Pathology of Upper GIT

1. Pathology of Upper GIT Stand up, be bold, be strong, Takethe whole responsibility on yourshoulder, and know that you are thecreator of your own destiny.- - Swami Vivekananda.

2. CPC 4.2.5: Feeling dreadful…!• Worsening abdominal pain. 12h, sudden, 9/10.• Cramping  constant, severe, Nausea, vomiting, NSAID.• Blood in vomit, 8kg loss/3m, dark stool 2m.• Heart burn, NSAID use (backpain), stress, 10 cig/day,• Pale, sweaty, HR 125, faint pulse, BP 90/56 – shock*Differential Diagnosis: (acute compl.)• Perforated ulcer, Gastric Ca, Apendicitis, Dirverticulitis.• Acute Cholecystitis, Pancreatitis, Ruptured aneurysm.Investigations:• WBC 33.3, Hb 8.2, MCV 80,  urea/creat, Lipase Nor.• USS – free fluid, X-Ray – free air shadow.CASE STUDY:Mr E.K. 55-year-old Torres Strait Islander man.“I had a bit of a pain in my gut yesterday but today it is much worse and I feel really dreadful”. CPC 4.2.5: Feeling dreadful…!• Worsening abdominal pain. 12h, sudden, 9/10.• Cramping  constant, severe, Nausea, vomiting, NSAID.• Blood in vomit, 8kg loss/3m, dark stool 2m.• Heart burn, NSAID use (backpain), stress, 10 cig/day,• Pale, sweaty, HR 125, faint pulse, BP 90/56 – shock*Differential Diagnosis: (acute compl.)• Perforated ulcer, Gastric Ca, Apendicitis, Dirverticulitis.• Acute Cholecystitis, Pancreatitis, Ruptured aneurysm.Investigations:• WBC 33.3, Hb 8.2, MCV 80,  urea/creat, Lipase Nor.• USS – free fluid, X-Ray – free air shadow.CASE STUDY:Mr E.K. 55-year-old Torres Strait Islander man.“I had a bit of a pain in my gut yesterday but today it is much worse and I feel really dreadful”.

3. Top differential diagnosis ?1 2 3 4 50% 0% 0%91%9%1. GORD with bleeding.2. Bleeding PUD.3. PUD + GORD4. Perforated peptic ulcer.5. Acute cholecystits+stones. Top differential diagnosis ?1 2 3 4 50% 0% 0%91%9%1. GORD with bleeding.2. Bleeding PUD.3. PUD + GORD4. Perforated peptic ulcer.5. Acute cholecystits+stones.

4. Most likely Aetiology?1 2 3 4 527%0%64%9%0%1. H.pylori2. Obesity3. Genetic4. Smoking5. NSAID use Most likely Aetiology?1 2 3 4 527%0%64%9%0%1. H.pylori2. Obesity3. Genetic4. Smoking5. NSAID use

5. Most likely Risk factor?1 2 3 4 50% 0%91%9%0%1. Stress2. GORD3. Hiatus hernia4. Smoking5. NSAID use Most likely Risk factor?1 2 3 4 50% 0%91%9%0%1. Stress2. GORD3. Hiatus hernia4. Smoking5. NSAID use

6. Next step?1 2 3 4 50% 0% 0%0%0%1. Stop NSAID & counsel.2. Surgical referral.3. Stool occult blood test4. Breath test for H.pylori5. Stop soking & counsel. Next step?1 2 3 4 50% 0% 0%0%0%1. Stop NSAID & counsel.2. Surgical referral.3. Stool occult blood test4. Breath test for H.pylori5. Stop soking & counsel.

