Degenerative arthritis in spine
Their theoretical advantage, however, is that they will cause significantly less toxicity than conventional NSAIDs, particularly in the GI tract. degenerative arthritis in spine Testicular pain. This theoretical enhanced safety profile will be a significant advantage in the management of all patients but especially those at high risk for peptic ulcers. Nonsteroidal anti-inflammatory drugs (NSAIDs) exert their anti-inflammatory effect primarily by inhibiting an enzyme called cyclooxygenase (COX), also known as prostaglandin (PG) synthase. COX catalyzes the conversion of the substrate molecule, arachidonic acid, to prostanoids. degenerative arthritis in spine Alternative pain relief products. Prostanoids consist of prostaglandins E, D and F2a, prostacyclin and thromboxane. The major inflammatory vasoactive prostanoids are PGE2 and prostacyclin. Thromboxane is critical for platelet clotting, while PGD2 is involved in allergic reactions and PGF2a in uterine contraction. degenerative arthritis in spine Chronic pain pharmacies. Non-steroidal Anti-inflammatory Agents The mechanism by which NSAIDs exert their anti-inflammatory and analgesic effects is via inhibition of the prostaglandin-generating enzyme, cyclooxygenase (COX) (see image above). In addition to their inflammatory potential, prostaglandins also contribute to important homeostatic functions, such as maintenance of the gastric lining, renal blood flow, and platelet aggregation. Reduction of prostaglandin levels in these organs can result in the well-recognized side effects of traditional non-selective NSAIDs - that is, gastric ulceration, renal insufficiency, and prolonged bleeding time. The elderly are at higher risk for these side effects. For example, adults over the age of 60 who are taking NSAIDs have a 4-5 fold higher risk of gastrointestinal bleeding or ulceration then their age-matched counterparts. Other risk factors for NSAID-induced GI bleed include prior peptic ulcer disease and concomitant steroid use. Potential renal toxicities of NSAIDs include azotemia, proteinura, and renal failure requiring hospitalization. Hematologic and cognitive abnormalities have also been reported with several NSAIDs. Therefore, in elderly patients, and those with a documented history of NSAID-induced ulcers, traditional non-selective NSAIDs should be used with caution, usually in lower dose and in conjunction with a proton pump inhibitor. Renal function should be monitored in the elderly. In addition, prophylactic treatment to reduce risk of gastrointestinal ulceration, perforation and bleeding is recommended in patients > 60 years of age with: prior history of peptic ulcer disease; anticipated duration of therapy of > 3 months; moderate to high dose of NSAIDs; and, concurrent corticosteroids. Misoprostol, at a dose of 200 mg four times daily, constitutes effective anti-ulcer prophylaxis but is often poorly tolerated due to diarrhea. Omeprazole, and other proton pump inhibitors, are also very effective anti-ulcer prophylactic agents, although cost can be limiting.
Degenerative arthritis in spine
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