1. New GIT 1 Dr Basu Part I: Oral Cavity diseases, Vocal cord, salivary gland Part II: Esophagus Stomach Dr Amitabha Basu MBBS, MD

2. Part I Oral Cavity diseases, Vocal cord, salivary gland

3. Oral Cavity diseases Tumors and tumor like condition

4. Tumors and tumor like condition: Oral cavity PapillomaEpithelial tumor, Benign lesion (a Squamous papilloma) LeukoplakiaIrregular white mucosal plaque

5. Squamous papilloma has fibro vascular stalk Also seen in vocal cord : singers nodules: where talking/ singing is a profession !

6. Leukoplakia Description → Leathery, white, discrete areas of mucosal thickening. Microscopy → Hyperkeratosis + dysplasia or carcinoma in situ of squamous epithelium. Risk factors → Chronic friction, Alcohol abuse. Types → Hairy leukoplakia, Verrucous leukoplakia, Erythroplasia.

7. Hairy leukoplakia: facts Etiology: Almost exclusive to HIV infection, Often EBV infection also Morphology: “Hairy” white plaques on oral mucosa caused by epithelial thickening Lab: CD 4 cell count (low below 200 cells/cumm).

8. Carcinoma of oral cavity Risk factors →Leukoplakia, Alcohol abuse, Tobacco use, HPV (types 16, 18, and 33), Protracted irritation. Molecular pathology Activation of cyclin-dependent kinase. Type of neoplasm→ Squamous cell carcinoma

9. HPV infection: koilocytosis Squamous cells with white cytoplasmic vacuole and curved nuclei Study other similar picture

10. Prognosis Lips and early detection –Lower lip - commonest 90% survive for 5 years without recurrence. –Floor of mouth, Base of tongue, pharynx : Poor prognosis Favored site for metastasis : cervical Lymph node

11. Neoplasms of vocal cords Benign: Squamous papilloma: –in vocal cord and larynges: singers nodule. –HPV infection: koilocytic change. Singers nodule Malignant tumor of vocal cord: large white necrotic mass : Squamous cell carcinoma.

12. Salivary gland lesions Sialadenitis: inflammation Neoplasms

13. Sialadenitis : Etiology Viral –Mumps (esp. parotids) –Other organ involvement in mumps Acute Pancreatitis ( ↑ serum amylase) Mumps Orchitis ( infertility) Bacterial: due to –Ductal obstruction –Dehydration Immunological : Sjogren's syndrome

14. Sialadenitis Acute Bacterial infection Neutrophils infiltrating the parotid gland. Chronic autoimmune (Sjogren's / Sicca syndrome). Dry mouth and eye Fibrosis, lymphoid infiltrates & Acinar atrophy. Type of ANA present = SS-A and SS-B autoantibody

15. Tumors of salivary glands Pleomorphic adenoma Parotid gland, and other glands MOST common Benign. Can recur, Malignant transformation rare Papillary Cystadenoma Lymphomatosum Or, Warthin tumor Benign, may be bilateral

16. Pleomorphic adenoma A mixed tumor Gross: Capsulated Micro: –Chondroid region + myoepithelial cells in myxoid stroma

17. Gross and micro C myxoid stroma myoepithelial cells

18. WARTHINS TUMOR SECOND MOST COMMON SALIVARY GLAND TUMOR Gross: capsulated Micro: 1.Double layer epithelial (oncocyte) CELLS. 2.LYMPHATIC STROMA WITH GERMINAL CENTERS.

19. 2 layers of oncocyte or oxyphilic cells, lymphoid stroma

20. Let us relax : Part II

21. Esophagus 1.Tracheoesophageal fistula 2.Esophageal web 3.Esophageal Achalasia 4.Mallory Weiss Syndrome 5.Esophageal varices 6.Gastroesophageal reflux 1.Esophagitis 2.BARRETT ESOPHAGUS

22. Esophagus Tracheoesophageal fistula Associated with Artesia of esophagus. Complication: aspiration of gastric content after birth and LUNG abscess. Esophageal web Plummer Vinson syndrome Weblike protrusion of esophageal mucosa. Morphology: Dysphagia.

