NSAIDs and paracetamol Flashcards
NSAIDs MOA
Inhibit COX1 and COX2 enzymes having analgesic, antipyretic, and anti-inflammatory effect
–> reduce prostaglandin synthesis and secretion
COX 1 - house keeping enzyme
COX 2 - induced by inflammatory stimuli
Pharmacological effects and therapeutic uses of NSAIDs
- reduce pain associated with inflammation e.g. gout, RA
- reduce pain
- reduce fever
- anti-thrombotic effects (low dose aspirin)
Non-selective vs selective COX-2 NSAIDs
Non-selective - inhibit both COX1 and COX2 –> block production of both good and bad prostaglandins –> can cause GI ulcer, reduce renal functioning etc.
Selective NSAIDs - only inhibit COX2 enzyme –> block production of bad prostagaldins –> stop pain and inflammation
HOWEVER ADVERSE EFFECTS STILL SAME COMMONALITY DUE TO CONSITUTIVE NATURE OF SELECTIVE NSAIDS
NSAID side effects
- GI bleeding and ulceration (prostaglandins produced by COX1 help form protective mucosal barrier)
- Increased bleeding risk - LDA inhibit platelet aggregation
- reduced renal function - reduced renal compensatory mechanisms
- reduced airway functioning - increased bronchospasm
- can reduce fertility
- prevents oxygen delivery to foetus in pregnancy
Why should NSAIDs be used with caution in some patient groups?
- pregnant women - foetal risks due to poor oxygen delivery
- women trying to become pregnant - poor ovary fertilisation
- asthma - risks of bronchospasm
- renal disease - reduced renal compensatory mechanisms, drug-drug interactions
- cardiac failure - increased bleeding risk
- elderly patients
- hypertension - drug-drug interactions
Pharmacological effects of paracetamol
Analgesic and anti-pyretic effect
- does not exert any anti-inflammatory activity
- contraindicated with NSAIDs
- better tolerated
- drug interactions with warfarin (INR monitoring required)
Paracetamol overdose and its treatment
Overdose can lead to hepatic failure, cell toxicity, renal failure and possibly death,
Treatment - NAC as an antidote
