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Rheumatoid arthritis pathophysiology
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Rheumatoid arthritis (RA) is an autoimmune disorder in which the immune system attacks the joints and surrounding tissues, leading to inflammation and joint damage. The exact cause of RA is unknown, but a combination of genetic, environmental, and hormonal factors is thought to contribute to its development.

In RA, immune cells, such as T cells and B cells, produce inflammation-promoting cytokines that cause the synovial membrane (the tissue lining the joints) to thicken, resulting in the accumulation of fluid and the formation of soft tissue nodules. This inflammation damages the joint tissues, including cartilage and bone, leading to joint pain, stiffness, and loss of function.

Over time, the inflammation can also lead to erosions and destruction of the joint structures, resulting in progressive joint damage and deformities. In addition to affecting the joints, RA can also cause systemic symptoms, such as fatigue, fever, and weight loss, and can increase the risk of comorbidities, such as cardiovascular disease.

Treatment of RA typically involves a combination of medications, such as nonsteroidal anti-inflammatory drugs (NSAIDs), disease-modifying antirheumatic drugs (DMARDs), and biologic agents, to reduce inflammation, prevent joint damage, and improve quality of life.
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