Gastrointestinal System

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Gastrointestinal System

Common diseases of the esophagus, the stomach, and the small and large intestines include functional disorders, inflammation, infections, and tumors.

Diseases of the Esophagus

Esophageal diseases of various kinds are characterized by fairly uniform clinical symptoms of dysphagia (swallowing difficulties), heartburn (retrosternal pain), and vomiting (with or without blood). The most frequent causes are inflammatory or neoplastic diseases. Other esophageal problems that should be considered in differential diagnosis include diverticula and fistulas, atresia in the newborn, motility changes (e.g., achalasia), and a number of diseases that affect the esophagus secondarily (e.g., Mallory-Weiss lacerations in alcoholism, varices in hepatic cirrhosis, esophageal sclerosis in primary systemic sclerosis, and bulemia).

Diseases of the Stomach

Congenital diseases of the stomach, such as congenital pyloric stenosis, congenital hernias, diverticula, and cysts, are rare. The 2 most frequent disorders affecting large numbers of patients are inflammation of the stomach (gastritis) and epithelial tumors (carcinoma). These are discussed in more detail here, in addition to the frequent adult hernias, a common cause of reflux esophagitis and, potentially, esophageal cancer.

Nontumorous Diseases of the Small and Large Intestines

Congenital disorders of the intestines are uncommon and are discussed in Table 4-1 and malabsorption syndromes in Table 4-4.

TABLE 4-1

DEVELOPMENTAL INTESTINAL DISEASES

Disease	Features
Small intestine
Atresia	Complete occlusion of intestinal lumen secondary to intraluminal diaphragm or disconnected blind ends (occurs in fetuses of mothers with polyhydramnios)
Stenosis	Partial occlusion (stricture) of the intestinal lumen secondary to incomplete intraluminal diaphragm, external adhesions (e.g., secondary to [transient] volvulus)
Duplications	Tubular or cystic structures (enteric cysts) that may communicate with the intestinal lumen (most common in ilium; may contain gastric mucosa and cause peptic ulcer similar to Meckel diverticulum)
Meckel diverticulum	Partial persistence of the vitelline duct, 60–100 cm before the ileocecal valve, with all layers of intestinal or gastric mucosa
Large intestine
Malrotation	Abnormal positioning of colon in abdominal cavity (e.g., cecum in left upper quadrant); may give rise to volvulus
Hirschsprung disease	Congenital megacolon secondary to aganglionic segment (lack of Auerbach and Meissner plexus preferentially in sigmoid colon and rectum)

Infectious enterocolitis (IEC) and food poisoning are diseases of worldwide prevalence characterized by diarrhea and (gastro)intestinal inflammation with increased intestinal secretion and reduced absorption. Mucosal necrosis, hemorrhage, and ulceration develop according to local or systemic toxic influences of the causative agent. Loss of fluid and toxic side effects are especially dangerous for children and the elderly. Etiologic agents frequently identified in acute IEC are viruses (rotavirus, Norwalk agent) and bacteria (enterotoxic Escherichia coli); however, in up to 50% of cases, no organism is identified. In the United States, the most common causative agents in fatal IEC, in order of frequency, are Salmonellae, Listeria, Toxoplasma, Norwalk agent, E. coli, and Campylobacter.

The most common vascular lesions of the small and large bowel are phlebectases (hemorrhoids) and ischemic and thrombotic disorders; less common are local vasculitis accompanying systemic vasculitis and collagen-vascular diseases as well as angiodysplasia.

Tumors of the Small and Large Intestines

Benign tumors of the intestines are most often epithelial in nature and are referred to clinically as polyps. They usually are rare in the small intestine but frequent in the large intestine (colonic polyps increase in frequency from approximately 20% before the age of 40 years to 50% beyond the age of 60 years). The clinical entity polyp is subclassified pathologically into polyps as such (i.e., reactive lesions, such as hyperplastic, hamartomatous, or inflammatory polyps) and adenomas (i.e., benign neoplastic lesions, such as tubular or villous adenomas). The pathologic entity polyp does not possess malignant potential, whereas adenomas (also referred to as adenomatous polyps) do. Depending on their size, there is a 10% to 15% risk of cancer development within 5 years in tubular adenomas and a 30% to 40% risk in villous adenomas. The risk of malignancy increases with the number of adenomas; especially prone for malignant change are familial polyposis syndromes (e.g., Gardner syndrome) in which the occurrence of cancer approaches 100% by midlife.

Other more infrequent benign lesions of the intestines are lipomas, leiomyomas, neurofibroma, and hemangioma, which may also impress clinically as polyps and rather rarely may cause complications (e.g., erosion, bleeding and anemia, obstruction, or intussusception).

Malignant tumors of the small intestine account for less than 0.1% of tumors diagnosed at autopsy, or less than 5% of all gastrointestinal (GI) tumors. They consist primarily of adenocarcinomas, malignant lymphomas, and carcinoid tumors (CTs). Even less frequent are stromal tumors, such as leiomyosarcoma and gastrointestinal stromal tumors (GIST). By contrast, adenocarcinomas of the colon and the rectum are among the most common malignant tumors in the Western world, accounting for approximately 15% of all cancer deaths in the United States (approximately 150,000 new cases diagnosed every year, with a peak incidence at the age of 60-70 years). Other malignant tumors of the large bowel include CTs and, rarely, malignant lymphomas and (anal) melanomas. As in the small intestine, stromal tumors occasionally occur.

