1-OTC painkillers Flashcards
What are prostaglandins
sensitive nociceptors to the effects of other pain-causing stimuli
which NSAID is not anti-inflammatory
acetaminophen
name 5 examples of OTC NSAIDS
naproxen (aleve), ibuprofen (advil), acetylsalicytic acid (bayer aspirin), acetominophen (tylenol), diclofenac (voltaren)
what do CGRP and Substance P do
cause vasodilation and histamine release
what is the prostaglandin synthesis pathway
arachidonic acid released from cell membranes
COX enzymes turn them into PGH2
then they get isomerated into different compounds (TxA2, PGE2…)
A.A –COX12–> Prostaglandins
which COX promotes gastric mucous secretion
COX 1
which COX promotes inflammation
COX 2
which COX promotes platelet aggregation and vasoconstriction of vessels
COX 1
which COX is known for the good side effects of inhibition by NSAIDS
COX 2
which COX is known for the bad side effects of inhibition by NSAIDS
COX 1
first NSAID sold
acetylsalicytic acid (aspirin)
NSAID Structure (3 things)
weak acid with carboxy group, hydrophobic, non-specific
why is it good that NSAIDS are hydrophobic
allows them to enter active sites
what class is aspirin in
salicylate
what class is ibuprofen in
propionic
what class acetaminophen
aminophenol
what class diclofenac
acetic acid
what class naproxen
propionic
how does aspirin work
irreversibly modifies COX enzymes by donating acetyl group to ser529 (cox1) and ser516(cox2)
what are other NSAIDS competitive inhibitors of
arachidonic acid
what do interleukins do
released from immune, induces COX2 in CNS and results in PGE2 formation
where are PGE2 receptors found
hypothalamus
what does PGE2 activation in hypothalamus cause
fever
how do NSAIDS stop fever
dont let COX2 make PGE2 (interleukin pathway)
how do NSAIDS stop headache
reduction in prostaglandins that cause vasodilation
why can NSAIDS be bad to tummy
because they stop COX1 which make gstric mucose and inhibit acid secretion
what so special about celecoxib
COX2 inhibition 30:1 over COX1
why they make coxibs
so that you only get COX2 inhibition, but not really as good as you would want because it increases bad heart things
who has a bigger active site, COX1 or COX2
COX2
which drug is the leading cause of liver failure
acetaminophen tylenol!
what does acetaminophen get turned into in the liver
toxic metabolite NAPQI (by CYP enzymes)
how is acetaminophen’s toxic metabolite usually detoxified
glutathione addition/conjugation
how is aspirin primarily used
decreasing thrombotic events by inhibiting thromboxane A2 in platelets
what is salicylism
symptoms from aspirin overdose
what is acetaminophen primarily used for now
analgesic and antipyretic, weak anti-inflammatory
how does acetaminophen work
inhibit COX3
which drugs boosts the endocannabinoid system
acetaminophen