7. Type of anemia ? Why?1 2 3 4 50% 0% 0%0%0%1. Acute Blood loss2. Nutritional (B12+Iron)3. Iron deficiency4. Megaloblastic.5. Hemolytic (NSAID) Type of anemia ? Why?1 2 3 4 50% 0% 0%0%0%1. Acute Blood loss2. Nutritional (B12+Iron)3. Iron deficiency4. Megaloblastic.5. Hemolytic (NSAID)

8. PUD: KFP questions• Why name peptic ulcer? Common locations of ulcer?• What are the normal defense mechanisms in stomach ?• What are the causes & risk factors for peptic ulcer?• Briefly describe pathogenesis of peptic ulcer?• Briefly describe microbiology & diagnosis of H.pylori?• Why chronic, single, punched out, clean ? Multiple..?• Why radiating folds in benign not in malignant ulcer?• List Microscopic features?• List complications – short & Long term?• Briefly outline management?• Zollinger-Ellison syndrome? PUD: KFP questions• Why name peptic ulcer? Common locations of ulcer?• What are the normal defense mechanisms in stomach ?• What are the causes & risk factors for peptic ulcer?• Briefly describe pathogenesis of peptic ulcer?• Briefly describe microbiology & diagnosis of H.pylori?• Why chronic, single, punched out, clean ? Multiple..?• Why radiating folds in benign not in malignant ulcer?• List Microscopic features?• List complications – short & Long term?• Briefly outline management?• Zollinger-Ellison syndrome?

9. CPC-2.4– KFP Questions:• Pathogenesis & pathology of Barrett’s oesophagus.• Which H. pylori-infected patients should be treated?• Does eradication of H. pylori infection benefit the patientwith peptic ulcer disease? Discuss.• What is the relationship between H. pylori infection andgastric malignancy?• Pyloric stenosis: causes, presentation & pathology.• H. pylori induced other disorders ?• Carcinoma esophagus & Stomach• Etiology, pathogenesis, Morphology & Complications. CPC-2.4– KFP Questions:• Pathogenesis & pathology of Barrett’s oesophagus.• Which H. pylori-infected patients should be treated?• Does eradication of H. pylori infection benefit the patientwith peptic ulcer disease? Discuss.• What is the relationship between H. pylori infection andgastric malignancy?• Pyloric stenosis: causes, presentation & pathology.• H. pylori induced other disorders ?• Carcinoma esophagus & Stomach• Etiology, pathogenesis, Morphology & Complications.

10. . Pathology CLI:• Major:– Acute Abdomen – Overview differential diagnosis.• Appendicitis, Intestinal Obstruction,  Self study.– GORD, Barrett’s & oesophageal cancer.– Peptic ulcer disease & Gastric cancer.• Minor:– Oesophagitis – Acute / Chronic.– Achalasia, Rings, Mallory Weiss,– Hiatus hernia, varices, plummer-Vinson sy.– Acute & Chronic gastritis.– Zollinger Ellison sy.– Pyloric stenosis,

11. . "Each time you are honest and conductyourself with honesty, a success forcewill drive you toward greater success.Each time you lie, even with a littlewhite lie, there are forces pushing youtoward failure."- -Joseph Sugarman, Author and Marketing Specialist

12. . Commitment to Excellence…Pathology of Upper GI:Oesophageal DisordersDr. Venaktesh M. ShashidharA/Prof. & Head of PathologySchool of Medicine

13. . Introduction:• Anatomy, Histology• Function – motility,digestion, enzymes.• Common disorders.– Oesophagitis.– GORD.– obstructions– Achalasia.– Barrett’s– PUD– MalignancyOesophagusStomachNormalName the parts ?????????

14. . Esophagus & Stomach NormalGlandular – Gastric  Normal  Squamous Oesophagus

15. . Dysphagia• Dysphagia: Difficulty in swallowing.– Odynophagia: painful swallowing – inflam, ulcer,Carcinoma.• Sites:– oropharyngeal, esophageal, esophagogastric, andparaesophageal .• Symptoms:– Solids – Mechanical Obstruction – tumors/strictures.– Solids & Liquids – Motility disorders – Achalasia.– Liquids – Pharyngeal disorders.• Causes:– Local, Systemic, central.– Mechanical, neural, functional.– ulcers, tears, webs, rings, tumors, strictures,paralysis abnormal peristalsis. (stroke),

16. . Esophageal Disorders:• Reflux Oesophagitis.• Barrett’s• Stricture – Inflam.• Mallory-Weiss.• Varices• Hernia• Zenker diverticulum• T-E Fistula.• Web – IDA – P-V Sy.Herniations