TABLE 4-2

HISTOLOGIC CLASSIFICATION OF GASTRITIS

Type of Gastritis	Histologic Features	Course
Common acute gastritis	Mucosal edema Neutrophilic infiltration with or without erosions Petechiae with or without mild lymphoplasmacytic infiltration Epithelial regeneration in neck region of glands	Usually transient
Eosinophilic gastritis	Eosinophilic infiltrates of all layers, frequently with muscular hypertrophy	Incidental or recurrent (may be related to allergies or ingestion of chemical irritants)
Chronic type B gastritis (more common)	Superficial lymphoplasmacellular infiltrate Neutrophils if erosive, with or without lymph follicles Colonization by Helicobacter pylori Elongation of glandular necks with epithelial regeneration Intestinal metaplasia in late phase	Chronic persistent or recurrent May predispose to carcinoma or lymphoma
Chronic type A gastritis	Patchy lymphocytic infiltrate with invasion of crypt epithelia and epithelial degeneration Loss of acidophilic cells Intestinal metaplasia	Chronic aggressive Decreased vitamin B₁₂ resorption may predispose to cancer*

^*Decreased vitamin B₁₂ resorption is followed by various B₁₂ deficiency diseases, such as pernicious anemia, spinal cord demyelination, and others.

TABLE 4-3

PATHOGENESIS OF CARCINOMA OF THE STOMACH

Factors	Prevalence and Examples
Nutritional factors	Apparently account for geographic variations in cancer incidence: large amounts of smoked fish, pickled vegetables, highly salted foods; diets low in fruits and vegetables (i.e., in protective antioxidants) Identified carcinogens: nitrosamines, benzpyrene
Infections	Chronic Helicobacter pylori infection as cofactor (see above)
Genetic factors	Approximately half of cancer patients possess blood group A No clearcut genetic traits identified Changes in tumor suppressor gene activity (e.g., p53), germline mutations, and genetic mismatch repair similar to cancer of the colon (see there)
Other factors	Low socioeconomic status (probably related to nutritional factors and infection)

TABLE 4-4

PATHOGENESIS OF MALABSORPTION SYNDROMES *

Major Cause of MAS	Specific Disturbance
Defective intraluminal digestion	Deficiency in bile or pancreaticenzymes or both
	Inactivation of pancreatic enzymes by excess gastric acid
	Disturbed resorption by bacterial overgrowth
Defective intestinal digestion	Deficiency in hydrolytic enzymes and peptidases secondary to bacterial overgrowth with mucosal atrophy
Defective transepithelial transport	Abetalipoproteinemia
Reduction in resorptive surface	Gluten-sensitive enteropathy (celiac sprue)
	Crohn disease
	After surgery (gastrectomy, bypass, short bowel)
Specific infections	Whipple disease
	Tropical sprue
	Parasitic infestations
	Tuberculosis
Malignancies	Intestinal lymphoma (IPSID)

^*IPSID indicates immunoproliferative small intestinal disease; MAS, malabsorption syndrome.

Figure 4-1 Esophagitis
Esophagitis, which affects up to 20% of people in developed countries, is usually caused by gastric reflux (reflux esophagitis). Reflux esophagitis follows a “chemical” irritation by gastric fluids containing acid and pepsin (peptic esophagitis), which is secondary to improper closure of the lower esophageal sphincter. The tonus of the lower esophageal sphincter may be decreased by hiatal hernia of the stomach; voluminous intake of fatty foods; increased chocolate, alcohol, or nicotine consumption; hormonal factors (estrogen therapy, pregnancy); or treatment with central nervous system (CNS) depressants such as diazepam or opiates. Pathologically, acute reflux esophagitis shows hyperemia and mild degenerative changes such as ballooning of epithelial cells, occasional mild superficial erosion, and occasionally eosinophilic (rarely neutrophilic) infiltration. Chronic disease results in fibrosis and stenosis.

Figure 4-2 Chronic Reflux Esophagitis and Barrett Esophagus
Chronic reflux esophagitis is classified into stages of severity. Stage I is characterized by epithelial hyperplasia and keratosis (clinical finding: leukoplakia) with sparse submucosal lymphocytic infiltrate. Stage II resembles stage I, with the addition of superficial erosion and neutrophilic infiltration. Stage III resembles stage II, with epithelial ulceration and more pronounced epithelial regeneration (elongated epithelial papillae). Complications of chronic reflux esophagitis include fibrous scarring and stenosis, mucosal metaplasia, and cancer. Barrett esophagus (BE) is the focal replacement of stratified squamous epithelium by metaplastic columnar epithelium with goblet cells. BE appears grossly as velvety, pink islands of mucosa in the lower third of the esophagus. Besides the intestinal-type mucosa, gastric mucosal elements (cardia- or fundus-type glands, including parietal and chief cells) are frequent. BE is associated with a greatly increased incidence of adenocarcinoma.

Figure 4-3 Esophageal Cancer: Squamous Cell Carcinoma
Malignant neoplasms of the esophagus account for up to 2% of cancer deaths in the United States annually. Certain ill-defined genetic predispositions, exposure to food carcinogens (e.g., nitrosamines), tobacco smoke, chronic alcoholism, and chronic esophagitis (especially with BE) seem to be important pathogenetic factors. Loss of p53 tumor suppressor gene function is one of the most frequently observed molecular changes in esophageal cancer. Squamous cell carcinoma usually impresses as a plaquelike or fungating white lesion in the upper or medial part of the esophagus. The tumor infiltrates the esophageal wall deeply, penetrates into the mediastinum, and spreads via lymphatic channels. Invasion of the bronchial tree may occur with fistulation. Severe dysphagia and anorexia cause pronounced cachexia. The 5-year survival rate is 10% for patients with squamous cell carcinoma.

Figure 4-4 Esophageal Cancer: Adenocarcinoma
Adenocarcinomas

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