Week 2 Altered Physiology Scenario 4a 65-Year-Old Obese Afri

Week 2 Altered Physiologyscenario 4a 65 Year Old Obese African Ameri

This case study involves a 65-year-old obese African American male presenting with crampy left lower quadrant pain, constipation, and fever of 101°F. He has a history of recurrent episodes over 15 years, often responding to bowel rest and antibiotics, but has refused colonoscopy despite risk factors, including chronic inflammatory bowel disease (diverticulitis), sedentary lifestyle, and low-fiber diet. Family history of colon cancer further elevates his risk. He eventually undergoes colonoscopy, revealing multiple polyps, some of which are diagnosed as adenocarcinoma of the colon.

The purpose of this analysis is to evaluate the potential reasons underlying the patient's presenting symptoms, identify genetic factors involved in the disease development, and explain the impact of immunosuppression on body systems.

Paper For Above instruction

The patient's presenting symptoms—crampy left lower quadrant pain, constipation, and fever—are characteristic of diverticulitis, a common complication of diverticular disease. Diverticulitis occurs when herniated colonic mucosa and submucosa through weak points in the muscular wall (diverticula) become inflamed or infected. The patient's recurrent episodes over years suggest ongoing diverticular disease exacerbated by his diet low in fiber, which increases intracolonic pressure and promotes diverticula formation (Peery et al., 2012). His age and obesity are additional risk factors, as both contribute to increased colonic pressure and inflammation, augmenting the risk of diverticulitis (Moritz et al., 2015). The inflammatory process manifests as localized pain, and systemic signs like fever reflect infection or inflammation within the diverticula.

Genetically, several genes have been associated with increased susceptibility to colon adenocarcinoma. Mutations in tumor suppressor genes such as APC (adenomatous polyposis coli) are central in the pathogenesis of familial and sporadic colon cancers. Loss of APC function leads to unchecked cell proliferation and the formation of adenomatous polyps, precursors to invasive carcinoma (Kinzler & Vogelstein, 1996). Other genetic alterations involve mismatch repair genes like MLH1 and MSH2, whose mutations predispose to microsatellite instability, a hallmark of Lynch syndrome, which elevates colon cancer risk (Lynch et al., 2009). The patient's multiple polyps identified during colonoscopy suggest a genetic predisposition compounded by environmental factors like diet and sedentary lifestyle. Such genetic mutations, coupled with chronic inflammation from diverticulitis, escalate the risk of malignant transformation into colon adenocarcinoma.

Immunosuppression is a state where the immune system's ability to recognize and eliminate pathogens or abnormal cells is diminished. This can result from disease processes, medications, or emerging from neoplastic conditions themselves. When immunosuppressed, body systems—particularly the immune, lymphatic, and hematopoietic systems—are compromised. The immune function reduction impairs defenses against infections, increases susceptibility to opportunistic pathogens, and diminishes immune surveillance against tumor cells (Kumar et al., 2018). Specifically, in the context of colon cancer, immunosuppression hampers the immune system's role in detecting and destroying neoplastic cells, aggravating tumor progression. Moreover, immunosuppressed individuals display a higher incidence of infections and a diminished response to vaccines, further compromising overall health. The chronic inflammation linked to diverticulitis and genetic predispositions to cancer may also exacerbate immunosuppressive effects, creating a cycle that promotes tumorigenesis and hampers recovery.

References

  • Kinzler, K. W., & Vogelstein, B. (1996). Lessons from hereditary colorectal cancer. Cell, 87(2), 159–170.
  • Kumar, V., Abbas, A. K., & Aster, J. C. (2018). Robbins Basic Pathology (10th ed.). Elsevier.
  • Lynch, H. T., et al. (2009). Hereditary non-polyposis colorectal cancer (Lynch syndrome): Clinical features, genetic testing, and management. Journal of Clinical Oncology, 27(2), 276–283.
  • Moritz, E. D., et al. (2015). Obesity and diverticulitis: A systematic review and meta-analysis. Annals of Surgery, 262(1), 16–24.
  • Peery, A. F., et al. (2012). Risk factors for diverticulosis and diverticulitis: A systematic review. Gastroenterology, 142(2), 252–260.