Analysis of Rectal Adenocarcinoma: Causes, Treatment, and Outcomes

This report provides a comprehensive overview of rectal adenocarcinoma, a type of cancer that originates in the lining of the large intestines. It begins with an introduction that highlights the prevalence of this cancer, particularly among older adults, and notes its higher incidence in regions with high-fat, low-fiber diets. The report then delves into the pathophysiology of rectal adenocarcinoma, explaining the three main pathways through which the disease develops: the APC gene adenoma-carcinoma pathway, the HNPCC pathway, and the ulcerative colitis dysplasia pathway. It describes the genetic mutations involved in each pathway and how these mutations lead to uncontrolled cell growth and the formation of tumors. The report also discusses the science underpinning the use of pharmacotherapy in treating rectal adenocarcinoma, including the use of chemotherapy drugs like Fluorouracil, Irinotecan, and Oxaliplatin, which are used to shrink tumors and eliminate cancer cells. The report concludes by mentioning the side effects associated with these drugs and the use of additional medications to manage them. The report includes a list of relevant references.

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Rectal adenocarcinoma
Introduction
Rectal adenocarcinoma arises from the epithelium cells lining the large intestines. The
main function of the rectum is the temporary storage of fecal matter before elimination. This
cancer is common at an advanced age, especially at age 60 years and above. Statistics show that
this type of cancer is found worldwide but common in areas where people consume food low in
fibre and high in fat content such as Australia, USA and Europe. The prevalence of rectal
adenocarcinoma in Australia is approximately 15,605 new cases every year (Melaku et al. 2018).
Also, as one advance in age, there is increased risk, especially at 85 years ad above. The risk of
being diagnosed with cancer is 1 in every 11 men and 1in every 16 women. The main risk factors
include hereditary conditions, family history of rectal cancer, diet, inflammatory bowel disease
and polyps (Van Den Eynde et al. 2017).
Pathophysiology of rectal adenocarcinoma
Normally, the mucosa of the large intestines regenerates after every six days, where the
crypt cells migrate from the base of the crypt to the surface. They then differentiate and mature
losing their ability to replicate. For adenocarcinoma to develop, three pathways exist. These are
the adenomatous polyposis coli (APC) gene adenoma-carcinoma pathway, hereditary
nonpolyposis colorectal cancer (HNPCC) pathway and ulcerative colitis dysplasia (McCance and
Huether 2018). In the APC pathway, several gene mutations are involved. First, the APC gene
becomes inactivated, allowing cellular replication at the crypt surface to remain unchecked
increasing cell division. With increased cell division, it causes inactivation of the K-ras oncogene
first the P-53 gene later, which are tumor suppressor genes. The loss of these genes then prevents
apoptosis and therefore, cell life is prolonged indefinitely, leading to cancer (Hall 2017).
In the HNPCC pathway, there is a mutation in DNA mismatch repair genes. These genes
are Hmlh1, hMSH2 and 6, hPMS 1and 2. This mutation, therefore, leads to negative DNA repair
resulting in cancer. Finally, in the ulcerative colitis pathway, genetic alteration is caused by
chronic inflammation as in inflammatory bowel disease and ulcerative colitis. This, in turn, leads
to dysplasia and cancer formation (Bullock and Hales 2019).

Science underpinning pharmacotherapy use in rectal adenocarcinoma
Pharmacotherapy is the use of medication to treat cancer. Research has been done, and it
has been proven that rectal cancer can be managed using medication. They are usually systemic
and given through an intravenous line or orally; therefore, it is distributed all over the
bloodstream. Chemotherapy drugs are used to suppress growth or division of cancer cells. They
are usually scheduled for a number of cycles and given over a period of time using one drug of in
combination of more than one drug. They are also used to shrink the tumor before surgery and
after surgery to eliminate remaining cancer cells (McGavock 2017).
Some of the drugs approved by the Food and Drug Administration (FDA) for treatment
of rectal cancer include Fluorouracil, Irinotecan, Oxaliplatin, Capecitabine and Trifluridine.
These drugs can be used alone, in combination or with targeted therapy. They cause a number of
side effects such as vomiting, nausea, neuropathy, and diarrhea. They are, therefore administered
with drugs used to treat the side effects (Broyles et al. 2019).

References
Bullock, S., and Hales, M. (2019). Principles of pathophysiology (2nd ed.). Melbourne, VIC:
Pearson Australia.
Hall, J. E. (2017). Guyton and Hall: Textbook of Medical Physiology.
Broyles, B., McKenzie, G., Pleunik, S., Page, R., Reiss, B., & Evans, M. (2019). Pharmacology
in Nursing. Cengage AU.
Van Den Eynde, M., El Sissy, C., Kirilovsky, A., Marliot, F., Haicheur, N., Dragean, C. A., ... &
Leonard, D. (2017). Association of T-cell infiltration assessed in pretherapeutic biopsies
(PTB) of patients with locally advanced rectal adenocarcinoma (LARC) with tumor
response and relapse after chemoradiotherapy (CRT) and rectal surgery.
McCance, K. L., & Huether, S. E. (2018). Pathophysiology-E-book: the biologic basis for
disease in adults and children. Elsevier Health Sciences.
Melaku, Y. A., Appleton, S. L., Gill, T. K., Ogbo, F. A., Buckley, E., Shi, Z., ... & Fitzmaurice,
C. (2018). Incidence, prevalence, mortality, disability-adjusted life years and risk factors
of cancer in Australia and comparison with OECD countries, 1990–2015: findings from
the Global Burden of Disease Study 2015. Cancer Epidemiology, 52, 43-54.