Pain Relievers for your CV
For patients on aspirin heart therapy, recommend TYLENOL® for pain relief because it doesn't interfere with the cardiovascular benefits of aspirin like ibuprofen can.1
Extra Strength TYLENOL® Dosing Explained
Find out why the labeled total daily dose is 3000 mg and when you can recommend up to 4000 mg at your discretion.Note: Video pertains to Extra Strength TYLENOL® dosing only, not to Regular Strength TYLENOL® or TYLENOL® 8 HR Arthritis Pain dosing.
Ibuprofen may compete with aspirin to occupy COX-1 receptors, potentially compromising aspirin’s cardiovascular benefits.1 (Excerpt)
NSAID inhibition of COX-1 can diminish the COX-1 mediated role in gastric mucosal protection, which can lead to GI side effects such as irritation and bleeding.2-5 (Excerpt)
In kidneys with some degree of dysfunction, NSAID inhibition of COX-1 and COX-2 can further compromise renal function.6 (Excerpt)
Acetaminophen & NSAIDs:
MOAs and Clinical Considerations (Unabridged)
Scientific animation demonstrates the clinical implications of the Mechanisms of Action (MOAs); commentary explores how to counsel patients on their selection and use of OTC analgesics.
Acetaminophen & NSAIDs:
MOAs and Clinical Considerations (Abridged)
Scientific animation shows how the Mechanisms of Action (MOAs) of acetaminophen and NSAIDs can have important implications for patient care. Introduction by pain specialist Bruce D. Nicholson, MD.
Metabolism in the Liver
Acetaminophen is metabolized in the liver through 3 distinct pathways, all of which ultimately yield non-toxic metabolites when acetaminophen is taken at recommended doses.7-10
Counseling Patients about Acetaminophen Use
Clinical rationales and counseling messages for promoting patients' proper use of acetaminophen and other OTC analgesics. (Excerpt)
TYLENOL® Future Care Scholarship
For over 20 years, the makers of TYLENOL® have supported students pursuing degrees in healthcare by awarding a total of $250,000 in scholarships each year to forty exceptional students. Learn more from Meghan, a medical student and 2011 scholarship recipient.
References: 1. Catella-Lawson F, Reilly MP, Kapoor SC, Cucchiara AJ, DeMarco S, Tournier B, Vyas SN, FitzGerald GA. Cyclooxygenase inhibitors and the antiplatelet effects of aspirin. N Engl J Med. 2001;345(25):1809-1817. 2. American College of Cardiology. ACCF/ACG/AHA 2008 expert consensus document on reducing the gastrointestinal risks of antiplatelet therapy and NSAID use. Circulation. 2008;1894-1909. 3. Hirschowitz BI. Nonsteroidal anti-inflammatory drugs and the gastrointestinal tract. Gastroenterol. 1994;2(3):207-223. 4. Blot WJ, McLaughlin JK. Over the counter non-steroidal anti-inflammatory drugs and risk of gastrointestinal bleeding. J Epidemiol Biostat. 2000;5(2):137-142. 5. Cheatum DE, Arvanitakis C, Gumpel M, Stead H, Geis GS. An endoscopic study of gastroduodenal lesions induced by nonsteroidal anti-inflammatory drugs. Clin Ther. 1999;21(6):992-1003. 6. DeMaria AN, Weir MR. Coxibs—beyond the GI tract: Renal and cardiovascular issues. J Pain Symptom Manage. 2003;25(2S):S41-S49. 7. Mitchell JR, Thorgeirsson SS, Potter WZ, Jollow DJ, Keiser H. Acetaminophen-induced hepatic injury: protective role of glutathione in man and rationale for therapy. Clin Pharmacol Ther. 1974;16(4):676-684. 8. Patten CJ, Thomas PE, Guy RL, et al. Cytochrome P450 enzymes involved in acetaminophen activation by rat and human liver microsomes and their kinetics. Chem Res Toxicol. 1993;6(4):511-518. 9. Raucy JL, Lasker JM, Lieber CS, Black M. Acetaminophen activation by human liver cytochromes P450IIE1 and P450IA2. Arch Biochem Biophys. 1989;271(2):270-283. 10. Thummel KE, Lee CA, Kunze KL, Nelson SD, Slattery JT. Oxidation of acetaminophen to N-acetyl-p-aminobenzoquinone imine by human CYP3A4. Biochem Pharmacol. 1993;45(8):1563-1569.