Flashcards in Painkillers + Paracetamol Deck (12):
How do NSAIDs work?
Inhibit cox-1 & 2, reducing amount of prostaglandins produced in body
What are the good effects of NSAIDs
- Reduce fever -> Il-1 usually triggers PgE to cause reset of thermostat in hypothalamus
- Reduces pain -> Prostaglandins usually sensitise nociceptors to painful sitmuli
- Reduce inflammation - Prostaglandins cause vasodilation and increased vascular permeability
Give 3 main ADRs of NSAIDs
- Reduced PgE2 leads to more permeable gastric mucosa and increases chances of ulcer formation
- Reduced PgE2 leads to constriction of the afferent arteriole in glomerulus, reducing GFR. Can cause Na+/K+/Cl- and H20 retention
- Prolongation of bleeding time (platelet inhibition)
Which COX causes all the bad side-effects of NSAIDs
Give three DDIs of NSAIDs
Warfarin - Increase in concentration -> Increased bleeding
Methotrexate - Increase in concentration
Sulphonylureas - Increase conc -> Hypoglycaemia
How does aspirin inhibit Cox-1?
How is paracetamol usually metabolised?
Glucoronide (60%) or sulphates (30%) in Phase II metabolism
What happens if you take paracetamol overdose/
Enters phase one metabolism
Conjugates with glutathione
Hepatocellular necrosis occurs
How do you treat paracetamol overdose
0-4 hrs -> Charcoal
0-36 hours -> N-acetylcysteine
How do opioids work?
Act pre-synaptically -> Open K+ channels, hyperpolarising neurone and decrease synaptic transmission
Also close voltage gates Ca2+ channels, inhibits release of substance P neurotransmitter
Give three ADRs of opiates