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KEY POINTS
Treatment goals for osteoarthritis (OA) should be identified prior to beginning treatment and should be individualized on a patient-by-patient basis. An acceptable balance between minimizing pain and side effects, while maximizing functionality and quality of life, should be targeted.
Optimal treatment of OA includes both pharmacologic and nonpharmacologic therapies. Adherence to nonpharmacologic treatment should be assessed at each medication therapy management (MTM) encounter.
Given the significant adverse effects of chronic treatment with nonsteroidal anti-inflammatory drugs (NSAIDs), reassessment of risk factors such as cardiovascular risk and risk of gastrointestinal bleeding should be conducted during each MTM encounter to ensure safety of continued treatment and potential need for additional medications to reduce risk (eg, proton-pump inhibitors for risk of gastrointestinal bleeding).
Assessment of potential adverse effects from analgesic therapy should be determined during each MTM encounter. Importantly, bleeding from NSAIDs or constipation, sedation, and/or respiratory depression associated with opioids should be monitored frequently.
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Osteoarthritis (OA) is the most common form of arthritis. OA is characterized by damage to the joint and joint structures, commonly in weight-bearing joints such as the hips and knees (Figure 29-1). OA may also occur in non-weight-bearing joints such as the hands. OA affects approximately 27 million Americans,1 and since the prevalence of disease increases with age, the number of individuals suffering from OA is estimated to increase significantly in the near future.2 Women are more commonly affected than men, and they also tend to have more joints involved. The prevalence of OA is similar in both African-Americans and Caucasians, although Caucasians are more likely to experience severe disease.
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The development of OA is multifactorial and results when biomechanical weaknesses and risk factors combine in a susceptible individual. Increasing age is the most significant risk factor for OA. Other risk factors include a history of trauma, obesity, involvement in certain sports, occupations with repetitive and/or strenuous movements, female gender, and genetic factors.3
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OA can be broadly categorized as primary or secondary (Table 29-1). Primary OA does not have an identifiable cause and can be further classified as localized, generalized, or erosive. Secondary OA can be attributed to an identifiable cause such as trauma, inflammatory conditions, congenital disorders, endocrine disorders, metabolic disorders, or other conditions that contribute to or increase the risk of developing OA.3
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