutathione

Question 46

specific antidote for acetaminophen poisoning and timeline

Answer 46

N-acetylcysteine w/in 10 hours

Question 47

Which NSAID? Hx of PUD, but not active

Answer 47

celecoxib NSAIDs + misoprostol or prazols

Question 48

Which Analgesic? active PUD

Answer 48

acetaminophen or opioids

Question 49

COX1 or COX2? produces G protective PG production promotes platelet aggregation and vasoconstriction

Answer 49

COX-1

Question 50

COX1 or COX2? Promotes inflammation inhibits platelet aggregation promotes vasodilation

Answer 50

COX-2