Peptic ulcer disease

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  • DU1 st part within 3 cm of pylorus GU occasionally it can be on greater curvature or ant and post walls
  • Duodenum—smaller<1 cm but there also occasionally 3 to 6 cm large Occasionally gastric ulcers are larger than this
  • Ill defined, aching sensation or as hunger pain
  • Peptic ulcer disease

    1. 1. PEPTIC ULCER DISEASE --Dr. Mansi
    2. 2. What is PEPTIC ULCER????? <ul><ul><ul><ul><ul><li>Breaks in mucosal surface </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>>5mm in size </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Depth till submucosa </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>In any part of GI tract exposed to aggressive action of acid pepsin juices. </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Can be acute or chronic </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Both can penetrate muscularis mucosae.. </li></ul></ul></ul></ul></ul>
    3. 3. SITES <ul><ul><ul><ul><ul><li>Gastric and duodenal – 98 % </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Ratio of 1:4 </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Duodenum:1 st part >95% </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li> :ant & post walls </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>Gastric :junctn b/w antrum &acid secr. mucosa </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>:lesser curvature </li></ul></ul></ul></ul></ul><ul><ul><ul><ul><ul><li> </li></ul></ul></ul></ul></ul>
    4. 4. Pathomorphology <ul><li>Round </li></ul><ul><li>Punched out craters </li></ul><ul><li>2 to 4 cm diameter </li></ul>Margins – Perpendicular - No Elevatn or Beading Mild oedema of immediate adj. mucosa Surrounding Mucosal folds Radiate like Wheel Spokes Base Remarkably Clean
    5. 5. Duodenal ulcer Gastric ulcer Patho physiology <ul><li>Major </li></ul><ul><li>causes </li></ul><ul><li>Gastric </li></ul><ul><li>acid </li></ul><ul><li>Gastric </li></ul><ul><li>emptying </li></ul>increasd decreased rapid delayed Bicarbonate secretion remarkably decreased H.pylori & NSAID H.pylori & NSAID Abnormal resting & stimulated Pyloric sphincter pressure
    6. 6. ETIOLOGY <ul><ul><li>Predisposing factors </li></ul></ul><ul><ul><li>Age :young in DU and peak inc. at 6 th decade in GU. </li></ul></ul><ul><ul><li>Sex :GU commoner in males </li></ul></ul><ul><ul><li>Causes </li></ul></ul><ul><ul><li>H.Pylori </li></ul></ul><ul><ul><li>NSAID </li></ul></ul><ul><ul><li>Infection: CMV,herpes simplex,etc.. </li></ul></ul><ul><ul><li>Other drug/toxin: bisphosphonates, chemo, clopidogrel , glucocorticoids </li></ul></ul><ul><ul><li>Misc.:crohn,neoplasm,ashemia,infiltrating diseases,duodenal obstruction,etc.. </li></ul></ul>
    7. 7. <ul><li>Smoking </li></ul><ul><li>Genetic : increased freq of blood group O and non secretor status </li></ul><ul><li>Stress </li></ul><ul><li>Diet : alcohol and caffeine </li></ul><ul><li>Associations </li></ul><ul><li>Systemic mastocytosis </li></ul><ul><li>CRF, nephrolithiasis </li></ul><ul><li>Hyperparathyroidism </li></ul><ul><li>Cirrhosis </li></ul><ul><li>Alpha antitrypsin deficiency </li></ul><ul><li>CAD, pancreatitis, polycythaemia vera </li></ul>Pathogenetic factors not related to h.pylori & NSAID
