Inflammation Lecture 2 Flashcards
What is the mechanism of action of aspirin
Non selective inhibition of COX 1 and 2 receptors
Irreversible inhibition of COX-1 (anti platelet)
What is the mechanism of action of Naproxen, Diclofenac and ibuprofen
Non selective inhibition of COX 1 and 2
What are COX-2 selective inhibitors
Celecoxib
Etoricoxib
Describe how the pyretic effect occurs and how NSAIDS block this (antipyretic effect)
- PG formation (PGE2) in hypothalamus triggered by fever causing pathogens (bacterial endotoxin, IL-1)
- NSAIDs prevent prostaglandin production- reduce temperature (anti-pyretics)
How do NSAIDS have an analgesic effect
Reduction of formation of prostaglandins that sensitise pain nociceptors- they increase or sensitise pain produced by other inflammatory mediators like bradykinin
What inflammatory mediators do NSAIDS effect to reduce vasodilation
PGE2 and PGI2
Where are the unwanted gastric effect from NSAIDS coming from
Inhibition of COX-1 derived prostaglandin functions
COX-1 normally decreases acid secretion and promotes mucosa formation
What is the flowchart of inflammation starting from phospholipid
Phospholipid is converted to Arachidonate via phospholipase A2
Arachidonate is converted to cyclic endoperoxides via cycloxygenase
Cyclic endoperoxides are converted to PGI2 (Vasodilator, stop platelet aggregation) or TXA2 (thrombotic vasoconstrictor)
PGI2 stimulates vasodilation and stops platelet aggregation
How do corticosteroids have its anti-inflammatory effect
Reduces prostaglandin synthesis
reduced COX-2 expression
Reduced PLA2 activity
Reduced cytokine generation- movement of neutrophils from blood to inflammatory sites
Reduced production of NO
What are the unwanted effect of glucocorticoids
Suppression of immune system- infection susceptible
Osteoporosis
Reduced wound healing
CUSHING SYNDROME- too much cortisol in body
