Analgesic-Antipyretic & Anti-Inflammatory Drugs

Front 1

General mechanism of NSAIDs

Back 1

--inhibition of PG biosynthesis

--inhibits PG synthetase (cyclooxygenase)

Front 2

Major differences between NSAID analgesics and narcotic analgesics

Back 2

(1) NSAIDs have much lower maximal effects than do opiods
(2) no addiction associated w/ NSAIDs
(3) free of unwanted CNS effects of the opiods
(4) treat low - moderate intensity pain

Front 3

List general side effects of analgesic-antipyretic and anti-inflammatory agents.

Back 3

--GI ulceration, intolerance = most common!

--block platelet aggregation
--inhibit uterine motility
--analgesic abuse nephropathy
--hypersensitivity

Front 4

Which two side effects of nonselective COX inhibitors are NOT shared by selective COX-2 inhibitors?

a) inhibition of platelet function
b) alteration in renal funciton
c) inhibition of labor induction
d) GI ulceration and intolerance

Back 4

These 2 COX-1 inhibitor side effects are NOT shared by COX-2 inhibitors..
(a) inhibition of platelet function
(d) GI ulceration and intolerance

The other side effects (renal function inhibition and labor induction inhibition) are common to both COX-1 and COX-2 inhibitors.

Front 5

Aspirin

--mechanism
--uses
--contraindications

Back 5

Aspirin

Mechanism: irreversible acetylation of COX

Uses: analgesic, antipyretic, anti-inflammatory

(also juvenile RA, dec incidence of colon cancer & MI)

Contraindications: ulcer, gout, asthma, flu

Front 6

Aspirin

--side effects
--signs of intoxication

Back 6

Aspirin

SE's: tinnitus, dec renal function, GI intolerance, hypersensitivity, hepatotoxicity

Intoxication: respiratory alkalosis followed by metabolic acidosis, headache, mental confusion, ringing in ears

Front 7

Diflunisal does not have which of the following effects:

(a) anti-pyretic
(b) anti-inflammatory

Back 7

(a) anti-pyretic

Diflunisal has no anti-pyretic effect but has a greater anti-inflammatory potency compared to aspirin.

Front 8

This NSAID is used to treat IBD.

Back 8

Mesalamine

Front 9

Of the following aspirin effects, which one is NOT shared by acetaminophen?

(a) anti-pyretic
(b) anti-inflammatory
(c) analgesic

Back 9

(b) anti-inflammatory

Acetaminophen is a weak anti-inflammatory drug.

Front 10

Give this antidote within 10 hours of acetaminophen OD..

Back 10

N-acetylcysteine

Front 11

Acetaminophen can be metabolized to these 3 non-toxic metabolites

Back 11

(1) sulfate
(2) glucoronide
(3) glutathione compound which is eventually converted to mercapturic acid

Front 12

This severe adverse effect can result from acetaminophen OD.

Back 12

fatal hepatic necrosis

Front 13

TRUE or FALSE

Chronic alcoholism can increase the risk of acetaminophen toxicity.

Back 13

TRUE

Chronic alcoholism induces P-450 enzymes, which is the key player in forming a toxic metabolite that can cause hepatic necrosis.

Front 14

Indomethacin

--uses
--adverse effects
--what drug inhibits indomethacin renal secretion?

Back 14

Indomethacin

--tx: acute gout, ankylosiing spondylitis, management of patent ductus arteriosus

--adverse effects: GI, CNS severe frontal headache

--probenecid inhibits renal secretion of indomethacin

Front 15

Sulindac

--uses
--rare complication

Back 15

Sulindac

--tx: RA, osteoarthritis, ankylosing spondylitis, acute gout suppress polyp formation in colon cancer

Rare complication: renal stone

Front 16

These 2 drugs can reduce the synthesis of both prostaglandins and leukotrienes.