23. Tracheoesophageal fistula Esophageal web Microcytic hypo chromic anemia, chance of Cancer.

24. Esophageal Achalasia Definition: Failure of relaxation of LES Etio-pathogenesis: Loss of ganglion cells in myenteric plexus (often by Trypanosoma Cruzi- south America) Gross: proximal dilatation of esophagus. Clinical: Progressive dysplasia and regurgitation.

25. X- ray and gross: rat tail (bird beak) appearance of lower esopgahous Study other similar picture

26. MALLORY WEISS SYNDROME Def: Longitudinal Tears of the mucosa of esophagus at GE Junction Occur after violent retching or vomiting. Cause: –Retching IN ALCOHOLIC stupor –Also in non alcoholic without any history [Hiatal hernia]. Study other similar picture

27. Clinical: Sudden Hematemesis: fresh blood ( usually not profuse ) Blood mixed with gastric contents or mucus Light-headedness, dizziness, or syncope Complication: Boerhaave syndrome (is rupture of the esophagus- massive hematemesis may occur )

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29. Esophageal varices Def: Dilated submucosal esophageal veins in lower third of esopgahous. Cause: Portal hypertension following alcoholic cirrhosis. Effect: Result in massive upper GI hemorrhage when ruptured.

30. Gross and micro Dilated and thrombosed vessels on the sub mucosa

31. Gastroesophageal reflux disease Etiology: Sliding Hiatal hernia and incompetent lower esophageal sphinter, alcohol, Scleroderma. Complications: Reflux Esophagitis, Barrett esophagus Clinical: heart burn, relieved by antacids.

32. BARRETT ESOPHAGUS Morphology: columnar epithelial metaplasia of esophageal squamous epithelium. Complications: esophageal adenocarcinoma (lower 1/3 rd of esophagus).

33. Columnar epithelial metaplasia with goblet cells or, Intestinal metaplasia → adenocarcinoma

34. Esophageal Squamous cell Carcinoma EtiopathogenesisAlcohol, tobacco, HPV ( High risk groups), smoking. Type of tumorSquamous cell carcinoma MorphologyUpper 2/3 rd of esophagus. Gross: tumor with central necrosis and microscopy of SCCA ClinicalProgressive weight loss, dysphagia.

35. central necrosis Study other similar picture

36. End of esopgahous

37. Disease of Stomach

38. Stomach Pyloric stenosis Menetrier disease Gastritis Peptic ulcer Malignant tumors

39. Pyloric stenosis Congenital. More in male Cause: hypertrophy of the circular muscle Clinical: –Outlet obstruction, Projectile vomiting. –First 2 weeks of life. –Oval mass upper abdomen. –Association with Turner syndrome (45, X0) / Edward syndrome (Trisomy 18).

40. Multifactorial inheritance If present in female – more chance (than male) that she will pass this disease to her offspring. So, If a child with PS is female: –the likelihood of having a future son with PS is one in five. –the likelihood of having a future daughter with PS is one in 14.

41. Gastritis Acute hemorrhagic gastritis Chronic gastritis

42. Acute hemorrhagic gastritis Def: acute inflammation, erosion and hemorrhage in present in gastric mucosa. Cause : aspirin, NSAIDs, smoking, burns, brain injury, stress, uremia, post surgery.

43. Gastric erosion: acute gastritis

44. Time for chronic gastritis Chronic inflammation → atrophy of gastric mucosa = atrophic gastritis

45. Autoimmune gastritisHelicobacter pylori associated gastritis Pernicious anemia: site: fundus Site: antrum Reduced acid secretion Curved, gram negative and silver stain (GMS) positive rod In duodenum Auto-antibodies to parietal cell or intrinsic factors are present in the serum. Megaloblastic amenia. Peripheral (nerve) myelin loss.

