PEPTIC ULCER disease (PUD) Dr. Gehan Mohamed Dr. Abdelaty Shawky
Learning Objectives • Recognize the typical clinical presentation and risk factors for peptic ulcer disease. • Understand pathophysiology of PUD focusing on H. pylori. • List the four layers of peptic ulcer seen by microscope. • Identify the complications of PUD.
Ulcers are defined as a breach in the mucosa of the alimentary tract, which extends through the muscularis mucosa into the submucosa or deeper. ( An erosion differs from an ulcer in being more superficial than ulcers and partially affecting surface epithelium).
Definition of peptic ulcer: • Peptic ulcers are chronic most often solitary, lesions that occur in any portion of the gastrointestinal tract exposed to the aggressive action of acid-peptic juices.
* Clinical presentation: • Relapsing lesion • Most often diagnosed in middle aged to older adults but may first become evident in young adult life. • Epigastric burning or aching pain. • Pain worse at night and 1 to 3 hours after meal specially in doudonal ulcer.
May radiate to the back (consider penetration) • Relieved by antacids (duodenal), or vomiting (gastric). • Dyspepsia. • Nausea, vomiting, bloating , and weight loss occur. • Hematemesis or melena with GIT bleeding.
* Sites of peptic ulcer: • Duodenum: First portion. Anterior wall is more often affected. • Stomach: Usually antrum. Lesser curvature (common) . • At the margins of a gastroenterostomy (stomal ulcer) • In the duodenum, stomach or jejunum of patients with Zollinger-Ellison syndrome. • Within Meckel’s diverticulum that contains ectopic gastric mucosa.
* Pathogenesis of peptic ulcer: Peptic ulcers are produced by an imbalance between the gastro-duodenal mucosal defense mechanisms and damaging forces.
* Mucosal defense mechanisms: • Bicarbonate secretion • Mucous secretion • Tight adherence between epithelial cells to prevent any acid leakage to the inside. • Good blood supply to the mucosa • Renewal of damaged epithelial cells.
* Damaging agents: • H. pylori • Gastric acid • Pepsin • Superimposed injury from environmental or immunologic agents.
Role ofH. Pylori infection in the pathogenesis of peptic ulcer: H. pylori infection is present in almost all patients with duodenal ulcers and 70% of cases with gastric ulcers. * Mechanism: 1. H. pylori secretes urease (generates ammonia), protease (breaks down glycoprotein in the gastric mucus) or phospholipases. 2. Bacterial lipopolysaccharide attracts inflammatory cells to the mucosa. Neutrophils release myeloperoxide. 3. A bacterial platelet-activating factor promotes thrombotic occlusion of surface capillaries.
Damage of the protective mucosal layer. The epithelial cells are exposed to the damaging effect of acid-peptic digestion. • Inflammation of the gastric mucosa. • Chronically inflamed mucosa more susceptible to acid- peptic injury and prone to peptic ulceration.
* Other Causes of peptic ulcer: • Chronic use of NSAIDs (aspirin) an corticosteroids. • Cigarette smoking. • Psychological stress. • Ischemia.
* Gross features: Site: Gastric ulcers are located at the antrum toward the lesser curvature. The duodenal ulcer is usually located at the 1st part anteriorly. Shape: Round, oval. Size: Usually less than 2cm in diameter. • Lesions less than 0.3 cm are likely to be shallow erosions. • Giant ulcers are usually greater than 3cm in diameter. • Size does not differentiate benign from malignant ulcer.
Base of ulcer: • Firm (formed of bundles of muscles and fibrous tissue). Floor: Clean (gastric juice digest any food particles at the floor. Margin (Surrounding gastric mucosa): Edematous and reddened due to gastritis. Depth of the ulcer: • Superficial ulcer penetrate the mucosa reaching up to the muscularis mucosa. • Deeply excavated ulcers having their bases on the muscularispropria.
Biopsy of peptic ulcer • Biopsy is necessary to distinguish between benign and malignant ulcers. • Biopsy should be taken from the ulcer edge, at least from each quadrant. • Up to 10-12 biopsies may be taken to exclude cancer.
* Microscopic features: - Four distinct layers are present in a peptic ulcer in the same sequence starting from the luminal side : 1. Surface coat of exudate and necrotic debris. 2. Fibrinoid necrosis. 3. Granulation tissue. 4. Fibrosis replacing the muscle wall and extending into subserosa.
* Complications of PUD : 1. Hemorrhage: hematemesis or melena. 2. Perforation 3. Healing by fibrosis causing obstruction. 4. Malignant transformation: rare (0.5% of gastric peptic ulcer).