This organism, formerly known as Campylobacter pylori, is now known as Helicobacter pylori, a curved bacterium that colonizes the gastric mucosa. H. pylori has been found in 90% of patients with chronic gastritis, 95% with duodenal ulcer disease, and 70% with gastric ulcer. Chronic gastritis is defined as the presence of chronic inflammatory changes in the mucosa leading to mucosal atrophy and epithelial metaplasia. The two main causes of chronic gastritis are infection by H. pylori and autoimmune gastritis. Left untreated, chronic gastritis increases the risk of peptic ulcer disease and gastric adenocarc

1. This organism, formerly
known as Campylobacter
pylori , is a curved
spirochete-like bacterium, of
which two major genotypes
exist.This organism colonizes
the gastric mucosa
(particularly the antrum and
cardia) in a variety of ways:
free in mucus, surface
adhesion, and intercellularly.
Chronic Gastritis f
H. pylori has been found in 90% of patients with chronic gastritis, 95% with
duodenal ulcer disease, 70% with gastric ulcer, and 50% with gastric carcinoma.
Lecture 7

2. Stomach
Anatomical Regions: Cardia, Fundus, Body, Pyloric antrum, Pylorus.
Lesser curvature, Greater curvature.
Histological Layers: Serosa, Muscularis m, Submucosa , Mucosa.
Microscopic types of Gastric Mucosa: Cardiac, Fundic, Pyloric (antral).
Glands of Stomach: Cardiac, Fundic, Pyloric.
Cells of Fundic Epithelium: Mucous neck cells, Parietal cells, Chief cells,
Enteroendocrine cells, Stem cells.
Gastric gland are comprised of two major components: foveola (crypt,
pit) and secretory portion (adenomere).

4. Definition
Chronic gastritis is defined as the
presence of
chronic inflammatory changes in the
mucosa leading eventually to
mucosal atrophy
&
epithelial metaplasia.
The two main features of this disease are infiltration of the lamina propria
by inflammatory
cells and atrophy of the glandular epithelium.

5. Etiology/types/classification
B
Body-predominant
Less than 10%
Antral-predominant
90%
Nonimmune gastritis

6. Less common etiologies
• RADIATION INJURY,
• CHRONIC BILE REFLUX,
• MECHANICAL INJURY, AND
• SYSTEMIC DISEASE
such as Crohn disease, amyloidosis, or graft-versushost disease.

7. Nonimmune Gastritis

8. Body Predominant
Autoimmune gastritis is characterized by:
• Antibodies to parietal cells (Oxyntic Cells) and
intrinsic factor
• Reduced serum pepsinogen I concentration
• Antral endocrine cell hyperplAsiA
• Vitamin B12 deficiency
• Defective gastric acid secretion
(achlorhydria )

9. Pathogenesis
Autoimmune gastritis is associated with
loss of parietal cells,
which are responsible for secretion of gastric acid
(HCl) and intrinsic factor.
The absence of acid production stimulates gastrin
release, resulting in hypergastrinemia and
hyperplAsiA of antral gastrin-producing
G cells.

10. • Lack of intrinsic factor disables ileal vitamin B12
absorption, leading to B12 deficiency and a slowonset megaloblastic anemia
pernicious
anemia ).
(
• The reduced serum pepsinogen I concentration
results from chief
destruction.
cell (Zymogenic cells or Peptic cells)

11. clinical features
• Chronic gastritis usually causes few or no
symptoms;
1.Upper abdominal discomfort
2.Nausea
3.Vomiting
4.symptoms of anemia
5.atrophic glossitis,
6. diarrhea.
7.peripheral neuropathy (B12 deficiency).

12. The median age at diagnosis
is 60 years. Slightly more
women than men are
affected.

13. Antral-predominant
>90%
Pan-gastritis

14. Epidemiology
associated with :
Poverty,
Household crowding,
Llimited education,
African-American or MexicanAmerican ethnicity,
Residence in rural areas .

