NURS6501.Advanced_Pathophysiology_week_2_discussion_2.

NURS6501.Advanced_Pathophysiology_week_2_discussion_2.Pathophysiology of Rheumatoid Arthritis Rheumatoid arthritis is an inflammatory disease which is distinguished by synovitis and destruction of the joints. Although the impacts of genetic factors are obvious, the genetic bases are not sufficient to explain the activation of immune insult witnessed. The prevailing aspect is basically synovium inflammation whereby the synovial membrane grows to be hyperplasic in RA. Immune and inflammatory cells which are known types of synoviocytes are infiltrated. These inflammatory cells include; plasma cells, macrophages, dendrite cells, B- and Tlymphocytes moreover there are elevated levels of cytokines. Cytokines has been found to accelerate synovial inflammation. The response of chronic inflammatory conjoined with continued joint destruction is found to persist in RA patients despite continued use of diseasemodifying drugs and anti-inflammatory agents. This is thought to be as a result of unsuitable retention, continuous recruitment, and weakened apoptosis (Poole, et al. 1994). Pathophysiology of Osteoarthritis Osteoarthritis is a disease associated with the degenerative joint which culminates to morphological damage and total cartilage loss. OA is also linked to damage of other joint tissues, as well as the occurrence of delicate biochemical changes during the onset of OA. A healthy cartilage has a balanced water content achieved by driving water out by compressive force and uses osmotic and hydrostatic pressure to drawing water in. thus when OA manifests, proteoglycan content around the cartridge decrease which disorganizes the collagen matrix. There is an increase in the content of water as a result of the collapse of collagen fibers and loss of proteoglycan which consequently decreases osmotic pull which is prevailed over by collagen loss. Having lost the proteoglycan protection, collagen fibers within the cartilage are exposed to