INTRODUCTION

• Acid peptic disease” is a collective term used to include many

conditions such as gastro-esophageal reflux disease (GERD),
gastritis, gastric ulcer, duodenal ulcer, esophageal ulcer.
• The commonest ulcers are the gastric and the duodenal ulcers.
• Symptoms of peptic ulcers include abdominal pain, nausea, heart
burn, regurgitation, vomiting, loss of appetite and weight loss.
• Excessive secretion of acid and pepsin or a weakened stomach
mucosal defense is responsible for damage to the delicate
mucosa and the lining of the stomach, esophagus and duodenum
resulting in ulceration.
CAUSES
• Helicobacter pylori: H.pylori is responsible for around 60%-90% of all
gastric and duodenal ulcers.
• NSAIDs: Prostaglandins protect the mucus lining of the stomach. Non
steroidal anti-inflammatory drugs (NSAIDs) such as aspirin, diclofenac
and naproxen prevent the production of these prostaglandins by
blocking cyclo-oxygenase enzyme leading to ulceration and bleeding. 
• Smoking, alcohol and tobacco: Cigarettes, alcohol and tobacco cause
an instant and intense acid production.
• Blood group O: People with blood group “O” are reported to have
higher risks for the development of stomach ulcers as there is an
increased formation of antibodies against the Helicobacter bacteria,
which causes an inflammatory reaction and ulceration.
• Heredity: Patients suffering from peptic ulcer
diseases usually have a family history of the
disease, particularly the development of duodenal
ulcer which may occur below the age of 20.
• Steroids/Other medicines: Drugs like
corticosteroids, anticoagulants like warfarin
(Coumadin), niacin, some chemotherapy drugs,
and spironolactone can aggravate or cause ulcers.
• Diet: Low fiber diet, caffeinated drinks and fatty
foods are linked to peptic ulcer.
• Other diseases: Chronic liver, lung and kidney diseases
especially tumors of the acid producing cells all predispose to
peptic ulcers.
• Zollinger-Ellison Syndrome (ZES) is a rare pre-cancerous
condition which causes peptic ulcer disease. It is a syndrome
disorder wherein tumors in the pancreas and duodenum also
known as gastrinomas produce a large amount of gastrin which
is a hormone that stimulates gastric acid secretion.
• Endocrine disorders such as hyperparathyroidism are also
implicated in the development of peptic ulcers.
• Stress: Stress and neurological problems can also be associated
with the Cushing ulcer and peptic ulcer.
HELICOBACTER
• Curved gram-negative rod
• Colonizes stomach
• Associated with peptic ulcer disease and gastric
carcinoma.
• H. cinaedi & H. fennelliae are intestinal rather
than gastric organisms and cause diarrheal
disease
Pathogenesis
Colonization of the Gastric Mucosa
- 50% of the world’s population (30% in developed & nearly 80% in
developing countries)
 Colonization favored by :
• ™Acid-resistance:
- Urease enzyme - catalyzes urea hydrolysis to produce ammonia
buffers the gastric acid
- Amidase and arginase - production of ammonia
- Ure-I protein: regulates passage of urea across the cell membrane
into cytoplasm.
Pathogenesis
• ™Motility:
- 4 to 8 unipolar flagella
- Allows to remain in the viscous environment of the mucus
layer
• Adhesins: - Blood group antigen-binding adhesin &
Adherence-associated lipoprotein
• ™Resistance to oxidative stress: detoxifying enzymes.
Pathological Changes
• Vacuolating cytotoxin (VacA): VacA induces formation of
vacuoles in cytoplasm of epithelial cells
• ™Cytotoxin-associated Gene A (CagA): Pathogenicity island –
encodes type IV secretion system – allows bacterium to
modulate certain aspects of host cell’s metabolism including:
- Cytoskeletal rearrangements
- Host-cell morphological changes
- Expression of proto-oncogenes
- Release of proinflammatory cytokines from gastric epithelial
cells.
Pathogenesis
• Molecular mimicry: LPS is identical to Lewis blood group antigen
expressed on gastric parietal cells 
- Immune tolerance by downregulating T cells
- Induction of autoantibodies that cross-react with mucosal epitopes and
contribute to the development of chronic active gastritis.
• Alteration in gastric mucus
• ™Host factors: People with polymorphisms in cytokine genes (e.g.
interleukin 1) or genes coding Toll-like receptors - gastric
adenocarcinoma
• ™Environmental risk factors - „Smoking, Diets high in salt and
preserved foods
Clinical Manifestations
• ™Acute gastritis
- Antral gastritis (MC) - predisposes to duodenal ulcers
- Pangastritis: predisposes to adenocarcinoma
• Peptic ulcer disease: 80% duodenal and 60% of gastric ulcers due
to H. pylori
• Chronic atrophic gastritis
• ™Autoimmune gastritis
• ™Pernicious anemia
• ™Adenocarcinoma of stomach
• ™Non-Hodgkin’s gastric lymphoma
Protective Role for H. pylori
• Colonization of H. pylori has an inverse relation with the
occurrence of:
• ™Gastroesophageal reflux disease (GERD)
• ™Barrett’s esophagus
• ™Adenocarcinoma of esophagus
• ™Allergic disorders including asthma
 Laboratory Diagnosis
Invasive Tests
• Endoscopy-guided
multiple biopsies (antrum
and corpus)
• Histopathology with
Warthin Starry silver
staining - immunostaining
to improve sensitivity
Laboratory Diagnosis
• Microbiological methods
- „Gram-staining: Curved gram-negative bacilli with seagull-
shaped morphology
- Culture media
• Skirrow’s media
•  Chocolate agar
• Incubated at 37°C under microaerophilic condition (5% O2,
10% CO2 & 85% nitrogen)
Laboratory Diagnosis
• Biochemical tests:
- Oxidase, catalase and urease tests - positive
- Biopsy urease test (also called rapid urease test): rapid,
sensitive and cheap.
Laboratory Diagnosis…Noninvasive Tests
• ™Urea breath test:
- Most consistent and accurate test
- Most sensitive, quick and simple
- Used to monitor treatment response
• Stool antigen (coproantigen) assay
- Used to monitor treatment response
- Useful for screening of children.
• ™Antibody (IgG) detection by ELISA:
- Screening before endoscopy, Seroepidemiological study.
Treatment
• Treatment is not recommended for asymptomatic colonizers
or primary prophylaxis for gastric cancer
• Indications- duodenal or gastric ulceration, low-grade gastric
B-cell lymphoma
• Multidrug regimens are used
Treatment regimen for H. pylori infections:
• 1st line triple drug therapy (OCM or OCA regimen):
Omeprazole + Clarithromycin + Metronidazole
or Amoxicillin given for 7–14 days.
↓
Urea breath test is done after 1 month’s gap
↓
If 1st line regimen fails (Urea breath test is +ve)
↓
Treatment regimen for H. pylori infections:
2nd line quadruple drug therapy (OBMT regimen):
Omeprazole + Bismuth subsalicylate + Metronidazole +
Tetracycline given for 14 days
↓
If 2nd line quadruple drug therapy fails, then:
Culture of endoscopy-guided biopsy is done and treatment is
given based on antimicrobial susceptibility test
Monitoring Patients during Treatment
• Perform urea breath test after completion of treatment
regimen.
• If tests positive, repeat the treatment course with the same
quadruple regimen
• If urea breath test still remains positive, treatment is instituted
based on culture of endoscopy guided biopsy, followed by
antimicrobial susceptibility report.
THANK YOU..!