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Colorectal Cancer - Discovering the Riddles - Research Paper Example

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The paper "Colorectal Cancer - Discovering the Riddles" describes the preventable type of cancer that is often treatable when diagnosed at an early stage. The paper narrates on complexities of the disease, causes, risk factors, pathology, clinical manifestations, diagnostic studies, and treatment…
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Colorectal Cancer - Discovering the Riddles
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Human Anatomy August, Colorectal Cancer: Discovering the Riddles Colorectal cancer now ranksthird as the most commonly diagnosed cancer type in men and second in women in the US, with over 1.2 million new cancer cases and 608,700 deaths estimated to have occurred in 2008 (Jemal et. al. 2011). Specifically, about 72% of cases arise in the colon and about 28% in the rectum. Modifiable and non- modifiable risk factors are associated with this type of cancer and are seen as the backbone of its preventive measures. Actually, colorectal cancer is a preventable type of cancer and is often treatable especially when diagnosed at an early stage. With this finding, it is imperative to learn about the complexities of the disease, including the causes and risk factors, pathology, clinical manifestations, diagnostic studies, and treatment modalities. Causes and Risk Factors Several causes have been attributed to cancer. It points out that there is no single factor that can cause cellular aberrations at the level of the lower gastrointestinal tract. Currently, medical research literature is saturated with its possible involvement in genetic, environmental, dietary, lifestyle, and overall health status. Some people are at increased risk because they have inflammatory bowel disease, a personal or family history of colorectal polyps or colorectal cancer, or genetic syndromes like familial adenomatous polyposis (FAP) or hereditary non-polyposis colorectal cancer (also known as Lynch syndrome) (“Screen for Life” 2). Advancing age is also a significant factor in the development of tumors that could later develop into colorectal cancer. Overall, 91% of new cases and 94% of deaths occur in individuals 50 and older. Based on the most recent data by the Surveillance Epidemiology and End Results (2008), the incidence rate of colorectal cancer is more than 14 times higher in adults 50 years and older than in those younger than 50. Furthermore, gender is considered as a risk factor for colorectal cancer. According to SEER (2008), colorectal cancer incidence and mortality rates are 35% higher in men than in women. The reasons why risk is higher for men than for women are not completely understood, but may reflect higher frequency of abdominal obesity, smoking, and drinking in men, as well as hormonal differences (American Cancer Society 3). In the same research data by SEER (2008), race also plays a role in the statistics of mortality rates in colorectal cancer. Colorectal cancer incidence and mortality rates are highest in African American men and women. Moreover, several studies have documented that African American patients are more likely to be diagnosed after the disease has spread beyond the colon. In addition, African Americans with colorectal cancer are less likely than white patients to receive recommended surgical treatment and adjuvant therapy (Du et.al. 2007). Nevertheless, having a past medical history of colorectal cancer is a significant finding in redeveloping the disease. Precancerous and cancerous tumors surgically removed can reemerge due to irritation in the area. Also, virtually not every tumor is removed in a single operation, and smaller tumors may grow after the removal of the larger and most obvious ones. Lifestyle- related factors, including physical inactivity, smoking, high fat diet, obesity, alcohol- intake are also significant factors in developing cellular and tissue malignancy aside from colorectal cancer. Pathophysiology Like any other types of cancer, alteration in the normal physiologic process in the lower gastrointestinal tract is the culprit of colorectal cancer. Deletion of genes is linked to the transformation of normal colon epithelial cells to benign and malignant adenomas. Normally, the cell regeneration rate should occur at a rate almost equal to cell death. However, mutations of tumor suppressors, oncogenes, and repair genes cause an increase of underdeveloped and undifferentiated cells transforming gradually into tumors and polyps. Prolonged contact with fecal matter in the area also promotes this mutation. Colorectal polyps are closely associated with development of cancer. A polyp, or papilloma, is a finger- like projection arising from the mucosal epithelium. Most polyps are benign. Neoplastic polyps are pedunculated (stalk) adenomatous polyps or sessile (papillary or villous) adenomas. Once the malignant cells of an adenoma transverse