Peptic Ulcer Disease.pptx

Peptic Ulcer

1. Peptic Ulcer Disease Dr. Sachit Koirala [Resident, 1 st Year] Facilitator : Dr. Mahipendra Tiwari KIST Medical College Lalitpur Nepal 2078-04-31

2. Introduction Peptic ulcers : Focal defects in the gastric or duodenal mucosa that extend into the submucosa or deeper. ‘Peptic’ : Associated with Pepsin But, Peptic Ulcer Disease (PUD) does not occur in the absence of acid Responsible for up to two-thirds of upper GI bleed imbalance between mucosal barriers and other aggravating factors Common sites : Duodenum and lesser curvature of stomach Less common sites : Esophagus , Meckel diverticulum

3. Arterial supply to stomach

4. Vagal nerve supply to stomach

5. M : Muscarinic receptor ECL : Enterochromaffin Like H : Histamine receptor G : Gastrin receptor

6. Pathogenesis

7. H. pylori 77% of duodenal ulcers are associated with H. pylori infection Gram – ve spiral like flagellated organism, first studied by Warren and Marshall (both got Nobel prize) No. 1 carcinogen in Gastric Carcinoma Releases Urease  Urea to ammonia  alkalinization of acidic environment  survival of bacteria in gastric lumen Bacterial colonization and attachment to epithelial cells  Release of cytotoxins ( eg. cagA toxin) urease, catalase, vacuolating cytotoxin, lipopolysaccharide more common in lower socioeconomic group

8. NSAIDs NSAIDs inhibit cyclooxygenases (i.e., COX-1 and COX-2) Impairs prostaglandin synthesis Decrease mucosal blood flow Inhibit the release of nitric oxide (NO) and hydrogen sulfide (H2S) Enhances neutrophil adherence 15-20% incidence with regular use of NSAIDs

9. Duodenal and pre-pyloric peptic ulcers : Gastric acid level is higher Gastric ulceration : Gastric acid level is relatively normal Severe physiologic stress Cushing ulcers  brain tumor or injury, single, deep ulcers, prone to perforation, associated with high gastric acid output, stomach Curling ulcers  Extensive burns, prone to perforation, 1 st part of duodenum Gastrinoma (Zollinger-Ellison syndrome) or multiple endocrine neoplasia type I (MEN-I) Smoking: Smokers are about twice as likely to develop PUD as nonsmokers Alcohol : No confirmatory data

10. Other risk factors Physiologic risk factors Increase in BAO [OR 3.5] Increase in MA no correlation between acid secretion and the severity of PUD Genetics 20% have family history Uremic gastropathy Cytomegalovirus infection Bile gastropathy Granulomatous gastritides ( eg , sarcoidosis, histiocytosis X, tuberculosis) 5-fluorouracil (5-FU), methotrexate (MTX), and cyclophosphamide Use of crack cocaine : Juxtapyloric , Perforation

11. History Sex: Duodenal Ulcer – M:F = 2:1; Gastric Ulcer – M:F=1:1 Age: Gastric Ulcer Pts are older than Duodenal Ulcer Pts Pain >90% pts with PUD Mechanism of pain is unclear Epigastric May Radiate to back (Bailey & Love, 27 th ed); Non radiating (Schwartz, 11 th ed) Duodenal Ulcer : 2-3 hrs after meal and at night (2/3 rd : Awaken from sleep) Gastric Ulcer : Occurs with eating, doesn’t awaken from sleep

12. History Abdominal pain is acute, severe and sharp if perforation occurs Periodicity Nausea Bloating Hematemesis or melena resulting from gastrointestinal bleeding. Weight loss Occult blood in stool Symptoms suggestive of anemia like fatigue or dyspnea

13. Physical examination Unperforated Peptic Ulcer Disease Epigastric tenderness Melena Succussion splash due to gastric outlet obstruction Perforated Peptic Ulcer Disease Fetal position Generalized tenderness rebound tenderness Guarding Rigidity Hypotension Tachycardia Anuria Septic Shock

14. Gastric Ulceration : Modified Johnson Classification Type I: Ulcer along the body of the stomach, most often along the lesser curve at incisura angularis. Type II: Ulcer in the body in combination with duodenal ulcers. Type III: In the pyloric channel within 3 cm of pylorus. Type IV: Proximal gastroesophageal ulcer. Type V: Can occur throughout the stomach. Associated with the chronic use of NSAIDs

