Rectal Cancer

Rectal Cancer

    * Introduction
    * Signs and symptoms
    * Diagnosis
    * Treatment
Rectal adenocarcinomas including most cancers. Other rare forms of cancer include rectal carcinoid, lymphoma and sarcoma. Squamous cell carcinomas can develop in the transition from the anus and rectum are considered anal carcinomas.
Most rectal cancers produce no symptoms and are discovered on routine examination of digital or proctoscope. Bleeding is the most common symptom of rectal cancer. Changes in bowel habits may include diarrhea, constipation, change in size and shape of the seat. Partial intestinal obstruction can cause colicky abdominal pain and bloating. If the cancer invades the bladder urine output changes can occur. Other presentations include perforation, jaundice with liver metastases.
Approximately 75% of colorectal cancers are sporadic and develop the private persons without risk factors. Most rectal cancers develop in patients with a family medical history positive for colorectal cancer or polyps. As a recognized risk factors: diet, alcohol, smoking, bile acids, hereditary factors, hereditary adenomatous polyposis, hereditary colorectal cancer and inflammatory bowel disease nonpolipozic: ulcerative colitis and Crohn's disease.
Although radical resection of the rectum is the main therapy, surgery as a single therapy has a high recurrence rate. Rectal adenocarcinomas are sensitive to radiation therapy. It can be applied preoperatively, intraoperatively and postoperatively, with or without chemotherapy. Adjuvant therapy includes administration of chemotherapy and is especially useful in treating liver metastases. Local Recurrence is more common in rectal cancers than in the colon. The disease recurs in 5-30% of patients in the first year after surgery. Factors that influence the development of the appellant include variability surgery, primary tumor grade and stage, primary tumor location and the ability to obtain negative resection margins.
Pathogenesis of cancer of the rectum Carcinomas are found in 4% of neoplastic polyps. Cells must accumulate 4-5 molecular defects, including activation of oncogenes and inactivation of tumor suppressor genes to turn malignant. In normal mucosa, the surface epithelium is regenerated to 6 days. Cells in the crypts migrate from the crypts to the surface, where sufferers cell differentiation, maturation and eventually lose their ability to multiply.
In adenomas, several genetic mutations alter this process, beginning with the inactivation of the APC gene, allowing the surface crypt cell replication. Mutations occur with increased cell division in November forcing oncogene K-RAS activation in the early stages of p53 mutations in late stages. The cumulative loss in suppressor gene function prevent apoptosis and cell gives eternal life.
Causes and risk factors for rectal cancer The etiology of rectal cancer is unknown, but appears to be multifactorial in origin and include environmental factors and genetic makeup. Diet can play a causative role, especially one that contains fat.
Environmental factors include: Excess fat-diet without dietary fiber, especially animal fats and vegetable oils saturated unsaturated -Oils containing omega-3 and omega-6 monounsaturated fatty acids appear to be less carcinogenic Long-term diets with red meat or processed meat seems to increase risk of distal colon cancer Fiber-rich food intake seems to be protective against cancer, accelerating intestinal transit and shorten the time of contact with harmful substances lining Calcium-increasing food has a protective effect for colorectal mucosa by binding bile acids and fatty acids -Selenium, carotenoids and vitamin A, C, E have protective effects by binding to oxygen free radicals in the colon -Alcohol-daily drinkers had an increased risk of cancer 2 times Smoking and smoking-particularly that begins at an early age increases the risk of colorectal cancer Bile acids, bile acids after cholecystectomy increased exposure to circulating factors continued degradation of intestinal bacteria.
Hereditary factors include: Medical-family history of colorectal-cancer risk is increased in first degree relatives of affected patients -Personal history of polyps or colorectal cancer among patients with colorectal cancer, 30% type synchronous adenomatous lesions, 40-50% have polyps at colonoscopy, malignancy occurs in 2-5% of patients.
Genetic Diseases: -Familial adenomatous polyposis is an autosomal dominant hereditary syndrome that causes the development of more than 100 adenomatous polyps and a variety of extraintestinal manifestations Individual-risk malignant polyps were not higher than that of polyps in the general population, increased number of polyps, however, predispose patients to an increased risk of cancer, colorectal cancer develops in untreated 100% of them until the age of 40 years Nonpolipozic hereditary colorectal cancer-an autosomal dominant syndrome, patients have the same number of polyps in the general population but are more prone to malignant polyps -And these patients have an increased incidence of endometrial cancer, brain, stomach and thyroid.
Inflammatory bowel disease: Ulcerative colitis-malignizarii-incidence increases with time after 10 years the incidence of colorectal cancer is 1% per year Crohn's disease-colorectal-cancer incidence in these patients is 4-20 times higher than the general population.