the muscularis mucosae, the tumor becomes invasive and highly malignant. When detected early, the submucosa may not be penetrated for several years. Having larger polyps increase the risk of colorectal cancer. Although lesions larger than 1.5 cm occur less often, they are more likely to be malignant than those smaller than 1.0 cm (Huether and McCance 1015). Most colorectal cancers are moderately differentiated adenocarcinomas. These tumors have a long preinvasive phase, and when they invade, they tend to grow slowly. Colorectal carcinoma starts in the glands of the mucosal lining. Because the lymphatic channels are located under the muscularis mucosae, the lesions must traverse this layer before metastases can occur. Carcinomas may also be located primarily in the rectal area. Rectal carcinomas are defined as tumors occurring up to 15 cm from the anal opening. Tumors of the rectum can spread to the rectal wall to nearby structures: the prostate in men and the vagina in women. Penetration occurs more readily in the lower third of the rectum because it has no serosal covering. Systematic and pulmonary metastases occur through the hemorrhoidal plexus, which drains into the vena cava. Clinical Manifestations The clinical manifestations of colorectal cancer actually depend on the location of the tumors. Generally, the categorization of the clinical signs and symptoms evolve into two distinct tumor types. On the right side the lesions are polypoid and extend along one wall of the cecum and ascending colon. Because of this location, clinical manifestations include pain, palpable mass in the lower right quadrant, anemia, and dark- reed or mahogany- colored blood mixed with the stool. These large, bulky tumors become necrotic and ulcerated, contributing to persistent blood loss and anemia. Obstruction is unusual because the growth does not readily encircle the colon (Huether and McCance 1016). On the other hand, tumors of the left, or descending colon start as small, elevated, button- like masses. This type grows circumferentially and spreads along the entire bowel wall, eventually ulcerating in the middle as the tumor penetrates the blood supply. Obstruction is common but occurs slowly. Manifestations include progressive abdominal distention, pain, vomiting, constipation, need for laxative, cramps, and bright red blood on the surface of the stool. According to the American Cancer Society (2008), clinical signs and symptoms usually do not manifest in early stages of the disease, which is why screening is very important (11). However, some carefully selected early warning signs warrant screening for tumors in the lower gastrointestinal tract. These signs may include bleeding from the rectum, blood in the stool or in the toilet after having a bowel movement, a change in the shape of the stool, cramping pain in the lower stomach, a feeling of discomfort or an urge to have a bowel movement when there is no need to have one, new onset of constipation, and abnormal weight loss. Medical specialists and other medical researchers argue with the list of the early signs and symptoms. Some individuals do not manifest these signs rendering the list inefficient to the total public. But generally, the American Cancer Society, the proponent of the “Early Warning Signs of Cancer”, still remains as the leader in cancer research. Diagnostic and Screening Tests Advanced medical research has already introduced empirical screening tests to determine the presence of cancer cells in the colon and rectum, and accurately place each individual into stages and grades. Because of the altered integrity of the internal environment in the lower GI tract, a Fecal Occult Blood Test (FOBT) is used as a screening test for colorectal cancer. Also called as the Guaiac Smear Test, it is the most common test for detecting fecal occult blood. The Guaiac test reacts to the peroxidase activity of heme, but this makes the test liable to reaction with other peroxidases in the feces, such as those from certain fruits, vegetables, and red meat. Dietary restrictions are therefore necessary to avoid false-positive results (World Gastroenterology Organization 2007). Currently, fecal occult blood testing using the Guaiac smear is being replaced in many countries by fecal immunochemical tests (FIT or IFOBT), which detect hemoglobin using sensitive and specific techniques. Such tests obviate the need for dietary restrictions. Aside from detecting the presence of blood in the stool, Stool DNA is a new test that specifically detects cancer cell DNA in the stool. Another laboratory assessment for the detection of colorectal cancer is the level of carcinoembryonic antigen (CEA). CEA is seen to be elevated in 70% of people with colorectal cancer. However, this elevation cannot be equated to the cancer stage since the value also rises in the presence of other benign and malignant diseases. Radiographic analysis through double- contrast barium enema also demonstrates polyps and small lesions in the colon and rectum. In