Pathology, Chronic Gastritis ,Gastric Cancer

Helicobacter pylori gastritis
Helicobacter pylori gastritis
presents as a predominantly antral gastritis with high acid production, despite
hypogastrinemia. The risk of duodenal ulcer is increased in these patients. In a subset of patients
the gastritis progresses to involve the gastric body and fundus. This pangastritis is associated
with multifocal mucosal atrophy, reduced acid secretion, intestinal metaplasia, and increased risk
of gastric adenocarcinoma.

H. pylori
These spiral-shaped or curved bacilli are present in gastric biopsy specimens of almost all patients with duodenal ulcers and the majority of individuals with gastric ulcers.

polymorphisms in the gene encoding the pro-inflammatory cytokine interleukin-1? (IL-1?)
correlate with the development of pangastritis after H. pylori infection.

Helicobacter pylori gastritis Clinical Presentation
may manifest as non-ulcer gastric pain, nausea,
anorexia, bloating or significant weight loss

Helicobacter pylori gastritis Pathology
H. pylori is concentrated within the superficial mucus
overlying epithelial cells in the surface and neck regions. The distribution can be irregular, with
areas of heavy colonization adjacent to those with few organisms.

Helicobacter pylori Localization
found in the gastric antrum; cardia is the second most common
localization. Thus, an antral biopsy is preferred for evaluation of H. pylori gastritis.

H. pylori-infected antral mucosa
is usually erythematous on endoscopy. The inflammatory
infiltrate includes neutrophils within the lamina propria, including
some that cross the basement membrane to assume an intraepithelial location and accumulate in
the lumen of gastric pits to create pit abscesses. In addition, the superficial lamina propria
includes large numbers of plasma cells, often in clusters or sheets, and increased numbers of
lymphocytes and macrophages. Intraepithelial neutrophils and subepithelial plasma cells

Gastric mucosal gland secretory function/ H pylori chronic gastritis is characterized by
increased serum PGI and normal levels of serum gastrin. Parietal cell and intrinsic factor autoantibodies and pernicious anemia are absent

Chronic Gastritis
Nausea and upper abdominal discomfort may occur, sometimes with
vomiting, but hematemesis is uncommon. The most common cause is infection with the bacillus Helicobacter pylori

Autoimmune gastritis
is an inflammatory disorder of the stomach mucosa due to an autoimmune reaction targeting the parietal cells and affects the mucosa of gastric body and
corpus fundus; gastric antrum is spared.It is associated with serum antiparietal
cell and anti-intrinsic factor antibodies.

Autoimmune gastritis Pathogenesis
is associated with loss of parietal cells, which are
responsible for secretion of gastric acid and intrinsic factor. The absence of acid production
stimulates gastrin release, resulting in hypergastrinemia and hyperplasia of antral gastrinproducing
G cells. Lack of intrinsic factor disables ileal vitamin B12 absorption, leading to B12
deficiency and a slow-onset megaloblastic anemia (pernicious anemia). Chief cells are lost along
with parietal cells, resulting in reduced serum pepsinogen I concentration and achlorhydria.

The autoimmune reaction targeting the parietal cells is effected by
CD4+ T cells which are the
principal agents of injury. CD4+ T cells attack parietal cell components, including the H+
-K ATPase (proton pump).Autoantibodies to parietal cells and to intrinsic factor are not involved in
the pathogenesis of autoimmune gastritis

Autoimmune gastritis Pathology
is characterized by diffuse mucosal damage of the acidproducing
mucosa within the gastric body and fundus. Damage to the antrum and cardia is typically absent or mild. Glandular units in the acid-producing (oxyntic) mucosa of the body are destroyed and lost, resulting in fibrosis of the lamina propria. The acid-producing mucosa undergoes atrophy; fundus appears markedly thinned, and rugal folds are lost. Loss of parietal
and chief cells is extensive.

Autoimmune gastritis Pathology
Autoimmune gastritis Pathology
Metaplastic replacement of native parietal glands occurs:
areas of intestinal metaplasia develop, characterized by the presence of goblet cells and columnar
absorptive cells. Areas of pseudopyloric metaplasia also develop characterized by presence of
pyloric cells.Hyperplasia of the antral G (enterochromaffin-like) cells develops in most patients.Over time, hypergastrinemia
can stimulate G cell hyperplasia in the fundus and body.

Autoimmune gastritis Clinical Presentation
Antibodies to parietal cells and to intrinsic factor are present early in the disease course. Progression to gastric atrophy probably occurs over 2 to 3 decades, and
anemia is seen in only a few patients.The median age at diagnosis is 60 years.

Pernicious anemia and autoimmune gastritis are
often associated with other autoimmune diseases including Hashimoto thyroiditis, type I diabetes mellitus, Addison disease,
Graves disease, vitiligo, myasthenia gravis, and Lambert-Eaton syndrome.

Autoimmune gastritis Clinical presentation may be linked to symptoms of anemia
vitamin B12 deficiency
may cause atrophic glossitis, in which the tongue becomes smooth and beefy red. Demyelination involving the dorsal columns. Later, axonal degeneration and neuronal death occurs. Numbness, weakness, and
paresthesia of the extremities that primarily affects legs and less often arms.Later, this myelopathy progresses
to unsteady gait, poor coordination, and bowel or bladder dysfunction. At physical examination,
signs of dorsal column involvement include loss of position and vibration sense and ataxia. Lateral column involvement includes Vision changes and change of mental state.

