PEPTIC ULCER AND NON ULCER DYSPEPSIA

1. PEPTIC ULCER AND NON ULCER DYSPEPSIA DR BANU NISA ABDUL HAMID MASTER IN FAMILY MEDICINE 1ST YEAR POSTGRADUATE , UKM

2. Objective • most likely causes of dyspepsia • risk factors of recurrent peptic ulcer disease • role of Helicobacter pylori in the pathogenesis of peptic ulcer • disease and its relationship to ulcer relapses • manage patients presented with dyspepsia • role of available drugs for the treatment of dyspepsia • recognise the indications for long-term maintenance therapy • manage patients with PUD and concomitant high CVD risk needing antiplatelet therapy

3. DYSPEPSIA • Defination: • having one or more symptoms of epigastric pain, burning, post-prandial fullness, or early satiation.

4. 5 MAJOR CAUSE • Gastro-esophageal reflux (GERD) • Medications • Functional dyspepsia (FD) – non ulcer dyspepsia • Peptic ulcer disease (PUD) • Malignancy

5. Some medications that commonly cause dyspepsia • NSAIDS • Cox-2 inhibitors • Bisphosphonates • Erythromycin • Tetracyclines • Iron • Potassium supplements • Acarbose • Digitalis • Theophylline • Orlistat • Aspirin

6. FUNCTIONAL DYSPEPSIA

7. FUNCTIONAL DYSPEPSIA • Rome III working group defined FD presence of symptoms thought to originate in gastro-duodenal region, in the absence of any organic, systemic ,or metabolic disease that is likely to explain them.[Tack et al. 2006].

8. FUNCTIONAL DYSPEPSIA

9. Rome III diagnostic criteria for functional dyspepsia At least 3 months of one or more of the following: • bothersome postprandial fullness • early satiation • epigastric pain • epigastric burning AND • no evidence of structural disease (including upper endoscopy) that is likely to explain the symptoms.

10. Pathophysiological mechanism • Delayed gastric emptying • Impaired gastric accommodation to a meal • hypersensitivity to gastric distention • H. pylori infection • altered duodenal response to lipids or acid • abnormal duodenojejunal motility • central nervous system dysfunction [Tack et al. 2004].

11. Pathophysiologic mechanisms in functional dyspepsia. H+, acid exposure. CNS modulation  stress,illness Visceral hypersensitivity (fat, ,wall distension) Acid hypersensitivity Decrease fundic accommodation Vagal neuropathy Abnormal distribution of Igastric contents Inflammation gastric contents [bacteria (H. pylori), viruses, etc.] Gastric dysarrhytmias Delayed gastric emaptying/ Antral hypomotility Overdistended antrum Duodenal hypersensitivity Small bowel dysmotility

12. Diagnostic criteria: PDS 1. Bothersome postprandial fullness, occurring after ordinary sized meals, at least several times per week AND/OR 2. Early satiation that prevents finishing a regular meal Supportive criteria 1. Upper abdominal bloating, postprandial nausea or excessive belching can be present 2. Epigastric Pain Syndrome may coexist

13. Diagnostic criteria: EPS 1. Pain or burning localized to the epigastrium of at least moderate severity at least once per week AND 2. The pain is intermittent AND 3. Not generalized or localized to other abdominal or chest regions AND 4. Not relieved by defecation or passage of flatus AND 5. Not fulfilling criteria for gallbladder and sphincter of Oddi

14. Diagnostic criteria: EPS Supportive criteria 1. Upper abdominal bloating, postprandial nausea or excessive belching can be present 2. The pain is commonly induced or relieved by ingestion of a meal but may occur while fasting 3. Postprandial distress syndrome may coexist

15. FD Management of functional dyspepsia. PPI Promotility agents H.pylorieradiacation Nonresponders Alternative therapies Promotility agents Tricyclics SSRI

16. PEPTIC ULCER DISEASE

17. PEPTIC ULCER • Defination: mucosal lesions that penetrate the muscularis mucosae layer and form a cavity surrounded by acute and chronic inflammation.

