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Colorectal Cancer 2
Colorectal Cancer

Introduction
Colorectal carcinoma is the third leading form of carcinoma and the second most common cause of carcinoma death rates in both women and men in the United States. Metastatic illness is typically the cause of death in CRC. Although efforts to detect CRC at an earlier stage have been increased through screening programmes, over 25 percent of sick people are still detected with the metastatic disorder and another 25 percent progress to metastases (Hashiguchi et al., 2019). Nurses can assist patients in identifying symptoms such as gastrointestinal bleeding, unusual weight loss, abdominal upset, or changes in stool routines, and they should advise them on screening. They must also provide patient education on diverse screening methods, such as stool testing, gene testing, and colonoscopy. It serves as a reference point for several patients who require accurate and reliable guidance to address many concerns and doubts that inevitably occur after having been invited to the prevention strategy (Keum & Giovannucci, 2019).
This paper focuses on colorectal cancer, its pathophysiology, critical care problems, medical diagnostics, and nursing diagnosis.

Pathophysiology
CRC pathogenesis includes both colitis-associated and sporadic CRC molecular mechanisms. The epithelial cells that cover the rectum or colon cause sporadic instability. Colorectal cancer develops from the epithelial cells that line the rectum or colon of the digestive tract, most commonly as a consequence of Wnt signalling system mutations that augment signalling activity. Mutations can either be acquired or inherited. The APC gene is a mutated gene in colorectal cancer. Several mutations should occur in addition to the abnormalities in the Wnt signalling process for the cell to become carcinogenic (Thanikachalam & Khan, 2019).
The TP53 gene codes for the p53 protein, which regulates cell division as well as encourages apoptosis in the event of cell defects. Mutations cause apoptosis, or the loss of power over cellular division. DCC and TGF-β are normally involved in apoptosis, but they are deactivated in CRC. Oncogenes promote cell division. Cell proliferation is overactivated as a result of mutations. Colorectal cancer expresses roughly 70 percent of every human gene, with slightly more than 1 percent having high expression when compared to other types of cancer (Davidson et al., 2021). Consequently, a lack of MMR proteins can sometimes lead to a failure to identify and restore genetic damage, enabling additional cancer-causing genetic changes to happen as well as colorectal cancer to advance. The traditional concept of colorectal cancer pathophysiology has been the polyp to carcinoma advancement succession. Gene mutations, local inflammatory variations, and epigenetic alterations are pivotal to a polyp to colorectal carcinoma cancer sequence (Siegel et al., 2020).
Epigenetic changes are far more common in colon carcinoma than mutational changes. A typical colon carcinoma has just 1-2 oncogene genetic variations and 1–5 tumour suppressor genetic variants, with approximately 60 additional "passenger" mutations (Xi & Xu, 2021). Other common forms of epigenetic mechanisms in carcinomas that modify gene expression patterns involve direct hypomethylation or hypermethylation of CpG regions of the protein-encoding genome, as well as modifications in chromosomal architecture and histones that impact gene expression. Epigenetic decreases in enzyme expression of DNA repair are expected to result in the epigenomic and genomic instability associated with...