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Peptic ulcer disease

1. ANATOMY

2. GASTRIC ULCER

Epidemiology/Etiology

  • 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
  • Low socioeconomic group

Pathogenesis

Factors involved in gastric ulcer formation

  • Duodenogastric reflux – contains bile salts and lysolecithin
    • Breaks the mucosal barrier making it more vulnerable for injury
  • Ischemia of gastric mucosa

Pathology

  • The ulcer’s floor is formed by the muscular layer
  • Posteriorly it can penetrate into the pancreas
    • Can cause torrential bleeding by eroding left gastric or splenic arteries
  • Anteriorly it can perforate into the liver – causing hour glass contracture or tea-pot deformity
  • Microscopic – ulcer crater with chronic inflammatory cells, granulation tissue and epithelial proliferation
  • Grossly, margin of benign ulcer is clear, deep, near lesser curvature
  • Gastric ulcer >3cm has a higher chance of malignant transformation
  • 95% of benign gastric ulcers occur toward the lesser curvature as it takes more burden of passage of food, therefore more wear and tear
  • Acute ulcer – confined to mucosa and submucosa. Due to NSAIDs
  • Chronic ulcer – penetrates muscularis layer of stomach

Classification of Types of Gastric Ulcer –  Daintree Johnson Classification  

  • Type I – in the antrum, near the lesser curvature (normal acid level)
  • Type II – combined gastric and duodenal ulcer (high acid level)
  • Type III – prepyloric ulcer (high acid level)
  • Type IV – ulcer in the cardia or proximal stomach (normal acid level)

Clinical Features

  • Pain in epigastric region after food
  • Relieved by vomiting
  • Periodicity – symptom free interval for 2-6 months
  • Weight loss
  • Aversion to spicy, fried foods

Investigations

  • Barium meal XR – to see  niche and notch
  • Gastroscopy – location, type of ulcer, biopsy
  • US abdomen – rule out other disease

Differential diagnosis

  • Hiatus hernia, cholecystitis, chronic pancreatitis, dyspepsia, carcinoma stomach

Treatment

  • H2 blockers – promote ulcer healing by reducing acid secretion
    • Cimetidine, ranitidine, famotidine (most potent)
  • Proton pump inhibitors – inhibits parietal cell H+/K+ATPase enzyme responsible for acid secretion
    • Omeprazole, lansoprazole, pantoprazole
  • Surgery – partial gastrectomy and Billroth I gastroduodenal anastomosis
  • Type IV proximal ulcer is difficult to manage – treated by subtotal gastrectomy
    • Pauchet’s procedure – sleeve like extension cut along the lesser curve to remove the ulcer

Complications

  • Hour glass contracture – the stomach is divided into two compartments
    • Clinical features – loss of periodicity, persistent pain, vomiting, loss of appetite and weight
    • Diagnosis – barium meal, shows filling only in the proximal stomach
    • Treatment – partial gastrectomy and Billroth I anastomosis is done
  • Tea-pot deformity (hand-bag stomach) – due to cicatrisation and shortening of lesser curve
  • Perforation
  • Bleeding – erosion into left gastric and splenic arteries. Most common in type II and III ulcers
  • Penetration – posteriorly into pancreas and anteriorly into liver
  • Malignant transformation – adenocarcinoma of stomach is the most common

3. DUODENAL ULCER

Epidemiology/Etiology

  • Most common in blood group O +ve
  • Stress, anxiety
  • H.pylori infection
  • NSAIDs, steroids
  • Endocrine causes – Zollinger-Ellison syndrome , MEN syndrome , hyperparathyroidism

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Pathogenesis

  • Duodenal ulcers occur in first part of duodenum – involve the muscular layer
  • Eventually shows cicatrisation causing pyloric stenosis
  • Serosa overlying the site of ulcer shows petechial haemorrhages with speckled red dots – cayenne pepper
  • Microscopic – chronic inflammation with granulation tissue, gastric metaplasia of duodenal mucosa
  • Kissing ulcers – 2 opposing ulcers, one over the anterior surface and one over the posterior surface of the duodenum
  • Anterior ulcer perforates commonly
  • Posterior ulcer bleeds or penetrates commonly

Clinical features

  • Pain relieved by food – increased appetite so patients are more likely to gain weight
  • Night pains are common
  • Heart burn and vomiting
  • Periodicity is more common than in gastric ulcer
  • Melaena, haematemesis

Investigations

  • Barium XR – deformed or  absent duodenal cap
  • Gastroscopy – type and location of ulcer; biopsy to look for H.pylori
  • Serum gastrin level

Treatment

  • General measures – avoid alcohol, NSAIDs, smoking, spicy food

Drugs

  • H2 Blockers
  • Proton pump inhibitors
  • Antacids – neutralise HCl to form water and salt
    • Aluminium hydroxide
  • Sucralfate – aluminium salt which provides protective coat to ulcer crater and promotes healing
  • Anti H.pylori regimen – triple therapy
    • Omeprazole, clarithromycin, amoxicillin

Surgery

  • Highly selective vagotomy (HSV)
    • Only fibres supplying the parietal cells are ligated, reduces acid secretion so ulcer heals
  • Truncal vagotomy with gastrojejunostomy

Complications

  • Pyloric stenosis – due to scarring of first part of duodenum
  • Bleeding, perforation
  • Penetration into pancreas
  • Residual abscess

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