Analgesics- acetaminophen & NSAIDs Flashcards
Acetaminophen
AEs
Hepatotoxicty
-leading Cause of acute live failure: nasty metabolite NAPQI destroys liver proteins and causes tissue damage
-most incidental ODs
Risk factor: high doses, alcohol use, chronic liver disease
-limit max dose for patients over 65
Lower side effects vs NSAIDs but liver damage is bad!!
NSAIDs
Inhibit central and peripheral prostaglandin synthesis via COX 1 and 2 inhibition
- work in brain and at local injury
- alter local and center PG synthesis
- lower fever
- systemic inflammatory response
NSAIDs
Toxicity
Significant toxicities
-most risk of side effects in the USA
-25% of accidental overdoses are from NSAIDs
- most hospitalizations per year due to GI bleeds
-HTN, decrease renal function, decrease platelet function, fluid retention, bronchospasm, hepatotoxicty
Cardiac toxicity (with cox 2 inhibitors)
Acetaminophen
Analgesic
Works in brain (ONLY) by inhibiting central prostaglandin synthesis (alters perception of pain signal)
-widely used drug in the world
-fever reducer
NSAIDs
COX enzymes
Cox 1: expressed in body at all times
Cox 2: selectively expressed (cells make only when there is an injury)
NSAIDs inhibit normal PG functions
PG functions: protect the GI tract, increase mucosal mucus and bicarbonate secretion, Lower acid secretion, vasodilation, lower the ability for platelets to aggregate
NSAIDs
Two types
Non selective: IBprofin (etc)
-all work on COX 1
COX 2 inhibitors
- Celcocib ( Celebrex)
- only work on COX 2
- less AE, less risk of GI issues
- increase risk of heart attack
NSAID related GI bleeding
Patients at high risk: use of aspirin, warfarin or steroids, prior ulcer or GI bleed, > 65 years old
Treatment: misoprostal, PPI, change to a COX 2 agent
Why do NSAIDs cause ulcers?
Bc they reduce the PGs functions in stomach
Ketorolac ( Toradol)
NSAID (toxicity)
Guidelines: limit use to max of 5 days, dose adjustments for patients over 65
Do not use if: prior ulcer, renal disease, high bleeding risk, use of ASA, NSAID
* most potent of all NSAIDs
- equivalency to morphine pain relief
Migraine headaches
Many treatments but two specific
Ergot alkaloids
Serotonin receptor agonists
Ergot Alkaloids
-non selective 5-HT1 agonists
Constrict intracranial blood vessels, inhibit neurogenic inflammation
-N/V, abdominal pain, fatigue, weakness, muscle pain, diarrhea
* ergotism: cold, numb painful extremities
Ergot Alkaloids
Can cause physical dependence
Do not use within 24 hours of a specific serotonin receptor agonist (triptan)
Avoid with: renal/hepatic impair money, hypertension, heart disease, PVD, CVD, pregnancy
Metabolized by cyp3a4
Used post birth to control bleeding
Serotonin receptor agonists “triptans”
Selective 5-HT receptor agonists
- normalize dilated intracranial arteries
- peripheral neuronal inhibition
- paresthesias, fatigue, dizziness, flushing, chest symptoms (15-50%)
- avoid within 24 hours of ergot alkaloids, avoid 2 weeks ofMAOIs
- risk with heart disease and vascular disease
Almotriptan Eletriptan Frovatriptan Rizatriptan Sumatriptan Zolmitriptan
Serotonin Receptor Agonists “triptans”