Peptic (Gastric & Duodenal) Ulcer

Peptic (Gastric & Duodenal) Ulcer

Symptoms & Signs

·        Gastric & duodenal usually indistinguishable clinically

·        Uncomplicated: can be silent, epigastric pain after food, relived by antacids, and waking at night due to pain, weight change

·        Complicated: haematemesis/melaena, vomiting, severe pain Þ pancreatitis or perforation (but 50% of patients with fatal complications present without ulcer pain), shock, anaemia, peritonitis

Epidemiology

·        10% of the population have one at some time in their lives

·        M>F 3:1

·        Genetic risk (50% twin concordance)

Aetiology

·        Need mucosal injury

·        H. Pylori infection. Damages D cells ® ­gastrin ®­acid & pepsin ® metaplasia + helicobacter damage ® ulcer

·        Smoking, alcohol, etc

·        NSAIDs

·        If neither H. Pylori infection nor NSAIDs then ulcer very unlikely

·        Not due to ­acid (except for Zollinger-Ellison syndrome)

·        Macroscopic appearance: well demarcated, punched out, with radiating mucosal folds. Most <4 cm diameter

·        Microscopic appearance – 4 layers/zones:

o   Exudative zone: fibrin, debris, neutrophils, etc

o   Necrotic zone: necrotic debris

o   Granulation tissue zone

o   Zone of fibrous tissue

o   Adjacent: blood vessel thickening, mucosal hyperplasia, chronic inflammation

Helicobacter Pylori

·        Curved gram negative organisms in gastric mucus

·        From contaminated water

·        Prevalence in NZ 30% but declining, 20% in Wellington, lower in Dunedin. Causes 60% of antral gastritis (other causes include bile reflux)

·        H. Pylori infection in 70-80% of gastric ulcers, 95% of duodenal

·        Also associated with gastric adenocarcinoma and gastric MALT lymphoma (i.e. it‟s a carcinogen)

·        Lives beneath gastric mucus: pH of 5 – 7 (compared with 1 – 2 in stomach lumen)

·        H. Pylori always gives gastritis, usually in the antrum, but usually asymptomatic. Eradication only of benefit if ulcer‟s present

·        Microscopic appearance: chronic atrophic gastritis. Chronic inflammatory infiltrate ® gland atrophy over time, intestinal metaplasia of remaining glands

Investigations

·        Bloods: FBC (anaemia), amylase

·        Refer for endoscopy if > 45 years or alarm symptoms

·        At endoscopy check for H Pylori, CLO test from biopsy sample, or histology/culture, and biopsy from antrum of stomach. 1% of gastric ulcers are cancers – always biopsy – but ulcers don‟t predispose to cancer

·        Urease breath test (gold standard): swallow C13 labelled urease and check for expired labelled CO₂. H. Pylori has Urease to turn urea ® NH₂ + CO₂

·        CXR: subdiaphragmatic gas in perforation

·        Contrast Xray (less accurate than endoscopy)

Differential

·        Pain: Reflux, gastric ulcer, gastric cancer, gallbladder disease, chronic pancreatitis, IBS

·        Acute Severe Pain: acute pancreatitis, bilary colic, aortic dissection, MI

·        Zollinger-Ellison syndrome: uncontrolled gastric acid secretion driven by ­plasma gastrin released by a gastrinoma - 50% malignant ® multiple peptic ulcers

·        Crohn‟s, Lymphoma, CMV

Treatment

·        If on NSAIDs: stop them.  Normally curative

·        Antacids

·        H₂ receptor antagonists: good healing over 4 – 8 weeks (ranitidine, cimetidine)

·        PPIs: for unresponsive ulcers  - superior to H₂RA for healing and maintenance

·        Triple therapy for H. Pylori:

o   75% effective under normal conditions.  Reinfection is rare (< 1%)

o   2 weeks optimal – 7 days pretty good 

o   pH has effect on antibiotic bioavailability: want to ­pH (e.g. omeprazole)

o  Bismuth (De-Nol) + tetracycline & metronidazole + ranitidine, or Clarithromycin & metronidazole + ranitidine, or

o  Amoxycillin + metronidazole + omeprazole

o  Treatment of H. Pylori in non-ulcer dyspepsia has little effect. Only proven benefit of eradication is in ulcer disease and MALT lymphoma

·        Always re-scope an ulcer to check healing.  You want to be sure it‟s not a cancer missed on histology

·        (and PPIs will mask symptoms)

Complications

·        Only time surgery is involved

·        Haemorrhage: 2.5% of PU per year ® occult, melaena or haematemesis.  10% mortality

·        Perforation: 1% of PU per year, usually NSAID users

·        Penetrating: pancreas, liver, biliary

·        Obstruction: of pylorus due to chronic scarring/stenosis ® functional obstruction