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  • Image not available. Millions of Americans have osteoarthritis (OA). OA prevalence increases with age; women more commonly affected than men.
  • Image not available. Contributors to OA are systemic (e.g., age, gender, genetics, hormonal status, obesity, and occupational or recreational activity) and/or local (e.g., injury, overloading of joints, muscle weakness, or joint deformity).
  • Image not available. OA is primarily a disease of cartilage that reflects a failure of the chondrocyte to maintain proper balance between cartilage formation and destruction. This leads to loss of cartilage in the joint, local inflammation, pathologic changes in underlying bone, and further damage to cartilage triggered by the affected bone.
  • Image not available. The most common symptom associated with OA is pain, which leads to decreased function and range of motion. Pain relief is the primary objective of medication therapy.
  • Image not available. Manifestations of OA are local, affecting one or a few joints, usually the knees, hips, and hands. Osteophytes (bony proliferation of affected joints) are often found, in contrast to the soft-tissue swelling of rheumatoid arthritis.
  • Image not available. Nonpharmacologic therapy is the foundation of the pharmaceutical care plan and should be initiated before or concurrently with pharmacologic therapy.
  • Image not available. Based upon efficacy, safety, and cost considerations, scheduled acetaminophen, up to 4 g/day, should be tried initially for pain relief in OA. If this fails, a nonsteroidal antiinflammatory drug (NSAID) may be tried, if there are no contraindications.
  • Image not available.NSAIDs are associated with gastrointestinal (GI), renal, cardiovascular, liver, and central nervous system toxicity. Monitoring with complete blood count, serum creatinine, hepatic transaminase levels, and blood pressure readings can be valuable in detecting potential toxicity.
  • Image not available. Strategies to reduce NSAID-induced GI toxicity include the use of nonacetylated salicylates, cyclooxygenase-2 (COX-2])–selective inhibitors, or the addition of misoprostol or a proton pump inhibitor. COX-2–selective inhibitors vary in their ability to prevent GI toxicity, and concomitant use of aspirin largely negates the gastroprotective effect of COX-2–selective inhibitors.
  • Image not available. COX-2–selective inhibitors can increase the risk of cardiovascular events. This may be a class effect, but the extent of this risk varies among COX-2–selective inhibitors, and traditional NSAIDs may also pose risks. This hazard, in addition to the GI toxicity possible with all NSAIDs, underscores the importance of using NSAIDs only as needed and after assessing the individual patient's risk. New guidelines to reduce GI and cardiovascular risk for those who require treatment with NSAIDs have been developed.
  • Image not available. Other agents useful in treating OA include topical NSAIDs or capsaicin, glucosamine and chondroitin in combination, and intraarticular injections of corticosteroids or hyaluronic acid.

After reviewing this chapter the reader should be able to:

  • 1. Describe two physical and/or chemical characteristics of articular cartilage that make it suitable for its role in joint function.
  • 2. List three risk factors for the development of osteoarthritis (OA).
  • 3. Explain the basic pathophysiology of OA.
  • 4. List three elements essential for the appropriate diagnosis of OA.
  • 5. Explain three nonpharmacologic interventions for OA.
  • 6. Explain the mechanism of action of acetaminophen in the treatment of OA.
  • 7. Explain the mechanism ...

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