Autoimmune gastritis Laboratory Studies
(a) antiparietal and anti-intrinsic factor (IF) antibodies in the serum; (b) achlorhydria,
both basal and stimulated; (c) low serum pepsinogen I concentrations and low pepsinogen
I/pepsinogen II ratio; (d) hypergastrinemia which reflects G cell hyperplasia; and (e) low serum
cobalamin (vitamin B12) levels (< 100 pg/mL).

Gastric fundic-gland polyps
most common type of polyp detected by endoscopy in
Western countries.

Gastric hyperplastic polyps
Gastric hyperplastic polyps
are benign polyps occurring exclusively in the fundus and
asymptomatic. They are usually less than 1 cm in size .They are sessile,shiny and pale or erythematous, resembling the surrounding mucosa. They are composed of
cystically dilated glands lined by normal cell types of the acid-secreting mucosa, with a mixture
of parietal cells, chief cells, and mucus neck cells. The lining cells appear flattened and difficult to recognize when markedly dilated. Inflammation is typically absent or minimal

Fundic gland polyps (FGPs) occur
either sporadically, in association with proton pump inhibitor
(PPI) treatment or in individuals with familial adenomatous polyposis (FAP). FAP is an
autosomal dominant inherited cancer syndrome caused by a germline mutation of the adenomatous polyposis coli gene (APC).

familial adenomatous polyposis FAP-associated Fundic gland polyps (FGPs)
This type of polyps demonstrate germ-line mutations in the APC gene. Also shows low grade dysplasia

PPI-associated sporadic -associated Fundic gland polyps (FGPs)
Shows activating ?-catenin mutations. Rarely shows dysplasia.

A polyp is a small growth with a stalk, protruding from a mucous membrane.Hyperplastic polyps have been associated mostly with longstanding H.pylori chronic gastritis and
autoimmune gastritis. They result from hyper-regenerative epithelium in response to an
underlying chronic inflammatory stimulus. The hyperplastic polyps were described as pedunculated.The hyperplastic glands in these polyps are lined by foveolar epithelium.As these polyps are typically antral. The lamina
propria shows variable degrees of chronic inflammation including lymphocytes and plasma cells. Polyps larger than 1.5 cm should be surgically removed and
examined histologically.

Gastric adenomatous polyps
Gastric adenomatous polyps
These polyps are benign epithelial neoplasms that arise from the epithelial cells lining the stomach.

Gastric adenomatous polyps microscopic Findings
consist of dysplastic epithelium
with pseudostratification, nuclear abnormalities, and mitotic figures overlying cystically dilated
glands without dysplastic changes. The dysplastic cells show elongated, pencil-shaped nuclei
with hyperchromasia and clumped chromatin

Tubular Adenomas
cells proliferate generating tubular-shaped glands,

Gastric adenomas with intestinal phenotype
are lined by a dysplastic intestinal-type
epithelium (goblet cells and/or Paneth cells).Arise in association with background of H.
pylori gastritis with intestinal metaplasia and gastric atrophy

Gastric adenomas with gastric phenotype
they are lined by dysplastic gastric-type epithelium (gastric foveolar cells
containing neutral mucin). Tend to develop in apparently
normal, non-atrophic mucosa

Gastric adenomas (particularly those of intestinal phenotype) arise
predominantly through mutational inactivation of
APC gene

Gastric Adenocarcinoma
Is the most common malignant tumor of the stomach.

Hereditary syndromes with a predisposition for stomach cancer
include hereditary
nonpolyposis colorectal cancer, Li-Fraumeni syndrome, familial adenomatous polyposis, and
Peutz-Jeghers syndrome

A diet rich in pickled vegetables, smoked fish, salt, and smoked meats correlates with an
increased incidence of gastric cancer

Gastric Adenocarcinoma Location
Gastric Adenocarcinoma Location
most often found in the distal stomach, the lesser curvature of the antrum and the prepyloric region.

Polypoid (fungating) gastric carcinoma
It is a solid mass, often several centimeters in diameter that projects
into the stomach lumen.

Ulcerating gastric carcinoma
Ulcerating gastric carcinoma
They have shallow ulcers of variable size. The ulcer’s lateral margins are irregular and
its base is ragged. Surrounding tissues are firm, raised and nodular.

Scirrhous gastric carcinoma (also diffuse or infiltrating adenocarcinoma)
Scirrhous gastric carcinoma (also diffuse or infiltrating adenocarcinoma)
No true tumor mass is seen. Instead, the
stomach wall is diffusely thickened and firm. If the entire stomach is involved, it is called a
linitis plastica tumor. In this particular cancer, the invading tumor cells evoke a desmoplastic
reaction consisting in extensive fibrosis in the submucosa and muscularis that stiffens the gastric

linitis plastica
has a leather bottle-like appearance

well-differentiated adenocarcinoma
is presumed to arise from intestinalized gastric mucosa. The liver is the most common
site of metastases.

poorly-differentiated carcinoma
The histology is remarkable for diffusely infiltrating cells showing
no gland formation or signet-ring cells.Metastases are commonly found in the serosa or lymph nodes.

Sister Mary Joseph nodule
Gastric tumors can also metastasize to the periumbilical region to form a
subcutaneous nodule.

Peritoneal spread
The ovaries (Krukenberg’s tumor) and the rectal shelf (Blumer’s
tumor) are typically involved by this particular spread. Other sites of this particular spread include the
pancreas, the transverse colon, and the undersurface of the diaphragm.

loss of E-cadherin
is a key
step in the development of gastric cancer.

Loss-of-function mutations in CDH1
present in
about 50% of sporadic diffuse gastric tumors .

Gastric Cancer Clinical Presentation
loss, and persistent abdominal pain. Nausea or early satiety

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