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COX inhibitor drugs: NSAIDs and Acetaminophen pharm exam 3
Terms in this set (68)
general uses of COX inhibitor drugs
arthritis, bursitis, mild-moderate pain, fever, menstrual and premenstrual symptoms
preventative uses of aspirin
reduces the risk of myocardial infarctions and cerebral vascular accidents (aka strokes). prevents arteriole clots
categories of COX inhibitors
anti-inflammatory drugs and non anti-inflammatory drugs
antiinflammatory COX inhibitor drugs
aka NSAIDs. include aspirin, ibuprofen, naproxen, and celecoxib.
divisions of anti-inflammatory COX inhibitor drugs
divided into first generation and second generation NSAIDS
non antiinflammatory COX inhibitor drugs
include acetaminophen (fever and pain relief but no reduction of inflammation
uses of first generation NSAIDS
reduction of pain, fever, inflammation.
MOA of first generation NSAIDS
irreversibly inhibits COX 1 and COX 2. desired effects stem from COX 2 inhibition while adverse effects stem from COX 1 inhibition
inhibition of COX 2
decreases inflammation, pain, fever, delays and prevents colon cancer
inhibition of COX 1
tissue damage and GI distraction because COX 1 does lots of tissue protection.
first generation NSAID prototype
MOA of aspirin
irreversibly inhibits COX 1 and COX 2
uses of aspirin
inflammation reduction, analgesia, fever reduction, dysmenorrhea, reduction of platelet aggregation (for MI and CVA prevention)
do not give aspirin to children because if they have an existing viral infection this can lead to Reye's syndrome. do not give aspirin to pregnant women because of the risk to the mom and baby.
contraindications with aspirin
patients with peptic ulcer disease, bleeding disorders, and aspirin/NSAID hypersensitivity. due to aspirin causing further gastric damage and anti platelet activity.
administration of aspirin
PO, rapid and complete metabolism
metabolism of aspirin
quickly metabolizes into salicylic acid, an active metabolite. salicylic acid is highly bound to albumin, and crosses all membranes easily (aka crosses BBB). salicylic acid is highly effected by ph, so more basic ph means faster excretion because of ionization
adverse effects of aspirin
GI - gastric distress, bleeding, ulcers. general excessive bleeding, renal impairment, salicylism, and hypersensitivity.
patient education while on aspirin
watch out for any signs of early bleeding like bloody or tar colored stool, bruising.
aspirin and other anticoagulant drugs (warfarin, heparin)
increased bleeding risk
aspirin and glucocorticoid drugs
both damage the gastric lining
aspirin and alcohol
increased gastric bleeding and GI damage
aspirin and other NSAIDS
can block the anti platelet effect of aspirin. teach a patient that if they are in pain, to take more aspirin and not another pain reducer if you are using aspirin daily for anti platelet activity.
symptoms of salicylism
sweating, headache, dizziness, hyperventilation, respiratory alkalosis (kidneys should compensate).
acute poisoning of aspirin
takes about 20-25 grams of aspirin. is a medical emergency
symptoms of acute poisoning of aspirin
respiratory depression, respiratory acidosis, hyperthermia, stupor, coma (increase temp, sweating, dehydration, decreased LOC)
treatment of acute poisoning of aspirin
needs stomach pumped or a decrease in the pH or the urine to excrete it faster.
plain, buffered, and enertic coated tablets
chemical added to normalize the pH of aspirin
enteric coated tablets of aspirin
slows the rate of dissolution. tablet dissolves in the small intestine instead of the stomach to protect the stomach lining
dosing of aspirin
daily dosing of 80/81 mg or 325 mg for platelet aggregation prevention
surgeries with patients on daily aspirin
have them stop taking the aspirin immediately because the decreased platelet clotting activity can take 5-7 days to come back to normal.
