and women equally; however, is more severely expressed by women (Huether & McCance, 2012, p.996). OA is manifested in any synovial joint, or weight-bearing areas and primarily affects hands, hips, and spine (Huether & McCance, 2012, p. 996). The primary defect of OA is a loss of articular cartilage: thereby, losing its glistening appearance, and becoming yellow-gray or brownish gray (Huether & McCance, 2014, p. 1565). The disease progresses surface areas of the cartilage flake off with deeper areas develop fibrillation; thereby, causing the cartilage to thinand become absent leaving the subchondral bone unprotected causing it to become dense and hard (Huether & McCance, 2014, p. 1565). Huether & McCance (2012) state the articular cartilage loss is the results of a cascade of cytokine and anabolic growth factor pathways. Furthermore, enzymatic process assists in breaking macromolecules of proteoglycans, glycosaminoglycans, and collagen into large diffusible fragments (Huether & McCance, 2012, p.997). Huether & McCance (2014) state inflammatory cytokines, IT-1 and TNF degrade cartilage through induction of nitric oxide synthase (inos) and nitric oxide (NO). Treatment is based on symptom severity involving rest to involved joint, low impact aerobic exercises, to prevent joint capsule contraction; and analgesic and anti-inflammatory drug therapy to reduce the pain and swelling (Huether & McCance, 2014, p. 1568). Noted clinical
manifestations are manifested during the fifth or sixth decade of life with noted articular surface changes after the age of 40 (Huether & McCance, 2014, p. 1566).ReferencesHammer, G. G., & McPhee, S. (2014). Pathophysiology of disease: An introduction to clinical medicine. (7th ed.) New York, NY: McGraw-Hill Education.Huether, S. E., & McCance, K. L. (2014). Pathophysiology: The biological basis for disease in adults and children. (7thed.). St. Louis, MO: Mosby.Huether, S. E., & McCance, K. L. (2012). Understanding pathophysiology (5th ed.). St. Louis, MO: Mosby.
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