Stomach
Ulcers
Peptic ulcer disease
Author: Elliot Weisenberg, M.D.
Last author update: 1 August 2012
Last staff update: 18 May 2023
Copyright: 2003-2024, PathologyOutlines.com, Inc.
PubMed Search: peptic ulcer disease[title]
Table of Contents
Definition / general | Clinical features | Pathophysiology | Sites | Treatment | Gross description | Microscopic (histologic) description | Microscopic (histologic) images | Differential diagnosisCite this page: Weisenberg E. Peptic ulcer disease. PathologyOutlines.com website. https://www.pathologyoutlines.com/topic/stomachpud.html. Accessed December 18th, 2024.
Definition / general
- Ulcer:
- Breach in muscularis mucosa of GI tract
- Erosion is more superficial breach
- Ulcers begin as erosions, but not all erosions progress to ulcers
Peptic ulcer:- Chronic, usually solitary, due to acid-peptic juices
- Causes:
- Mucosal injury due to Helicobacter pylori infection, NSAID use, Zollinger-Ellison syndrome (multiple peptic ulcerations in stomach, duodenum and jejunum due to excess gastrin secretion by a tumor), ischemia, bile / pancreatic juice reflux
- Alcohol, smoking, COPD and corticosteroids use may exacerbate peptic ulcer disease and impair healing
- Hyperacidity present in minority of duodenal ulcers and only rarely in gastric ulcers
- H. pylori has nearly universal association for duodenal ulcers; present in 65% of gastric ulcers and 90% of gastric ulcers not related to NSAID use or Zollinger-Ellison syndrome
Clinical features
- Incidence in US of 4 million, 350,000 new cases / year
- 3,000 deaths per year
- Affects 10% of American men, 4% of women (M/F = 3:1 for duodenal ulcers, 1.5-2:1 for gastric ulcers)
- Incidence has decreased recently for duodenal ulcers, not for gastric ulcers
- Usually in pyloric-type mucosa along lesser curvature
- 20% have coexisting duodenal ulcer
- 5% are multiple
- Mean age 50 years, but may occur in children
- Multiple (~10) biopsies recommended to rule out malignancy
- Symptoms:
- Epigastric burning
- Pain worse at night, within 1-3 hours after meals
- Pain may decrease with food / alkali
- Perforation associated with pain in back, left upper quadrant, chest
- Usually impairs life but doesn’t shorten it
- Heals in 15 years without treatment versus weeks with treatment
- Complications: perforation, hemorrhage, obstruction, surgery
Pathophysiology
- H. pylori related ulcers:
- Produces urease (to protect it from acid), protease (breaks down glycoproteins in gastric mucus), phospholipase (damages epithelial cells, may release leukotrienes)
- Attracts neutrophils that produce myeloperoxidase (turns HCl into hypochlorous acid, combines with NH3 to form monochloramine)
- Both hypochlorous acid and monochloramine destroy mammalian cells
- NSAID related ulcers:
- Usually moderate / severe foveolar hyperplasia, edema, vascular ectasia (indicative of reactive / chemical gastropathy), all more prominent than in non-NSAID ulcers (Mod Pathol 1999;12:592, Endoscopy 2004;36:42, Endoscopy 2006;38:2)
Sites
- Duodenum, antrum, lesser curvature near incisura most common site in stomach, GE junction, margins of gastrojejunostomy, adjacent to Meckel diverticulum containing ectopic gastric mucosa, lower esophagus
- 98% in stomach or duodenum
- Duodenum:stomach 4:1
- Gastric ulcers on greater curvature or not in antrum are more likely to be related to NSAID use, ulceration may also be caused by tumors, infections (other than H. pylori) especially in immunocompromised patients
Treatment
- Antibiotics if H. pylori induced promote healing of ulcers and reduce greatly recurrences, proton pump inhibitors, discontinuation of NSAIDS and corticosteroids, smoking cessation
Gross description
- 90% < 4 cm, 50% < 2cm, clean base (due to peptic enzymes), surrounded by erythematous mucosa, may see blood vessel in ulcer base
- Usually sharply punched out defect with straight walls, NO heaped up margins
- Size doesn’t predict malignancy
Microscopic (histologic) description
- Generally associated with H. pylori gastritis, may see reactive gastropathy if history of NSAID use
- Ulcer may be transmural or limited to mucosa and submucosa
- Muscle wall replaced by fibrous tissue
- Serosal fibrosis
- Hyperplasia of adjacent lymph nodes
- Proximal mucosa may be overhanging
- Distal mucosa may have ladder-like configuration
- Accompanied by active and chronic inflammation, unless NSAID related
- Active ulcers have 4 prototypical zones:
- Surface neutrophils, bacteria, necrotic debris and possibly Candida
- Fibrinoid necrosis at base and margins
- Granulation tissue with chronic inflammatory cells
- Fibrous or collagenous scars in muscularis propria with thickened blood vessels showing endarteritis obliterans
- Healing ulcers:
- Have regenerating epithelium over the surface
- May have intestinal metaplasia, marked reactive changes
- Rarely exhibits hyalinization (severe thickening, usually of submucosa, Arch Pathol Lab Med 1982;106:472)
Microscopic (histologic) images
Images hosted on other servers:
Various images
Differential diagnosis
- Acute gastric ulcers due to severe systemic stress
- Carcinoma (radiologically)
