Pathophysiology of cancer tumours refers to the physiological changes leading to the formation of tumours and the functional changes which are observed after the disease. Cancer is associated with approximately 150 disease processes which involve unrestricted proliferation and expansion of cells. Cancer is developed as a consequence of varying tissue responses which result in uncontrolled cell growth. Cancer tumour is a generically used term for neoplasm and is generally classified into two categories which include malignant and benign tumours (Pathology, 2017). While a benign tumour is generally devoid of any harmful impacts and is curable, a malignant tumour indicates the existence of cancerous symptoms.
Malignant tumour is prominently associated with the impact on cell differentiation and change. The cancer tumours are responsible for limiting the essential tissue functions which gradually result in notable differences such as lowered immunity. The malignant types of tumours have been observed to exhibit a considerable degree of resistance towards the different forms of treatment and are associated with consequential outcomes such as recurrence after treatment and the increased probabilities of the growth of the tumour (Dr Ananya Mandal, 2017).
Benign tumours are associated with limited portions of the body and do not spread to other parts of the body other than the localized region. The incapability of benign cancer tumours for metastasis can be considered as the major reason for their localization. The treatment of benign tumours is possible in the initial stages due to their flexible response to the treatment. However, negligence in treatment could increase in size of the tumour, thereby increasing the risks of damage to vital organs and organ systems (NCHPAD, 2017).
It is also necessary to apprehend the genetic changes associated with the cancer tumours which account for a significant aspect of the pathophysiology of the same. Oncogenes are defined as cancer-causing genes and include the impact of the existence of normal genes in high proportions in the case of patients afflicted with cancer (Pathology, 2017).
In other cases, oncogenes are also associated with the transmutation of normal genes resulting in cancerous changes in tissues. Tumour suppressor genes are significant for the inhibition of surplus cell division alongside limiting the survival of cells with indications of damage to the DNA. The genetic changes are responsible for the transformation of normal cells into cancer cells (Dr Ananya Mandal, 2017).
Betty’s biopsy results suggest moderately differentiated adenocarcinoma grade 3. The pathophysiology of colorectal cancer alongside the evaluation of the biopsy results could help in preparing a viable plan for prognosis and treatment of Betty’s health conditions. The pathophysiology of colorectal cancer suggests its proliferation in three sequential stages such as initiation, promotion and progression. The initiation is associated with consistent mutations in DNA which lead to cancerous growth (Fakhoury et al., 2014).
In the case of Betty, the adenocarcinoma suggests the cancerous growth of the epithelium i.e. colorectal lining. Genes associated with tumour growth include oncogenes, mutator genes and tumour-suppressing genes. Therefore colorectal cancer in the case of Betty can be related to the sequence of genetic alterations which leads to permanent and progressive depreciation in normal control of cell differentiation and growth. The grade 3 tumour observed in the biopsy of Betty indicates that she has moderately differentiated adenocarcinoma in which the cancerous growth is found to be associated with characteristics of undifferentiated and well-differentiated cancer cells (Huether & McCance, 2015).
However, the indication of grade 3 is indicative of poor differentiation in which the cancerous cells are more aggressive and could require a strenuous prognosis. Since the grading of tumours is a standard for establishing the plan for prognosis, the grading of Betty’s colorectal cancer has to be taken into consideration. The poor differentiation of cancer cells observed in the case of Betty could be responsible for the expansion of the cancerous cell growth along major pathways. The pathways include the proliferation of cancer through inflammatory bowel disease, familial adenomatous polyposis and associated polyposis syndromes, hereditary colorectal cancer, familial non-polyposis colorectal cancer and sporadic colorectal cancer (McCance & Huether, 2015).
The pathophysiology of colorectal cancer in the context of Betty’s biopsy results indicates that her recommended modes of treatment could include surgery followed by chemotherapy to prevent the growth of cancerous cells. The size of the tumour has to be estimated to consider the alternative of radiation for the treatment of moderately differentiated Adenocarcinoma grade 3 (Tchernof & Després, 2013).
The case of Betty involves stage 3 colorectal cancer which is also categorized as Duke’s C hence the chances of a 5-year survival rate work in favour of Betty (Ncin.org.uk, 2017). However, the first step in the treatment of colorectal cancer is to identify the stage of the cancer which helps in determining the type of treatment i.e. chemotherapy, surgery or radiation. Chemotherapy is intended for the restriction of uncontrolled growth of cancer cells and the two commonly adopted chemotherapy methods include neoadjuvant and adjuvant chemotherapy. Neoadjuvant chemotherapy is recommended by healthcare professionals for the treatment of colorectal cancer in which the size of the tumour is larger and unsuitable for surgery (Tchernof & Després, 2013).
The objectives of adjuvant chemotherapy are indicative of restricting the growth of cancerous cells in the colorectal lining after surgery. The process of adjuvant chemotherapy is also associated with the promising outcome of restrictions on the expansion of colorectal cancer to other parts of the body. The colorectal cancer of Betty is limited to the nearby lymph nodes and therefore it has not expanded to other parts of the body.
Therefore the suitable chemotherapeutic treatment for Betty would be adjuvant chemotherapy followed by surgery. While surgery is assumed as an unlikely measure for the limitation of cancer growth, the localized nature of colorectal cancer of Betty creates opportunities for surgery. The surgery would involve the removal of the affected section of the colon alongside the affected lymph nodes nearby. Removal of the nearby lymph nodes can be termed a partial colectomy and subsequently, Betty has to be monitored for remaining traces of cancer in the colorectal lining (Tursi, Papa & Danese, 2015).
The most commonly used drugs for administering chemotherapy for stage 3 colorectal cancers include different regimens or groups of drugs. One regimen includes capecitabine and oxaliplatin known as Cape Ox and the other comprises three drugs such as oxaliplatin, 5-FU and leucovorin known as FOLFOX. The alterations in the regimens of FOLFOX could also include administration of 5-FU with capecitabine or leucovorin distinctly. The variations in the different forms of adjuvant chemotherapy could also be used as promising inputs for determining the relevant chemotherapy treatment for Betty (Waldner & Neurath, 2014).
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Waldner, M. J., & Neurath, M. F. (2014, February). The master regulator of intestinal disease: IL-6 in chronic inflammation and cancer development. In Seminars in Immunology (Vol. 26, No. 1, pp. 75-79). Academic PressOrder Now