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Lecture 8.1 Gastrointestinal pathology Week of december 1, 2013

Lecture 8.1 Gastrointestinal pathology Week of december 1, 2013. PNU Dep’t of Health Science Dr Shai’ RAD 240 PATHOLOGY. GI overview. ESOPHAGUS STOMACH SMALL/LARGE BOWEL APPENDIX, PERITONEUM. OESOPHAGUS. Congenital Anomalies Achalasia Hiatal Hernia Diverticula Laceration Varices

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Lecture 8.1 Gastrointestinal pathology Week of december 1, 2013

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  1. Lecture 8.1 Gastrointestinal pathology Week of december 1, 2013 PNU Dep’t of Health Science Dr Shai’ RAD 240 PATHOLOGY

  2. GI overview • ESOPHAGUS • STOMACH • SMALL/LARGE BOWEL • APPENDIX, PERITONEUM

  3. OESOPHAGUS • Congenital Anomalies • Achalasia • Hiatal Hernia • Diverticula • Laceration • Varices • Reflux • Barretts • Esophagitis • Neoplasm: Benign, Sq. Cell Ca., Adenoca.

  4. ANATOMY • 25 cm. • UES/LES • Upper and lower esophageal sphincter • Mucosa/Submucosa/Muscularis/Adventitia*

  5. Inf. Thyroid Arts. R. Bronch. Art. Thoracic. Aor. Variations: Inf, Phrenic Celiac Splenic Short Gast. Left Gastric Art.

  6. DEFINITIONS • Heartburn (GERD/Reflux)‏ • Dysphagia • Hematemesis • Esophagospasm (Achalasia)‏

  7. CONGENITAL ANOMALIES • ECTOPIC TISSUE (gastric, sebaceous, pancreatic)‏ • Atresia/Fistula/Stenosis/”Webs” • Schiatzki “Ring” in lower esophagus MOST COMMON

  8. MOTOR DISORDERS • Achalasia • Hiatal Hernia (sliding [95%], paraesophageal)‏ • “ZENKER” diverticulum • Esophagophrenic diverticulum • Mallory-Weiss tear

  9. ACHALASIA • “Failure to relax” • Aperistalsis • Incomplete relaxation of the LES • Increased LES tone • INCREASE: Gastrin, serotonin, acetylcholine, Prostaglandin F2α, motulin, Substance P, histamine, pancreatic polypeptide • DECREASE: N.O., VIP • Progressive dysphagia starting in teens • Mostly UNCERTAIN etiology

  10. HIATAL HERNIA • Diaphragmatic muscular defect • WIDENING of the space which the lower esophagus passes through • IN ALL cases, STOMACH above diaphragm • Usually associated with reflux • Very common Increases with age • Ulceration, bleeding, perforation, strangulation

  11. DIVERTICULA • ZENKER (HIGH)‏ • TRACTION (MID)‏ • EPIPHRENIC (LOW)‏ • TRUE vs. FALSE?

  12. DIVERTICULUM

  13. LACERATION • Tears are LONGITUDINAL (lower esophagus) • Usually secondary to severe VOMITING • Usually in ALCOHOLICS • Usually MUCOSAL tears • By convention, they are all called: • MALLORY-WEISS

  14. VARICES • THREE common areas of portal/caval anastomoses • Esophageal • Umbilical • Hemorrhoidal • 100% related to portal hypertension • Found in 90% of cirrhotics • MASSIVE, SUDDEN, FATAL hemorrhage is the most feared consequence

  15. VARICES

  16. VARICES

  17. ESOPHAGITIS • GERD/Reflux Barrett’s • Barrett’s • Chemical • Infectious

  18. REFLUX/GERD • DECREASED LES tone • Hiatal Hernia • Slowed reflux clearing • Delayed gastric emptying • REDUCED reparative ability of gastric mucosa

  19. REFLUX/GERD • Inflammatory Cells • Eosinophils • Neutrophils • Lymphocytes • Basal zone hyperplasia • Lamina Propria papillae elongated and congested, due to regeneration

  20. REFLUX/GERD

  21. BARRETT’S ESOPHAGUS • Can be defined as intestinal metaplasia of a normally SQUAMOUS esophageal mucosa. The presence of GOBLET CELLS in the esophageal mucosa is DIAGNOSTIC. • SINGLE most common RISK FACTOR for esophageal adenocarcinoma • 10% of GERD patients get it • “BREACHED” G-E junction

  22. BARRETT’S ESOPHAGUS

  23. BARRETT’S ESOPHAGUS • INTESTINALIZED (GASTRICIZED) mucosa is AT RISK for glandular dysplasia. • Searching for dysplasia when BARRETT’s is present is of utmost importance • MOST/ALL adenocarcinomas arising in the esophagus arise from previously existing BARRETT’s

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