NSAIDS and Gout Flashcards
NSAIDs-function characteristics
Analgesia
Antipyretic
Anti-inflammatory
NSAID primary target
COX-1 and COX-2 inhibitor=>stop prostaglandin production
NSAIDS clinical uses
Mild/moderate pain Fever Inflammation Antithrombotic Miscellaneous=>menstrual cramps, closure of patent ductus arteriousos, MI/stroke, others.
Aspirin pharmacokinetics
Absorbed into GI tract, hydrolyzed into salicylic acid
Bound to plasma proteins, so potential for drug interactions
Low dose aspirin
analgesic and antipyretic
High dose aspirin
Anti-inflammatory
Aspirin anti-pyretic effects
Blocks prostaglandins in CNS=> resets temperature control in the hypothalamus
Fall of temp is caused by dilation of superficial blood vessels
Aspirin Anti-coagulant effects
Prolongs bleeding time=>inhibition of Thromboxane (TX)
Aspirin Adverse
GI Tract upset=>cox-1 inhibition, dyspepsia, epigastric pain, nausea, vomiting, cramping
GI irritation due to inhibition of cytoprotective PGs (PGE2 and PGI2)
Platelet Inhibition
Decreased kidney function
Main differences between other NSAIDs and aspirin
Duration of action and potency
Non-Selective COX inhibitors
Aspirin Ibuprofen Idomethacin=> gout Ketorolac Naproxen Oxaprozin Piroxicam Sulindac
Cox-2 selective inhibitors
Have analgesic, antipyretic, and anti-inflammatory effects w/ less GI adverse effects
No impact on platelet aggregation=>higher incidence of CV thrombotic events
COX-2 selective inhibitor approved for rheumatoid arthritis and osteoarthritis
Celecoxib
Acetaminophen actions/uses
Pain reliever and fever reducer, but no anti-inflammatory properties
NOT an NSAID
-Used in children and elderly
Acetaminophen safety/adverse
Hepatotoxicity at high doses=>narrow therapeutic index
150mg/kg=>liver necrosis
350mg/kg=:>liver failure
