This document provides tips and instructions for using a PowerPoint presentation on Helicobacter pylori. Some key points: - Blank slides are included to allow adding notes and engaging students by asking questions. The presentation is meant to be an active learning session conducted over multiple revisions. - Topics covered include the microbiology of H. pylori, its role in diseases like peptic ulcers and gastric cancer, pathogenesis, clinical diagnosis using invasive and noninvasive tests, and treatment using antibiotic-based triple therapy. - Futuristic areas discussed are preventive vaccination, the potential role of probiotics and gut microbiome, and research exploring both harmful and protective effects of H. pylori colonization

1. Tips on using my ppt.
1. You can freely download, edit, modify and put your
name etc.
2. Don’t be concerned about number of slides. Half the
slides are blanks except for the title.
3. First show the blank slides (eg. Aetiology ) > Ask
students what they already know about ethology of
today's topic. > Then show next slide which enumerates
aetiologies.
4. At the end rerun the show – show blank> ask questions >
show next slide.
5. This will be an ACTIVE LEARNING SESSION x
three revisions.
6. Good for self study also.
7. See notes for bibliography.

2. Aetiology
• Idiopathic
• Congenital/ Genetic
• Nutritional Deficiency/excess
• Traumatic
• Infections /Infestation
• Autoimmune
• Neoplastic (Benign/Malignant)
• Degenerative/ lifestyle
• Iatrogenic
• Psychosomatic
• Poisoing/ Toxins/ Dtug induced

3. Aetiology
• Idiopathic
• Congenital/ Genetic
• Nutritional Deficiency/excess
• Traumatic
• Infections /Infestation
• Autoimmune
• Neoplastic (Benign/Malignant)
• Degenerative/ lifestyle
• Iatrogenic
• Psychosomatic
• Poisoing/ Toxins/ Dtug induced

4. Introduction & History.

5. Introduction & History.
• Peptic ulcer disease is thought to be a lifestyle
disease caused by “hurry, worry and curry.
• It has been known for more than a century that
bacteria are present in the human stomach.
• These bacteria, however, were thought to be
contaminants from digested food rather than true
gastric colonizers.
• Persistence of a pathogen in an environment long
thought to be sterile is not likely.

6. Introduction & History.
• Robin Warren and Barry Marshall thought
and later proved that H. pylori is
pathogenic.
• This discovery resulted in the awarding of
the 2005 Nobel Prize in Physiology or
Medicine to Robin Warren and Barry
Marshall for their “discovery of the
bacterium Helicobacter pylori and its role
in gastritis and peptic ulcer disease.”

7. Relevant Microbiology
•

8. Relevant Microbiology
• H. pylori is a gram-negative bacterium,
measuring 2 to 4 μm in length and 0.5 to 1
μm in width.
• spiral-shaped,
• It has 2 to 6 unipolar, sheathed flagella
• Microaerophilic.
• It has 2 to 6 unipolar, sheathed flagella
• Urease positive. Those organisms that are
capable of hydrolyzing urea to produce
ammonia and carbon dioxide.

9. Relevant Microbiology
• Urease is thought to allow short-term
survival in the highly acidic gastric lumen,
whereas motility is thought to allow rapid
movement toward the more neutral pH of
the gastric mucosa; this may explain why
both factors are prerequisites for
colonization of the gastric mucosa.

10. Pathophysiology

11. Pathophysiology
Helicobacter pylori causes
1. Transient Acute Gastrits.
2. Chronic active gastritis,
3. Peptic ulcer disease,
4. Distal gastric adenocarcinomas
• Gastric lymphomas Gastric MALT
lymphoma form of lymphoma involving
the mucosa-associated lymphoid tissue
(MALT)

12. Pathology

13. Pathology
• Colonization with H. pylori virtually always leads
to infiltration of the gastric mucosa in both antrum
and corpus with neutrophilic and mononuclear
cells
• This Chronic Active Gastritis is the primary
condition related to H. pylori colonization, and
other H. pylori-associated disorders in particular
result from this chronic inflammatory process.

14. Pathology
• Atrophic gastritis, intestinal metaplasia, and
gastric cancer.
• Chronic H. pylori-induced inflammation can
eventually lead to loss of the normal gastric
mucosal architecture, with destruction of gastric
glands and replacement by fibrosis and intestinal-
type epithelium.
• This process of atrophic gastritis and intestinal
metaplasia occurs in approximately half of the H.
pylori-colonized population,
• they increase the risk for gastric cancer by 5- to
90-fold depending on the extent and severity of
atrophy

15. Peptic ulcer disease
• Gastric or duodenal ulcers (commonly
referred to as peptic ulcers) are defined as
mucosal defects with a diameter of at least
0.5 cm penetrating through the muscularis
mucosa
• Gastric ulcers mostly occur along the lesser
curvature of the stomach, in particular, at
the transition from corpus to antrum mucosa
• Duodenal ulcers usually occur in the
duodenal bulb, which is the area most
exposed to gastric acid.

16. Peptic ulcer disease
• Duodenal ulcers are approximately fourfold
more common than gastric ulcers;
Duodenal ulcers in particular occur between
20 and 50 years of age, while gastric ulcers
predominantly arise in subjects over 40
years old.

