portion of the gastric body that protrudes over a horizontal line drawn from the esophagogastric junction (Fig. 4.4). It blends into the gastric body, which constitutes most of the stomach. The body is demarcated from the distal portion, called the pyloric antrum, by a notch in the lesser curvature, the incisura angularis. Numerous longitudinal, grayish pink mucosal folds (called rugae) lie parallel to the lesser curvature (Fig. 4.5) and characterize the mucosa of the gastric body.
FIG. 4.2 Unopened stomach demonstrating its classic J shape. Esophagus and duodenum are also present.
FIG. 4.5 Gastric rugae. When the normal stomach is opened, the rugae appear as coarse folds of the mucosa.
longitudinal, the middle circular, and the inner oblique layer. Only the middle circular layer is complete. It is the strongest of the three muscle layers, and it becomes hypertrophic proximally and distally at the sphincters. The pyloric musculature consists of two layers: a thick inner circular layer and a thin outer longitudinal layer. The muscularis mucosae consists of two or three muscle layers.
FIG. 4.6 Regional gastric lymph node drainage. The node groups are perigastric nodes (1-6), left gastric (7), along the splenic artery (10,11), along the hepatoduodenal ligament (12), para-aortic (9,16), and intra-abdominal nodes (8,13-15).
and a single inconspicuous nucleolus (Figs. 4.7 and 4.8). Ovoid, spherical, mucin-containing, membrane-bound granules pack the supranuclear cytoplasm. The mucin stains strongly with the periodic acid-Schiff (PAS) stain (Fig. 4.9); it is negative or only weakly positive with mucicarmine stains. Numerous spot desmosomes and gap junctions maintain intercellular communication between the surface mucous cells, regulate cell differentiation (7), and help maintain mucosal barrier integrity. The surface mucous cells are produced in the mucous neck region, migrate upward, and extrude from the surface.
TABLE 4.1 GASTRIC EPITHELIAL CELLS AND THEIR PRODUCTS
to cardiac and pyloric glands, oxyntic glands are straight rather than coiled. Up to three gastric glands empty into the base of a gastric pit. Oxyntic mucosa contains six different cell types: surface foveolar cells, isthmus mucous cells, parietal cells, mucous neck cells, chief cells, and endocrine cells (Fig. 4.10). The gland neck contains undifferentiated, mucous neck, and parietal cells; the glandular bases contain parietal, chief, and endocrine cells.
TABLE 4.2 COMPARISON OF ANTRAL AND CARDIAC GLANDS
reverses. The canaliculi collapse, the microvilli recede, and cytoplasmic tubulovesicular structures become prominent again as the cell returns to its resting state.
macrophages that break through the basement membrane of oxyntic glands.
and postepithelial mechanisms (Fig. 4.14). Adherent mucus provides a stable unstirred layer that supports surface neutralization of acid by mucosal bicarbonate and acts as a permeability barrier to luminal pepsin (12). (Surface mucus is hydrophobic and water repellent). Surface-active phospholipids are produced by mucous neck cells and parietal cells. Parietal cells pump one HCO3– ion across the basal membranes for every H+ they secrete into the canaliculi (13). HCO3– is picked up by mucosal capillaries and carried to the basal part of surface foveolar cells. The bicarbonate ions are then secreted into the overlying mucous layer, where they are trapped by glycoproteins in the mucus, increasing the pH in the unstirred layer from approximately pH 2.0 in the gastric lumen to approximately 7.0 at the mucosal surface. This creates a pH gradient that traps and neutralizes most hydrogen ions as they enter the unstirred mucous layer (6). Maintenance of the pH gradient depends on both the secretion rate of bicarbonate and the thickness of the mucous gel layer (14). Mucus also lubricates the stomach facilitating food movement along the gastric lining, without causing mucosal abrasions. Its glycoproteins play a major role in resistance to injury by maintaining the viscoelastic and permeability properties of the mucous gel. Foveolar cells secrete lipid into the mucus that coats the epithelium lining the gastric lumen with a nonwettable surface, protecting the mucosa against the action of water-soluble H+ and pepsin (15) (pepsin can destroy the polymeric structure of this glycoprotein layer, solubilizing the surface mucous gel and liberating degraded glycoprotein subunits into the gastric lumen).
EGF, TGF-&agr;, and insulinlike growth factor directly stimulate gastric mucosal growth (24,25). EGF is ideally suited to participate in gastric repair because it is acid stable and stimulates epithelial migration, DNA synthesis, and gastric mucus production. TGF-&agr; shares 35% homology with EGF and mimics its mitogenic effects (26). EGF and TGF-&agr; also modulate parietal cell function and inhibit gastric hydrochloric secretion (27).
TABLE 4.3 LESIONS COEXISTING WITH GASTRIC DUPLICATIONS
first part of the duodenum lies on the left side. Dextrogastria affects approximately 1 of every 6,000 to 8,000 births (37). Situs inversus affecting only the stomach and duodenum (with the remainder of the thoracic and abdominal viscera lying in their normal positions) is extremely rare (37). The stomach lies either completely behind the liver or above it. Although abnormally positioned, gastric structure and function are normal.
antral diverticula should be carefully evaluated to exclude the presence of an underlying pathologic process such as gastritis, peptic ulcer disease (PUD), or neoplasia.