18. Two types:

19. In Malaysia • Few reports on the pattern of peptic ulcer in Malaysia. • Male are more prone than female • In both sexes, GU –older age grp compare to DU • Of the 3 main Malaysian ethnic grp, Chinese of both sexes had the highest frequency of peptic ulcer. • Chinese female had the highest frequency of DU. (Source: Profile of PUD in Malaysia,M V Kudva)

21. Risk factor • Major risk factor: Helicobacter pylori infection NSAIDS ASA

22. Etiology and risk factors for peptic ulcer disease Odds Ratio

23. Clinical Manifestation • Night time awakening /episodic epigastric pain relieved following food intake (most specific clinical sign) • Epigastric pain describe as episodic , dull, burning (dyspepsia) pain. • 46% of patients had reflux symp (heartburn, acid regurgitation) ~ GERD

24. Clinical manifestation

25. Clinical manifestation • Most common symp of PUD (> 80 yo) : • Epigastric pain (74%) • Nausea (23%) • Vomiting ( 20%) • Less common features: • Indigestion • Belching • Vomiting • Associated with gastric/pyloric stenosis • LOA • Intolerance to fatty foods • Positive FHX

26. Definitive diagnosis • direct visualization of the ulcer via radiography (upper GI barium swallow, double contrast) or upper GI endoscopy (EGD). • Referral to EGD should be considered in all patients: • 50 years of age or older, with persistent symptoms, anorexia, weight loss, vomiting, • and in the presence of signs of GI bleeding.

27. Differential diagnosis of peptic ulcer disease

29. Common Complication

30. GI Bleeding • 80 %stop spontaneously- only supportive Rx required • Asymptomatic/hemate-mesis,coffee ground emesis,malena, tachycardia,shock. • Urgent OGDS –detect cause of bleeding, start on appropriate therapy. • Shock present- aggressive resuscitation & blood transfusion needed. • Surgery remains a definate indication and best Rx – OGDS/interventional radiology fails.

31. Perforation • Lifetime prevelance of perforation in PUD pts ~5%. • Cause: NSAIDS, H.pylori • Bleeding, sudden onset of sudden severe, sharp abdominal pain/ epigastric pain • Abd : generalized tenderness, guarding, rigidity, rebound tenderness • S/S of septic shock tacycardia,hypotension,lethargy,anuria,cyanosis • Simple surgical closures, intensive medical treatment, H pylori eradication, NSAID withdrawal have been reported to result in very low recurrence rates.

32. Gastric outlet obstruction • more commonly due to malignancy than PUD. • nausea, vomiting, bloating, indigestion, epigastric pain, and weight loss. • endoscopy has the advantage of being diagnostic and can rule out possible malignancy. • Malignant obstruction is reported in 66% of patients. • Outcomes may be improved with effective ulcer therapy with acid reduction and eradication of H pylori. • Surgery is associated with significant morbidity and mortality and should be reserved for endoscopic treatment failures. • Surgical palliation for malignant disease has poor results and high rates of morbidity and mortality.

33. HELICOBACTER PYLORI

34. HELICOBACTER PYLORI (HP) • Gram negetive spiral bacteria • Transmitted: fecal-oral ,oral-oral, mother to child routes, iatrogenic. • Highly prevalent in developing country & lower socioeconomic . • HP +ve subjects have 10-20% lifetime risk of developing PUD.

36. PIC of halicobacter

37. Common Treatment Regimn

38. Overall ,tripletherapy for 14 days has been shown to be more effective at eradication of H pylori than dual therapy. • A recent meta-analysis did not find a difference in H pylori eradication rate between quadruple (PPI +bismuth +metronidazole + tetracycline for 10–14 days) and triple therapy (PPI+clarithromycin +azithromicin for 7–14 days).

39. H. pylori has been found more frequently in dyspeptic patients than in controls and has been shown to affect acid secretion and, to a lesser extent, gastric motility . • “Test and treat strategy”(< 50YO, no alarming symp) • In areas of low H. pylori prevalence (< 20%), the empirical use of PPIs alone is considered to be an equal option for symptom relief .

