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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
Gastric heterotopia
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[object Object],[object Object],[object Object],MORPHOLOGY
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Histopathology usually demonstrates increased numbers of eosinophils
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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
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[object Object],[object Object],[object Object],[object Object],MORPHOLOGY   A Steiner silver stain demonstrates the numerous darkly stained  H. pylori  organisms along the luminal surface of the gastric epithelial cells. Note that there is no tissue invasion by bacteria.
[object Object],[object Object],[object Object],[object Object],[object Object],Free powerpoint template: www.brainybetty.com
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Chronic gastritis with lymphoid follicle formation in the gastric mucosa (arrow) Some gastric glands are still found (arrowhead).
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)
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[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],GASTRIC ULCERATION
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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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[object Object],[object Object],[object Object],[object Object],[object Object],Multiple stress ulcers of the stomach, highlighted by the dark digested blood in their bases. MORPHOLOGY
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[object Object],[object Object],[object Object],[object Object],[object Object],Clinical Features
Normal  Acute gastritis  Chronic  gastritis  Atrophic gastritis  Intestinal  metaplasia Dysplasia Cancer
[object Object],[object Object],[object Object],[object Object],[object Object],Figure 3). Necrotic fibrinoid debris and inflammatory infiltrate in the ulcer base.
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
(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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Etiology of PUD Normal Increased Attack Hyperacidity, Zollinger Ellison syndrome. Weak defense Stress, drugs, smoking Helicobacter pylori *
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[object Object],[object Object],[object Object],[object Object],[object Object],Pathogenesis
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Bacteria over  epithelial cells
 
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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.
 
 
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[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Histologic Appearance
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Diagram of aggravating causes of, and defense mechanisms against, peptic ulceration.
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Sharp edges, converging folds of mucosa in the upper half. The ulcer bed is covered by fibrinopurulent exudate.
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( Figure 1) Peptic ulcer of stomach (arrow). The whole mucosa and part of  submucosa are denuded.(M: mucosa, SM: submucosa, MP: muscularis propria)
Pancreas Ulcer Mucosa
( Figure 6). Fibrosis in the muscularis propria (arrow). Chronic inflammatory  cell infiltration is also noted (arrowhead).
(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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Lect 4- gastric disord

  • 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
  • 4.
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  • 7. Free powerpoint template: www.brainybetty.com
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  • 13. Free powerpoint template: www.brainybetty.com
  • 14. Histopathology usually demonstrates increased numbers of eosinophils
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  • 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
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  • 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)
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  • 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
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  • 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).
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  • 52. Etiology of PUD Normal Increased Attack Hyperacidity, Zollinger Ellison syndrome. Weak defense Stress, drugs, smoking Helicobacter pylori *
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  • 60. Bacteria over epithelial cells
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  • 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.
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  • 80. Diagram of aggravating causes of, and defense mechanisms against, peptic ulceration.
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  • 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)
  • 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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  • 92. Free powerpoint template: www.brainybetty.com I wish to eat nacy lemak noooooooooooooooooooow lah