17. . Oesophagus motility Disorders:Hernia: 30% incidence over 50years. (mostly asymptomatic)Achalasia: Lack of relaxation of lower sphincter.95% 5%Achalasia Hernia-Sliding Hernia-Rolling

18. . Mallory-Weiss Tear (Syndrome)• Severe/forced vomiting.• Longitudinal mucosaltear.• Chronic Alcoholics,• Over eating• Hiatal hernia in 75%.• Spontaneous healing.• Boerhaave syndrome –with rupture (Pacific Islands)

19. . Esophageal Varices:• Dilated veins – lower part.• Pathogenesis: Portalhypertension (Cirrhosis) Porta-Systemic Shunts open varices of - lower esophagealveins, peri-umbellical, Rectal V• Rupture  massive bleeding.

20. . Oesophagitis:• Acute: errosive, alcohol, infection.• Chronic: Acid reflux (GERD),chemical, alcohol, smoking,candida, radiation, idiopathic(eosinophilic).• Endoscopic view Microscopy:• Acute inflammation.• Eosinophils: Few (reflux) more inEosinophilic.Candida

21. . I know where Im going and I knowthe truth, and I dont have to bewhat you want me to be. Im free tobe what I want.-- Muhammad Ali

22. . Commitment to Excellence…Pathology of GORD / GERD(Gastro O/esophageal Reflux Disease)Dr. Venaktesh M. ShashidharA/Prof. & Head of PathologySchool of Medicine

23. . GORD: Acid reflux disorders• Gastric Acid pH-1 (million times more than blood…!)• Oesophagus protected by Lower Sphincter.• Defective sphincter  Reflux of acid  Inflam.• Clinical Stages:1. Functional Heartburn.2. NERD – Non Erosive RD3. MERD – Minimal change RD4. GORD.5. Barrett’s Oeophagus.6. Adenocarcinoma

24. . GORD: Clinical ClassificationGORDHeartburnOesophagitis24%Barrett’s1%Non-ErosiveReflex Disease (NERD)(normal endoscopy)75%Endoscopy24-hr pH StudyAET +veSI +veAET -veSI +veAET -veSI –ve? MERDAET: Acid Exposure IndexSI: Symptom Index.MERD: minimal change.. RDEtiology: (LES)• Alcohol, Tobacco,• Obesity,• CNS depressants,• Pregnancy,• Hiatal hernia• Delayed gastric emptying• increased gastric volume

25. . Pathogenesis & Stages:ABCDBasalHyperplasia1. Acid reflux Symp.2. Inflammation3. Regeneration (basal).4. Metaplasia (Barretts)5. Mild Dysplasia6. High grade Dysplasia7. Adeno-CarcinomaAdenocarcinoma

26. . GERD: Pathogenesis.Normal  Hyperplasia  Dysplasia  CarcinomaNormalSq. Ep.MetaplasticCol. Ep.InflammedSq. Ep.Basal cell hyperplasia

27. . Squamous Carcinoma - Adenocarcinoma.• Less common• Upper end• Tobacco, diet, toxins.• More common• Lower end• Reflux disease (Barretts)TumourNormalTumourNormal

28. . Squam. Ca. - Adeno. Ca.K. Pearl GlandsPleomorphic, Hyperchromatic cells forming glands / keratin pearls(Infiltration, inflammation, hemorrhage, necrosis)

29. . "Learn to enjoy every minute of your life.Be happy now. Dont wait for somethingoutside of yourself to make you happy.Precious is the time you have, whether itsat work or leisure. Every minute should beenjoyed and savored."Earl Nightingale1921-1989, Radio Announcer, Author and SpeakerHakuna Matata….!

