GASTRITIS

GASTRITIS :it is a general term for group of condition with

one thing in common i-e Inflammation of lining of the
stomach
TYPES
Acute gastritis
It is sudden inflammation or swelling of stomach lining
Chronic gastritis
It is progressive long term inflammation of stomach lining
ACUTE GASTRITIS
• Gastritis results from mucosal injury. When neutrophils
are present, the lesion is referred to as acute gastritis.
When cell injury and regeneration are present but
inflammatory cells are rare or absent, the term
gastropathy is applied
CLINICAL FEATURES :Both gastropathy and acute
gastritis may be asymptomatic or cause variable
degrees of epigastric pain, nausea, and vomiting. In
more severe cases, there may be mucosal erosion,
ulceration, hemorrhage, hematemesis, melena, or
rarely, massive blood loss.
PATHOGENESIS /ETIOLOGY
• The gastric lumen is strongly acidic, with a pH close to 1 . Multiple
mechanisms have evolved to protect the gastric mucosa
1)Mucin secreted by surface foveolar cells forms a thin layer of mucus . The
mucus layer also promotes formation of an “unstirred” layer of fluid over the
epithelium that protects the mucosa; it has a neutral pH as a result of
secretion of bicarbonate ions by surface epithelial cells.
• 2) Finally, the rich blood supply of the gastric mucosa efficiently buffers and
removes protons that back diffuse into the lamina propria. Gastropathy,
acute gastritis, and chronic gastritis can occur after disruption of any of
these protective mechanisms. The main causes
include:
i) Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit cyclooxygenase
(COX)-dependent synthesis of prostaglandins E2 and I2, which stimulate nearly
all of the above defense mechanisms. Although COX-1 plays a larger role than
COX-2, both isoenzymes contribute to mucosal protection. Thus, while the risk
for development of NSAID induced gastric injury is greatest with nonselective
inhibitors, such as aspirin, ibuprofen, and naproxen, selective COX-2 inhibition,
for example, by celecoxib,can also result in gastropathy or gastritis.
ii) Those infected with urease-secreting H. pylori may be
due to inhibition of gastric bicarbonate transporters by
ammonium ions.
iii) Hypoxemia and decreased oxygen delivery may account
for an increased incidence of gastropathy and acute
gastritis at high altitudes.
iv) Ingestion of harsh chemicals, particularly acids or bases,
leads to severe gastric mucosal damage as a result of direct
injury to epithelial and stromal cells. Direct cellular
damage also contributes to gastritis induced by excessive
alcohol consumption and radiation therapy. Agents that
inhibit DNA synthesis or the mitotic apparatus, including
those used in cancer chemotherapy, may cause generalized
mucosal damage due to insufficient epithelial renewal.
MORPHOLOGY: In gastropathy and mild acute gastritis
the lamina propria shows only moderate edema and
slight vascular congestion. The surface epithelium is
intact, but hyperplasia of foveolar mucus cells is
typically present.
• Neutrophils, lymphocytes, and plasma cells are not
prominent. With more severe mucosal damage,
erosions and hemorrhage develop. Hemorrhage
may manifest as dark punctae in an otherwise
hyperemic mucosa.
• Concurrent presence of erosion and hemorrhage is
termed acute erosive hemorrhagic gastritis.
• STRESS RELATED MUCOSAL INJURY :Stress-related gastric injury occurs in patients with
severe trauma, extensive burns, intracranial disease, major surgery, serious medical
disease, and other forms of severe physiologic stress. Examples are as follows:
• Stress ulcers affecting critically ill patients with shock, sepsis, or severe trauma.
• Curling ulcers occur in the proximal duodenum and are
• associated with severe burns or trauma.
• Cushing ulcers arise in the stomach, duodenum, or esophagus of those with intracranial
disease and have a high incidence of perforation.
PATHOGENESIS
• The pathogenesis of stress-reis most often due to local ischemia. This may be caused by
systemic hypotension or reduced blood flow resulting from stress-induced splanchnic
vasoconstriction.
. Cushing ulcers are thought to be caused by direct stimulation of vagal nuclei resulting acid
hypersecretion.