    8. 8. <ul><li>Gram –ve </li></ul><ul><li>S-shaped , flagellate </li></ul><ul><li>Lies b/w mucous layer & gastric epithelium </li></ul><ul><li>1 st antrum then proximal segments. </li></ul><ul><li>Dormant state – coccoid form </li></ul><ul><li>Genome—1500 proteins </li></ul><ul><li>Transmission:oral-oral/faeco-oral </li></ul>H.pylori
    9. 9. Cytokines-IL 1 α / β , IL6,IL2, IL8(recruits act. neutrophils) TNF- α ,IFN- γ <ul><li>HOST FACTORS </li></ul><ul><li>Duration </li></ul><ul><li>Location </li></ul><ul><li>Apoptosis </li></ul><ul><li>Cag PAI </li></ul><ul><li>Mucosal nd systemic </li></ul><ul><li>humoral response </li></ul>cagA into host cells <ul><li>BACTERIAL FACTORS </li></ul><ul><li>1st : Outer membrane proteins </li></ul><ul><li>2 nd :gastric residence-- Urease </li></ul><ul><li>3 rd :Mucosal damage </li></ul><ul><ul><ul><li>vacA </li></ul></ul></ul><ul><ul><ul><li>cagA </li></ul></ul></ul><ul><ul><ul><li>Pathogenecity island cag </li></ul></ul></ul><ul><ul><ul><li>Catalase, lipase, adhesins, </li></ul></ul></ul><ul><ul><ul><li>platelet activating factors </li></ul></ul></ul><ul><li>Proteases nd phospholipases </li></ul><ul><ul><ul><li>Breaks glycoprotein lipid complex of mucous gel </li></ul></ul></ul><ul><ul><ul><li>Damage surface epi. cells </li></ul></ul></ul><ul><li>inflammatn </li></ul><ul><li>Chronic gastritis </li></ul><ul><li>Peptic ulcer </li></ul><ul><li>Gastric MALT lymphoma </li></ul><ul><li>Gastric adenocarcinoma </li></ul>V I R U L E N C E Pathophysiology of H.pylori ulcer
    10. 10. <ul><li>Gastric metaplasia </li></ul><ul><li>Increased acid production </li></ul><ul><li>Decreased duodenal mucosal bicarbonate production </li></ul>Then how does it cause Ulcers in duodenum?????
    11. 11. <ul><li>Endothelial defects </li></ul><ul><li>Stasis--ischemia </li></ul>Direct toxicity by Ion trapping <ul><li>Epithelial effects </li></ul><ul><li>Due to PG depletion </li></ul><ul><li>HCL </li></ul><ul><li>mucin </li></ul><ul><li>bicarbonate </li></ul><ul><li>Epi. cell </li></ul><ul><li>proliferation </li></ul>ULCER erosions Healing (spontaneous Or therapeutic) NSAID induced PUD Pathophysiology Epithelial effects Due to PG depletion
    12. 12. Clinical features <ul><li>Abdominal pain * </li></ul><ul><li>Epigastric </li></ul><ul><li>Burning or gnawing discomfort* </li></ul><ul><li>90 min to 3 h after meal </li></ul><ul><li>Frequently relieved by antacids or food in DU.* </li></ul><ul><li>Awakes the pt from sleep b/w midnight & 3 am. </li></ul><ul><li>Nausea </li></ul><ul><li>Weight loss </li></ul><ul><li>Dyspepsia </li></ul><ul><li>if not relieved by food antacids , </li></ul><ul><li>radiates to back—penetrating ulcer </li></ul>
    13. 13. <ul><li>Perforation: </li></ul><ul><li>Gastric outlet obstruction </li></ul><ul><li>Bleeding </li></ul>Symptom : sudden continuous generalized abd pain Examn : severly tender board like abdomen Common in elderly and with NSAID Penetration Complications Symptoms : Pain worsening with meals, nausea and vomiting of undigested food Examn : succusion splash Symptoms : Tarry stools or coffee ground emesis Acute hematemesis Anemia Examn : tachycardia and orthostasis suggesting dehydration
    14. 14. <ul><li>NUD : non ulcerative dyspepsia </li></ul><ul><li>D/D OF ULCER LIKE SYMPTOMS </li></ul><ul><li>Proximal GI tumors </li></ul><ul><li>Gastro esophageal reflux </li></ul><ul><li>Vascular disease </li></ul><ul><li>Pancreaticobiliary disease </li></ul><ul><li>Crohn’s disease </li></ul>Differential diagnosis
