NSAIDS Flashcards
What are the 3 classes of prostanoid?
Prostaglandins, prostacyclin and thromboxanes
What do NSAIDS cause?
Inhibition of down stream products of arachidonic acid
What is arachidonic acid derived from?
linoleic acid, converted in the liver
Where is arachidonic acid found?
throughout the body, particularly muscle, brain and liver
Why do PGI2 and TXA2 oppose each other?
PGI2 inhibits platelet aggregation and TXA2 promotes platelet aggregation
What is the difference between COX-1 and COX-2?
COX-1 is constitutively active in most tissues and COX-2 is inducible in chronic inflammation, it also has a larger substrate channel
What type of receptor do prostanoids signal through?
GPCRs ( many types)
Name 2 autocoids
Bradykinin and histamine
What is the common mode f action for an NSAID?
Inhibition of COX, decreasing prostanoid synthesis, by competing with arachidonic acid for hydrophobic site of COX
How does an NSAID work as an anelgesic?
Reduces PGE2 synthesis in dorsal horn, reducing neurotransmitter release and therefore reducing excitability of neurones in pain pathway
How do NSAIDS work as an anti-inflammatory?
Reduce production of prostaglandins preventing vasodilation and oedema
How do NSAIDS work as an antipyretic?
Inhibition of hypothalamic COX-29(usually stimulated by pyrogens), preventing prostaglandin synthesis and reducing temperature
Name 3 ADRs
Dyspepsia, nausea, peptic ulceration, bleeding and perforation
How do NSAIDS affect the kidneys?
Cause reversible reduction in GFR and renal blood flow, prevent vasodilation of afferent arteriole
What is a problem with selective COX-2 inhibitors?
Inhibit PGI2 but not TXA2 potentially leading to unapposed aggregatory effects