40. NICE guidelines recommend initiation of a 4 week trial of full dose PPI therapy in patients with uninvestigated dyspepsia.

41. Test available for H.pylori: • Blood antibody test (enzyme-linked immunosorbent assay [ELISA]). This test detects exposure to H pylori but cannot be used to confirm successful treatment. • Urea breath test. This test is adequate for screening and for confirming cure following treatment. The use of PPIs within 2 weeks of testing can interfere with the results. • Stool antigen test. This test is adequate for screening and for confirming cure following treatment. • Stomach biopsy. Gold standard. It is adequate for screening and for confirming cure. Results depend on the number of biopsies and the experience of the pathologist.

42. RELATIONSHIP WITH ULCER RELAPSES • Studies showed that the rate of Helicobacter pylori "reappearance" and of duodenal ulcer relapse up to 6 years after eradication of H. pylori. (Archimandritis A, Balatsos V.  'Bacteriology and epidemiology of Helicobacter pylori infection. J Clin Gastroenterol. 1999;28(4):345.) •  Recent studies have suggested that the eradication of H. pylori affects the natural history of duodenal ulcer disease such that the rate of relapse decreases markedly. (Asaka M, Ohtaki T, Kato M. Causal role of Helicobacter pylori in peptic ulcer relapse. Gastroenterol. 1994 Jul;29 Suppl 7:134-8.)

43. Chronic PUD was almost exclusively due to H. pylori infection with up to 90% of duodenal ulcers and 70% of gastric ulcers attributed to this bacterium. • However, NSAIDs and aspirin are now responsible for most ulcer disease in developed countries. (d2- advances in public health, effective H.pylori eradication therapy).

44. EGD (Esophagogastroduodenoscopy)

45. Alarm symptoms that require prompt EGD in dyspeptic patients. • Anemia • Evidence of acute/chronic bleeding • Previous history of peptic ulcer • Odynophagia • Dysphagia • Recurrent or persistent vomiting • Unintentional weight loss

46. Prompt endoscopy is recommended in patients with alarm symptoms or patients over a threshold age (35-55 years). • Men , younger age ↑prevalence at diagnosis of upper GI malignancy • Once failed a 48 week trial of PPI therapy (in an area of low prevalence of H. pylori)/ failed to respond to eradication of H. pylori (in an H. pylori endemic region) upper endoscopy is indicated. • Performing upper endoscopy during a symptomatic period especially while the patient is off acid-suppressant therapy is important to making a diagnosis of functional dyspepsia by excluding other potential causes of symptoms.

47. Upper GI barium radiography: inferior to upper endoscopy and is generally not recommended as part of the work up for dyspepsia.

48. Management of dyspepsia

49. Dyspepsia Age>50 or alarm symptoms Age<50 and no alarm symptoms EGD Use of NSAIDs or other probable offending medication Dyspepsia without GERD or offending medication Typical GERD symptoms High or intermediate Prevalence of H. pylori (>20%) Trial off medication or change to an alternate medication Full dose PPI trial Continued symptoms despite adequate PPI trial Symptom resolution Yes No Negetive Treat as GERD Test and treat for H. pylori (Stool antigen or breath test off PPI for >2 weeks) Empiric trial of PPI 4–6 weeks Full dose PPI trial

50. Test and treat for H. pylori (Stool antigen or breath test off PPI for >2 weeks) Empiric trial of PPI 4–6 weeks No respond No response EGD Abnormal EGD Normal EGD Treatment based on endoscopic findings 1. Biopsy for H. pylori (unless negative H. pylori stool antigen or breath test OFF PPI for greater than 2 weeks) 1. Reassurance 4. Evaluate and treat for IBS 2. Consider alternate causes of abdominal pain 3. Consider trial of low dose trycydic antidepressant or antispasmotic Note: diagnostic algorithm may differ based on regional cancer risk, gender, and age of patient at presentation.