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Professional Practice: Application of Integrated Care

Pathophysiology of Cancer Tumours

In normal human cells, the segment of DNA i.e. genes, determine expansion, maturation & annihilation of cells by hereditary modifications in the gene which can be appeared at various stages via inherited mutation (National Cancer Institute, 2017). The two main classes of genes that are altered with these modifications are oncogenes and tumour suppressor genes. Oncogenes are cancer-causing agents that can be normal genes, asserted inadequately at greater stages in the one, suffering from cancer, or can be an alteration of normal genes. But in both forms, these genes bring out cancerous modifications in body tissues. The tumour suppressor genes typically obstruct cell distribution & avert the durability of cells that have impaired DNA and more often, but these genes get disabled and lead to the development of cancer. The cancerous/cancer tumour is having the capability to develop a fast pace & metastasize into additional body tissues (Mandal, 2019).

Cancer tumours are malignant tumours, consisting trillions body cells, which can metastasize, escalate, or infect surrounding tissues. Malignant tumours or neoplasm occur through hereditary modifications, hormonal modifications or environmental agents which lead to destruction and collapse of DNA naturally which further leads to mutation (inheritable change) in the genome. The inheritable or sudden change in genome causes stimulation of growth-boosting oncogenes and deactivation of tumour suppressor genes which consequently leads to uncontrolled cell proliferation and modifications in genes that control apoptosis. This process further leads to decreased apoptosis. These resultant factors cause colonial expansion, further leading to tumour progression, which causes the formation of malignant neoplasm or tumour among patients (NIH, 2015).

Pathophysiology of Colorectal Cancer Disease

The case study revealed that Betty is suffering from colorectal cancer where the various risk factors provoke parasympathetic behavior and cause an irritation in the lining of intestine turning into inflammation (Cipriano, n.d.). This leads to the glut fat changes the natural flora of intestine and consequently, polymorphic leukocytes lead to an abscess. This further increases the inflammation and necrosis and results in ulcerative lesions colon. The repetition of this process as in time leads to dysplasia and then, the hereditary mutation (sudden/inheritable) in cellular DNA leads to the formation of cancer and manifests the symptoms of pain, irregular bowel movement, constipation & increment of tumour in the colon (Cipriano, n.d.).

The colonoscopy results in the case study revealed Betty’s Adenocarcinoma of descending colon with stage 3A (Duke’s C). Adenocarcinoma initiates in the mucus-producing cells which facilitate lubrication in the colon (Akkoca et al., 2014). This level of colorectal cancer develops and metastasizes over the internal lining of colon & is termed as infiltrating adenocarcinoma (American Cancer Society, n.d.). The Dukes staging system is used as a classification for colorectal cancer and according to the stage 3, A (Dukes C) in the case represents that Betty's cancer has grown enough and crossed the inner lining of the intestine and reaches to the muscle layer (Akkoca et al., 2014). In this stage, it is clear that cancer has spread up to at least one to three lymph nodes close to the bowel. The chances of survival during this stage reach 30% with a maximum of 5 years (Radiopaedia. n.d.). 

FOLFOX Treatment

FOLFOX is the combination of three drug components, i.e., folinic acid, fluorouracil & oxaliplatin, which is used in the treatment of bowel cancer. The initials of these drugs have named the treatment as FOLFOX treatment. Folinic acid is also known as leucovorin and is also used as an antidote in methotrexate poisoning (Vodenkova et al., 2019). During the day of chemotherapy, anti-emetics are administered before the administration of chemotherapy medication. The chemotherapy drugs can be given through the cannula/central line/PICC line. Then, the infusion of folinic acid & oxaliplatin is administered over 2 hours. Then, a small dose of5-fluorouracil, as an injection is administered in the line & the rest of the dose is given through a small pump which is connected to the line. FOLFOX is administered after every 2 weeks/14 days of treatment, in which, the first day of treatment initiates by the infusion of oxaliplatin & folinic acid for 2 hours and 5-fluoro uracil, administered as an injection in the line. 5- fluorouracil, administered through the pump for either 46 hours in a run or in 24 hours partially with the continuation of remaining dose for the next day (Macmillan Cancer Support, n.d.).

5-fluorouracil converts into fluorouracil monophosphate which further converts into fluorouracil diphosphate. Fluorouracil diphosphate converts into fluorouracil triphosphate & in the presence of RRM-1, forms fluorodeoxyuridine diphosphate, which converts to fluorodeoxyuridine triphosphate (Vodenkova et al., 2019). Fluorouracil triphosphate causes RNA damage, CDDP leads to inter or intra DNA strand crosslinks and FdUTP causes destruction of replication forks (Vodenkova et al., 2019). This way, it helps in preventing replication and serves as a function of effective anti-cancer therapy.

References for Cancer Pathophysiology, Diagnosis, Aetiology and Common Treatment Options

Akkoca, A. N., Yan?k, S., Özdemir, Z. T., Cihan, F. G., Sayar, S., Cincin, T. G., ... & Özer, C. (2014). TNM and Modified Dukes staging along with the demographic characteristics of patients with colorectal carcinoma. International Journal of Clinical and Experimental Medicine7(9), 2828. Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4211795/

American Cancer Society. (n.d.). Understanding your pathophysiology report: Invasive adenocarcinoma of the colon. Retrieved from: https://www.cancer.org/treatment/understanding-your-diagnosis/tests/understanding-your-pathology-report/colon-pathology/invasive-adenocarcinoma-of-the-colon.html

Cipriano, C. (n.d.). Pathophysiology of colon cancer. Retrieved from: https://www.scribd.com/doc/100733263/Pathophysiology-of-Colon-Cancer-1

Macmillan Cancer Support. (n.d.). FOLFOX. Retrieved from: https://www.macmillan.org.uk/cancer-information-and-support/treatments-and-drugs/folfox

Mandal, A. (2019). Cancer Pathophysiology. Retrieved from: https://www.news-medical.net/health/Cancer-Pathophysiology.aspx

National Cancer Institute. (2017). The genetics of cancer. Retrieved from: https://www.cancer.gov/about-cancer/causes-prevention/genetics

NIH. (2015). What is cancer? Retrieved from: https://www.cancer.gov/about-cancer/understanding/what-is-cancer

Radiopaedia. (n.d.). Dukes staging system for colorectal cancer. Retrieved from: https://radiopaedia.org/articles/dukes-staging-system-for-colorectal-cancer

Vodenkova, S., Buchler, T., Cervena, K., Veskrnova, V., Vodicka, P., &Vymetalkova, V. (2019). 5-fluorouracil and other fluoropyrimidines in colorectal cancer: Past, present and future. Pharmacology & Therapeutics, 107447. Retrieved from: https://doi.org/10.1016/j.pharmthera.2019.107447

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