May act at the site of injury and decrease inflammation (NSAIDS)
May alter nerve conduction (L.A)
May modify transmission in the dorsal horn(opioids, antidepressants)
Affect the emotional aspects and central component of pain(opioids, antidepressants)
what is ASA half life? absorption? peak levels?
what may happen if ASA given to a child?
Half life 2-19 hrs, Good po absorption, peak levels after 1 hour
Reyes syndrome may occur if given to a febrile child-may cause seizures, coma and death
what type of pain is acetaminophen used for? what is protein/lipid binding? MOA? does it cross BBB?
for mild/mod pain, weak antiinflammatory, highly lipid soluble, poor protein binding, crosses BBB
MOA via central noradrenergic/serotonergic system, modulates dynorphin & K receptor function. Direct inhibition of COX 2 PGE 2 release, spinal inhibition of NO generating impairment of NMDA release
is acetaminophen COX 1, 2 or 3? peak effects?
what type of pain is it good for?
main adverse effect?
weakly inhibits CoX 1 and 2, inhibits COX 3
first drug od choice for mild/moderate pain
main adverse effect is hepatic centrilobular necrosis
almost entirely metabolized by the liver, greater toxicity with P450 induction
what is the IV version of tylenol?
used for mild to moderate pain and moderate to severe pain with adjunctive opioids
what type of pain are NSAIDS used for? lipid solubility and protein binding? BBB crossing? metabolized how? excreted where? dosing for hepatic or kidney problems?
mild to moderate pain in combo with other analgesics for inflammatory pain
highly lipid soluble and poorly protein bound
crosses BBB esp (indomethacin)
metabolized in liver excreted via kidneys
hepatic or renal disease requires lower doses
are NSAIDS analgesics?
no they function as antiinflammatories & analgesics providing synergism to opioid analgesics
what is the MOA of NSAIDS?
COX 1 products maintain the integrity of gastric mucosa
COX 2 inhibition (prostaglandin inhibition) causes analgesic & antiinflammatory effects by 1.reducing conversion of AA to prostaglandin 2. inhibition of prostaglandin E 3.inhibiton of prostacyclin and thromboxane 4.
what is the final MOA of NSAIDS?
decrease recruitment of phagocytes, decrrease free radicals, decrease phospholipase C activity in macrophages, decreased rheumatic factor production & block NO synthase
what are the adverse effects of NSAIDS? what increases the r/o adverse effects?
increase myocardial effects of rofecoxib, increase hepatic transaminase levels, renal effects ( NA reabsorption, tubular dysfunction, nephritis, and renal failure