MORPHOLOGY
• Stress-related gastric mucosal injury ranges from shallow erosions caused by superficial
epithelial damage to deeper lesions that penetrate the depth of the mucosa. Acute ulcers
are rounded and typically less than 1 cm in diameter. The ulcer base frequently is stained
brown to black by acid-digested extravasated red cells.,
• acute stress ulcers are found anywhere in the stomach and are often multiple. They are
sharply demarcated, with essentially normal adjacent mucosa, although there may be
suffusion of blood into the mucosa and submucosa and some inflammatory reaction..
CHRONIC GASTRITIS : ETIOLOGY
I)infection bacillus helicobacter pylori
2)Autoimmune gastritis
3)Chronic NSAID use is a third important cause of
gastritis
4) Less common causes include radiation injury and
chronic bile reflux.
CLINICAL FEATURES
• The signs and symptoms associated with chronic
gastritis typically are less severe but more persistent
than those of acute gastritis. Nausea and upper-
abdominal discomfort may occur, sometimes with
vomiting, but hematemesis is uncommon.
HELICOBACTER PYLORI GASTRITIS :H.pylori infection most often presents as
an antral gastritis with increased acid production. The increased acid
production may give rise to peptic ulcer disease of the duodenum or
stomach. While in most cases H. pylori gastritis is limited to the antrum, in
some individuals it progresses to involve the gastric body and fundus,
resulting in reduced parietal cell mass and acid secretion. Reduced acid
output results in hypergastrinemia, as in autoimmune atrophic gastritis
• PATHOGENESIS . Four features are linked to H. pylori virulence:
• Flagella, which allow the bacteria to be motile in viscous mucus
• • Urease, which generates ammonia from endogenous urea, thereby
elevating local gastric pH around the organisms and protecting the
bacteria from the acidic PH of stomach
• Adhesins, which enhance bacterial adherence to surface foveolar cells
• Toxins, such as that encoded by cytotoxin-associated
• gene A (CagA), that may be involved in ulcer or cancer development
• These factors allow H. pylori to create an imbalance between
gastroduodenal mucosal defenses and damaging forces that overcome
those defenses
• MORPHOLOGY :The organism is concentrated within mucus
overlying epithelial cells in the surface and neck regions.
• The inflammatory reaction includes a variable number of
neutrophils within the lamina propria
• The superficial lamina propria includes large numbers of
plasma cells, often in clusters or sheets, as well as increased
numbers of lymphocytes and macrophages. When intense,
inflammatory infiltrates may create thickened rugal folds.
Lymphoid aggregates, some with germinal centers, are
frequently present and represent an induced form of mucosa-
associated lymphoid tissue (MALT) that has the potential to
transform into lymphoma.
• Intestinal metaplasia, characterized by the presence of goblet
cells and columnar absorptive cells , also may be present and
is associated with increased risk of gastric adenocarcinoma.
AUTOIMMUNE GASTRITIS . In contrast H. pylori-associated
gastritis,autoimmune gastritis typically spares the antrum and induces
marked hypergastrinemia . Autoimmune gastritis is characterized by the
following:
• Antibodies to parietal cells and intrinsic factor that can be detected in
serum and gastric secretions
• Reduced serum pepsinogen I levels
• Antral endocrine cell hyperplasia
Vitamin B12 deficiency leading to pernicious anemia and neurologic
changes
• • Impaired gastric acid secretion (achlorhydria)
• PATHOGENESIS Autoimmune gastritis is associated with immune-
mediated loss of parietal cells and subsequent reductions in acid and
intrinsic factor secretion. Deficient acid secretion stimulates gastrin
release, resulting in hypergastrinemia and hyperplasia of antral gastrin-
producing G cells. Lack of intrinsic factor disables ileal vitamin B12
absorption, leading to B12 deficiency and a particular form of
megaloblastic anemia called pernicious anemia
MORPHOLOGY :Autoimmune gastritis is characterized
by diffuse damage of the oxyntic (acid-producing)
mucosa within the body and fundus.
• Damage to the antrum and cardia typically is absent
or mild. With
diffuse atrophy, the oxyntic mucosa of the body and
fundus appears markedly thinned, and rugal folds are
lost.
Neutrophils may be present, but the inflammatory
infiltrate more commonly is composed of
lymphocytes, macrophages, and plasma cells