Chemistry of NSAIDs Flashcards
What are the effects that NSAIDs have
Analgesic, antipyretic (fever reducing), anti-inflammatory effects
What is the precursor to aspirin, more bioabailable alternative that is easier on the stomach
Salicylic acid, acetylsailicylic acid
What is the precursor for certain imflammation mediators, what enzyme is inhibited by NSAIDS
Archidonic acid, cyclooxygenase (COX)
Which products from COX are most likely to be effected by NSAIDS
PGE2: inflammation, fever and pain/ PGI2: anti-aggregatory and hyperalgesic/ TXA: platelet aggresgation
What are concerns with COX-2 selective inhibition, products of COX affected
Increase the risk of heart attack (promote thrombosis), less PGI2 and TXA
T/F: Parietal gastic cells allow for proton pums and superficial epithelial cells interact for mucus production
True
What is the dual insult of prostaglandins with regards to the GI system
Increased gastric acid secretion and diminished mucus secretion on epithelial mucosa
What class of NSAIDs are more potent than salicylic acid, why
Fenamates, two aromatic rings
What are the msot selective COX-2 inhibitors
Meloxicam, Nimesolide, Celecoxib, Etodolac, Rofecobix
How do NSAIDs prevent activation of COX, how is acetylsalicylic acid different
Competitive inhibition, acetylates the enzyme
T/F: APAP is an NSAID
False” APA has little to no binding to the COX-1 and COX-2 enzymes therefore having no antiinflammatory action
What is the theory behind APAP not having anti-inflammatory function
APAP is oxidized by peroxides not allowing tyrosine to be oxidized for PGG2 synthesis
