NSAIDs Flashcards
What are the NSAIDs?
They are heterogeneous group having anti-inflammatory, analgesic and antipyretic effects.
Prototype NSAID:
Aspirin
Non selective NSAIDs:
ibuprofen, naproxen, diclofenac, piroxicam and indomethacin.
Selective Cox-2 inhibitor:
Celecoxib
Analgesic-antipyretic with weak anti-inflammatory action:
Paracetamol
Mainly constitutive Cyclooxygenase enzyme that respnsible for forming protevtive PGs in GIT and kidney
Cox-1
Cox Inducible in inflammation, constitutive in endothelium and kidney:
Cox-2
Mechanism of aspirin:
Aspirin ireversibly inhibits (acetylates) cyclooxygenase enzymes (cox1, cox2)》inhibit PG and TXA2 production.
Paracetamol mechanism:
It inhibits PG synthesis mainly in CNS
May act on cox3 (weak anti-inflammatory effect
Its action may involve interaction with the serotonergic and endogenous opioid system
The NSAIDs lower body temp in patients with fever by :
Blocking PGE2 synthesis and release.
NSAIDs have no effect on normal body temp..
True
PGE2 pain mechanism:
It is throught to sensitize nerve endings to the action of bradykinin, and histamine
NSAIDs in pain:
They are mainly for management of pain of low to moderate intensity arising from musculoskeletal disorders rather than that arising from viscera
Advantages over opioid analgesics:
No dependence, no respiratory depression in theraputic doses
Anti-inflammatory action of NSAIDs
– leukocyte migration and – release of lysosmal enzymes.
They inhibit inflammation in arthritis, but they neither arrest the progress of the disease nor induce remission
Common unwanted effects of NSAIDs:
Epigastric distress, ulceration, hemorrhage and iron deficiency anemia
Which PG inhibits gastric acid secretion?
Prostacyclin I2
Which PG stimulate synthesis of protective mucus
PGE2 and PGF2
How to diminish the gastric damage
