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Peptic Ulcer Disease

  • Definition – ulcer in lower stomach or duodenum. Can be acute or chronic; both penetrate the muscularis mucosae but acute ulcer shows no sign of fibrosis. Anterior penetrates and posterior bleeds.

Etiology

  • Gastric ulcer (GU)
    • Imbalance between protective and damaging factors of gastric mucosa
    • Atrophic gastritis, bile reflux, gastric stasis, abnormalities in acid and pepsin secretion
    • Smoking, alcohol, NSAIDs, steroids
    • H. Pylori – G-, spiral, multiple flagella
    • Low socioeconomic group
  • Duodenal ulcer (DU)
    • MC in blood group O +ve
    • Stress, anxiety
    • H.pylori infection
    • NSAIDs, steroids
    • Endocrine causes – Zollinger-Ellison syn, MEN syn, hyperparathyroidism

Pathogenesis – commonly H pylori/NSAIDs

H.pylori

  • Strongly associated with H.pylori infection – increases with age and developing countries
    • Person to person contact
    • Most colonised people are healthy and asymptomatic
  • 90% of DU and 70% of GU pts are infected
    • The remaining are caused by NSAIDs, especially in developed countries
  • Motile – allows it to burrow and live beneath mucus layer adherent to the epithelial surface
    • Adhesion molecule BabA binds to Lewis b Ag on epithelial cells
    • Releases urease to neutralise any acidity >> produces ammonia >> raises the pH around bacterium
  • Causes chronic gastritis by provoking a local inflam response – depends on expression of
    • cagA gene – injected into epithelial cells, interacts with cell-signalling pathways involved in cell replication and apoptosis
    • vacA gene – pore forming protein, causes increased cell permeability, efflux of micronutrients from the epithelium, induction of apoptosis and suppression of local immune cell activity
  • causes increases gastrin release from G cells >> hypergastrinemia >> increased acid prod by parietal cells
  • rarely can cause pangastritis >> gastric atrophy and hypochlorhydria
    • allows other bacteria to proliferate within the stomach >> predisposes to gastric cancer
  • effects of H.pylori are more complex in GU than DU

http://www.scielo.br/img/revistas/abc/v94n4/en_a19tab01.gifNSAIDs

Gastric Ulcer

Duodenal Ulcer

Clinical features

ALARM symptoms – (urgent gastroscopy)

Diagnosis

  • Barium meal XR – niche + notch (GU), absence of duodenal cap (DU)
  • Gastroscopy (need to stop PPI 2 weeks before procedure)
  • Forrest classification is used to assess risk and intervention by endoscopic procedures.
  • Abdominal US
  • Biopsy – on all gastric ulcers
    • Ulcers on greater curvature assumed to be malignant unless proved otherwise
  • FBC – T2/T3 ulcers show HCl hypersecretion

Differential diagnosis

  • Hiatus hernia, cholecystitis, chronic pancreatitis, dyspepsia, carcinoma stomach, gastrinoma, cushing/curling ulcers, Crohns, TB, Zollinger-Ellison syndrome

Treatment

  • H.pylori eradication
    • PPI + 2 abx of: amoxicillin, clarithromycin and metronidazole for 7d
      • Omeprazole 20mg + amoxicillin 1g, clarithromycin 500mg
    • Quadruple therapy – in case of eradication failure
      • PPI, bismuth subcitrate, metronidazole, tetracycline for 14d (OBMT)
  • General measures – cig, aspirin, NSAIDs should be avoided
  • Antacids – aluminium hydroxide
  • Surgery –
    • Partial gastrectomy with Billroth I anastomosis (gastroduodenostomy)
    • Highly selective vagotomy may be performed to decrease acid secretion. (parietal cells ligated)

Complications

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