Psoriasis is a common skin disorder affecting millions of people. It affects 2 to 3% of the Caucasian population, usually in individuals between 15 and 30 years old. (Liu, Krueger, & Bowcock, 2007). There are several different forms of the disease. The most common type is chronic plague psoriasis. It presents itself as silvery-scaled patches usually on the knees, elbows, lower back, and scalp. Outbreaks can be triggered by infection, such as strep throat, drug-use, psychological stress, hormonal changes and skin injury. The exact cause is still unknown; however, research has provided some interesting insights into the pathophysiology of psoriasis. The most evident pathophysiological change leading to psoriasis is hyperproliferation and abnormal differentiation of keratinocytes. Keratinocytes are cells in the epidermis that produce keratin, a “protein that helps protect the skin and underlying tissues from heat, microbes, and chemicals.” (Tortora & Derrickson, 2006). Patients with psoriasis shed and replace these cells every two to six days. This is quite a bit faster than normal which is 21 to 28 days so a buildup of dead and living cells is created. (Reid, 2007). This is what causes the flaky, red patches seen in psoriasis patients. “The most common explanation for keratinocyte hyperproliferation is that it is mediated by pro-inflammatory cytokines (regulatory molecules) produced by T cells and dendritic cells that accumulate in diseased skin.” (Jullien, 2006). Psoriasis can be classified as an auto-immune disease. An autoimmune disease is “produced by failure of the immune system to recognize and tolerate self-antigens.” (Fox, 2008). Psoriasis is considered a T-cell mediated, Type-1 autoimmune disease. T cells are activated by mistake and infiltrate the skin causing the hyperproliferation and differentiation of keratinocytes. Most of the T cells that are activated...
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