15. Differential diagnosis Acute Cholecystitis and Biliary Colic Acute Coronary Syndrome Acute Gastritis Esophageal rupture and tears Gastroesophageal Reflux Disease Inflammatory Bowel Disease Gastric Carcinoma Nonulcer dyspepsia (NUD) or functional dyspepsia

16. Investigations Testing for H. pylori : All patients with active or past history of peptic ulcer disease (unless previous cure of HPI has been documented). (1) Rapid Urease Test Urea breath test Fecal antigen test or Biopsy-based testing The 2017 American College of Gastroenterology (ACG) guidelines for the treatment of H pylori infection (HPI)

17. Investigations Chest Xray to look for perforation

18. Investigations Upper gastrointestinal (GI) endoscopy : preferred diagnostic test. ‘Gold standard’ – Bailey & Love Gastric Ulcers Duodenal Ulcers Most occur at the junction of the fundus and antrum, along the lesser curvature discrete mucosal lesions punched-out smooth ulcer base filled with whitish fibrinoid exudate solitary and well circumscribed Malignancy relatively more common >95% in 1 st part of duodenum well-demarcated break in the mucosa may extend into the muscularis propria Malignancy uncommon

19. Benign gastric ulcer Malignant gastric ulcer Mucosal folds Converging mucosal folds up to the margin Effacing mucosal folds Site 95% lesser curve Greater curvature Margin Regular margin Irregular margin Floor Granulation tissue in floor Necrotic slough in floor Edge Not everted; punched or sloping Everted edge Surrounding area Surrounding area and rugae are normal Surrounding area shows nodules, ulcers and irregularities Size and extent Small, deep up to part of muscle layer Large and deep

20. Forrest classification

21. Duodenal Ulcer Ia Duodenal Ulcer IIa

22. Duodenal Ulcer IIb Gastric Ulcer IIc

23. Duodenal Ulcer III Gastric Ulcer III

24. Investigations Ultrasonography Transabdominal USG is helpful to identify conditions mimicking PUD, like Biliary colic. Endoscopic ultrasound (EUS) : useful in the evaluation of gastric mass lesions Barium meal X-ray Gastric Ulcer : Niche on lesser curvature, Notch on greater curvature Duodenal Ulcer : Absence of duodenal cap, Trifoliate duodenum CT Scan with oral contrast Preferred over Barium meal Provides anatomical information like in case of rolling hiatus hernia

25. Arrows: Tumor infiltrating through Serosa Arrowheads: Enlarged LN

26. Treatment Proton Pump Inhibitors (PPI) Mainstay of treatment of PUD Renders the patient achlorhydric All benign ulcers heal, majority within 2 weeks H. pylori eradication therapy : Triple Therapy Proton pump inhibitor (PPI) Clarithromycin (500 mg) or metronidazole 500 mg BID (when Clarithromycin resistance is increasing) Amoxicillin 1000 mg BID or metronidazole 500 mg BID

27. Surgical treatment of duodenal ulcer Indications Perforation Obstruction Bleeding Intractability or nonhealing

28. Treatment Billroth I Billroth II Gastrojejunostomy

29. Truncal Vagotomy Highly Selective Vagotomy

30. Heineke Mikulicz Pyloroplasty

31. Complications Bleeding by erosion into the left gastric and rarely splenic vessels or to vessels in the wall of ulcer Common in type II and III gastric ulcers Surgery Oversewing of the ulcer with or without vagotomy and drainage Vagotomy + Antrectomy

32. Complications Perforated Peptic Ulcer Most common site is anterior wall of duodenum Anterior or incisural gastric ulcer may also perforate Investigations: Erect Chest Xray : Gas Under Diaphragm Serum amylase : Elevated but not diagnostic CT scan is diagnostic

33. Treatment of Perforated Peptic Ulcer Resuscitation Analgesia Systemic antibiotics Surgery

34. Hx : History Rx : Investigation HSV : Highly Selective vagotomy TV/D : Truncal Vagotomy & Drainage Bx : Biopsy

35. Other Complications Duodenal Ulcer Gastric Ulcer Pyloric stenosis Hourglass contracture Penetration to pancreas Teapot deformity Malignant transformation (5-10%)

36. Thank you