Gastrointestinal System
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) |
Tumors of the Small and Large Intestines
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* |
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.

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.

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.

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.