Peptic Ulcer Disease

Overview

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.

Definitions
Dyspepsia: “indigestion”; describes symptoms such as bloating & nausea, thought to originate from the upper GIT; a chronic or recurrent abdominal pain or discomfort centered in the upper abdomen
Ulcer: breach/ defect in mucosal lining of the stomach or duodenum that extends through the muscularis mucosae into the submucosa or deeper
Erosions: breech in epithelium of the mucosa only; do not penetrate muscularis mucosae
Metaplasia: a change in phenotype of differentiated cells in which one cell type is replaced by another cell type; may result in reduced functions or increased propensity for malignant transformation

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

Remember Intrinsic factor is needed for Vitamin B12 absorption.

Watch Gastric Physiology (Acid, Ulcer, Relfux)

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

Signs and Symptoms

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

Remember 3 notable characteristics: localization to the epigastrium, relationship to food, episodic occurrence

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

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.

Side note H. Pylori infection has reduced. This result in ↓ duodenal ulcers (almost always assoc with H. pylori infection) and ↑ in gastric ulcers (main site of ulcers caused by NSAIDs).

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).

Pathophysiology of H. Pylori associated peptic ulcer

Watch Helicobacter Pylori and Peptic ulcers pathophysiology

Management

Management

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

Pharmacology

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

Side Note Peptic ulcer penetration occurs when chronic ulcer penetrates the entire thickness of the stomach or duodenal wall, into an adjacent organ such as the pancreas, but without free perforation into the peritoneal cavity

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