Tumours of the Intestine

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Primary tumours of the small intestine are rare

The small intestine rarely develops primary tumours, but among those that do arise are stromal tumours; in particular, leiomyoma or lipoma may develop in the small bowel wall.

Carcinoid (neuroendocrine) tumours, derived from the neuroendocrine cells in the small intestinal crypts, are most common in the jejunum and ileum.

Malignant lymphomas, derived from mucosa-associated lymphoid tissue of the small bowel, are usually B-cell lymphomas. Coeliac disease is a major predisposing factor. Tumours may be multi-focal, and spread is to local lymph nodes.

Primary adenocarcinoma of the small bowel is very rare. It usually presents as an ulcerating strictured lesion, producing small bowel obstruction.
Adenomata of the large bowel appear as polyps

Adenomata derived from the glandular epithelium of the large bowel manifest as one of three different patterns of polyp categorized as tubular, villous or tubulovillous. Such polyps are important because they frequently develop into a carcinoma. There is much evidence to suggest that most carcinomas of the colon develop from previous adenomata, and the well-established progression from adenoma to carcinoma is the basis of the polyp-cancer sequence for development of carcinoma of the colon. The risk of malignant change is greatest where large lesions are present.

Adenocarcinoma of the colon is common

Carcinoma of the colon is the second most common cause of death from neoplasia. These tumours are adenocarcinomas derived from the glandular epithelium of the large bowel mucosa.

The epidemiology of carcinoma of the colon shows great geographic variation, which has been related to environmental factors rather than genetic factors in local populations. Although there has been great interest in the role of dietary fats, fibre, processed sugar, and bile acids, none has been conclusively shown to be important in pathogenesis.

The main risk factors for development of a carcinoma are the presence of multiple sporadic adenomatous polyps, ulcerative colitis, and familial adenomatous polyposis. The fact that adenomatous polyps are a precursor lesion for development of carcinoma has led to implementation of screening programmes to detect occult blood in the stools, derived from ulceration of adenomatas.

Carcinoma of the colon has a peak incidence in those aged between 60 and 70 years, and is rare under the age of 40. When young individuals develop the disease, inflammatory bowel disease or inherited polyposis syndrome should be suspected as predisposing causes.

Both sporadic and inherited forms of colonic adenoma are recognized

Sporadic adenomata increase in incidence with age.and are assumed to be related to environmental agents consumed in the diet. They may appear as any one of the patterns of adenoma.


Familial adenomata are seen in familial adenomatous polyposis (FAP), an autosomal dominant condition due to a mutation in a tumour suppressor gene termed the 'APC gene' (adenomatous polyposis coli gene). Patients develop innumerable adenomata of the large bowel from about the age of 25, with 100% risk of developing a carcinoma of the colon by the age of 45 {\I (Fig. 11.12).} Other forms of inherited polyposis syndromes are listed in {\I Fig. 11.13} on the blue button below.

 Colorectal carcinoma has several morphological patterns

There are several well-recognized morphological types of carcinoma of the colon and rectum, each associated with different clinical patterns of presentation. The main presenting features are attributable to obstruction (colicky abdominal pain and distension with later vomiting) or blood loss (acute or chronic bleeding leading to development of anaemia).

50% of tumours occur in the rectum and sigmoid.

30% of tumours occur in the caecum and right colon.

20% of tumours occur in the descending and transverse colon.

Because the faeces is fluid in the right side of the colon, a lesion may grow to a large size before causing obstruction. Carcinomas of the right side are mainly large, polypoid exophytic lesions, which grow into the lumen of the bowel. Carcinomas of the left side cause obstruction early because the faeces is more solid. Left-sided lesions are of two main types: annular carcinomas, which are small but cause stenosis; and ulcerating tumours, which present mainly with bleeding.

Colonial carcinomas vary in differentiation

Spread of carcinoma of the colon is by three main routes. There is local spread through the bowel wall, when invasion of the serosa of adjacent bowel or bladder may occur; lymphatic spread to draining nodes; and blood spread to the liver and other sites such as lung.

Infiltrative carcinoma of the colon is a rare pattern caused by signet-ring cell carcinoma that is virtually identical to that seen in the stomach. It is often associated with carcinoma that develops in association with inflammatory bowel disease.

Macroscopically carcinomas are raised red lesions with a rolled edge and frequent central ulceration. Lesions are composed of solid, white tissue, and invasion into the wall of the bowel may be seen.

Histologically, the majority of lesions have a glandular pattern composed of pleomorphic neoplastic epithelial cells.

Prognosis of carcinoma of the colon is related to stage
The prognosis of carcinoma of the colon is related to the stage of disease, which is assessed using a modification of a staging system originally proposed for carcinoma of the rectum by Dukes. Following surgical resection, it is particularly important to determine adequacy of resection margins, particularly lateral extension to pelvic side wall or adjacent structures, which is associated with a poor outcome.

Dukes staging is shown here in its most simple and widely used form. Many modifications are in use, and some workers split stage B into B1 (extending into muscle) and B2 (extending through muscle); likewise, C1 (limited to wall with involved nodes) and C2 (through wall with involved nodes). It is important to check which modification of Dukes staging is locally in use to avoid misunderstandings.

Neuroendocrine tumours occur throughout the gut

Tumours derived from the neuroendocrine cells of the gut (carcinoid tumours) occur most commonly in the appendix and small bowel, but also arise in the stomach, colon, rectum, and oesophagus. The biological behaviour of the tumour appears to differ according to the site.
Lesions in the small bowel, colon and stomach are slow-growing, low-grade, and malignant. Some are multicentric. Tumours appear as yellow mucosal or mural masses, and metastasis is most commonly via the portal vein to the liver.
Lesions in the rectum and appendix almost never metastasize, appearing as tumour nodules composed of firm, yellow tissue.
A small proportion of lesions in the oesophagus appear as small-cell anaplastic carcinomas that are histologically identical to oat-cell carcinoma of the lung.
Depending on the nature of the neuroendocrine cells in the tumour, patients may develop a syndrome caused by hormone secretion. Some of these tumours secrete 5-hydroxytryptamine (5-HT), and its breakdown product, 5-hydroxyindolacetic acid (5-HIAA), can be detected in excess in the urine. Hepatic metastasis can produce the carcinoid syndrome, with symptoms due to excessive secretion of 5-HT (particularly facial flushing, bronchospasm and diarrhoea). Tumours secreting gastrin may stimulate excess gastric acid secretion, causing peptic ulceration (Zollinger-Ellison syndrome).
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