NSAIDS

Question 1

Arachidonic acid

Answer 1

essential fatty acids

most abundant and important precursor of eicosanoids

released from the membrane phospholipids by PLA2

corticosteroids suppresses the productions PLA2

Question 2

Oxygenation of arachidonic acid

Answer 2

COX: prostaglandins and thromboxanes

Lipoxygenase: Leukotrienes

Epoxygenase: epoxides

Free radicals: isoprostanes

Question 3

PGH synthase

Answer 3

both cyclooxygenase and hyper peroxidase activities

COX reactions requires a free radical

Hydroperoxidase reaction converts OOH to OH

Question 4

COX 1 vs. COX 2

Answer 4

COX 1 is expressed in various tissues
Housekeeping function

COX 2 is expressed upon stimulus in inflammatory and immune cells
stimulated by GF, tumor promoters, and cytokines

Inhibited by NSAIDS

Question 5

Prostaglandins vs. Thromboxanes

Answer 5

PGI2: vascular epithelia, vasodilator, blocks platelet aggregation

TXA2: platelets, vasoconstrictor, induce platelet aggregation

Question 6

Mechanism of action of NSAIDs

Answer 6

inhibitor of PGHs or COX which catalyzes the production of prostaglandins

Question 7

Salicylates

Answer 7

aspirin

Question 8

Arylacetic acids

Answer 8

indomethacin

Question 9

Arylproprionic acids

Answer 9

ibuprofen

Question 10

Non-carboxylate NSAIDs

Answer 10

meloxicam

Question 11

COX-2 selective NSAIDs

Answer 11

celecoxib

Question 12

Side effects of NSAIDs

Answer 12

dyspepsia, nausea, vomiting

blood loss, ulcer, GI hemorrhage

Blood coagulation

renal

hypersensitivity

Reye’s syndrome: specific to aspirin

CNS

Question 13

Aspirin

Answer 13

only NSAID that irreversibly inhibits COX 1 by acetylating a serine residue in the active site

Blocks TXA2; increases the risk of bleeding but also reduces the risk of MI

Question 14

Selective COX 2 inhibitors

Answer 14

valine binding site of COX2 is sunsituted for isoleucine in that of COX1