NSAIDS

Question 1

Non selective NSAIDS

Answer 1

Aspirin
Diclofenac
Ibuprofen
Indomethacin
Ketorolac
Piroxicam
Tolmetin
Acetaminophen (not NSAID)

Question 2

COX-2 Selective

Answer 2

Celecoxib
Etoricoxib
Meloxicam (not as selective)

Question 3

What happens when you inhibit COX

Answer 3

Decreased PGs and TXA

Question 4

Which COX is constitutive

Answer 4

1

Question 5

Where is COX-2 constitutive

Answer 5

Kidney

Brain

Question 6

What naturally induces COX-2

Answer 6

Growth factors
Tumor promoters
Cytokines

Question 7

What effects do NSAIDs have

Answer 7

Antipyretic
Analgesic
Anti-inflammatory

Question 8

Blocking which COX can cause GI damage

Answer 8

1

Question 9

What does endothelial COX-2 activation lead to

Answer 9

Vascular Prostacyclin

Question 10

What sensitizes nerve endings to pain

Answer 10

PGE2

Question 11

NSAIDs or opioid better for inflammatory pain

Answer 11

NSAIDs

Question 12

What is responsible for fever

Answer 12

COX-2 –> PGE2

Question 13

What are NSAIDs useful for treating

Answer 13

RA
OA
Gout

Question 14

DOC closing ductus arteriosis

Answer 14

Indomethacin

Question 15

DOC gout Sx

Answer 15

Indomethacin

Question 16

Why can Celecoxib cause HS reactions

Answer 16

Sulfonamide

Question 17

What happens if you give child with viral fever, Aspirin

Answer 17

Reye’s

Question 18

What do you give child with viral fever

Answer 18

Acetaminophen/Ibuprofen

Question 19

Contraindication

Answer 19

Pregnancy

Aspirin is Category D

Question 20

DOC OA and pregnancy

Answer 20

Acetaminophen

Question 21

Tx for Colon cancer

Answer 21

Aspirin

Question 22

Give for niacin flushing

Answer 22

Aspirin

Question 23

Tx GI ulceration from COX-1 inhibition

Answer 23

Misoprostol
PPIs
H2 blockers

Question 24

Lowest risk of GI ulceration

Answer 24

Celecoxib

Question 25

Highest risk of GI ulceration

Answer 25

Piroxicam

Question 26

Why are there CVS AEs with NSAIDs

Answer 26

Imbalance of TXA2 and PGI2

Question 27

Higher CV risk but lower GI effects

Answer 27

COX-2 inhibitors

Question 28

What are the CVS AE of NSAIDs

Answer 28

Vasoconstriction
Platelet aggregation
Thrombosis

Question 29

Renal AE of NSAIDs

Answer 29

Decreased RBF
AIN
Analgesic nephropathy

Question 30

What happens with decreased PGE2

Answer 30

Sodium and water retention (Decreased GFR)

Question 31

What happens with decreased PGI2

Answer 31

Hyperkalemia and ARF

Question 32

What is the most common cause of AIN

Answer 32

NSAIDs and ABX

Question 33

What is the effect of chronic NSAID use

Answer 33

Analgesic nephropathy and papillary necrosis

Question 34

Aspirin effect on uric acid

Answer 34

Low dose reduces secretion

High dose inhibits reabsorption

Question 35

What is seen in Aspirin HS

Answer 35

Rhinitis
Edema
Asthma

Question 36

Why does Aspirin HS occur

Answer 36

Excess LT synthesis

Question 37

Which NSAIDs are irreversible

Answer 37

Aspirin/Salicylates

Question 38

What happens with Aspirin induced uncoupling of oxidative phosphorylation

Answer 38

Increased CO2 and respiration
Hyperventilation (resp centre at high doses)
Resp paralysis (toxic levels)

Question 39

How does Aspirin/Salicylates increase BT

Answer 39

Decreased TXA2 in platelets but unaffected PGI2 levels

Question 40

What kind of elimination does Aspirin undergo

Answer 40

Zero order

Question 41

What can chronic Aspirin use cause

Answer 41

Hepatic injury

Question 42

What is Salicylism

Answer 42

HA
Confusion
Tinnitus
Dizziness

Question 43

Acid/Base effects of Aspirin

Answer 43

Resp alk

Metab acid