46. Autoimmune gastritis Atrophic gastric mucosa + intestinal metaplasia (goblet cells) + few lymphocytes Increased chance of gastric carcinoma

47. Helicobacter pylori associated gastritis Mucosa shows acute and chronic inflammatory cells+ atrophy + silver stain positive curved organism. ↑ chance of both gastric carcinoma / lymphoma

48. Peptic ulcer Location Etiology Pathogenesis Morphology Complication

49. Peptic ulcer Location: 1.Duodenum : first portion [ common] 2.Stomach, usually antrum 3.In Zollinger-Ellison syndrome [multiple non healing ulcers] 4.Meckel diverticulum that contains ectopic gastric mucosa. Peptic ulcer of the duodenum

50. Etiology and pathogenesis 1.Etiology: 1.H. pylori ( more with duodenal ulcer than gastric ulcer), chronic use of NSAIDs, Aspirin, Cigarette smoking, Corticosteroids. 2.Pathogenesis: Increased secretion of hydrochloric acid and pepsin and reduced mucosal defence.

51. Duodenal peptic ulcer- DU More common than gastric Etiology : –H.pylori (100%), Blood group O –Zollinger-Ellison syndrome ( gastrinoma): multiple non healing ulcer. –Increased gastric emptying Location: Anterior wall: first portion of duodenum C/F: Pain which is relieved by food.

52. Gastric ulcer Small, oval ( 1-3 cm), single Punched out margins Clean ulcer base Benign or Malignant? C/F: Pain aggravated by food.

53. Benign vs malignant gastric ulcer Small, oval ( 1-3 cm), single Large Punched out marginsRolled up ( heaved up) margins Clean ulcer baseNecrotic base

54. Complications: Peptic ulcer Bleeding: more with DU Perforation: more with DU Obstruction : due to edema and scarring: more with DU Cancer: more with gastric ulcer.

55. Time for gastric tumors Menetrier disease Adenocarcinoma

56. Menetrier disease Enlarged gastric rugal fold- like brain. Massive foveolar hyperplasia Reduced gastric acid Reduced serum protein ( protein loosing enteropathy- edema, low plasma protein).

57. Gastric tumors: facts Age: >50 years Sex: Men, Blood Group A: frequent Geographic Location: More in Japan, Finland, Iceland, less in USA. Anatomical location: The lesser curvature of the antropyloric region.

58. Etiology: Gastric CA 1.H.Pylori (Chronic atrophic gastritis) 2.Nitrosamine: smokes fish and vegetable, pickle ( preservative > Japan). 3.Increased salt and low fresh food intake.

59. Morphology Adenocarcinoma ( always) Early – Early gastric carcinoma-is defined as a lesion confined to the mucosa and submucosa. Advanced –neoplasm that has extended below the submucosa into the muscular wall.

60. Morphology of advanced Gastric carcinoma Gross Micro Etiology Exophytic ( polypoid) Intestinal type of malignant glands Associated with H.Pylori Infiltrating or diffuse Signet ring cells in all layers of stomach Not associated with H.Pylori

61. Intestinal type of malignant glands

62. Infiltrating or diffuse Also known as: linitis plastica Diffuse infiltration of malignant cells in the stomach. Produce ‘leather bottle’ stomach: small shrunken stomach.

63. linitis plastica Diffuse type: signet ring cells (contain mucin in the cytoplasm): poorly differentiated

64. Other facts Metastasis –To the left supraclavicular sentinel (Virchow) node: hypothetical first lymph node. Metastasize to both ovaries : Krukenburg tumor. Prognosis: poor Hematemesis and melena- black stool +.

65. Prognosis depends on Grading Well differentiated tumor : well formed glands, small in size, less mitosis : good prognosis. Moderate differentiated (more irregular glands but still identifiable) : intermediate prognosis. Poorly differentiated (predominant unrecognizable glands and cells): bad prognosis Undifferentiated : barely recognizable primary tissue: very bad prognosis Anaplastic: bizarre and large cells, more mitosis: worse prognosis

66. Thank you