nsaids Flashcards
(29 cards)
what do nsaids do?
inhibit cox
what do prostacyclin do
causes vasodilation, inhibit platelet aggregation
What do prostaglandins do
vasodilation, vascular permeability, pain
Has certain roles on GI as well
- reduce gastric acid secretion
- increase mucosal blood flow
- increase mucus secretion
- increase bicarbonate secretion
whatdo thromboxanes do
increase platelet aggregation and vasoconstriction
What is aspirin
acetylsalicylic acid
What does aspirin do
analgesic, anti pyretic, antiplatelet
how does aspirin achieve its analgesic effect
block prostaglandin which sensitises the nociceptive fibers to stimulation by other inflammatory mediators
why is there an analgesic ceiling for aspirin
because other mediators like bradykinin and leukotriene can also activate and stimulate the nociceptive fibers
What are the adverse effects of aspirin
normal dose can cause Gastric intolerance, bleeding, hypersensitivity.
mild dose can cause
- tinnitus, uricosuric, fever dehydration, metabolic acidosis, central hyperventilation respiratory alkalosis
sever can cause coma, vasomotor collapse, hypothrombinaemia, renal and respiratory failure.
Reye’s syndrome- encephalitis and liver, vomitting, personality changes, delirium, listlessness, convulsions.
When is reyes syndrome’s risk increased
when taken by children with viral infections
What are some other examples of NSAIDS
- Naproxen
- indomethacin
- diclofenac
What are the properties of indomethacin
strongly anti-inflammatory due to additional steroid like phospholipase A inhibition
can have CNS effect 15-25% confusion or depression, psychosis, hallucination
What is naproxen used for
dysmenorrhoea
What is diclofenac used for
used for inflammatory joint disease as they have longer half life in synovial fluid
What are the GI effects when NSAIDS block COX
- dyspepsia, nausea vomiting
- ulcer formation, potential hemorrhage risk in chronic ulcers
What are the renal effects of NSAIDS
inhibiting PGE2 results in sodium retention. Because PGE2 inhibits Na+ reabsorption in the thick ascending limb where 25% of Na is reabsorbed.
inhibiting PGI2 results in suppression of renin and aldosterone secretion, as well as acute renal failure.
- Leading to hyperkalemia. Because aldosterone increase K+ excretion, suppressing it results in K+ retention in the blood
Why does inhibiting PGI2 results in supression of aldosterone, but Na+ reabsorption is still increased?
Because it prevents reabsorption of only 1-2% at teh DCT, cannot correct for the absorption of 25% in the thick ascending limb
What are some other adverse effects of NSAIDS
- pseudo allergic reactions
- bleeding, failure of hemostasis which leads to bleeding
- asthma, can trigger bronchospasms
why might effects be stronger for aspirin as compared to other nsaids
because aspirin is a irreversible cox inhibitor
when is cox 2 induced
when there is an inflammation
What are some examples of COX2
parecoxib, parecoxib, etoricoxib
why are cox 2 selective inhibitors better
they reduce adverse GI effects
Where is cox 2 constitutive in
CNS, Kidney, female reproductive tract, synovium of joint
which of the following do cox-2 inhibitors inhibit?
TXA2, PGI2, PGE2
PGI2, PGE2
