gastric disorder

1. SMS 2044

2. Stomach Condition Comment Pyloric stenosis 1 in 300 to 900 live births Male to female ratio 3:1 Pathology: muscular hypertrophy of pyloric smooth muscle wall Symptoms: persistent, nonbilious projectile vomiting in young infant Diaphragmatic hernia Rare Pathology: herniation of stomach and other abdominal contents into thorax through a diaphragmatic defect Symptoms: acute respiratory embarrassment in newborn Gastric heterotopia Uncommon Pathology: a nidus of gastric mucosa in the esophagus or small intestine ("ectopic rest") (The Latin word for "nest“) Symptoms: asymptomatic, or an anomalous peptic ulcer in adult

3. Gastric heterotopia

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14. Histopathology usually demonstrates increased numbers of eosinophils

21. Schematic presentation of the presumed action of H. pylori in the development of chronic gastritis and peptic ulceration. The histologic features of the two disease conditions are depicted

34. Chronic gastritis with lymphoid follicle formation in the gastric mucosa (arrow) Some gastric glands are still found (arrowhead).

35. Chronic gastritis with chronic inflammatory cell infiltration and lymphoid follicle formation (arrowhead) in the gastric mucosa. Atrophy of the gastric glands is seen.(arrow). (M: mucosa, and SM: submucosa)

41. Neurogenic or catecholamine-induced vasoconstriction Mucosal ischemia D amage the mucosal barrier D irectly injure mucosal cells by oxygen or metabolic deprivation

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47. Normal Acute gastritis Chronic gastritis Atrophic gastritis Intestinal metaplasia Dysplasia Cancer

49. Figure 4). Granulation tissue in the ulcer base. New blood vessels lined by plump endothelial cells (arrow). Edema and inflammatory infiltrate are also seen. (Figure 5). Fibrotic tissue beneath the ulcer base

50. (Figure 8) Intestinal metaplasia in chronic gastritis. The gastric foveolar epithelium (arrowhead) is replaced by intestinal type of epithelium (arrow). The intestinal epithelium has goblet cells. Chronic inflammatory cell infiltration is also seen. (Figure 7) Chronic gastritis with intestinal metaplasia (arrow) seen in the mucosa around the peptic ulcer. The mucinous gastric foveolar epithelium (arrowhead) is replaced by intestinal type of epithelium (arrow).

52. Etiology of PUD Normal Increased Attack Hyperacidity, Zollinger Ellison syndrome. Weak defense Stress, drugs, smoking Helicobacter pylori *

60. Bacteria over epithelial cells

69. Peptic ulcer of the duodenum. Note that the ulcer is small (2 cm) with a sharply punched-out appearance. Unlike cancerous ulcers, the margins are not elevated. The ulcer base shows a small amount of blood but is otherwise clean. Compare with the ulcerated carcinoma . Medium-power detail of the base of a nonperforated peptic ulcer, demonstrating the layers of necrosis (N), inflammation (I), granulation tissue (G), and scar (S) moving from the luminal surface at the top to the muscle wall at the bottom.

80. Diagram of aggravating causes of, and defense mechanisms against, peptic ulceration.

82. Sharp edges, converging folds of mucosa in the upper half. The ulcer bed is covered by fibrinopurulent exudate.

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86. ( Figure 1) Peptic ulcer of stomach (arrow). The whole mucosa and part of submucosa are denuded.(M: mucosa, SM: submucosa, MP: muscularis propria)

87. Pancreas Ulcer Mucosa

88. ( Figure 6). Fibrosis in the muscularis propria (arrow). Chronic inflammatory cell infiltration is also noted (arrowhead).

89. (Figure 8) Intestinal metaplasia in chronic gastritis. The gastric foveolar epithelium (arrowhead) is replaced by intestinal type of epithelium (arrow). The intestinal epithelium has goblet cells. Chronic inflammatory cell infiltration is also seen. (Figure 7) Chronic gastritis with intestinal metaplasia (arrow) seen in the mucosa around the peptic ulcer. The mucinous gastric foveolar epithelium (arrowhead) is replaced by intestinal type of epithelium (arrow).

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