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According to Karch (2013), the etiology of RA is indefinite. However, Karch (2013) notes that pathogenesis of RA has long been exposed and explicated by researchers. RA is exhibited in human beings when "synovial cells resembling a localized tumor invades and destroys articular cartilage, subchondral bone, tendons, and ligaments" (1035). In other words, RA arises as a result of the immune system attacking the body. Though the exact cause of RA is not yet known, it is believed that permutation of genes coupled with environmental changes may prompt the onset of RA (Firestein, n.d). In individuals genetically predisposed to RA, some researchers believe that bacterial or viral infections could also prompt the onset of the disease (Firestein, n.d).
According to Karrch (2013), RA development process commences with damage to small blood vessels accompanied by an elevation in the quantity of the cells making up the lining of the synovium. This is also accompanied by permeation of cells characterized by a single rounded nucleus, for instance, lymphocytes in blood vessels. Consequently, the synovium swells and subsequently extends above the surface of the joint thus forming protuberances (Karch, 2013).
Symptoms of RA are majorly concentrated the foot and ankle of the affected individual. Major symptoms include swelling, reddening, softness, rigidity of the affected joints, and the affected individual in most cases also experiences exhaustion or general body weakness (Baert and Grampp, 2008). It is worth noting that joint rigidity usually occurs in the morning. Secondly, it is also important to note that practically all joints are affected by RA and hence symptoms may present themselves in all joints. There are also permanent defects such as inability to straighten the knee, wrists or fingers shift or drift in the direction of the ulna, and swan neck deformity, which is a condition whereby
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