Analgesics Flashcards
Pathophysiology behind NSAIDs, steroids, opioids etc. (14 cards)
How is arachidonic acid formed?
formed from phospholipids from the cell membrane
What enzyme frees arachidonic acid from phospholipids?
phospholipase A2
What do steroids act on to cause an anti-inflammatory response?
they inhibit phospholipase A2 from forming arachidonic acid
What are the 2 possible pathways that come from arachidonic acid?
COX is used to make prostaglandins
LOX is used to make leukotrienes
What do NSAIDs and aspirin act on to cause an anti-inflammatory response?
they are COX inhibitors, so prevent prostaglandins being formed from arachidonic acid
Why can NSAIDs and aspirin potentially worsen asthma symptoms?
this is because COX is inhibited, so more arachidonic acid will go down the LOX pathway instead, and therefore be used to make leukotrienes, which are bronchoconstrictors
Name three things that prostaglandins promote
pain
fever
inflammation
What can COX 1 do that COX 2 cannot do?
produce thromboxane for pro-coagulation
produces prostaglandins that protect the stomach epithelium from HCL
Name the 2 different types of NSAID’s
classical
selective
Describe the mechanism of action of classical NSAID’s
these inhibit COX 1 and 2
therefore, they increase the risk of peptic ulcers and increase the risk of bleeding (as COX-1 inhibits these)
What are the side effects/risks of classical NSAID’s
increased risk of peptic ulcers
increased risk of bleeding
Name three examples of classical NSAIDs
ibuprofen
naproxen
diclofenac
Describe the mechanism of action of selective NSAID’s
only inhibits COX-2
therefore there is a reduced risk of peptic ulcers but an increased risk of clotting
What are the side effects/risks of selective NSAID’s?
COX-1 is still producing thromboxane, whilst COX-2 inhibition is reducing prostacyclin
this increases the risk of blood clots and therefore complications e.g., stroke, MI
