1. Pathology of GIT ESOPHAGUS Sept. 30 2015 Prof. Dr Faeza Aftan Col of Med. Aliraqia University

2. ESOPHAGUS Congenital Anomalies; atresia & fistula Diverticula mucosal webs (Plummer-Vinson syndrome, Paterson-Brown- Kelly ) Achalasia Laceration (Mallory-Weiss tears,) Esophagitis,  Reflux (GERD) Barretts Neoplasm

3. Obstruction Mechanical; - atresia, Fistula, duplication. - Inflammation & scarring. - tumor Functional; - Achalasia, (primary & secondary)

4. Normal esophageal-gastric junction

5. Esophageal atresia and Tracheoesophageal fistula. A, Blind upper and lower esophageal segments. B, Blind upper segment with fistula between lower segment and trachea. C, Fistula between patent esophagus and trachea. Type B is the most common. most commonMechanical Obstruction

6. Functional obstruction  Achalasia incomplete LES relaxation, increased LES tone, aperistalsis of the esophagus. failure of distal inhibitory neurons. 1ry; idiopathic, most common. 2ry ; cancer, Chagas dis. or fibrosis, amyloidosis, DM

7.  Achalasia LES are regulated by excitatory (ACH, substance P) & inhibitory (NO, VIP) neurotransmitters. achalasia lack inhibitory subst. The result is a nonrelaxed esophageal sphincter. Autopsy specimens, on L/M, shown an inflammatory response ( lymphocytes, eosinophils and mast cells), loss of ganglion cells, and neurofibrosis. Unknown cause. an autoimmune, hereditary, neurodegenerative, genetic and infections.

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

9. Esophageal diverticulum Zenker diverticulum Traction Epiphrenic diverticulum

10. Dilated portion of stomach protrudes above diaphragm Common! Usually asymptomatic. Heartburn, reflux esophagitis Danger: ulceration, bleeding Hiatal Hernia

11. Sliding (L) & rolling (R) hiatal hernias Hiatal hernias

12. 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

13. Esophagial Varices

14. Esophagitis Infective esophagitis viral, Bacterial, Fungal Non infective eophagitis Alcohol, Pills, Acid & alkali, chemotherapy & radiotherapy. Reflux esophagitis Laceration (Mallory-Weiss tears)

15. Candida esophagitis

16. ESOPHAGITIS - Herpes

17. Factors associated with the development of gastro-oesophageal reflux disease. Severe reflux oesophagitis Barrett’s oesophagus REFLUX/GERD

18. Barrett esophagus; long segment= >3 cm Vs. short segment< 3 cm is involved Barrett esophagus

19. Replacement of squamous epithelium by columnar epithelium with goblet cells Complication of long-standing reflux esophagitis Danger: risk of adenocarcinoma screen for high-grade dysplasia Barrett Esophagus

20. Barrett esophagus

21. Molecular studies suggest that Barrett epithelium may be more similar to adenocarcinoma than to normal esophageal epithelium, consistent with the view that Barrett esophagus is ???? a pre-malignant condition

22. LACERATION Tears are LONGITUDINAL Usually secondary to severe VOMITING Usually in ALCOHOLICS Usually MUCOSAL tears By convention, they are all called: MALLORY-WEISS

23. Mallory-Weiss tears

24. TUMORS BENIGN MALIGNANT – Squamous cell carcinoma – Adenocarcinoma

26.  SQUAMOUS CELL CARCINOMA >45 Years males 4X > females. underdeveloped areas. 50% occur in the middle 1/3 of esophagus

27. Tobacco, > 3/4 Alcohol polycyclic hydrocarbons, nitrosamines, fungus-contaminated foods, HPV radiation therapy Very hot beverages loss of tumor suppressor genes, including p53 and p16. Other: poverty, caustic esophageal injury, Achalasia, Plummer-Vinson syndrome, Nutritional deficiencies,

28. Esophageal Sq cell ca.

29. Squamous dysplasia

30. SQUAMOUS CARCINOMA DYSPLASIA  IN-SITU  INFILTRATION

31. Squamous Cell Carcinoma

32. Squamous cell carcinomas The rich submucosal lymphatic network promotes spread, even away from the principal mass. ca of up 1/3 of esophagus __ cervical LN. middle 1/3 __ mediastinal, paratracheal, & tracheobronchial LN; lower 1/3 spread to gastric and celiac LN.

33. ADENOCARCINOMA BARRETT’s Obesity Tobacco & alcohol H. pylori ‏ Female hormones

34. ADENOCARCINOMA Progression of Barrett esophagus to adenocarcinoma occurs through genetic and epigenetic changes. accumulate mutations.

35. ADENOCARCINOMA

36. Esophageal adenoca. Sq cell ca.

37. Adenocarcinoma Commonest type in US Risk factor: Barrett esophagus Distal 1/3 of esophagus Symptoms: late obstruction Squamous cell carcinoma Commonest type worldwide Risk factors: smoking, alcohol, genetics, esophagitis. Middle 1/3 of esophagus Symptoms: insidious onset; late obstruction Esophageal Carcinoma

38. Esophageal cancer. A, adenoca B, Sq cell ca.

39. BENIGN TUMORS LEIOMYOMAS POLYPS CONDYLOMAS (HPV)‏ LIPOMAS‏