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Rapid

pain relief for minor to severe pain. Basis of the WHO pain ladder. Well known safety profile.

Weak inhibitor of the synthesis of prostaglandins (PG)


MoA similar to those of the selective cyclooxygenase-2 (COX-2) inhibitors.
Serotenergic pathway activation (5HT3)
Endocannabinoid enhancement in the CNS - could lead to antipyretic effect too
Oddly, will decrease PG concentrations in vivo, but wont suppress rheumatoid arthritis inflammation.
Decrease swelling after oral surgery in humans and suppresses inflammation in rats and mice
Inhibition of nitrogen oxide (NO) formation (neurotransmitter of nociception, in the spinal cord)
(NO production is activated by substance P and NMDA receptors)

Multiple synergistic effects reported with opiates and NSAIDs like ibuprofen, some even report
effects with dexamethasone and lidocaine* - boosting analgesia.

With proper use & dose timings (4-6h to a max of 4g daily in adults >50kg) - paracetamol remains the
cornerstone of continued analgesia. It should not be stopped (unless indicated) in patients with pain, should you
escalate to more potent medications. IV to oral switch is a key consideration, but you will lose some of the
analgesic effect. It is an extremely important nursing/medical consideration to ensure timely doses at
appropriate intervals.
http://ceaccp.oxfordjournals.org/content/early/2013/10/10/bjaceaccp.mkt049.full
*http://www.sciencedirect.com/science/article/pii/S1110184915001026?np=y

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