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Peptic Ulcer Disease

Explore the case of a 30-year-old male with epigastric pain, differential diagnoses, complications, and diagnostic steps for peptic ulcer disease. Learn about H. pylori infection, risk factors, clinical presentations, complications, and treatment options in this comprehensive guide.

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Peptic Ulcer Disease

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  1. Peptic Ulcer Disease Cengiz Pata,MDDept. Gastroenterology,Yeditepe University, Medical center

  2. Case • 30 year old male • Epigatsric pain radiating to the back Questions? Possible diagnosisDeferential diagnosisPossible complications

  3. Case • Pain: • What type of pain? How often?Awakes at night? Relation to food? • Complications: • Vomiting? (obstruction?)Stools? (melena?) • Common deferential diagnosis: • Pnacreatobiliary diseaseDyspepsiaTumors

  4. Case • Next diagnostic step? • EndoscopyAbdominal USUGI? • DU Ulcer detected- next step? • Test for H. pyloriExclude NSAID use Rare – assess gastrin, mainly in unusual cases

  5. Benign gastric ulcer (B)

  6. Peptic Ulcer • A defect in the gastrointestinal mucosa extending through the muscularis mucosa. • Two main forms:1) Helicobacter associated 2) NSAID associated ( Steroids alone – no additional risk, Increased risk when combined with NSAIDS)

  7. Peptic Ulceration : Additional Causes • Acid hypersecretion:Gastrinoma ( ZE)Systemic mastocytosisBasophilia in myeloproliferative disorders • ViralHerpes simplex CMV ( mainly in immune compromised)

  8. Peptic Ulceration : Additional Causes • Vascular Insufficiency ( including due to crack cocaine) • Radiation induced • Chemotherapy induced • Stress ulceration

  9. Electron micrograph of H. pylori

  10. Prevalence of Helicobacter pylori in peptic ulcer

  11. Seroprevalence of H. pylori with increasing age in developed and developing countries Developing countries Developed countries 100 64-96% 75 10-75% 50 7-54% Prevalence (%) 6-39% 25 0 40-50 40-50 <20 <20 Age range (years) Adapted with permission from Heatley-Helicobacter pylori and Gastrointestinal Disease; Oxford, UK: Blackwell Scientific Publications

  12. Risk factors for H. pylori infection • Age • Country of origin • Socio-economic status • poor housing • bed sharing • overcrowding • large families

  13. Modes of transmission of H. pylori infection • Zoonosis unlikely • Environment unlikely • Person-to-person • oral-orallikely • gastro-orallikely • faecal-orallikely

  14. H. pylori infection and disease associations • Chronic gastritis • Duodenal ulcer • Benign gastric ulcer • Gastric carcinoma • Gastric MALT and non-Hodgkin‘s lymphoma • Ménétrier‘s disease

  15. Pattern of gastritis Duodenal ulcer Gastric ulcer Corpusitis * Antralgastritis *H. pylori colonizes areas of gastric metaplasia, leading to chronic duodenitis and eventually duodenal ulcer.

  16. NSAIDS • In the USA 30 bil OTC 20 mil prescriptions • 3-4% ulcerations • 20,000 die of NSAID complications • 80% have no preceding dyspepsia • Important to identify at risk populationsPrevious gastritisElderly

  17. PD & Systemic Diseases • COPD • Renal Failure • Cirrhosis • Mastocytosis

  18. Clinical Presentation • Abdominal Pain: Epigastric dull “hunger pain”DU- 11/2 –3 hrs postprandial relived by foodMay awake at night GU – May occur with meals • nausea weight loss more frequent in GU • Sudden pain – perforation? • Vomiting – obstruction?

  19. Clinical Presentation • Physical examination: • Poor predictive value, not specific • Pain may occur in RUQ ~ 20% • Detect complications: Tachycardia, orthostasis- bleeding?Radiation to the back- perforation?Succussion splash – outlet obstruction?

  20. Complications • Bleeding ~ 15% ( More in >60 yrs –NSAID) 20% - no warning sign • Perforation 6-7% FreePenetration: DU posterior to pancreas GU into Lt hepatic lobe Gastrocolic fistula

  21. Complications • Outlet obstruction 1-2%Inflammatory – reversible by TxScar tissue – balloon dilatation, Surgery • Presentation : Gradual onsetSudden

  22. Clinical manifestations of ulcer disease

  23. Differential Diagnosis • Non ulcer dyspepsia • Tumors of the UGIT • Biliary disease • Reflux disease • Vascular diseases • Pancreatitis • Coronary heart disease

  24. Diagnosis • Radiology:Single contrast 80% sensitivity Double 90%(worse for ulcers<0.5 cm, scar tissue) • Endoscopy: examination of choice good for small ulcersbiopsy samples for HP and malignancytherapeutic • Assay for HP infection

  25. Diagnostic methods for H. pylori Diagnostic method Main indication Sensitivity (%) Specificity (%) Histology Diagnosis 90 90 Culture 80-90 95 H. pylori antibiotic sensitivities Rapid urease test Endoscopy room diagnosis 90 90 Serology Screening and diagnosis 90 90 Urea breath test To confirm eradication 95 100

  26. The principle of the urease test NH2 2NH4++ HCO3- C O + 2H2O + H+ Urease NH2 Urea CLOtest pH change

  27. The principle of the 13C- or 14C-urea breath test Reproduced with permission from Mr Phil Johnson, Bureau of Stable Isotope Analysis, Brentford, UK.

