NSAID’s Flashcards
How do NSAID’s create an antipyretic effect (reduce fever)?
Inhibit PGE released from hypothalamus
What two eicosanoids are effected due to COX inhibition?
PGE2 and PGI2
They cause:
- vasodilation
-swelling
-pain
What effect does PGE1 and PGE2 have on pain?
Both sensitise nociceptive afferent nerve terminals to bradykinin
(In concentrations of Bradykinin too low on its own to cause pain)
What interacts with NSAID’s?
*anticoagulants
*ACE inhibitors
*lithium
*methotrexate
What is the role of PGE2 and PGI2 on the Gastric mucosa?
*keeps increased barrier thickness
What is the effect of PGE2 and PGI2 on the stomach?
Renders stomach susceptible to damage
What is the effect of PGE2 on the kidneys?
*maintains renal flow and electrolyte balance
*inhibition effects kidney function
What are the harmful effects of COX inhibition?
*gastric mucosa susceptible to damage (PGE2 and PGI2)
*impaired renal function (PGE2)
*reduced platelet function (TXA2)- increased bleeding time
What are the side effects of NSAID’s?
*GI complications
*renal failure
*platelet dysfunction- increased bleeding
*bronchospasm
*skin reactions
What are the GI side effects?
*heartburn, nausea, abdominal pain
*mucosal ulcers
*perforated ulcers, bleeding
What is the hypothesis for COX inhibition?
*inhibition of COX 2 = therapeutic effect, inhibition of COX 1 enzymes= side effects
What NSAIDs have the lowest risk of GI toxicity?
Ibuprofen and Diclofenac
Celecoxib and etoricoxib
What is the relationship between GI toxicity and selectivity?
The NSAID’s with highest COX 2 selectivity have the lowest risk of toxicity
Diclofenac
Ibuprofen
Suldinac
Indometacin
Piroxicam - most toxic but least COX 2 selective
What is an example of a COX1 specific inhibitor?
Aspirin
What are examples of non specific cox inhibitors?
Diclofenac and ibuprofen
