CoX inhibitors, NSAIDs, Aspirin, Acetaminophen Flashcards
(21 cards)
describe the COX-1 and COX-2 pathways
Video notes
which physiologic process is responsible for analgesia, anti-inflammatory activity, antipyeresis, bleeding tendencies, and gastric mucosal damage
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explain the expected outcomes if a medication inhibits COX 1 and/or COX 2
If a medication inhibits COX 1:
gastric erosision and ulceration, bleeding, renal impairment but also protection against MI/stroke
If a medication inhibits COX 2:
renal impairment, promotion of MI and stroke, but also suppression of inflammation, alleviation of pain, reduction of fever and protection against colorectal cancer.
After cellular damage, what role does cyclooxygenase play in the cascade leading to inflammation?
it catalyzes the synthesis of prostaglandins, which promote inflammation and sensitize receptors to painful stimuli.
it also promotes synthesis of prostacyclin, which causes vasodilation.
describe the beneficial and adverse actions of NSAIDs and the basic mechanism.
NSAIDs help by alleviating mild to moderate pain, suppress fever, relieve dysmenorrhea
NSAIDs hurt by posing a risk of serious harm d/t stomach ulcers.
The basic mechanism for NSAIDs is to inhibit the COX. 1st generation inhibit COX 1 & COX 2 and second generation inhibit COX 2 only.
explain how NSAIDs can lead to MI stroke. What is the main mechanism that promotes this risk?
due to their prothrombotic (blood clotting) properties, NSAIDs can lead to MI and stroke. The main mechanism that promotes this risk is the inhibition of the cyclooxygenase enzyme.
discuss the role of COX in synthesizing prostaglandins that increase blood flow and how a COX inhibitor can thus cause renal impairment
COX 1 synthesizes prostaglandins to increase blood flow to the kidneys, which supports the renal system. If COX 1 is inhibited, renal impairment occurs because the renal tubes are not dilated enough.
state the main difference between aspirin and other NSAIDs.
Aspirin’s effects are irreversible, whereas other NSAIDS are reversible.
differentiate the first generation NSAIDs from the second generation NSAIDs.
first generation NSAIDS inhibit COX 1 and COX 2
second generation NSAIDS inhibit just COX 2v
regarding the selective COX 2 inhibitor (celecoxib), describe the MOA, clinical use, and AEs.
MOA: Selective inhibition of COX-2, No inhibition of COX-1
clinical use: last choice for long term management of pain Osteoarthritis, Rheumatoid arthritis ,Acute pain
Dysmenorrhea, Familial adenomatous polyposis
AEs: Dyspepsia, Abdominal pain, Renal impairment, Sulfonamide allergy, Cardiovascular impact (stroke, MI, and other serious events)
why can a COX 2 inhibitor increase incidence of MI?
This has been attributed to their ability to inhibit endothelial COX-2 derived prostacyclin (PGI2), which leads to vasoconstriction and thrombus
list main drug interactions for aspirin, NSAIDs (ibuprophen, naproxen) and Tylenol
Tylenol:
Alcohol–regular alcohol use increases risk of liver injury (use less than 2,000 mg/day)
Warfarin
Vaccines
list main drug interactions for aspirin
anticoagulants–intensify effects
glucocorticoids–ulcer risk higher
alcohol–gastric bleeding risk
non-aspirin NSAIDS–other NSAIDs can reduce the antiplatelet effects of aspirin
ACE inhibitors and ARBs–can impair renal function and increase risk of acute renal failure
vaccines–can blunt the immune response to vaccines
list main drug interactions for ibuprofen
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list main drug interactions for naproxen
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considering acetaminophen, explain the MOA, beneficial and adverse effects
Selective inhibition of COX and limited to the CNS
Decreases prostaglandin synthesis in CNS so mainly treats fever/pain
beneficial effects: Analgesic, antipyretic
Does not have any anti-inflammatory or antirheumatic actions
Not associated with Reye’s syndrome, so safe with children
Does not increase platelet aggregation
Does not reduce blood flow to kidneys
No increase in GI ulcers
adverse effects: Very few at normal doses (use less than 4,000 mg/day)
Stevens-Johnson syndrome (SJS), acute generalized exanthematous pustulosis (AGEP), and toxic epidermal necrolysis (TEN)
Hepatotoxicity
With overdose or in patients with liver failure
Overdose: Hepatic necrosis
when is aspirin contraindicated?
in patients who have a known allergy to NSAIDs and also in pregnancy
alternative would be Tylenol
compare signs and symptoms of acute poisoning with aspirin and with acute toxicity acetaminophen, the time course and management
Acetaminophen:
Overdose: Hepatic necrosis
Signs and symptoms of hepatic failure, coma, death
Early symptoms: Nausea and vomiting, diarrhea, sweating, abdominal pain
Treatment for overdose: Acetylcysteine (Mucomyst)
aspirin: acute poisoning
Immediate threats to life: Respiratory depression, hyperthermia, dehydration, and acidosis. Treatment is largely supportive.
discuss the safety of NSAIDs with pts. who have chronic kidney disease
NO GIVING NSAIDs to pts. with chronic kidney disease because NSAIDs disrupt the compensatory vasodilation response of renal prostaglandins to vasoconstrictor hormones released by the body.
Inhibition of renal prostaglandins results in acute deterioration of renal function after ingestion of NSAIDs.
recognize the 4 step approach for the use of COX inhibitors for musculoskeletal pain.
step one: non drug measures
step two: initiate with acetaminophen or aspirin
step three: try other non-selective NSAIDs-naproxen, ibuprofen, or a nonacetylated salicylate
step four: as a last resort: try the selective COX-2 inhibitor celecoxib
summarize nursing implications and patient teaching for NSAIDs and acetaminophen
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