Pharm 3 Nsaids And Acetaminophen

Front 1

Cox-1

Back 1

Thromboxan TXA2 - platelets: causes platelet adhesion andvasoconstriction

prostacyclin PGI2 = endothelium: inhibits platelet adhesion and causes vasodilation, stomach mucoas: protects against acid.

Front 2

Cox-2

Back 2

leads to formation of inflammatory mediators

Front 3

Which NSAID does NOT inhibit both cox-1 and cox-2

Back 3

Celecoxib/Celebrex

Is relatively seelctive for Cox-2 and causes less GI toxicity than nonspecific COX inhibitors, but significant GI toxicity still occurs.

Front 4

AE

Back 4

Gi bleed

prostaglandins are protective of mucosa, so if you inhibit cox-1 it stops being protective and increase risk of bleeding.

Kidney fxn
- Prostaglandins help to open afferent arterioles to let more blood in and filter. If you block prostaglandins, stops it's ability to filter and increases Serum Cr

Front 5

Clinical use of NSAIDs/ASA

Back 5

Analgesic - has ceiling effect

Antipyretic - blocks prostaglandins that help to increase temp

Anti-inflammatory - prostaglandins are responsible for inflammation, increased vascular permeability, and is prevented from forming, reduces erythema, edema, etc.

Antiplatelet
Aspirin permanently inhibits COX, and inhibits TXA2 and PGI2

Front 6

Drug interactions for NSAIDs

Back 6

1. Warfarin - ASA inhibits platelet fxn, more bleeding.
2. Methotrexate - ASA blocks renal tubular secretion of methotrexate, increasing blood levels.
3. Co-admin of ibuprofen w/ ASA negates the anti-platelet activity of ASA - exceptions: celecoxib/celebrex, acetaminophen or with diclofenac

Front 7

NSAIDs - pt r/t var

Back 7

Hypersensitivity
Hx of GI intolerance ot salicylate or active GI lesion
Decreased effective circulatory volume
Renal dysfxn
Low platelet ct