NR 283 Pathophysiology Paper

Student Name

Chamberlain University

NR-283: Pathophysiology

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Introduction of Disease

Melanoma is a type of skin cancer with a high malignant potential. While it is not the most common form of skin cancer, it is considered the deadliest. Melanoma originates from melanocytes, which are the cells responsible for producing melanin, the pigment that gives skin its darker color. These melanocytes are located at the junction of the epidermis and dermis and produce melanin in response to ultraviolet (UV) radiation. According to Harting (2014), the occurrence of malignant melanoma has risen significantly in the past three decades, making it the fifth most common tumor in the population. Despite the increasing incidence, preventive measures are available that can reduce the likelihood of developing melanoma.

Etiology

The primary cause of melanoma and other forms of skin cancer is overexposure to UV radiation. While certain genes may play a role in influencing skin cancer susceptibility, no conclusive evidence has been found linking specific genes to skin cancer risk (Porth & Gaspard, 2014). Melanin acts as a partial barrier to UV radiation, which is primarily sourced from sunlight and artificial sources like tanning beds. UV exposure can occur both outdoors and indoors, with UV rays reflecting off surfaces like snow in winter, thus intensifying their harmful effects. Additionally, prolonged exposure through car windows can increase UV exposure, especially for those who spend a lot of time in vehicles. People with fair skin, particularly Caucasians, as well as individuals with light-colored hair (blonde or red), eyes (blue or green), and a high number of freckles or moles, are at a higher risk of developing skin cancer. Men generally face a higher risk of skin cancer than women, and other risk factors include a family history of skin cancer, severe childhood sunburns, and a previous diagnosis of melanoma (Harting, 2014).

Pathophysiology Processes

Malignant melanoma develops when melanocytes, the pigment-producing cells in the skin, undergo mutations due to UV radiation exposure. These mutations can damage the genetic material within skin cells, leading to uncontrolled cell growth and the formation of tumors. The process typically begins with dysplasia, where abnormal cellular changes occur, and may progress to anaplasia, characterized by further loss of cellular differentiation (VanMeter & Hubert, 2014). While some genetic predispositions to melanoma have been observed, there is no definitive link between specific genetic factors and the development of the disease (Harting, 2014). The body does have mechanisms to repair damaged DNA; however, if cell proliferation exceeds the repair capacity, these mutated cells may multiply rapidly, making it difficult for the body to correct the damage. Ongoing research is crucial for advancing the understanding of melanoma and improving prevention and treatment strategies.