15. the mode of h. pylori
transmission
is not well defined, but humans are the only
known host, making
Oral-oral,
Fecal-oral, and
Environmental spread
most likely routes of infection.
the

16. pathogenesis
• The most import cause is infection by
H. pylori.
Gastritis develops as a result of the combined
influence of
• bacterial enzymes (Urease,Protease,Phospholipase)and
• toxins (cagA, VacA) and release of
• noxious chemicals by the recruited
neutrophils.
Alcohol, tobacco, duodenal reflux (reflux gastritis),
allergy to foods, and various drugs (particularly antiinflammatory agents).

17. • After initial exposure to H.pylori, gastritis may
develop in
two patterns:
• 1. antral- type
with high acid production and
higher risk for the development of duodenal
(Hypersecretory)
ULCER,
and
• 2. pangastritis
(Environmental
with multifocal mucosal atrophy, with low
acid secretion and increased risk for
Gastritis)

18. Four features are linked to H. pylori
virulence:
1. flagella , which allow the bacteria to be
motile in viscous mucus
2.urease , which generates ammonia from
endogenous urea and thereby elevates local
gastric pH
3.adhesins that enhance their bacterial
adherence to surface foveolar cells
4. toxins , such as cytotoxin-associated gene A
(CagA), that may be involved in ulcer or cancer
development by poorly defined mechanisms

19. • Chronic Inflammatory cell infiltration
• Mucosal Atrophy
• Intestinal
metaplasia
Neutrophils, plasma cells
( Autoimmune Gastritis)
(Goblet Cell)
Seen in H Pylori & Autoimmune gastritis not chemical.
Intestinal metaplasia: Type I (complete), Type II (Incomplete)
Pyloric Metaplasia
Intestinal Metaplasia

22. Type B
Ant
Ant
Pan
Pan
Type A

23. Clinical Features /Diagnosis
Histologic identification of the organism,
Serologic test for antibodies to H. pylori,
Fecal bacterial detection,
The urea breath test based on the generation of ammonia by the bacterial urease.

24. • Gastric biopsy specimens can also be
analyzed by
• the rapid
UREASE test,
• bacterial culture, or
• bacterial DNA detection by PCR.

25. TreaTmenT
• Combinations of antibiotics and proton pump
inhibitors. Clarithromycin, Amoxicillin/ Flagyl, Omeprazole
• Individuals with H. pylori gastritis usually improve
after treatment, although RELAPSES
can occur after incomplete eradication or reinfection.
• Prophylactic and therapeutic vaccine
development is still at an early stage of
development.

27. Chronic superficial gastritis
• If the inflammatory infiltrate is limited to the
foveolar region and unaccompanied by glandular
atrophy, the condition is designated as chronic
superficial gastritis.
• Subtle epithelial abnormalities seen in this form
include a reduced amount of cytoplasmic mucin,
nuclear and nucleolar enlargement, and some
increase in foveolar mitoses.

28. UNCOMMON FORMS OF GASTRITIS
Reactive Gastropathy
Eosinophilic
gastritis
Lymphocytic
gastritis

29. Chronic atrophic gastritis
• When the inflammation is more extensive and
accompanied by glandular atrophy, the condition
is termed Chronic atrophic gastritis
and is further categorized as mild,
moderate,
or severe by roughly estimating the thickness of
the glandular portion in relation to the thickness of
the whole mucosa.

30. Consequences of Chronic Gastritis
• PEPTIC ULCER DISEASE
• Adenocarcinomas

31. CanCer risk
• The long-term risk of gastriC CarCinoma
for persons with H. pylori-associated chronic
five
gastritis is increased about
fold
relative to the normal population.
• For autoimmune gastritis, the risk for cancer is in
the range of 2% to 4% of affected individuals,
which is well above that of the normal population.

33. Other types of Gastritis
•
•
•
•
•
•
•
•
•
Nonspecific Gastritis
Acute infectious nonbacterial gastroenteritis
Hemorrhagic gastritis
Collagenous gastritis
Lymphocytic gastritis
Allergic gastroenteritis
Diffuse eosinophilic gastroenteritis
Granulomatous gastritis
Syphillis,, CMV, Cryptococcosis, Bacillary
angiomatosis, Graft-versus-host disease