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The Pathogenesis Of Brian Colorectal Cancer Add in library

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Describe the pathogenesis of Brian’s colorectal cancer from the initial cellular mutation to the diagnosis of stage IIA colorectal cancer?


In the case of colorectal cancer, discussing about the pathogenesis of colorectal cancer mutations in KRAS is defined as an initial event in the term of pathogenesis. It has been reported that mutation in KRAS demonstrated in 50% of adenomas and hence defined as a key genetic modification that is useful to the development of adenoma to colorectal cancer. It has been found that progression of KRAS mutation is a vital stage in the multistep phenomenon in cancer development. Mutation in KRAS is been associated with very fast and competitive metastatic action of liver metastases. It has been found that there are several liver metastases that were associated with the high expression of KI67 and KRAS have shorter time lapse to be detected as it has restriction with colon and poor survival. Mutation KRAS is associated with C12V is associated to hepatic metastasis along with several lung and colon metastasis. For the treatment module role of KRAS is very critical as it is associated with the deprived response rates of several therapeutic agents thus the mutational role of KRAS act as a deciding step in validating therapies for colorectal cancers. KRAS is associated with epidermal growth factor receptor (EGFR) which is a tyrosine kinase and present on maximum colorectal tumours as it is known to KRAS decrease the response of agents which are anti EGFR. Mutation in KRAS and their implementation in cancer biology have been validated for past decade. KRAS has second highest prevalence of colorectal cancer and this therapy may be well validated in coming durations and at present act has promising approach (Cong and Xiang, 2012)

Describe two (2) modifiable and three (3) non- modifiable risk factors for colorectal cancer and explain how these risk factors may have contributed to the development of Brian’s colorectal cancer.

There have been several evidences that denotes about several factors including several dietary and lifestyle factors that influences the risk of colorectal cancer. Physical inertness, overweight and a deposition of adiposity are consistent risk factors as these parameters serves as major contributors to the high rates of colorectal cancer in several nations. In the recent advancements study indicates the chronic hyperinsulinemia as a major risk factor as it increases the risk of colon cancer because insulin resistance and hyperinsulinemia is promotes by over intake energy and in terms of the Western food routine and culture (e.g., saturated fats and refined carbohydrates), it may be a termed of factors that increses the colorectal cancer. Over consumption of liquor in combination with diet possessing deficit in micronutrients like methionine and folate and smoking likely to increases risk of colorectal cancer especially folate is a nutrient that has been well explores and bears in randomized clinical trials (Giovannucci, 2002). Some of the other risk includes age, personal history of polyps and inflammatory bowel disease, possessing some kind of syndromes, ethnic background and diabetes. Person having past history of adenomatous polyps (adenomas) are at the high risk of colorectal cancer. In inflammatory bowel disease including Crohn's disease and ulcerative colitis where colon stays inflamed for long duration, if untreated turns to dysplasia where it possess growth of cells at lining of colon which in case of uncontrolled management turns to colorectal cancer. Individual having family history of adenomatous polyps or colorectal cancer are at high risk to be having colorectal cancers. Mutation in several genes may result in development of colorectal cancer like mutation in APC gene causes in Familial adenomatous polyposis (FAP) and defect in MLH1 or MSH2 gene leads to Hereditary non-polyposis colon cancer (HNPCC) (Al-Sukhni et al., 2008). A recent study reveals that mutations in the gene MUTYH causes MUTYH-associated polyposis (Schlussel et al, 2014)

Describe the action and mechanism of action of metronidazole (Flagyl) in relation to its administration to Brian.

Describe the action and mechanism of action of morphine in relation to its administration to Brian.

Metronidazole is the major component which is found in plasma along with 2-hydroxymethyl metabolites and circulating metronidazole is bound to plasma proteins. Metronidazole is the productive antianaerobic drug validated in an in-vitro condition. An extensive and wide clinical trial to analyse metronidazole along with neomycin towards erythromycin and neomycin as bowel composition showsd a remarkable reduction in anaerobic flora in individual bearing metronidazole (Hinchey et al, 1983). Morphine is developed as god standard for the pain relieve as it is one of the best drug available for the better pain management and it is clinically very effective in cancer pain. Morphine acts on the central nervous system directly for relieve in pain by activating the peripheral tissues as well as it help in migration and proliferation of tumour cells. morphine is found very important for the maintenance of neoplastic tissues (Gach et al, 2011) .


Discuss the nursing responsibilities with associated rationales in relation to administering Morphine to Brian.

For nursing care it requires multidisciplinary approach towards patient care to meet the expected care


Though the exact reason behind the development of colon cancer is unknown but still several risk factors have been identified that progresses after the age of 40 in both male and females. Ranging from formation of multiple adenomatous polyps to development of colorectal cancer extensive nursing care is involved


While diagnosis it nursing personnel should always remember that there is no outward symptom to identify the disease so minute observation for the initial symptom should be taken with deep concern. Abdomen pain, tarry stools, anaemia, intestinal obstruction and unexplained reduction in weight must be considered at initial examination. Proper radiological examination of abdomen must be done along with colonoscopy and faecal occult blood test must be done and if diagnosis is positive then barium enema and flexible sigmoidoscopy should be done for further follow ups.


Primary treatment for the colorectal cancer is colon surgery but the choice of surgery depends upon the tumour location and organ involved. Post-operative care which involves radiotherapy and chemotherapy must be done in proper nursing care.


Nursing staff should be enough efficient to teach the patients the positive and negative impact of the disease along with proper care. Drug management, pain management and timely maintenance of patient surrounding should be done to avoid post-operative complications.

Discharge planning

Nurses should instruct the patient about post-operative complication like erythema, chills, wound separation, fever, shortness of breath, and more and advised to visit as soon the complication appears again (Toth, 2006).



Giovannucci E. 2002. Modifiable risk factors for colon cancer. Gastroenterol Clin North Am.31(4):925-43.

Haggar FA and Boushey RP. 2009. Colorectal Cancer Epidemiology: Incidence, Mortality, Survival, and Risk Factors. Clin Colon Rectal Surg. 22(4): 191–197.

Cong Tan, Xiang Du. 2012. KRAS mutation testing in metastatic colorectal cancer. World J Gastroenterol.18(37): 5171–5180

Gach K, WyrÄ™bska A, Fichna J, Janecka A. 2011. The role of morphine in regulation of cancer cell growth. Naunyn Schmiedebergs Arch Pharmacol. 384(3): 221–230.

Hinchey EJ, Richards GK, Prentis J. 1983. Metronidazole as a prophylactic agent in wound infection after colon surgery. Surgery. 93(1-2):197-200.

Toth PE. 2006. Ostomy care and rehabilitation in colorectal cancer. Semin Oncol Nurs. 22(3):174-177.

Schlussel AT, Gagliano RA Jr, Seto-Donlon S, Eggerding F, Donlon T, Berenberg J, Lynch HT. 2014. The evolution of colorectal cancer genetics-Part 2: clinical implications and applications. J Gastrointest Oncol. 5(5):336-44.

Al-Sukhni W, Aronson M, Gallinger S. 2008. Hereditary colorectal cancer syndromes: familial adenomatous polyposis and lynch syndrome. Surg Clin North Am. 88(4):819-844


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