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.
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).
Chronic gastritis is defined as the
chronic inflammatory changes in the
mucosa leading eventually to
The two main features of this disease are infiltration of the lamina propria
cells and atrophy of the glandular epithelium.
Less than 10%
Less common etiologies
• RADIATION INJURY,
• CHRONIC BILE REFLUX,
• MECHANICAL INJURY, AND
• SYSTEMIC DISEASE
such as Crohn disease, amyloidosis, or graft-versushost disease.
Autoimmune gastritis is characterized by:
• Antibodies to parietal cells (Oxyntic Cells) and
• Reduced serum pepsinogen I concentration
• Antral endocrine cell hyperplAsiA
• Vitamin B12 deficiency
• Defective gastric acid secretion
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
• Lack of intrinsic factor disables ileal vitamin B12
absorption, leading to B12 deficiency and a slowonset megaloblastic anemia
• The reduced serum pepsinogen I concentration
results from chief
cell (Zymogenic cells or Peptic cells)
• Chronic gastritis usually causes few or no
1.Upper abdominal discomfort
4.symptoms of anemia
7.peripheral neuropathy (B12 deficiency).
The median age at diagnosis
is 60 years. Slightly more
women than men are
associated with :
African-American or MexicanAmerican ethnicity,
Residence in rural areas .
the mode of h. pylori
is not well defined, but humans are the only
known host, making
most likely routes of infection.
• The most import cause is infection by
Gastritis develops as a result of the combined
• bacterial enzymes (Urease,Protease,Phospholipase)and
• toxins (cagA, VacA) and release of
• noxious chemicals by the recruited
Alcohol, tobacco, duodenal reflux (reflux gastritis),
allergy to foods, and various drugs (particularly antiinflammatory agents).
• After initial exposure to H.pylori, gastritis may
• 1. antral- type
with high acid production and
higher risk for the development of duodenal
• 2. pangastritis
with multifocal mucosal atrophy, with low
acid secretion and increased risk for
Four features are linked to H. pylori
1. flagella , which allow the bacteria to be
motile in viscous mucus
2.urease , which generates ammonia from
endogenous urea and thereby elevates local
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
• Chronic Inflammatory cell infiltration
• Mucosal Atrophy
Neutrophils, plasma cells
( Autoimmune Gastritis)
Seen in H Pylori & Autoimmune gastritis not chemical.
Intestinal metaplasia: Type I (complete), Type II (Incomplete)
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.
• Gastric biopsy specimens can also be
• the rapid
• bacterial culture, or
• bacterial DNA detection by PCR.
• 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
Chronic superficial gastritis
• If the inflammatory infiltrate is limited to the
foveolar region and unaccompanied by glandular
atrophy, the condition is designated as chronic
• Subtle epithelial abnormalities seen in this form
include a reduced amount of cytoplasmic mucin,
nuclear and nucleolar enlargement, and some
increase in foveolar mitoses.
UNCOMMON FORMS OF GASTRITIS
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,
or severe by roughly estimating the thickness of
the glandular portion in relation to the thickness of
the whole mucosa.
• The long-term risk of gastriC CarCinoma
for persons with H. pylori-associated chronic
gastritis is increased about
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.