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STOMACH Cell types:

STOMACH Cell types:. Mucosal surface & foveolae: Surface foveolar cells - secrete mucous Mucous neck cells - progenitor cells Glands: Mucous cells - secrete mucous & pepsinogen II Parietal cells - secrete HCl & IF Chief cells - secrete pepsinogen I & II

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STOMACH Cell types:

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  1. STOMACH Cell types: • Mucosal surface & foveolae: • Surface foveolar cells - secrete mucous • Mucous neck cells - progenitor cells • Glands: • Mucous cells - secrete mucous & pepsinogen II • Parietal cells - secrete HCl & IF • Chief cells - secrete pepsinogen I & II • Endocrine cells - secrete peptide & amine hormones

  2. Congenital Anomalies

  3. CONGENITAL ANOMALIES • Diaphragmatic Hernia: • Defect in diaphragm, away from esophageal hiatus • Portions of stomach & SI herniate  pulmonary hypoplasia & respiratory impairment

  4. CONGENITAL ANOMALIES • Heterotopic rests: • Location: Anywhere in the GIT • MC: Pancreatic & gastric • S/S: Usually asymptomatic but may cause ulceration

  5. CONGENITAL ANOMALIES • Congenital Hypertrophic Pyloric Stenosis:CHiPs • M > F (3:1), 1 in 200 infant males, multifactorial inheritance • Cause: • Hypertrophy & hyperplasia of circular muscle of pylorus  regurgitation, projectile non- bilious vomiting commences at 2 - 6 wks of age • May be due to defective autonomic regulation • Dx: Visible peristalsis & palpable mass in RUQ • Tx: Pyloromyotomy is curative

  6. ACUTE GASTRITIS • Other Causes: • Ingestion of strong acids or alkali • Ca chemotx • Radiation • Ischemia & shock • NGTs

  7. - Reduced mucosal blood flow - Direct damage to mucosal epithelium

  8. ACUTE GASTRITIS • Clinically: • Asymptomatic to epigastric pain of varying severity, up to acute abdomen w/ hematemesis & shock • major cause of massive hematemesis (esp. alcoholics) • Common in those who take daily aspirin for RA

  9. ACUTE GASTRITIS • Morphology: • Mucosal edema & congestion, PMN infiltration (milder cases) • Erosions (not deeper than muscularis mucosa) & hges (acute erosive gastritis)

  10. / dysplasia

  11. CHRONIC GASTRITIS • Pathogenesis: • Autoimmune: Abs to parietal cells parietal cell destruction ( HCl & IF) • Environmental: • Chronic infection by H. pylori • Alcohol, tobacco, radiation, bile reflux, Crohn’s disease, uremia, gastric atony

  12. CHRONIC GASTRITIS • Gross: • Red mucosa (thickened or flattened) • Autoimmune  fundus & body • H pylori  antrum & body • Bile reflux  antrum

  13. Histology: Lympho & plasma cell infiltrates in LP (superficial or involving entire mucosal thickness) Others: Regenerative atypia Intestinal metaplasia Atrophy Dysplasia CHRONIC GASTRITIS

  14. CHRONIC GASTRITIS • Clinical: • Mild abdominal discomfort, nausea, vomiting, hypochlorhydria • Autoimmune gastritis: • Hypo- / a- chlorhydria, hypergastrinemia, ~ 10%  overt PA, long-term risk of Ca is 2-4%

  15. ~ 50% of asymptomatic American adults > 50 yrs are infected Dx: CLO test Diseases Association: Chronic gastritis PUD Gastric ca/ lymphoma Helicobacter pylori

  16. PEPTIC ULCERS • Usually solitary ~ 0.6 - 4 cm • MC: duodenum & antrum • Ratio of duodenal: gastric PU is ~ 4 : 1 • ~ 4 M Americans have PU • Life-time incidence in USA is 10% for men & 4% for women

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