Peptic ulcer disease per se does not impart increased risk for development of gastric cancer. However,
Figure 17-25Diagram of growth patterns and spread of gastric carcinoma. In early gastric carcinoma (A), the tumor is confined to the mucosa and submucosa and may exhibit an
exophytic, flat or depressed, or excavated conformation. Advanced gastric carcinoma (B) extends into the muscularis propria and beyond. Linitis plastica is an extreme form of flat or
depressed advanced gastric carcinoma.
Figure 17-26Gastric carcinoma. Gross photograph showing an ill-defined, excavated central ulcer surrounded by irregular, heaped-up borders.
Figure 17-27Gastric carcinoma. A, Intestinal type demonstrating gland formation by malignant cells, which are invading the muscular wall of the stomach. B, Diffuse type demonstrating
signet-ring carcinoma cells.
Figure 17-28Gastric MALT lymphoma. Note the lymphoepithelial lesions (arrows). (Courtesy of Dr. Melissa Li, University of Florida, Gainesville, FL.)
Figure 17-29Gastrointestinal stromal tumor. A, Gross photograph of the tumor arising from the muscularis propria of the gastric wall. B, Microscopic view of the tumor showing spindle
Figure 17-30 A, Normal small-bowel histology, showing mucosal villi and crypts, lined by columnar cells. B, Normal colon histology, showing flat mucosal surface and abundant
vertically oriented crypts.
Figure 17-31Meckel diverticulum. The blind pouch is located on the antimesenteric side of the small bowel.
TABLE 17-6-- Major Causes of Diarrheal Illnesses
Secretory Diarrhea
Infectious: viral damage to mucosal epithelium
• Rotavirus
• Caliciviruses
• Enteric adenoviruses
• Astroviruses
Infectious: enterotoxin mediated
• Vibrio cholerae
• Escherichia coli
• Bacillus cereus
• Clostridium perfringens
Neoplastic
• Tumor elaboration of peptides, serotonin, prostaglandins
• Villous adenoma in distal colon (nonhormone mediated)
• Secretory diarrhea: Net intestinal fluid secretion leads to the output of more than 500 mL of fluid stool per day, which is isotonic with plasma and persists during fasting.
• Osmotic diarrhea: Excessive osmotic forces exerted by luminal solutes lead to output of more than 500 mL of stool per day, which abates upon fasting. Stool exhibits an osmotic
gap (stool osmolality exceeds plasma electrolyte concentration by ³50 mOsm).
• Exudative diseases: Mucosal destruction leads to output of purulent, bloody stools that persist on fasting; stools are frequent but may be small or large volume.
• Deranged motility: Improper gut neuromuscular function may produce highly variable patterns of increased stool volume; other forms of diarrhea must be excluded.
• Malabsorption: Improper absorption of gut nutrients produces voluminous, bulky stools with increased osmolarity combined with excess stool fat (steatorrhea). The diarrhea