a non-aspirin first generation NSAID
MOA of ibuprofen
reversible inhibition of COX 1 and COX 2
uses of ibuprofen
pain relief, fever, anti-inflammatory, menstrual issues. however, does not prevent MIs or CVAs, may actually increase the risk.
main use of ibuprofen
a good choice for dysmenorrhea, is selective for COX in the uterine muscle.
benefits of ibuprofen over aspirin
better at treating dysmenorrhea, has less gastric bleeding issues than aspirin. shorter term effect than aspirin
disadvantages of ibuprofen over aspirin
not used to prevent CVAs or MIs, may actually increase the risk of them.
similarities between ibuprofen and aspirin adverse effects
both have about equal risk of renal impairment.
another non aspirin first generation NSAID
MOA of naproxen
fairly selective for COX 1, less incidence of GI problems and MI/CVAs than other non aspirin NSAIDS
dosing of naproxen
12-17 hour half life, allows less frequent dosing
uses of naproxen
pain, fever reducer, anti inflammatory, menstural pain. do not use to prevent MIs or CVAs.
adverse effects of naproxen
GI disturbances are most common
second generation NSAIDS
inhibit COX 2 only. the theory was that they would have reduced adverse effects since they are selective for COX 2. after a few years, saw a higher risk of cardiovascular events like MIs and strokes
second generation anti inflammatory NSAID prototype
MOA of celecoxib
inhibits COX 2
uses of celecoxib
arthritis, ankylosing spondylitis (where vertebrae fuse together), acute pain, dysmenorrhea
advantages of celecoxib
less GI problems than first generation NSAIDS like aspirin, ibuprofen, and nalproxen
disadvantages of celecoxib
increased risk of MIs and CVAs over first generation NSAIDS, can impair the kidneys.
dosing of celecoxib
use lowest effective dose for shortest possible time
precautions with celecoxib
not a good option for patients with heart disease or risk factors for it.
a non antiinflammatory COX inhibitor drug. used for pain and fever reduction. is the preferred drug for fever in children because no risk of reyes syndrome. has NO anti inflammatory properties
MOA of acetaminophen
COX inhibition, thought to be limited to the central nervous system
adverse effects of acetaminophen
few adverse effects but can be hepatotoxic at high doses
metabolism of acetaminophen
metabolized by two pathways in the liver, major and minor.
major pathway of metabolism of acetaminophen
is simple, acetaminophen is converted directly to a non toxic metabolite. how most of acetaminophen is metabolized.
minor pathway of metabolism of acetaminophen
has two steps. the first step is that CYP450 converts acetaminophen to a toxic metabolite. the second step is that glutathoine is required to convert the toxic metabolite to a non toxic metabolite.
excessive doses of acetaminophen
causes more of the drug to be metabolized by the minor pathway, and glutathione can be depleted. this can result in a buildup of the toxic metabolite.
maximum dosage for acetaminophen
4 grams in adults, 2 grams in adults who frequently drink, as alcohol induces acetaminophen to be metabolized by the minor pathway.
contraindications for acetaminophen
contraindicated in someone with liver failure. check liver function tests.
alcohols effect on acetaminophen
alcohol induces CYP450 meaning more acetaminophen is metabolized by the minor pathway, alcohol depletes glutathione, meaning more toxic metabolites build up, and alcohol causes general liver damage reducing the livers ability to handle acetaminophen.
client education of acetaminophen
make sure the patient is not on coformulated opioids and acetaminophens and taking acetaminophen PO for further pain relief as this can cause toxic levels.
the cause of 50% of acute liver failure. manifestations of liver injury appear 48-72 hours after overdose
symptoms of acetaminophen toxicity
neasuea, vomiting, diarrhea, sweating, abdominal pain/discomfort, may progress to hepatic failure (jaundice, elevated liver enzymes, pain localized to right upper quadrant), coma, and death
antedote for acetaminophen toxicity
the antidote for overdose of acetaminophen. is a substitute for glutathione.
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