A clue that the lesion represents heterotopic pancreatic tissue, rather than an adenomyoma, is the finding of hypertrophic circular and longitudinal smooth muscle cells arranged circumferentially around the ducts in a more or less normal fashion (Fig. 4.21). Secondary changes such as pancreatitis, cyst formation, or neoplasia (islet cell tumors, ductal dysplasia [Fig. 4.22], and adenocarcinoma) may also cause confusion, particularly when they distort the underlying tissue (48). Dilated ducts forming submucosal mucin pools containing epithelial clusters and variable degrees of inflammation, without obvious pancreatic tissue adjacent to the mucin, may suggest a diagnosis of mucinous carcinoma. One should not make a diagnosis of invasive cancer in the absence of significant cytologic atypia and stromal desmoplasia.
appearance to the mucosa (66). Lymphoid follicles regress after the successful eradication of H. pylori infection, but they do so very slowly and may be still evident months or even years after treatment (65).
of IM increase with patient age and often become confluent, replacing large areas of the gastric mucosa. This process can be highlighted by staining gastric resection specimens for alkaline phosphatase activity since only intestinal-type epithelium expresses the enzyme (Fig. 4.25). IM more frequently coexists with gastric cancer than with gastric ulcer, but it shows the same distribution when associated with either condition.
(MUC1, MUC5AC, and MUC6) mucins and cytokeratin (CK) immunoreactivity (75). These cells have a complete switch in their differentiation program from a gastric to an intestinal phenotype, and they have been termed small intestinal, complete, or type I IM (Fig. 4.26).
FIG. 4.26 Complete intestinal metaplasia. A: The brush border of the absorptive cells is present, as are numerous goblet cells. B: Brush border highlighted by a CD10 immunohistochemical stain.
FIG. 4.27 Incomplete intestinal metaplasia. A: Low-power view showing the haphazard arrangement of goblet cells reminiscent of colonic mucosa. B: Higher-power view.
FIG. 4.29 Ciliated metaplasia. Ciliated metaplastic cyst located near the muscularis mucosae. The cilia are difficult to see on hematoxylin and eosin stain.
international expert group of gastroenterologists and pathologists gathered in Parma, Italy, and devised a system called the Operative Link for Gastritis Assessment (OLGA).
TABLE 4.4 DEFINITIONS AND GRADING GUIDELINES FOR EACH OF THE HISTOLOGIC FEATURES TO BE GRADED IN THE SYDNEY SYSTEM
TABLE 4.5 CAUSES OF ACUTE GASTRITIS
nausea, vomiting, and severe, acute, noncolicky, epigastric pain. Commonly, peritonitis or pleural effusions develop. The clinical course resembles that of patients with a perforated viscus. The mortality rate approaches 100% unless the affected part of the stomach is resected. Some patients develop abscesses. The most common offending organisms belong to Streptococcus species.
FIG. 4.30 Emphysematous gastritis. Photograph of the gastric mucosa showing the presence of an inflamed, partially necrotic, gastric mucosa. Deep in the mucosa, one sees large, dilated, air-filled spaces.
patients within 24 to 72 hours, predominantly in the proximal stomach.
disease shows extreme vascular congestion with dilation and hemorrhage into the superficial lamina propria (Fig. 4.33) often associated with acute inflammation (Fig. 4.33).
TABLE 4.6 PATHOLOGY OF ACUTE EROSIVE GASTRITIS
there is acute inflammation, and if lamina propria separates the glands, one should be extremely cautious before making a diagnosis of malignancy, even in the face of extreme epithelial atypia.
infiltration and extensive epithelial proliferation (106). Aspirin-induced damage results from its direct toxic effects as well as by decreasing mucosal defenses (107). The physicochemical property of aspirin aids in its rapid absorption, mucosal accumulation, and mucosal barrier breaking effects. Salicylates in aspirin become trapped inside gastric epithelia interfering with ATPase-dependent processes and leading to increased membrane permeability. Eventually, osmotic swelling and cell death develop. Additionally, small aspirin fragments may become embedded in the mucosa. These produce circular erosions or ulcers surrounded by hemorrhagic zones. Adjacent erosions become linked by linear mucosal cracks. The aspirin particles then fall into the cracks and become walled off in mucus until they dissolve.
erosions because of their chronicity and their potential for perforation and significant bleeding.
FIG. 4.36 Diagram of the mechanism of nonsteroidal anti-inflammatory drug (NSAID) damage. Following NSAID absorption, there is uncoupling of mitochondrial oxidative phosphorylation leading to reduced adenosine triphosphate (ATP) levels, which in turn result in the loss of intercellular junctional integrity and increased mucosal permeability. Also, as a result of the mitochondrial oxidative phosphorylation uncoupling, an efflux of calcium and hydrogen ions from mitochondria occurs, further depleting ATP stores and promoting oxygen radical damage. The damaged cell releases arachidonic acid, but the conversion of arachidonic acid to prostaglandins is prevented by the NSAID inhibition of cyclooxygenase. As a result, the damage of the gastric mucosa is more prolonged than would ordinarily be the case. As a result of the damage, the mucosa becomes vulnerable to luminal aggressive factors, which include acid, pepsin, bile, and Helicobacter pylori.
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