NSAIDs Flashcards
NSAIDs definition
Non-steroidal anti-inflammatory drugs
Can be selective or non-selectibe for either COX1 or COX2
Side effects = GI bleeding, increased risk of CV disease (COX2 specific only)
NSAID effects
Periphery = decrease prostaglandin production, leading to desensitisation of nociceptors
Central = decrease prostaglandin production in the spinal cord
Paracetamol
Paracetamol is not an NSAID because it does not reduce inflammation
Main action is as an anti-pyretic and analgesic
Has no accepted mechanism of action
COX3 - paracetamol theory
Postulates that paracetamol is a COX3 inhibitor
COX3 has never been isolated in humans
Nitric oxide synthesis - paracetamol theory
Postulates that paracetamol may inhibit nitric oxide synthesis in the spinal cord
NAPQI- paracetamol theory
Postulates that a metabolite of paracetamol, NAPQI, inhibits neurotransmission, hence reducing pain
Histamine
Released from mast cells in piecemeal degranulation, exosome secretion and anaphylactic degranulation
Histamine receptors
H1 = Gq, causes bronchoconstriction
H2 = Gs, increases gastric acid secretion and heart rate
H3 = Gs, auto-receptor
H4 = Gs, mast cells
Antihistamines
H1 receptor antagonists
Older drugs have anti-muscarinic effect and are therefore sedative
Newer drugs cannot cross the blood brain barrier and so do not act as sedatives
Steroids
Target the glucocorticoid nuclear receptor
Results in a decrease in PLA2 activity and COX expression, limiting prostaglandin synthesis
Gout
Occurs when a joint becomes inflamed due to crystallisation of uric acid in the fluid of that joint
Typical of high meat intake and not drinking enough water
Treatment for gout
Once gout has occured, it cannot be reversed
Acute attacks = NSAIDs (not aspirin), colchicine
Long term = uricosuric drugs, allopurinol