  28. Therapy • Treat H. pylori • Healing by inhibition of acid secretion:H2 receptor antagonists (H2RA)Proton Pump inhibitors ( PPI)Anti Acid • CytoprotectionSucralfateAnti AcidBismuth-BasedProstaglandin Analogs

  29. Therapy of DU • H2RA – Cure in 80% at 4 wks ~95% at 8 wks Split and once daily equally effective • PPI- Cure in 60-93% at 2 wks 80- 100 % at 4 wks • Omeprazole Vs ranitidine 14% advantage at 2 wks 9% advantage 4 wks

  30. Therapy of GU • Suppress acid by H2RA or PPI • Advantage of PPI less apparent • Sucralfate comparable to H2RA • Prepyloric ulcers may resemble more DU in terms of response to acid suppression

  31. Risk stratification of Ulcer Pts • Low risk:Intermittent symptomsNonsmokerDiscontinued NSAIDUncomplicatedEasy healing

  32. Risk stratification of Ulcer Pts • High risk:Frequent recurrenceRefractory to TxSmokingContinued NSAIDGiant Ulcer ( DU >2 cm GU > 3 cm)AnticoagulationDeformity & scarringElderlyAcid hypersecretion

  33. General Scheme • HP positive – Eradicate • If Non complicated – No further Tx • If high risk: • Follow by acid suppression for 4-6 wks • Withdraw – NSAIDSmoking Excess Alcohol • In GU – Biopsy?Cost and effect- Most CAs detected in first round of endoscopy

  34. Refractory Ulcers • Consider refractory after 8-12 wks of Tx • Ensure that refractory symptoms= refractory ulcer ( endoscopy) • If no ulcer - investigate pain • Consider “silent” refractory ulcer in high risk pts ( ~25% of refractory ulcers)

  35. Refractory Ulcers - causes • Persistent HP infection • Persistent NSAID use • Poor pt compliance • Giant ulcers ( healing at 3 mm/wk) • Smoking • Under laying pathology ( ZE, bands, crohn’s,infections I.e. TB syphilis, Ly, scarcoidosis ) • Impaired response to PPI ( 5% of population)

  36. Refractory Ulcers - Approach • Seek causes: DU- HP, NSAIDS, r/o ZE ( gastrin levels)GU- main concern CARepeat multiple BxEvidence for malignancy: CT, EUSNo explanation - surgery

  37. Surgery - DU • Refractory bleeding (~5% of transfused Pts) • Perforation (2-3%) • Outlet obstruction • Vagotomy + antrectomy Rec.  (1%) Comp Vagotomy + pyloroplasty intermediate (10%)Highly selective vagotomy Rec.  Comp 

  38. Zollinger Ellison Syndrome • Severe peptic ulcer diathesis + gastric acid hypersecretion due to b-cell endocrine tumor • 0.1-1% of PUD patients • Sporadic, or associated with MEN type I (25%)

  39. Zollinger Ellison Syndrome • >80% Localized to gastrinoma triangle:cystic & common bile ducts, duodenum, junction head and body of pancreas. • 60 % malignant, up to 50% with metastasis • Clinical: PUD >90% (recurrent, multiple, refractory, complicated)

  40. Zollinger Ellison Syndrome • Esophageal complaints ~60% • Diarrhea ~50% (fluid overload, pancreatic enzyme dysfunction, epithelial dysfunction) • Combination should raise clinical suspicion

  41. Clinical features of Zollinger-Ellison syndrome

  42. MEN I • Autosomal Dominant:Parathyroid (~90%), Pancreas (40-80%)Pituitary (30-60%) • Contributory effect of hyperparathyroidism, hypercalcemia  hypergastrinemia  acid secretion • Higher incidence of carcinoids • Smaller and multiple duodenal gastrinomas

  43. Diagnosis of Gastrinoma • Combination of clinical signs • Fasting gastrin levels (> 150 pg/ml) • Avoid confounding factors(hypochlorhydria, PPIs, outlet obstruction, renal failure) • Assess acid secretion (if low- excludes) • Provocative tests (calcium, secretin)

  44. Treatment • Localization (EUS, Oct scan, MRI, CT) • Exclusion of metastasis • If positive – symptomatic cure • If negative attempt surgical resection ( less likely in MEN I ~ 6%)

  45. Case -2 • 70 year old lady , RA • Dizziness and weakness for the last week. • Mild abdominal pain • Questions?

  46. Case-2 • Stools? • Melena • Drugs? • NSAIDS • Next action? • Gastroscopy

  47. Gastric Ulcer with Stigma

  48. Treatment • H2RA • Oral PPI • Oral PPI + H2RA • IV PPI

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