Lecture 33 - Analgesic II

Question 1

NSAID function?

Answer 1

reversible inhibition of COX-1 and Cox-2, suppressing prostaglandin production

Question 2

Irreversibly inhibiting NSAID?

Answer 2

aspirin - irreversibly inactivates serine residue

Question 3

Effects of NSAIDS?

Answer 3

decrease inflamm and reliev mild pain (PGs), anti-pyretic, anti-coagulation

Question 4

Prostaglandins?

Answer 4

lipid, potent, short half life, all cells but RBC, autocrine signalling

Question 5

Archidonic Acid?

Answer 5

synthesised linoleate, esterified to cell membrane phospholipids, liberated by phospholipase activation

Question 6

Cox-1?

Answer 6

active in all cells, involved in homeostatic systems, undesireable inhibition by NSAIDS leads to homeostatic disruption

Question 7

Cox-2?

Answer 7

normally dormant, activated to produce excessive inflammation in prostaglandins, induced by cytokines, TNF and growth factor

Question 8

Side effects of COX-2 inhibitor?

Answer 8

gastric, heart attacks, stroke

Question 9

Pharmacokinetics of NSAID?

Answer 9

lipophilic, high bioavailability, high protein binding (low VoD), slow onset

Question 10

Interactions?

Answer 10

anticoag, methotrexate, anti-diabetic, thyroid hormones, digoxin, organic acids

Question 11

Prostaglandins + leukotrines?

Answer 11

eicosanoids

Question 12

Aspirin processing?

Answer 12

acetyl salicyclic acid, passive diffusion in stomach, hydrolysed to salicyclic acid in liver, bind to albumin, excreted in competition with uric acid

Question 13

low dose aspirin?

Answer 13

irreversible acetylates plateletes inhibiting platelet aggregation via cox 1, reducing risk of heart attack and stroke

Question 14

High dose aspirin?

Answer 14

inhibits prostacyclins (vasodilators), not ideal of IHD patients, more side effects

Question 15

NSAIDS and bleeding?

Answer 15

increase bleeding time, loss, risk of haematoma during epidural

Question 16

GI Tract side effect?

Answer 16

NSAIDs irrate mucosa directly, also inhibit synthesis of gastric cytoprotective prostanoid (PG) to protect against acid damage - increased bicarbonate/decreased acid secretion, increasing mucus synthesis

Question 17

Aspirin triad?

Answer 17

intolerance (rhinitis and flushing), severe asthma, nasal polyps

Question 18

Aspirin and asthma?

Answer 18

inhibition of Cox 1 and 2 -> decreased PGE2 (bronchodilator) -> lipoxygenase pathway (inflam)

Question 19

Reye’s syndrome?

Answer 19

encephalopathy, fatty liver, increased ammonia, half fatal, children prone after viral illness