17. Association with H. pylori.
• Both gastric and duodenal ulcer diseases are
strongly related to H. pylori.
• Approximately 95% of duodenal ulcers and
85% of gastric ulcers occurred in the
presence of H. Pylori infection
• Eradication of this bacterium strongly
reduced the risk of recurrent ulcer disease
• This has had a major impact on the
treatment and course of peptic ulcer disease
in daily clinical practice.

18. Association with H. pylori.
• In earlier days, this disease was a chronic,
recurrent disorder with high morbidity,
frequently requiring acid-suppressive
maintenance therapy or surgery.
• Approximately 50% of patients with H.
pylori-associated peptic ulcer disease
suffered ulcer recurrence within 1 year
• Eradication of H. pylori dramatically
changes the natural course of ulcer disease
and almost completely prevents ulcer
recurrence.

19. Demography

20. Demography
• H. pylori infection rates rise rapidly in the
first 5 years of life and remain constantly
high thereafter, indicating that H. pylori is
acquired early in childhood.
• Infection more commonly occurs in
childhood and lasts for life unless
specifically treated.

21. Transmission and Sources of Infection
• The exact mechanisms whereby H. Pylori is
acquired are largely unknown.
• It is found almost exclusively in humans
and some nonhuman primates.
• Rare occasions been isolated from pet
animals;
• Direct human-to-human transmission, via
either an oral-oral or fecal-oral route or
both.
• ?Contaminated food,

22. CLINICAL ASPECTS OF H. PYLORI-
ASSOCIATED DISEASES
• Colonization with H. pylori is not a disease
in itself but a condition that affects the
relative risk of developing various clinical
disorders of the upper gastrointestinal tract
and possibly the hepatobiliary tract.
• Testing for H. pylori therefore has no
relevance by itself but should be performed
to find the cause of an underlying condition,
such as peptic ulcer disease, or for the
purpose of disease prevention, such as in
subjects with familial gastric cancer

23. Prognosis

24. Prognosis
• Although gastric colonization with H.
pylori induces histologic gastritis in all
infected individuals, only a minority
develop any apparent clinical signs of this
colonization.
• H. pylori-positive patients have a 10 to
20% lifetime risk of developing ulcer
disease
• 1 to 2% risk of developing distal gastric
cancer.

25. Investigations

26. Investigations
• Laboratory Studies
– Routine
– Special
• Imaging Studies
• Tissue diagnosis
– Cytology
• FNAC
– Histology
– Germline Testing and Molecular Analysis
• Diagnostic Laparotomy.

27. Investigations
• The available tests are generally divided
into
1. Invasive tests and
2. Noninvasive tests

28. Invasive tests
• Based on gastric specimens for
1. Histology
2. Culture
3. Other methods

29. Noninvasive tests
• Based on peripheral samples, such as
1. Blood
2. Breath samples
3. Stools
4. Urine
5. Saliva

30. Noninvasive tests
• Detection of –
1. Antibodies
2. Bacterial antigens
3. Urease activity.

31. Investigations
• Endoscopic or invasive
1. Rapid urease test
2. Histopathology
3. Culture.
• Rapid urease tests are considered the
endoscopic diagnostic test of choice.

32. Investigations
• Urea breath tests detect active H
pylori infection by testing for the enzymatic
activity of bacterial urease. In the presence
of urease produced by H pylori, labeled
carbon dioxide (heavy isotope, carbon-13,
or radioactive isotope, carbon-14) is
produced in the stomach, absorbed into the
bloodstream, diffused into the lungs, and
exhaled.

33. Investigations
• Obtain histopathology, often considered the
criterion standard to establish a diagnosis
of H pylori infection, if the rapid urease test
result is negative and a high suspicion for H
pylori persists (presence of a duodenal
ulcer).

34. Investigations
• Antibodies (immunoglobulin G [IgG]) to H
pylori can be measured in serum, plasma, or
whole blood.

35. Treatment

36. Treatment
• Proton pump inhibitor (ppi)–based triple
and 4drug therapy.
• Two antibiotics with a ppi.
• Tetracycline
• Amoxicillin
• Imidazoles (predominantly metronidazole
and tinidazole)
• Few selected macrolides (in particular
clarithromycin, sometimes azithromycin)
• Bismuth

37. Futuristic

38. Futuristic
• Preventive vaccination
• Enteric helminth infection can modulate the
host's immune system to attenuate H.
Pylori-induced gastric ulceration, atrophy,
and cancer
• Probiotics prevent infection with pathogenic
bacteria both through activation of the host's
immune system and through direct
competition of the probiotic bacteria with
the pathogen.

39. Futuristic
• Nowadays, even barry marshall sees the
germ’ two faces – the dangerous and the
helpful.
• Skin allergies or hay fever
• The bacteria also seem to provide a certain
protection against coeliac conditions, also
known as wheat gluten intolerance.
• Connection between its eradication and the
growing obesity problem worldwide.

40. Get this ppt in mobile
1. Download Microsoft
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3. Open Google lens.
4. Scan qr code from
next slide.

42. Get this ppt in mobile
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3. Open Google lens.
4. Scan qr code from
next slide.

43. Get this ppt in mobile

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