NSAIDs Flashcards
what are the 3 therapeutic effects of NSAIDs
analgesia
anti-inflammatory
anti-pyretic
how do NSAIDs work
they competitively inhibit the active site for arachnionic acid on the COX 2 enzymes
how are prostaglandins synthesised
arachidonic acid is cleaved from cell membrane phospholipids. this is then converted into prostaglandins by cycle-oxygenase enzymes
which cox enzyme causes ADRs when blocked
cox 1
which cox enzymes slows for therapeutic effects when blocked
cox 2
describe the pain pathway
nociceptors detect pain and send signals through afferent C fibres
this travels in the spinothalamic tract to the somatosensory Cortex
how do prostaglandins produce pain
PGE2 binds to EP1 receptors on C fibres
this increases the activity of the fibre to cause pain
what happens to prolonged pain
- there becomes an increase in cox 2 and PGE2 synthesis to increase sensitivity to pain
- lack of production of glycine mean pain c fibres cant be inhibited
how do prostaglandins contribute to pyrexia
PGE2 binds to EP3 receptors to cause an increase in heat production and decreased heat loss
what stimulates PGE2 synthesis to cause pyrexia
the release of interleukin 1 from macrophages
what happens when sulphonylurea is given with NSAIDs
hypoglycaemia
what happens when warfarin is given with NSAIDs
increased bleeding
how do aspirin work differently to other NSAIDs
binds irreversibly to inhibit cox enzymes
how does aspirin affect the CVS system
inhibits platelet cox enzymes, preventing platelet aggregation - meaning its cardio protective
what are the 3 types of endogenous opioids
beta-endorphin
met-enkephalin
leu-enkephalin