    15. 15. <ul><li>D/D OF EPIGASTRIC PAIN </li></ul><ul><li>Gastric </li></ul><ul><li>Duodenal </li></ul><ul><li>Gall bladder </li></ul><ul><li>Pancreas </li></ul><ul><li>Colon </li></ul><ul><li>Superficial / radicular pain </li></ul><ul><li>Nervous dyspepsia </li></ul>
    16. 16. Diagnostic Evaluation
    17. 17. <ul><li>Barium studies of proximal GI </li></ul><ul><li>Endoscopy </li></ul><ul><li>Tests for detection of H.Pylori </li></ul><ul><li>Occasionally serum gastrin level </li></ul><ul><li>gastric acid analysis </li></ul><ul><li>screen for NSAIDs </li></ul>Non invasive: serology Urea breath test Stool antigen Invasive : rapid urease histology culture Duodenal ulcer Gastric ulcer
    18. 18. Treatment
    19. 19. <ul><li>Cimetidine 400mg bid </li></ul><ul><li>Ranitidine 300mg hs </li></ul><ul><li>Famotidine 40mg hs </li></ul><ul><li>Nizatidine 300mg hs </li></ul>: Magnesium Hydroxide ,Aluminum Hydroxide , Sodium Bicarbonate , Calcium Carbonate :100 – 150 meq/l 1 & 3 hrs after the meal & hs <ul><li>Acid Suppressing Drugs </li></ul><ul><li>Antacids </li></ul><ul><li>H2 Receptor antagonists </li></ul><ul><li>Proton Pump </li></ul><ul><li>Inhibitors (PPIs) </li></ul><ul><li>Omeprazole 20mg/day </li></ul><ul><li>Lansoprazole 30mg/day </li></ul><ul><li>Rabiprazole 20mg/day </li></ul><ul><li>Pantoprazole 40mg/day </li></ul><ul><li>Esomeprazole 20mg/day </li></ul>
    20. 20. <ul><li>Mucosal Protective Agents </li></ul><ul><li>Sucralfate </li></ul><ul><li>Prostaglandin Analogue </li></ul><ul><li>Bismuth Containing Compounds </li></ul>-Sucralfate – 1gm qid -Misoprostol - 200 μ g qid
    21. 21. Regimens for Eradication Of H.Pylori <ul><li>Triple Therapy </li></ul><ul><li>Bismuth Subsalicylate + -2 tablets qid </li></ul><ul><li>Metronidazole + -250mg qid </li></ul><ul><li>Tetracycline -500mg qid </li></ul><ul><li>2 . Ranitidine Bismuth Citrate + -400mg bid </li></ul><ul><li>Tetracycline + -500mg bid </li></ul><ul><li>Clarithromycin / Metronidazole -500mg bid </li></ul>
    22. 22. Regimens for Eradication Of H.Pylori 3. Omeprazole + - 20mg bid Claithromycin + -250/500mg bid Metronidazole / -500mg bid Amoxicillin - 1gm bid
    23. 23. <ul><li>Quadruple therapy </li></ul><ul><li>Treatment of complications </li></ul><ul><li>Therapy for NSAID injury </li></ul><ul><li>Surgical Therapy </li></ul>
    24. 24. Surgical Therapy <ul><li>Duodenal Ulcer </li></ul><ul><li>Vagotomy & Drainage (By Pyroloplasty , Gastrodudenostomy , Gastrojejunostomy) </li></ul><ul><li>Highly Selective Vagotomy (does not require drainage procedure) </li></ul><ul><li>Vagotomy with Antrectomy </li></ul>
    25. 25. Surgical Therapy <ul><li>Gastric Ulcer </li></ul><ul><li>Antral Ulcer – Antrectomy with Billroth I </li></ul><ul><ul><ul><ul><ul><li> anastomosis </li></ul></ul></ul></ul></ul><ul><li>Ulcer Excision with Vagotomy & Drainage </li></ul><ul><li>3.High GU – Csende’s Procedure </li></ul><ul><ul><ul><ul><ul><li>Subtotal Gastrectomy with a Roux-en-Y Oesophagogastrojejunostomy </li></ul></ul></ul></ul></ul><ul><li>Kelling Madlener Procedure </li></ul><ul><li>antrectomy + intraop. ulcer biopsy + </li></ul><ul><li>vagotomy </li></ul>
    26. 26. Surgical complications <ul><li>Recurrent ulceration </li></ul><ul><li>Afferent loop syndromes </li></ul><ul><li>Dumping syndromes </li></ul><ul><li>Post vagotomy diarrhea </li></ul><ul><li>Bile reflux gastropathy </li></ul><ul><li>Maldigestion & malabsorption </li></ul><ul><li>Gastric adenocarcinoma </li></ul>
    27. 28. THANK YOU

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