Instructions: Response must be at least 310 words written in current APA format with at least two academic references cited. References must be within the last five years. Response must exten, refute/correct, or add additional nuance.
The aim of this brief paragraph is to analyze as best as possible the profile of a patient recently diagnosed with pancreatic ductal adenocarcinoma. The patient’s name is abbreviated as J.C. and he is 82 years old with a past medical history of diabetes, hypertension and atrial fibrillation. Prior to proceeding to the analysis, it is important to explain that ductal adenocarcinoma constitutes a form of cancer. How is cancer defined?
According to McCance and Huether (2019), the term cancer can be construed as diseases in which abnormal cells, prompted by different factors, divide uncontrollably and are able to invade other tissues. It is important to note that cancers are generally named according to the cell type from which they are produced. Consequently, in order to understand J.C. ‘s type of cancer, one must establish that carcinomas derive from epithelial tissue and that adenocarcinomas originate from ductal or glandular structures. J.C.’s ductal adenocarcinoma was detected as a mass in the head of his pancreas. Moreover, a solid mass infiltrate was also observed in the superior mesenteric vein, which is a large blood vessel in the abdomen. Does this infer that J.C. ’s cancer is spreading there? It is also mentioned that a perilesional node, referring to lymph node swelling was detected. This information will be essential when proceeding to stage J.C. ’s pancreatic ductal adenocarcinoma.
At this point, one can attempt to answer questions of importance. Based on the light analysis of J.C.’s profile and based on review of cancer biology as presented by McCance and Huether (2019 ), J.C.’s pancreatic ductal adenocarcinoma is invading his stomach and his lymph nodes. The body is programmed to regulate the cell proliferation cycle through the operation of tumor-suppressor genes designed to inhibit proliferation resulting from growth signals, stop cell division when cells are damaged and prevent mutations. Tumor suppressor genes as such serve an important function in preventing abnormal cell growth. On the other hand, oncogenes are activated in cancer. Each individual has two copies of each tumor-suppressor gene, one from each parent. Both copies must be inactivated for oncogenes, affiliated with abnormal cancer growth, to take over.
As we continue to explore the topic of J.C’s cancer, it becomes relevant to understand tumor cell markers. They simply represent substances produced by both benign and malignant cells that are either present in or on tumor cells or found in blood, spinal fluid or urine. They are used to screen and identify individuals at high risk for cancer; to help diagnose the specific type of tumor based on the clinical manifestations relating to the tumor and to follow the clinical course of a tumor. In J.C.’s case, the symptomatology of abdominal discomfort, nausea, weight loss inclined a clinician to not exclude cancer. According to the TNM stage, J.C. is at T2 meaning his detected lesion was between 2-5 cm; N implying lymph node involvement (perilesional node) and M1 implying demonstratable metastases. At this point, it is imperative to stress that malignant tumors differentiate themselves from benign tumors by more rapid growth rates and specific microscopic alterations. They also present with loss of differentiation and absence of normal tissue organization. What could they possibly be used for within the defined machine that is the human body? To amplify the anomaly, the malignant cancer cells are often able to spread from the site of the original tumor to distant tissues and organs through the body. This process is termed metastasis. In J.C’s case, the pancreatic ductal adenocarcinoma is affecting his epithelial tissue.
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