Back 16

(1) diclofenac
(2) ketoprofen

These drugs inhibit both lipooxygenase and cyclooxygenase enzymes.

Front 17

This NSAID inhibits lipoxygenase and cycloxygenase and is not recommended for children, pregnant or nursing women.

Back 17

Diclofenac

(as a comparison, ketoprofen aslo inhibits lipoxygenase and cycloxygenase)

Front 18

This NSAID can be used short-term for moderate - severe pain.

Back 18

Ketorolac

Front 19

TRUE or FALSE

Ibuprofen has a more potent analgesic effect compared to its anti-inflammatory effect.

Back 19

TRUE

Larger ibuprofen doses are needed to produce anti-inflammatory effects.

Front 20

This NSAID is 20x more potent than aspirin and can cross the placenta.

Back 20

Naproxen

It is used to treat spondylitis, juvenile RA and acute gout.

Front 21

Naproxen

--uses
--potency
--main route of elimination

Back 21

Naproxen

--tx: juvenile RA, acute gout, akylosing spondylitis
--20x more potent than aspirin
--handled mainly by kidneys

Front 22

Name the 5 NSAIDs with (relatively) long half-lives.

Back 22

(1) naproxen -- 14hr
(2) meloxicam -- 20hr
(3) nabumetone -- 24hr
(4) oxaprozin -- 50hr
(5) piroxicam -- 55hr

Front 23

This NSAID is structurally distinct from other NSAIDs and has a long half life.

Back 23

Piroxicam

Front 24

This NSAID inhibits COX-2 over COX-1 and treats osteoarthritis.

Back 24

Meloxicam

(as a comparison, nabumetone also preferentially inhibits COX-2; nabumetone however is a non-acid NSAID and it is also a prodrug)

Front 25

This is the only nonacid NSAID. It preferentially inhibits COX-2 at low dose, but it is not purely selective.

Back 25

Nabumetone

Front 26

This drug is a COX-2 selective inhibitor that is approved for osteoarthritis and RA.

Back 26

Celecoxib

Front 27

List the 3 TNF-alpha blocking agents.

Back 27

(1) etanercept
(2) adalimumab
(3) infliximab

Front 28

Inhibition of lipoxygenase prevents the formation of this molecule.

Back 28

leukotrienes

Front 29

The inducible COX-2 enzyme is involved in the formation of this molecule.

Back 29

prostaglandins

Front 30

The housekeeping COX-1 enzyme is involved in the formation of these 2 molecules.

Back 30

COX-1 involved in formation of:
(1) prostaglandins
(2) thromboxane

Front 31

Name the specific NSAID that would treat each of the following..

(1) short term moderate - severe pain
(2) IBD
(3) management of patent ductus arteriosus
(4) suppression of polyp formation in colon cancer
(5) RA without effect on prothrombin time

Back 31

(1) moderate-severe pain: ketorolac

(2) IBD: mesalamine

(3) patent DA: indomethacin

(4) suppress polyp formation: sulindac

(5) no effect on prothrombin time: celecoxib

Front 32

Why is adminstering N-acetylcysteine appropriate in the case of acetaminophen overdose?

Back 32

In the case of acetaminophen OD, metabolism by conjugation becomes saturated, and the drug is oxidatively metabolized by the CYP enzymes into a toxic metabolite.

N-acetylcysteine is a precursor of glutathione and as such, increases glutathione conjugation of the toxic intermediate. Thus, the toxic intermediate is converted to a glutathione-containing compound rather than a toxic adduct that causes hepatocyte apoptosis and/or liver necrosis.

Front 33

Which 2 NSAIDs and which anti-rheumatic drug would be appropriate for treatment of juvenile RA?

Back 33

Used to treat juvenile RA:

--aspirin
--naproxen
--abatacept

Front 34

Which NSAIDs would be appropriate for treatment of ankylosing spondylitis?

Back 34

Used to treat ankylosing spondylitis..

--indomethacin
--sulindac
--naproxen