30. . Commitment to Excellence…Pathology ofGastric DisordersDr. Venkatesh M. ShashidharA/Prof. & Head of PathologySchool of Medicine JCU

31. . Damage vs. DefenseGastric defences:

32. . • Acute Gastritis:– Drugs, toxins, alcohol, Ischemia.– Infections (H.pylori transient)• Chronic Gastritis:– Autoimmune: Pernicious an.(autoantibody)– Chem: NSAIDs, Bile reflux,Alcohol.– Bacterial: Helicobacter pylori.Gastritis:Normal ↑← AcuteChronic ↓

33. . Stomach: Acute stress ulcers:Pathogenesis? PG…!• Acute Stress Ulcers:• Curling Ulcers: Burns/trauma, prox. Duodenum.• Cushing’s ulcers: Intracranial lesions, deep, chance of perforation.Complications:• Bleeding 20%• Perforation 5%• Obstruction 2%

34. . Chronic Gastritis• Bacterial: Helicobacter pylori. (PUD) > 90%• Autoimmune:– Atrophic, Pernicious anemia <10%.– Antibody to Parietal cell & intrinsic factor.• Radiation, Bile reflux, etc. Rare• Systemic diseases – Crohn’s, amyloidosis

35. . Normal – Chronic GastritisNot PUD

36. . “I never thought of losing, but now thatit s happened, the only thing is to do itright. Thats my obligation to all thepeople who believe in me. We all haveto take defeats in life”– Muhammad Ali, Champion Boxer

37. . Commitment to Excellence…Pathology ofPeptic Ulcer Disease (PUD)Dr. Venkatesh M. ShashidharA/Prof. & Head of PathologySchool of Medicine JCU

38. . PUD: Overview• Helicobacter pylori infection*• Hyperacidity• Drugs - anti-inflammatory(NSAIDs) & Corticostroids.• Cigarette smoking, Alcohol,• Rapid gastric emptying• Duodenal reflux.• Personality and stress• GeneticHurry, Worry, CurryH.Pylori on the surface ofgastric epithelial cells

39. . Helicobacter pylori:• Common infection• 10% of men, 4% women develop PUD *• Positive in 70-100% of PUD patients.• 1st Part of duodenum > antrum > G-E junction.• H.pylori related disorders:– Chronic gastritis – 90%– Peptic ulcer disease – 95-100%– Gastric carcinoma – 70%– Gastric lymphoma– Reflux Oesophagitis.– Non ulcer dyspepsia

40. . H. Pylori Gastritis - Silver stainBacteria overepithelial cells

41. . H. Pylori - PUD – Pathogenesis• Gram negative, Spirochete.• Does not invade cells• Colonize Acidic Gastric mucosa only *• Protease  Break down mucous  exposeepithelium for digestion + urea.• Urease  Breakdown urea  ammonia neutralise acid  reflex Hyperacidity.• Chronic infl.  Gastric Metaplasia Ulceration.• Complications: Bleeding, perforation, stenosis,Carcinoma.

42. . PUD - Diagnosis• Endoscopy – findings• Barium meal – contrast• Endoscopy, Biopsy/cytology, stains.• Culture – difficult – for research only.• HP fecal antigen test• Monoclonal antibody test on stool samples.Specific (98%) and sensitive (94%).• C13 urea breath test – Radioactive – common.• H.pylori serology – IgG – new.

43. . Peptic Ulcer Morphology:• Common in duodenum than stomach (4:1)• > 80% single ulcer• Round small, clean,• punched out, <2cm*.• Radiating folds.• Microscopy:– Superficial necrotic layer.– Inflammatory cells zone.– Granulation tissue zone - B– Collagenous scar zone - C.Note: Radiating mucosal folds from the ulcer.. Why?

44. . Endoscopic Appearance

45. . Gastric UlcerRarely large / irregular / multiple ulcers

46. . Gastric Peptic Ulcer

47. . Gastric Peptic ulcer: ScarNote: Radiating mucosal folds from the ulcer.. Why?

48. . Double Benign, Chronic, Gastric Peptic UlcerMultiple peptic ulcer / severe peptic ulcer ? Etiology.

49. . PUD Complications:• Chronic Bleeding – Anemia(IDA).• Acute Bleeding – Massive, shock,• Fibrosis, Stricture obstruction – pyloric stenosis.• Perforation – Peritonitis, pancreatitis.• Gastric carcinoma. (not duodenal ca)Pancreas

50. . Perforation Peritonitis