Peptic Ulcer Disease

Overview

Peptic ulcer refers to an ulcer in the lower oesophagus, stomach or duodenum. Incidence ↑ with age; both sexes are similarly affected. In the developed world, Helicobacter pylori incidence has been slowly ↓ over the past 50 yrs; Non-Steroidal Anti-Inflammatory drug (NSAID) use has ↑. Peptic ulcers remain common worldwide, especially in the developing world where H. pylori infection is prevalent.

Anatomy and Physiology

The stomach is a J-shaped organ located inferior to the diaphragm within the abdominal cavity. Stomach has three main function:

• Mixes food producing Chyme which is transferred to the dudoenum
• Secreting gastric juice
• Reservoir for food

The lower esophageal sphincter and pyloric sphincter separates the stomach from the oesophagus and duodenum respectively. The parts of the stomach include:

• Cardia – entrance from oesophagus into the stomach
• Fundus – upper portion of the stomach
• Body
• Antrum – exit of the stomach into the duodenum

Layers of the stomach

• Mucosa (most inner layer)
• Submucosa
• Muscularis Externa (3 layers inner → outer)
  • Oblique
  • Circular
  • Longitudinal
• Serosa

The inside of the stomach looks tortuous (Rugae) and forms gastric pits which contain many cells.

The stomach have a number of specialised cells that perform varies function

• Parietal Cells → HCl (Acid) and intrinsic factor
• Chief cells → Pepsinogen
• G-cells → Gastrin
• D-cells → Somatostatin
• Enterochromaffin cells → Histamine
• Post Parasympathetic Neurons → stimulates digestion

Pathophysiology

Peptic ulcers result from an imbalance between factors:

• Promoting mucosal damage
  • Gastric acid
  • Pepsin
  • Bile salts refluxed from the duodenum
  • H. pylori infection
  • NSAIDs)
• Promoting gastro-duodenal defense
  • Prostaglandins, mucus
  • Bicarbonate
  • Mucosal blood flow
  • Integrity of tight junctions between epithelial cells
  • Restitution (process where any break in epithelium is rapidly filled by adjacent epithelial → mucosal stromal cells migrating → flattening to fill the gap).

Aetiology and Risk Factors

Aetiology

• Infection by H. pylori (common)
• Use of aspirin or other NSAIDs (common)
• Gastric ischaemia (‘stress ulcers’ in pts with multi-organ failure in ICUs)
• Zollinger-Ellison syndrome (gastric acid hypersecretion caused by a gastrin secreting neuro-endocrine tumour)
• Medications (potassium chloride, bisphosphonates)
• Infections & Crohn’s disease.

Risk Factors

• H. pylori
• NSAIDs
• Smoking
• >Age
• History of peptic ulcer
• Family History of peptic ulcer
• Alcohol
• Patient in ICU on mechanical ventilation or with coagulopathy
• Chronic obstructive lung disease
• Chronic renal insufficiency

Clinical Manifestation

Clinical Presentation

• Epigastric pain +/- radiates to back (severe)
• Pain occurs shortly after eating with gastric ulcers and 2-3 hrs afterward with duodenal ulcers
• Nocturnal pain
• Pain relieved by drinking milk
• Nausea and vomiting

Examination

• Epigastric tenderness – may occur on palpation of the abdomen. But often there are no other signs on examination.
• ‘Pointing sign’ – the patient can generally show site of pain with one finger

Medical Emergency – Perforated Ulcer

• Sudden, severe abdominal pain
• Haematemesis/or melaena,
• Signs of peritonitis
• Signs of shock and anaemia

Differential Diagnosis

• Oesophageal Cancer
• Gastric Cancer
• GORD/GERD
• Gallstone Disease
• Acute Pancreatitis
• Coeliac Disease
• Irritable Bowel Syndrome
• Pericarditis
• Lower lobe Pneumonia 
• Achalasia

Investigations

• H.pylori breath test or stool antigen test
• Upper Gastro endoscopy
• FBC
• Fasting serum gastrin level – hypergastrinaemia in Zollinger-Ellison syndrome
• Abdominal X-ray
• Abdominal CT

Treatment

• Relieve symptoms
• Induce healing
• Prevent recurrence

Medical management (mainstay of treatment, unless complicated)

H. pylori eradication:

 Cornerstone of therapy for peptic ulcers  as this will prevent relapse & eliminate

need for long-term therapy in the majority of patients

Triple therapy: PPI taken with 2 antibiotics (clarithromycin, amoxycillin or metronidazole) for 14 days

Complications and Prognosis

Complications

• Penetration
• Perforation – perforation of ulcer usually anteriorly
• Bleeding – ulcer erodes into the wall of a gastroduodenal blood vessel usually posteriorly
• Gastric outlet obstruction – from chronic pyloric stenosis may occur as pyloric channel ulcers heal with scarring and oedema

Perforated Peptic Ulcer

Overview

Perforated Peptic ulcer is a surgical emergency. It is caused by erosion of the ulcer through the wall of the stomach or duodenum into the peritoneal cavity. The contents of the stomach escape into the peritoneal cavity → peritonitis (board-like rigidity). The commonest site of perforation is the anterior aspect of duodenum from a duodenal ulcer.

Clinical Presentation

• Severe and sudden abdominal pain
• Signs and symptoms of Peritonitis
• Signs and Symptoms of shock

Investigation

• FBC
• EUC
• Erect Chest X-ray – reveals air under the diaphragm
• Abdo X-ray
• CT scan – indicates free intraperitoneal air

Management – Surgical Emergency

• Resuscitation
• IV Analgesia
• Surgery – of a perforated duodenal ulcer is either simple closure or a definitive procedure to decrease gastric acidity.

References

A Colour Handbook of Gastroenterology
Oxford Clinical Handbook of Clinical Medicine
Sleisenger and Fordtran’s Gastrointestinal and Liver Disease 10th Ed.