Counseling Points - March 2008 - (Page 6)

gist to ensure the preparations will not interfere with RA medications they are currently taking.8 Patient Education Because of the unpredictability individuals with RA face on a daily basis, informative patient education programs are an effective complement to traditional medical therapy. Providing patients with disease and treatment information and strategies to protect joints and cope with the stress of a chronic condition has been found to decrease disability associated with the disease, increase psychosocial interaction, and ameliorate clinical prognosis, which improves quality of life.9 Some excellent resources for patient education and disease information appear in Table 2. Table 2. RA Patient Education Resources • The Arthritis Foundation, www.arthritis.org • Arthritis National Research Foundation, www.curearthritis.org • Johns Hopkins Arthritis Center, www.hopkins-arthritis.org/ physician-corner/education/acr/acr.html • The National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), www.niams.nih.gov • The Mayo Clinic, www.mayoclinic.com/health/ rheumatoid-arthritis • National Library of Medicine and National Institutes of Health, www.nlm.nih.gov/medlineplus/rheumatoid arthritis.html • American College of Rheumatology, www.rheumatology.org/ • Rheumatoid Arthritis Public Patient Education Fact Sheet, www.rheumatology.org/public/factsheets/ra_new.asp • Rheumatology Nurses Society, www.rnsnetwork.org/ Pharmacological Therapies There are three primary classes of medications used to treat RA: nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying antirheumatic drugs (DMARDs).10 NSAIDs and corticosteroids have relatively short onsets of action and are helpful to relieve pain and inflammation, particularly during the first few weeks of RA symptom onset. DMARDs, on the other hand, stop or slow progression of RA, but their effects can take several weeks or months to demonstrate a clinical benefit.10 are available under various trade names (Table 3). 11 Aspirin is the oldest and most often used NSAID on the market. Patented in 1900 by Bayer, Americans consume about 120 billion tablets of aspirin per year.12 NSAIDs work by controlling pain and inflammation through a channel of the metabolism of arachidonic acid.13 This essential fatty acid, when metabolized, results in the synthesis of substances that control many homeostatic functions and also stimulate the production of pain and inflammation. Two pathways evolve from the metabolism of arachidonic acid. Along one pathway, lipoxygenase acts as a catalyst to produce substances that help regulate allergic and primary inflammatory responses. On the alternate pathway, cyclooxygenase (COX) acts as a catalyst to synthesize prostaglandins, prostacyclin, and thromboxane. It is this second pathway that NSAIDs target by inhibiting COX from entering the cycle.13 When inflammation is present, activation of bradykinin, histamine, and other substances occurs. Prostaglandins are chemical messengers that sensitize nociceptors (sensory receptors of pain) making them more responsive to the pain-producing effects of bradykinin and histamine. Low doses of NSAIDs block COX, inhibiting prostaglandin synthesis and thereby eliminating the pathway of painful stimuli.13 Although all NSAIDs are COX inhibitors, the way each agent interacts with the isoenzymes of COX may differ depending on its specific formulation.14 COX-1 is the most common isoenzyme and can be found in any tissue that contains prostaglandin, whereas COX-2 is chiefly located in tissues where active inflammation is present. Older, traditional NSAIDs, such as aspirin, are nonselective, meaning they interrupt the COX pathway at any point, interacting mostly with COX-1 isoenzymes. Newer NSAIDs, such as celecoxib (Celebrex®), selectively target COX-2.14 NSAID Toxicity Toxicity to NSAIDs appears to be dose- and age-related, or secondary to pre-existing conditions, and is most likely to occur with long-term use. The two most common adverse reactions associated with traditional NSAIDs are ulcer and gastrointestinal (GI) bleeding.14 To comprehend the toxicity profiles of NSAIDs, it is important to understand the roles prostaglandins play in the body. Prostaglandins are chemical messengers that are responsible for many hemodynamic functions, including inflammation, blood clotting, renal function, wound heal6 NSAIDs Currently, a total of nine different formulations of NSAIDs, such as ibuprofen, naproxen, and nabumetone, COUNSELING POINTS™ http://www.arthritis.org http://www.curearthritis.org http://www.hopkins-arthritis.org/physician-corner/education/acr/acr.html http://www.hopkins-arthritis.org/physician-corner/education/acr/acr.html http://www.niams.nih.gov http://www.mayoclinic.com/health/rheumatoid-arthritis/RA99999 http://www.mayoclinic.com/health/rheumatoid-arthritis/RA99999 http://www.nlm.nih.gov/medlineplus/rheumatoidarthritis.html http://www.nlm.nih.gov/medlineplus/rheumatoidarthritis.html http://www.rheumatology.org/ http://www.rheumatology.org/public/factsheets/ra_new.asp http://www.rnsnetwork.org/

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Counseling Points - March 2008 Welcome Pharmacological and Nonpharmacological Treatment of Rheumatoid Arthritis

Counseling Points - March 2008

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