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Although H. pylori does not invade the tissues, it induces an intense inflammatory and immune response. There is increased production of proinflammatory cytokines such as interleukin (IL)-1, IL-6, tumor necrosis factor, and, most notably, IL-8. IL-8 is produced by the mucosal epithelial cells, and it recruits and activates neutrophils.Several bacterial gene products are involved in causing epithelial cell injury and induction of inflammation. Epithelial injury is mostly caused by a vacuolating toxin called VacA, which is regulated by the cytotoxin-associated gene A (CagA). This gene is a component of the Cag pathogenicity island, a cluster of 29 genes, some of which encode pro-inflammatory proteins. In addition, H. pylori secretes a urease that breaks down urea to form toxic compounds such as ammonium chloride and monochloramine. The organisms also elaborate phospholipases that damage surface epithelial cells. Bacterial proteases and phospholipases break down the glycoprotein-lipid complexes in the gastric mucus, thus weakening the first line of mucosal defense.H. pylori enhances gastric acid secretion and impairs duodenal bicarbonate production, thus reducing luminal pH in the duodenum. This altered milieu seems to favor gastric metaplasia (the presence of gastric epithelium) in the first part of the duodenum. Such metaplastic foci provide areas for H. pylori colonization.Several H. pylori proteins are immunogenic, and they evoke a robust immune response in the mucosa. Both activated T cells and B cells can be seen in chronic gastritis caused by H. pylori. The B lymphocytes aggregate to form follicles. The role of T and B cells in causing epithelial injury is not established, but T-cell-driven activation of B cells may be involved in the pathogenesis of gastric lymphomas
Suppression of mucosal prostaglandin synthesis, which increases secretion of hydrochloric acid and reduces bicarbonate and mucin production
Dyspepsia- Peptic Ulcer Diseases
defined as having one or more symptoms of
epigastric pain, burning, postprandial fullness, or
Loss of appetite
typically located near the angularis incisura on the lesser
curvature, close to the border between the antrum and the
body of the stomach. Patients with type I gastric ulcers
usually have normal or decreased gastric acid secretion.
a combination of stomach and duodenal ulcers and are
associated with normal or increased gastric acid secretion.
prepyloric and are associated with normal or increased
gastric acid secretion.
occur near the gastroesophageal junction, and gastric acid
secretion is normal or below normal.
Types of Gastric Ulcer
70% of gastric ulcer patients are infected with H. pylori.
Majority of colonised people remain healthy and
uses adhesin molecules (BabA) to bind to Lewis b antigen on
induces an intense inflammatory and immune response
IL-1, IL-6, tumor necrosis factor, IL-8
Production of ammonia by the enzyme urease
Toxic to epithelial cell
Increase gastrin release from G cells
Negative feedback loop for gastrin release is halted
stimulates increased acid production by parietal cells.
Direct chemical irritation & COX enzyme inhibition,
which prevent prostaglandin synthesis
increases secretion of hydrochloric acid and reduces
bicarbonate and mucin production
Damage gastric and duodenal mucosal barrier
increased risk of upper gastric ulcer, bleeding
Increased risk of gastric ulcer and duodenal ulcer to a
more likely to causing complication and less likely to
heal if the patient continues to smoke.
recurrent abdominal pain
localisation to the epigastrium
Relation to food
Anorexia & nausea
presented with anaemia for the first time
Recurrent acute bleeding without ulcer pain
Gnawing or burning sensation
occurs shortly after meals with gastric ulcer and 2-3 hours afterward
with duodenal ulcer.
Diagnostic value of individual symptoms for PUD is poor.
Upper GI endoscopy
Rapid urease tests
Fecal antigen testing
detecting the presence of H pylori antigens in stools
Urea breath test
testing for the enzymatic activity of bacterial urease.
detect free abdominal air when perforation is suspected.
upper GI contrast study
extravasation of contrast indicates gastric perforation
H. pylori eradication
proton pump inhibitor (PPI)–based triple therapy.
PPI, amoxicillin, and clarithromycin for 7-14 days.
Amoxicillin should be replaced with metronidazole in penicillin-
allergic patients only high rate of metronidazole resistance
American College of Gastroenterology (ACG ) guideline: test
for H pylori done in patients who started long-term NSAID
NSAIDs should be immediately discontinued in patients with
positive H pylori test results if clinically feasible
Patient with known history of ulcer and in whom NSAID use is
unavoidable, the lowest possible dose and duration of the
NSAID and co-therapy with a PPI or misoprostol are
Choice for a chronic non-healing gastric ulcer
partial gastrectomy to exclude an underlying cancer.
Duodenal ulcer and gastric ulcer both belong to the
family of peptic ulcer disease.
H. pylori infection is the major cause of duodenal
ulcer followed by NSAID
They share almost the same clinical features.
Symptoms do not
follow a consistent
than relieves pain
Gastric Ulcer vs Duodenal Ulcer
Tend to cause more
Pain can awaken the
patient at night.
Pain is relieved by
food, but recurs 2 to
3 hours after a meal
•Diagnosis by visible
•Sudden severe pain then
•Irritation of diaphragm
leading to shoulder tip
•Absent bowel sound
Harmon RC, Peura DA. Evaluation and Management of
Dyspepsia [Internet]. Medscape. [cited 2015 May 24]. Available
Robbins basic Pathology. 9th Ed.
BS Anand. Peptic Ulcer Disease Treatment & Management
[Internet]. [cited 2015 May 24]. Available from:
Davidson’s Principle & Practice of Medicine. 22nd Ed.