Pathological aspects of esophagus
and stomach-III (Chronic Gastritis)
Dr.Ashraf A.Fatah Deyab
Assistant Professor of Pathology
Pathological aspects of esophagus and
stomach-III (Objectives)
 I. Discuss Chronic Gastritis
 II. Enlist the common causative
agents in various age groups
 III. Explain the pathogenesis and
pathology of Chronic Gastritis
 IV. Enlist clinical features

Suggested reading: Robbin’s Basic Pathology, 8th
Ed. Page-588-589 & 591-597
I. Discuss Chronic Gastritis- Definition

Frequent disorders of the stomach in all
taken biopsies.

The term gastritis is used to denote
inflammation associated with mucosal injury.

Gastritis is mostly a histological term that
needs biopsy to be confirmed.

Gastritis is usually due to infectious agents
(such as Helicobacter pylori) and
autoimmune and hypersensitivity reactions.
Anatomical site
II. Common causative agents of Chronic Gastritis

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Infectious agents (Bacterial “bacillus
Helicobacter pylori=90%”, parasitic, fungal,
viral “CMV” infection).
Autoimmune diseases. atrophic gastritis(10%)
Hypersensitivity reactions.- rare
Direct injurious agent (chemical or drugs,
chemotherapy, radiation, alcohol etc..)
chronic irritants (tobacco, caffeine) & secondary to
other systemic diseases, malignancy& stresses.

Others Less common etiologies (elderly, chronic
bile reflux, mechanical injury- uremia, GVHD ).
Chronic Gastritis- types

1- H.pylori gastritis= 90%
 2.
Autoimmune gastritis= 10%
 3.
Eosinophilic gastritis
 4.
Lymphocytic gastritis.
 5.
Granulomatous Gastritis

Reactive gastropathy.
Chronic gastritis

Two major types:
1.
Autoimmune gastritis (in association
with pernicious anemia)
 Type A gastritis
 Also k/a fundic type
2.
Chronic active (H.pylori) gastritis
 Type B gastritis
 Also k/a antral type
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

HELICOBACTER PYLORI GASTRITIS
Most common cause of gastritis – H.pylori.
Spiral-shaped or curved bacilli gram negativefacilitate its passage through the mucus layer
of H. pylori has revolutionized
understanding of chronic gastritis (90% of causes).
 50% worldwide affected, most common bacterial
infection in human. It was believed lifestyle factors,
such as stress and diet types (spicy, acidic, fatty meals).
 H. pylori infection = found to be a\w increased
risk of gastric cancer.
 discovery
H.pylori gastritis Epidemiology
High prevalence (USA)
is a\w
 Poverty.
 Household crowding.
 Limited education.
 residence in rural
areas.

Age group:
In high-prevalence area
- Infection Acquired in
childhood and then
persists for decades.
Transmission:
-
-
not well defined.
humans are the only known
host
Oral-oral, fecal-oral, and
environmental spread .
III. H. PYLORI GASTRITIS- Pathogenesis
Started as Localized antral gastritis with ability
to spread to form Pangastritis (cardia, body, fundus)
 H.pylori: features are linked to virulence:
1) Flagella& 2) Adhesion: enhance motility &
invasion of mucosa (foveolar cells surface).
3) Urease: generate acid from endogenous ammonia

from urea& there elevates local gastric PH.
4) Toxins: such as cytotoxin-associated gene A (Cag A)-in
50% of bacteria , that may also be involved in ulcer or cancer
H.Pylori infection>> Increased acid production>
overcome gastro-duodenal defense protective mechanism
III. H. PYLORI GASTRITIS- Pathogenesis

Helicobacter pylori can cause damage by
(1) Secreting urease, protease, and
phospholipases.
 (2) Attracting neutrophils that release
myeloperoxidase.
 (3) Promoting thrombotic occlusion of
capillaries, leading to ischemic damage of
the epithelium

III. H.pylori gastritis- morphology

Predominantly antral gastritis with increase risk
of DU is increased in antral gastritis.

Pangastritis: then gastritis progresses to involve
the gastric body, fundus& cardia. (mechanism
may be due??): Host gene encode certin cytokines or
influenced by Genetic variation among H. pylori strains

Pangastritis: a\w

1) Multifocal atrophy – not a\w with perniciuos anemia.
2)Intestinal metaplasia 3) Increase risk of gastric ca.

