H. Pylori MCQs given on the right side of the article

By Dr Sijil Sivaraman MD DM Gastroenterologist Email for Questions: gastrospecialist@gatetomedicine.com




  • Conventional thinking before 1982/1983 was that no pathogen can live in stomach due to the acidic nature. Dr Barry J. Marshall and Dr J. Robin Warren of western Australia discovered Helicobacter pylori during their research about gastric ulcer and later awarded Nobel prize.


  • H pylori has some unique features suited to live in the acidic stomach. It is gram-negative spiral bacillus with multiple unipolar flagella and fastidious in terms of growth requirements with strictly micro-aerophilic requiring C02 for growth. It most commonly colonise in the gastric antrum and present in the mucus that overlies the mucosa  and move freely in gastric mucous layer. It produce large amount of urease which hydrolyze urea to alkaline ammonia and co2


  • It is the most common  chronic bacterial infection worldwide with more than 50 % of world population been infected. In developing countries it is more common and acquired during childhood and with life cycle of Spontaneous elimination and subsequent reinfection.

Risk factors of acquiring H pylori:

The important risk factors for acquiring H pylori are low socioeconomic status, housing density, crowded conditions  which leads to contaminated water. Major Reservoir of H pylori  is man and there is person to person transmission.

Where it colonise :

H. Pylori colonise in Gastric epithelium, gastric metaplasia of esophagus and duodenum and meckel’s diverticulum.

The natural history of chronic H. pylori infection includes  (1) superficial gastritis, (2) duodenal ulcer phenotype, and (3) gastric ulcer/gastric cancer phenotype

The pattern of colonization  is an important determinant of  H. pylori disease manifestations. Antral colonization leads to hyperacidity leads to duodenal ulcer. Gastric ulcers and gastric adenocarcinoma occur more often with is proximal colonization of the stomach.

Gastric adenocarcinoma remains the second major cause of cancer death in the world. The burden of risk of gastric cancer is considered largely attributable to H. pylori infection, with cag PAI–bearing strains having a higher association with gastric cancer .

The increased risk of development of gastric carcinoma depends on factors including the strain of bacteria, host genetic factors, the duration of infection, and the presence or absence of other environmental risk factors.

Infection by H. pylori is present in 90% of cases of gastric MALT lymphoma.


H. pylori has been strongly associated with  Peptic ulcer disease, Gastric carcinoma and MALT lymphoma.

Other well established Associations are coronary artery disease, Immune thrombocytopenia purpura and Iron deficiency anemia


Serology (qualitative immunoglobulin G [IgG]) Widely available and inexpensive
Urea breath test (13C or 14C) Identifies active infection, useful both before and after treatment
Stool antigen test Identifies active infection, useful both before and after treatment


Histology Excellent specificity and provides additional information about gastric mucosa
Rapid urease test Rapid results, it is accurate in patients not using PPIs or antibiotics
Culture It has high specificity and allows antibiotic sensitivity testing

Rapid Urease test

  • It is performed during endoscopy , with antral biopsy specimen placed into a medium containing urea and an indicator
  • The urease produced by the active H pylori hydrolyzes urea to ammonia, which raises the pH of the medium and changes the color of the specimen from yellow (NEGATIVE) to red (POSITIVE)

Helicobacter pylori Treatment:

Initial treatment for H. pylori, a 10- to 14-day course of standard PPI triple therapy. and appropriate alternative is  10-day sequential regimen. If infection persists after this, bacteria are likely resistant to clarithromycin so retreatment should be with one of the PPI triple regimens noted earlier that incorporates a different combination of medications or a bismuth-based therapy for 14 days.

Triple therapy :

PPI, clarithromycin, amoxicillin

PPI, clarithromycin, metronidazole

PPI, amoxicillin, levofloxacin

PPI, amoxicillin, rifabutin

Quadruple therapy:

PPI, bismuth subsalicylate/subcitrate, metronidazole, tetracycline

Sequential therapy:

PPI, amoxicillin followed by PPI, clarithromycin and Tinidazole

This regimen appears highly effective despite clarithromycin resistance

Dr Sijil Sivaraman MBBS, MD (Gen Medicine), DM (Gastroenterology) medical@gatetomedicine.com

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Q1) Who discovered H Pylori and was later awarded Nobel prize?

A) Dr Barry J. Marshall and Dr J. Robin Warren
B) Dr.Watson J.Marshall and Dr.Weber Jobs
C) Dr.Michael Cook and Dr.Watson J.Marshall
D) Dr.Edvard I. Moser and John O’Keefe

Answer - Click Here

Q2) H pylori colonises in all of the following tissues, except?

A) Gastric epithelium
B) Gastric metaplasia of esophagus and duodenum
C) Meckel’s diverticulum
D) Zenker diverticulum

Answer - Click Here

Q3) The burden of risk of gastric cancer is considered largely attributable to H pylori infection with strain?

A) PAI–bearing strains
B) PCI–bearing strains
C) API–bearing strains
D) BPI–bearing strains

Answer - Click Here

Q4) H pylori has been strongly associated with all of the following, except?

A) Peptic ulcer disease
B) Gastric carcinoma
C) MALT lymphoma
D) Burkitt lymphoma

Answer - Click Here

Q5) All of the following are used for the Triple therapy of H. pylori infection, except?

B) Rifabutin
C) Levofloxacin
D) Doxycycline

Answer - Click Here

Any questions for Dr Sijil email gastrospecialist@gatetomedicine.com

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