Pharm Exam 4, 2014

Front 1

Celecoxib, rofecoxib

Back 1

Selective COX 2 inhibitors

Front 2

Indomethacin, etodolac

Back 2

Acetic acid derivatives

Front 3

Prototype NSAID to which others are measured

Back 3

Indomethacin

Front 4

Potent COX 1 and 2 blocker

Back 4

Indomethacin

Front 5

High incidence of GI ulceration

Back 5

Indomethacin

Front 6

Semi selective COX 1,2 inhibitor. Will still produce GI effects at high doses.

Back 6

Etodolac

Front 7

Typical NSAIDS with short DOA

Back 7

Fenamates

Front 8

Mefanamic acid

Back 8

Fenamate class

Front 9

Not recommended for use in children or pregnant women

Back 9

Fenamates

Front 10

Good analgesic properties, poor anti-inflammatory effects

Back 10

Ketorolac

Front 11

Enolic acid class:

Back 11

Meloxicam

Front 12

Relatively COX 2 selective, close to celecoxib

Back 12

Meloxicam

Front 13

Greater COX 2 potency than most traditional NSAIDs

Back 13

Diclofenac

Front 14

Potentially less GI toxicity than traditional NSAIDS

Back 14

Diclofenac

Front 15

Potentially greater cardiac toxicity than traditional NSAIDS

Back 15

Diclofenac

Front 16

Diclofenac + misoprostol

Back 16

Arthrotec

Front 17

ASA intolerant people should not take:

Back 17

Ibuprofen

Front 18

Representative propionic acid derivative:

Back 18

Ibuprofen

Front 19

GI bleeding, decreased renal function, hepatitis, edema

Back 19

Ibuprofen adverse effects

Front 20

COX 2 inhibitors are approved for:

Back 20

Dysmenorrhea, OA, RA, acute post op pain

Front 21

COX 2 inhibitors are contraindicated in _____ allergy and _____ of pregnancy

Back 21

ASA; 3rd trimester

Front 22

Advantage of COX 2 inhibitors:

Back 22

Less GI ulcers, less effect on platelets and bleeding time

Front 23

COX 2 disadvantage:

Back 23

No more effective as analgesics than nonselective COX inhibitors

Front 24

Platelet aggregation promoter present in platelets that is not affected by COX 2 inhibitors

Back 24

Thromboxane A2

Front 25

Platelet aggregation inhibitor present in endothelium selectively suppressed by COX 2 inhibitors

Back 25

Prostacyclin (PGI2)

Front 26

COX 2 inhibitors: shifts ratio of TXA2/PGI2 toward exaggerated :

Back 26

Thrombotic response

Front 27

COX 2 inhibitors: higher dose and longer duration of tx increase:

Back 27

CV and renal toxicity

Front 28

No anti-inflammatory or anti-thrombotic effects

Back 28

Acetaminophen

Front 29

Weak prostaglandin inhibitor

Back 29

Acetaminophen

Front 30

Does not affect uric acid levels

Back 30

Acetaminophen

Front 31

Tylenol toxicity doses:

Back 31

10 g causes injury; 15 g probably fatal

Front 32

The intermediate metabolite of tylenol is:

Back 32

Toxic to the liver if it can not be cleared fast enough

Front 33

Initial tylenol OD s/s

Back 33

N/V, diarrhea, abd pain

Front 34

Progressive s/s of tylenol OD:

Back 34

Elevation of SGOT, LDH, and PT

Front 35

End s/s of tylenol OD:

Back 35

Renal failure d/t ATN

Front 36

Tylenol: half life of drug increases with:

Back 36

Liver damage

Front 37

Tylenol metabolism: Secondary metabolic pathway is via ______ which transform it to N-acetyl-benzoquinoneimine

Back 37

CYP enzymes

Front 38

Tylenol OD: do not administer _____

Back 38

Emetics

Front 39

Tylenol OD: give ____

Back 39

Activated charcoal

Front 40

____ helps the body detoxify the hepatotoxic metabolite by restoring depleted _______ levels (gives more precursors)

Back 40

NAC/ glutathione

Front 41

If tylenol ingestion is significant, begin ______ administration

Back 41

N-acetylcystine