addition, computed tomography, chest x- ray and liver scan are proven very helpful in demonstrating metastasis to distant sites other than the colon and rectal area. Endoscopic examination through sigmoidoscopy and colonoscopy can visualize the sigmoid and the entire length of colon, respectively. The ability to remove a small amount of tissue for biopsy makes endoscopy a definitive test for cancer. Although other tests may significantly show the presence of tumors, biopsy is still the gold standard of colorectal cancer confirmation. Colorectal Cancer Staging The results of diagnostic studies in colorectal cancer are clinically categorized into stages and grades. Particularly, colorectal cancer has five stages. In stage 0, cancer cells are located only in the inner lining of the colon or rectum. Typically, this is confined to the surface of a polyp (a growth that protrudes from a mucous membrane). It is also known as carcinoma in situ. In stage 1, cancer cells have spread from the inner lining into the middle layers of the muscular wall of the colon or rectum. When the cancer has spread to the outside surface of the colon or rectum, this is considered as Stage 2. This may involve nearby tissues but not the lymph nodes. Stage 3 cancer involves the nearby lymph nodes. When cancer has spread to other distant parts of the body, such as the liver or lungs, it is already in the stage 4, or the terminal stage. In addition to the cancer stage, it is also useful to determine the grade of the cancer. Comparing the cancer cells look and behavior to normal cells will enable a determination of the grade and help to estimate how quickly the cancer may be growing. Colorectal cancer has three grades. Grade 1 or low grade typically means that cancer is slow growing, also known as well differentiated. When cells still have intermediate differentiation, it is considered to be in the moderate grade, or Grade 2. Lastly, when the cancer cells are fast- growing and poorly differentiated, it is considered a high- grade, or Grade 3 (“Learning about Colorectal Cancer” 2). Treatment The treatment of colorectal cancer depends on the choice of the patient, but the stage and grade of cancer actually provide the physician the clinical decision whether to use surgery, radiotherapy, and chemotherapy (American Cancer Society 18-21). Surgery. Stage 0 Cancer can be effectively managed conservatively with surgical removal of pre and cancerous tumors in the area. However, when the tumor is too large, a resection of a segment of a colon is necessary. When there is an involvement of lymph nodes, these should be surgically removed together with the polyps. Chemotherapy. The use of drugs that could suppress the growth and proliferation of cancer cells is equally effective in controlling cancer. After surgical intervention and the physician thinks that there is still a greater chance of recurrence of tumors, then the use of chemotherapeutic drugs will be the practical option. Three new targeted monoclonal antibody therapies were recently approved by the US Food and Drug Administration (FDA) to treat metastatic colorectal cancer. Bevacizumab (Avastin) blocks the growth of blood vessels to the tumor and both cetuximab (Erbitux) and panitumumab (Vectibix) block the effects of hormone-like factors that promote cancer cell growth. Radiotherapy. Radiation therapy is usually a cocktail treatment with chemotherapeutic drugs when surgery cannot effectively manage rapid progression of cancer. Also, these therapies may also be needed prior to surgery to reduce the size of the tumor and reduce its vascularity. However, radiation and chemotherapy poses side- effects since normal cells in the area are also damaged leading to chronic irritation especially in the bladder, prostate in males, and vagina in females. Works Cited American Cancer Society. Colorectal Cancer Facts & Figures 2008-2010. Atlanta: American Cancer Society (2008): 1-32. Print. Du, X.L., Fang, S., Vernon, S.W., El-Serag, H., Shih, Y.T., Davila, J. “Racial disparities and socioeconomic status in association with survival in a large population-based cohort of elderly patients with colon cancer.” Cancer 110.3 (2007): 660-669. Print. Jemal, Ahmedin, Bray, Freddie, Center, Melissa, Ferlay, Jacques, Ward, Elizabeth and David Forman. “Global Cancer Statistics.” American Cancer Society, Inc. 61.2 (2011): 69- 90. Print. Huether, Sue E. and Kathryn L. McCance. Understanding Pathophysiology 4th ed. Singapore: Mosby, 2007. Print. “Learning About Colorectal Cancer.” Current Oncology. Canada: Multimed Inc., 2008. Print. “Screening for Life.” National Colorectal Cancer Action Plan. Center for Disease Control. 21.1029 (2009):1-2. Print. Surveillance, Epidemiology, and End Results (SEER). “SEER Stat Fact Sheets: Colon and Rectum.” SEER.Cancer.gov. National Cancer Institute. Nov. 2008. Web. 6 Aug. 2011. World Gastroenterology Organization. Colorectal cancer screening. WorldGastroenterology.org. 2007. Web. 7 Aug. 2011. Read More
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