Gastrin- either Normal to decreased
H.pylori gastritis- morphology


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Endoscopy: Gastritis( erythematous): 1) Localized
Antral or 2) Pan-gastritis (+\-) Atrophic
Gastric biopsy : 1) Dense chronic inflammatory
infiltrate (lamina propria, Intraepithelial + Cross
the BM ) + neutrphils+ pit abscesses+Subepithelial plasma cells+ glands destructionfibrosis +intestinal metaplasia
Lymphoid aggregates with germinal centers
H.pylori infection\colonies demonstrate in mucosa
H.pylori may be found in gastric mucosa in Barrett’s .
Chronic Atrophic Gastritis with intestinal metaplasia
IV. Chronic Gastritis- clinical features
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Asymptomatic or Symptomatic: mild but more
persistent.
Nausea and upper abdominal discomfort, +\vomiting.
Sequelae of H.pylori infection: Peptic ulcer,
adenocarcinoma.)
Investigations: (1) Urease test (2) breath test
(3) H.pylori Ag – fecal test (4) Antibodies 5) PCR
(6) Gastric biopsy histopathology .
(7) Endoscopy
(8) Antibodies to parietal cells
Chronic gastritis- Other types
AUTOIMMUNE GASTRITIS
10% of cases of chronic gastritis, typically
spare the Antrum, mainly affect body&
fundus. characterized by:
• (1) Antibodies to parietal cells , intrinsic
factor - found in serum & gastric secretion
• (2) Reduced serum pepsinogen I conc.
• (3) Antral endocrine cells hyperplasia.
hypergastrinemia (4) Vitamin B12 deficiency
(5) Defective gastric acid secretion (achlorhydria)

AUTOIMMUNE pathogenesis
 Loss
of Parietal cell (Ab. Damage)>
reduce acid production & IF-this lead
to enhance>>
(1) Gastrin secretion + hypergastrinemia
& hyperplasia.
 (2) IF lead to >> B12 deficiency.
 (3) Low acid > reduction PG1 (chief
loss among parietal cell destruction)
AUTOIMMUNE GASTRITIS

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Body& fundus involved
Diffuse body mucosal
damage& atrophy.
Loss of parietal cells
mucosa with rugal lost
loss of acid & intrinsic
factors secretion
Lymph, MQ, plasma
Neutrophils cells.
Lymphoid aggregates
Intestinal ,metaplasia
endocrine hyperplasia
AUTOIMMUNE GASTRITISclinical features
Slow onset, variable progressive gastric
atrophy, anemia – in a few patients.
 Median age for diagnosis 60 years old.
 F >M.
 A\W others autoimmune diseases , grave’s,
DM-1, myasthenia gravis, ect..
 Vit B12 deficiency, tongue – Atrophic
glossitis , smooth +Megaloblastosis+
neurologic

Chronic autoimmune gastritis

Complications
1.
Achlorhydria*

2.
Hypergastrinemia*
➱
3.
Loss of acid (HCl) production results in
Increased levels of gastrin (loss of negative
feedback)
Macrocytic anemia*
Due to lack of intrinsic factor causing vitamin B12
deficiency.
Increased risk for gastric adenocarcinoma**
Increased risk for gastric carcinoid (why?).

4.
5.
21
Eosinophilic Gastritis.
Tissue damage a\w dense infiltrates of
eosinophils in the mucosa and
muscularis, usually in Antral or pyloric
region.
 Associate with:
 1) GI eosinophilia.
 2) Peripheral eosinophilia with increased

serum IgE levels
 3)
Allergic reactions
 4) Parasitic infections 5) H. pylori infection
Lymphocytic gastritis
Lymphocytic gastritis: nonspecific
symptoms, idiopathic.
 40% of cases a\w celiac disease
(suggesting immune-mediated
pathogenesis).
 Histologically-l
 limited to body marked increase in number of Intraepithelial of T lymphocytes.

Lymphocytic gastritis
Granulomatous gastritis:
 Gastritis
contains granulomas, or
aggregates of epithelioid histiocytes
(tissue macrophages). a\w(:
 (1) Crohn disease 1st most common,
 (2) 2nd Sarcoidosis.
 (3) Infections by mycobacteria.
fungi , CMV, and H. pylori
Granulomatous gastritis
Reactive Gastropathy

Gastropathy: defined as epithelial cell damage
and regeneration without associated
inflammation.

Gastropathy foveolar hyperplasia, glandular
regenerative changes, and mucosal edema.
Neutrophils are not abundant.

Causes : irritants such as chemical or drugs
(eg, NSAID and alcohol), bile reflux., and
mucosal trauma.

Endoscopy shows- watermelon stomach.
Reactive Gastropathy – watermelon
endoscopy appearance
Reactive Gastropathy
Antral reactive
mucosa
 Dilated capillaries
containing fibrin
thrombi.

MAJOR ASPECTS OF H.pylori ( TYPE A) & Autoimmune
( TYPE B) GASTRITIS
FEATURE
TYPE A GASTRITIS TYPE B GASTRITIS
DISTRIBUTION
Fundus, diffuse
Pyloric antrum, focal
GASTRIC SECRETION
Reduced*
Noramal or + or -
ANTIBODIES TO PARIETAL CELLS Yes*
No
OTHER AUTOIMMUNE DISEASES
Yes*
No
VITAMIN B12
Low*
Normal
PERNICIOUS ANEMIA
+
-
GASTRIN
Increased*
Normal
ANTIBODIES TO H PYLORI
-
+
INCIDENCE
Less common
More common
CANCER RISK
Increased*
Increased*
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The end