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Peptic Ulcer

Disease
Meraj Ondhia

Definition

- Break in mucosa of stomach or duodenum >5mm in diameter


and to
submucosa
- Factors promoting mucosal damage (pepsin, gastric acid,
Helicobacter Pylori,
NSAIDs) overpower protective mechanisms:
Mucus: trap bicarbonate ions
Bicarbonate: neutralise H+
Mucosal blood flow: maintained by vasodilator neuropeptides,
nitric oxide and prostaglandins and provides bicarbonate ions
from basal border of parietal cells
Prostaglandins: stimulate phospholipid and mucus secretion
and vasodilatation

Epidemiology
-Prevalence of H. Pylori infection:
Developing countries: 80-90%
Developed countries: 20-50%
-Infection is usually acquired during childhood by
various routes: faecal-oral, oral-oral, kissing or
ingestion of contaminated vomit
-Prevalence of peptic ulcer disease:
Duodenal ulcers: 10-15% of adult population
Gastric ulcers: 3-4 times less common than duodenal
ulcers
Both are common in the elderly

Aetiology
- H. Pylori
- Non-Steroidal Anti-Inflammatory
Drugs
- Zollinger-Ellison syndrome
- Stress
- Crohns Disease

Pathology

-H. Pylori is a spiral Gram-negative flagellate -> uses flagella to


burrow into mucus lining of stomach -> produces urease which
converts urea into carbon dioxide and ammonia -> carbon dioxide
reacts with H+ and produces bicarbonate that neutralises gastric
acid
-H. Pylori binds via the BabA adhesin to the Lewis antigen
expressed on the surface of gastric epithelial cells -> causes
gastritis in infected
-Ulcers occur when infecting strain expresses Cytotoxic-associated
protein (CagA) and Vacuolating toxin (VacA) genes
-CagA is a section of genes that codes for the Cag pathogenicity
island -> injects CagA product into epithelial cells -> alterations in
cell morphology, replication and apoptosis
-VacA is a pore-forming protein -> increases host cell permeability,

Antral Gastritis
-Antral Gastritis is normal result of H. Pylori infection ->
inflammatory response to H. Pylori induces G cells in pyloric glands
to secrete gastrin -> gastrin stimulates parietal cells to produce
gastric acid
-Increased acid production is usually asymptomatic

Duodenal Ulcers
Pathology

-Causally associated with H. Pylori:


95% of people with duodenal ulcers are infected with H. Pylori in
the antrum
Eradication via antibiotics heals ulcer and stops recurrence
- Most common in 1st part of the duodenum/superior part of
duodenum/duodenal cap/ampulla
Pathophysiology:
-Increased acid secretion due to: increased gastrin secretion
(result of antral gastritis) -> increased parietal cell mass
-Smoking impairs mucosal healing
-Virulence factors: VacA (pore-forming protein, induces apoptosis,
suppresses local immune mechanisms and CagA (alterations in
cell morphology, cell replication and apoptosis)
-Antral gastritis reduces somatostatin synthesis
-Patients who have blood group O
-Duodenal bicarbonate production by Brunners glands is

Cushing and Curling


ulcers
Cushing ulcer
-Gastric ulcer caused by raised intracranial pressure
-Raised intracranial pressure stimulates vagus nuclei, vagus nerve
releases acetylcholine which increases gastric acid secretion

Curling ulcer
-Acute duodenal ulcer, complication of severe burns
-Reduced plasma volume leads to ischaemia and necrosis of
duodenal mucosa

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