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”
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”
Diclifenac Flurbiprofen Keterolac Nabumetone Sulindac Diflunisal IBprofin Meclofenamate Naproxen Tolmetin Etodolac Indomethacin Mefenamic acid Oxaprozin Asprin* Fenoprofen Ketoprofen Meloxicam Piroxicam
NSAIDs
