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Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
Pathology of Upper GIT
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Pathology of Upper GIT

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  • 1. 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”.
  • 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.
  • 4. 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
  • 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.
  • 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)
  • 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?
  • 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.
  • 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
  • 51. PUD - Perforation
  • 52. Barry J Marshal, 2005 Nobel Prize….!There were a lot of people whodidnt believe what we said butthey couldnt keep us quiet…!A.A.Press.. 4 Oct 2005.Barry J. Marshall & J. Robin Warrenwas a trainee at that time…..!
  • 53. Commitment to Excellence…Gastric CarcinomaDr. Venkatesh M. ShashidharA/Prof. & Head of PathologySchool of Medicine JCU
  • 54. Gastric Carcinoma:• Adeno Carcinoma (90%) Lymphoma (4%),Carcinoid & Stromal tumors rare.• Adenocarcinoma Intestinal & Diffuse types.• Early (limited to mucosa) & Advanced stage.• Morphology: (Fungating & Diffuse infiltrative)– Adenocarcinoma:• Intestinal type – fungating, Early diagnosis, better prognosis.• Diffuse type – diffuse infiltrating, late, poor prognosis.– Gastric Lymphoma (MALT) – B cell, H.pylori.– Carcinoid tumor.– GastroIntestinal Stromal Tumor (GIST) *sarcoma.
  • 55. Gastric Adeno Carcinoma:Intestinal Type• H.pylori Metaplasia• C. gastritis / atrophy• HER-2/NEU mutation• Well differentiated• No Signet ring cells.• Gland formation.• Better PrognosisDiffuse Type• Idiopathic/familial.• No precursor lesion• E-Cadherin mutations• Poorly differentitated• Signet ring cells• No gland formation,• Poor Prognosis
  • 56. Fungating Carconoma
  • 57. Diffuse Ca - FibroticLinitis Plastica / Leather bottle stomach.Malignant cells between fibrous stroma Endoscopy
  • 58. Gastric CarcinomaMalignantNormal Gland
  • 59. Be content with what you have;rejoice in the way things are.When you realize thatthere is nothing lacking,the whole world belongs to you…!--Lao Tzu
  • 60. Points to Remember: PUD• Peptic ulcer – Gastric/duodenum - acid & Pepsin.• Etiology: H. pylori, Gram –ve, Spirochete does not invadetissue. Protease & Urease• Mucosal damage – Inflammation – ulcer – cancer.• Perforation, stenosis, Ca (Not duodenal).• single, punched out, clean, radiating folds (not in ca).• Microscopy: spiral bacteria-silver stain, inflammation.• Ulcer : necrosis, inflammatory cells, granulation, fibrosis.• Treatment: antibiotics + Proton pump inhibitors.
  • 61. “Only a man who knows what it islike to be defeated can reach down tothe bottom of his soul and come upwith the extra ounce of power it takesto win when the match is even.”– Muhammad Ali, Champion Boxer
  • 62. Case: 1• A 62-year-old female presented at theclinic for evaluation of mild dry cough,affecting her sleep.• Her medical history includes osteoporosis,HTN, mild memory loss, involuntary weightloss, has significant leg swelling. She takes5 prescription medications for her medicalconditions. She lives alone. She smokesabout 1ppd and takes a glass of red wineto help sleep.
  • 63. Case: 1Questions:• Does the patient have GERD?• List risk factors from the history for GERD?• Does the patient exhibit any symptoms ofGERD?• How should this patient be treated?• How should the patient be monitored?• What is NERD? how is it different?
  • 64. Case 2• 72y white man at aged care nursing home,chronic obstructive pulmonary disease, chronicalcohol abuse, chronic dementia, and multipleepisodes of upper GI bleeding. He wasadmitted to the hospital with complaints oflightheadedness, syncope, and abdominalpain.• Thin elderly man in no acute distress. BP 96/72,pulse 104, respiratory rate 24, and temperature98.9°F. Hb 12.9%.• The abdominal examination revealed mildepigastric pain on palpation. The rectal andprostate examinations were unremarkable;• Black stool, tested positive for fecal blood.
  • 65. Case 2Questions:• Does the patient have GERD?• List risk factors from the history forGERD?• Identify symptoms of GERD in thispatient?• How should this patient be treated?• How should the patient be monitored?
  • 66. Barrett OesophagusA-B, Gross view of distal esophagus (top) and proximal stomach (bottom) showing (A) normal gastroesophagealjunction and (B) the granular zone of Barrett esophagus (arrow). C, Endoscopic view showing red velvetygastrointestinal-type mucosa extending from the gastroesophageal orifice. Note paler squamous esophageal mucosa.(C, Courtesy of Dr. F. Farraye, Brigham and Womens Hospital, Boston, Massachusetts.)NormBarrettBarrett
  • 67. Barretts Metaplasia:

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