Pathogenesis of Brian’s colorectal cancer †Free Solution

Questions: 1. Describe the pathogenesis of Brians colorectal cancer from the initial cellular mutation to the diagnosis of stage IIA colorectal cancer? 2. 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 Brians colorectal cancer? 3. Describe the action and mechanism of action of metronidazole (Flagyl) in relation to its administration to Brian. b) Describe the action and mechanism of action of Morphine in relation to its administration to Brian? 4. Discuss the nursing responsibilities with associated rationales in relation to administering Morphine to Brian? Answers: 1. Describe the pathogenesis of Brians colorectal cancer from the initial cellular mutation to the diagnosis of stage IIA colorectal cancer? The colorectal cancer originates from the epithelial cells that lines the colon or rectum. They are the outcome of mutations in the Wnt signaling pathway that causes an increase in the signaling activity. The mutation are inherited or acquired and occurs in intestinal crypt stem cells. The mutated gene is APC gene producing the APC proteins and preventing accumulation of -catenin. In absence of APC the -catenin gets accumulated in high levels and translocates in the nucleus and binding to DNA thereby activating transcription of proto oncogenes (Searke, David, 2006). The other mutations that arises are from p53 protein that comes from TP53 gene that analyses cell division and kills the cells with Wnt pathway defect. Thus a cell line causes a mutation in TP53 gene, transforming a benign epithelial tumor in to epithelial cell cancer. The other proteins that are responsible for cell death are deactivated in the colorectal cancer are TGF- and DCC. The former has a deactivating mutation in almost half the colorectal cancer cases. Sometimes instead of this the SMAD is deactivated. DCC contains a deletion segment in the chromosome in such cases (Xie Itzkowitz,(2008). The genes that are oncogenes are overexpressed in the colorectal cancer (Shaib, Mahajan El-Rayes, 2013). It includes the genes encoding protein like PI3K, RAF, KRAS. It stimulate cell division cell division along with the growth factors and acquire up the mutation that results in overactive of cell proliferation. Sometimes the chronological sequence also matters like if in past a APC mutation has occurred than KRAS mutation will lead to a colorectal cancer than to a self limiting hyperplastic lesion. PTEN is a kind of tumor repressor that inhibits PI3K and sometime which become mutated and deactivate (Stein, Atanackovic Bokemeyer, 2011). 2. 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 Brians colorectal cancer? The modifiable risk factors for the colorectal cancer are as follows: Lifestyle management: less or no physical activity increases the chances of colorectal cancer. Smoking or high alcohol intake also has significant effects on the disease (Robsahm, Aagnes , Hjartker , Langseth, Bray and Larsen, 2013). Diet: The diet that has high red meat like of beef, pork, lamb, liver and the processed meat of hot doge, luncheon meats also increases the risk of the colorectal cancer. Cooking the meat at very high heat or temperature by frying, grilling or boiling produces chemicals that increments the risk of colorectal cancer. The diet that high in fat also have an adverse effect. The diet low in vegetable, green leafy, fruits also gives a negative effect. The non-modifiable risk factors are as follows: Age: The young generation can have colorectal cancer but the prevalence increase after fifty years. Approximately 9 out of 10 individual have colorectal cancer have attained the age of 50. Family history: If somebody has past history of adenomatous polyps or colorectal cancer the prevalence also increases, but most of the cases does not have a family history (Yin, Grandi, Raum, Haug, Arndt Brenner, 2011). People having a history of colorectal cancer in 1 or more first degree relative are at high risk. The risk is twice if the first degree relative has an history. Inherited syndromes: Approximately 10% who have inherited gene defects can have family cancer syndrome and may face death. These syndromes are linked to the polyps. The common type of syndromes that are inherited and are capable of causing colorectal cancer are familial adenomatous polyposis, hereditary non-polyposis colorectal cancer, Peutz-Jeghers syndrome, Turcot syndrome and MUTYH-associated polyposis. 3. Describe the action and mechanism of action of metronidazole (Flagyl) in relation to its administration to Brian. b) Describe the action and mechanism of action of Morphine in relation to its administration to Brian? Metronidazole is a amoebicidal, bactericidal and trichomoncidal. It is reduced by low redox potential electron transfer proteins to polar product which does not have the nitro group (Brayfield, 2014). The reductional products are to be responsible for the cytotoxic and antimicrobial effect of metronidazole which causes the DNA to disrupt and inhibits the synthesis of nucleic acid (Rossi, 2013). Morphine bind to the opioid receptor. The molecular signaling activate the receptors to carry out the action. There are three kinds of receptors (Franklin, 2014). First is Mu receptor that causes pain decrement, sedation, constipation and physical dependency. Second is kappa receptor. It also has the same effect as mu receptor (Okie, 2010). Third is delta receptor. It has analegesic and antidepressant effect and also causes respiratory depression (Mercadante Arcuri, 2005). 4. Discuss the nursing responsibilities with associated rationales in relation to administering Morphine to Brian. The nursing responsibilities and the rationales for administrating Morphine are as follows: Assessment of the patient incision. Assessing the patient respiratory vitals. Monitoring the heart rate of the patient. Clarifying the amount of does with the physician The rate and the depth of respiration and pulse oximetry. Rationale: Before the administration of an opioid analgesic like morphine the nurse should completely assess the respiratory status of the individual as these drugs can cause respiratory depression (White et al, 2006). It is not compulsory to clarify the dose amount as morphine 4mg IV is already in the appropriate amount. It is also not necessary to monitor up the heart rate of the individual. References Brayfield, A, ed. (14 January 2014). "Metronidazole". Martindale: The Complete Drug Reference. Pharmaceutical Press. Retrieved 3 April 2014. Franklin, G. M. (29 September 2014). "Opioids for chronic noncancer pain: A position paper of the American Academy of Neurology". Neurology 83 (14): 12771284 Okie S (November 2010). "A flood of opioids, a rising tide of deaths". N. Engl. J. Med. 363 (21): 19815. Mercadante S, Arcuri E (2005). "Hyperalgesia and opioid switching". Am J Hosp Palliat Care 22 (4): 2914. Robsahm TE, Aagnes B, Hjartker A, Langseth H, Bray FI, Larsen IK (November 2013). "Body mass index, physical activity, and colorectal cancer by anatomical subsites: A systematic review and meta-analysis of cohort studies.". Eur. J. Cancer Prev. 22 (6): 492505 Rossi, S, ed. (2013). Australian Medicines Handbook (2013 ed.). Adelaide: The Australian Medicines Handbook Unit Trust. Searke, David (2006). Cancer Epidemiology and Prevention (3 ed.). Oxford University Press. p. 809. Shaib, W; Mahajan, R; El-Rayes, B (2013). "Markers of resistance to anti-EGFR therapy in colorectal cancer". Journal of gastrointestinal oncology 4 (3): 30818. Stein A, Atanackovic, D, Bokemeyer, C (Sep 2011). "Current standards and new trends in the primary treatment of colorectal cancer". European journal of cancer (Oxford, England : 1990). 47 Suppl 3: S3124. White M, Shah N, Lindley K, Lloyd-Thomas A and Thomas M (2006) Pain management in fulminating ulcerative colitis. Pediatric Anaesthesia 16: 1148 - 1152. Xie J, Itzkowitz, SH (2008). "Cancer in inflammatory bowel disease". World journal of gastroenterology : WJG 14 (3): 37889. Yin L, Grandi, N, Raum, E, Haug, U, Arndt, V, Brenner, H (Jul 2011). "Meta-analysis: Serum vitamin D and colorectal adenoma risk". Preventive medicine 53 (12): 106