Gastritis is inflammation of the lining of the stomach and has many possible causes.
Common causes of gastritis are excessive alcohol consumption or prolonged use of nonsteroidal
anti-inflammatory drugs such as aspirin or ibuprofen.
Gastritis may also develop after major surgery, traumatic injury, burns, or severe infections.
Gastritis may also occur in those who have had weight loss surgery resulting in the banding
or reconstruction of the digestive tract.
Chronic causes are infection with bacteria, primarily Helicobacter pylori, chronic bile
reflux, and stress; certain autoimmune disorders can cause gastritis as well.
The most common symptom is abdominal upset or pain.
Other symptoms are indigestion, abdominal bloating, nausea, and vomiting and pernicious
anemia.
Some may have a feeling of fullness or burning in the upper abdomen.
An esophagogastroduodenoscopy, blood test, complete blood count test, or a stool test
may be used to diagnose gastritis.
Treatment includes taking antacids or other medicines, such as proton pump inhibitors
or antibiotics, and avoiding hot or spicy foods.
For those with pernicious anemia, B12 injections are given, but more often oral B12 supplements
are recommended.
Signs and symptoms
Many people with gastritis experience no symptoms at all.
However, upper central abdominal pain is the most common symptom; the pain may be dull,
vague, burning, aching, gnawing, sore, or sharp.
Pain is usually located in the upper central portion of the abdomen, but it may occur anywhere
from the upper left portion of the abdomen around to the back.
Other signs and symptoms may include: Nausea
Vomiting Belching
Bloating Early satiety
Loss of appetite Unexplained weight loss
Morphological patterns Acute
Erosive gastritis is a gastric mucosal erosion caused by damage to mucosal defenses.
Alcohol consumption does not cause chronic gastritis.
It does, however, erode the mucosal lining of the stomach; low doses of alcohol stimulate
hydrochloric acid secretion.
High doses of alcohol do not stimulate secretion of acid.
NSAIDs inhibit cyclooxygenase-1, or COX-1, an enzyme responsible for the biosynthesis
of eicosanoids in the stomach, which increases the possibility of peptic ulcers forming.
Also, NSAIDs, such as aspirin, reduce a substance that protects the stomach called prostaglandin.
These drugs used in a short period are not typically dangerous.
However, regular use can lead to gastritis.
Chronic Chronic gastritis refers to a wide range of
problems of the gastric tissues.
The immune system makes proteins and antibodies that fight infections in the body to maintain
a homeostatic condition.
In some disorders the body targets the stomach as if it were a foreign protein or pathogen;
it makes antibodies against, severely damages, and may even destroy the stomach or its lining.
In some cases bile, normally used to aid digestion in the small intestine, will enter through
the pyloric valve of the stomach if it has been removed during surgery or does not work
properly, also leading to gastritis.
Gastritis may also be caused by other medical conditions, including HIV/AIDS, Crohn's disease,
certain connective tissue disorders, and liver or kidney failure.
Since 1992, chronic gastritis lesions are classified according to the Sydney system.
Metaplasia Mucous gland metaplasia, the reversible replacement
of differentiated cells, occurs in the setting of severe damage of the gastric glands, which
then waste away and are progressively replaced by mucous glands.
Gastric ulcers may develop; it is unclear if they are the causes or the consequences.
Intestinal metaplasia typically begins in response to chronic mucosal injury in the
antrum, and may extend to the body.
Gastric mucosa cells change to resemble intestinal mucosa and may even assume absorptive characteristics.
Intestinal metaplasia is classified histologically as complete or incomplete.
With complete metaplasia, gastric mucosa is completely transformed into small-bowel mucosa,
both histologically and functionally, with the ability to absorb nutrients and secrete
peptides.
In incomplete metaplasia, the epithelium assumes a histologic appearance closer to that of
the large intestine and frequently exhibits dysplasia.
Etiology Coffee
Coffee can irritate and damage the lining of the gastrointestinal tract, increasing
the risk of gastritis and ulcers.
The consumption of coffee is not recommended for people with gastritis, colitis, or ulcers.
Helicobacter pylori Helicobacter pylori colonizes the stomach
of more than half of the world's population, and the infection continues to play a key
role in the pathogenesis of a number of gastroduodenal diseases.
Colonization of the gastric mucosa with Helicobacter pylori results in the development of chronic
gastritis in infected individuals, and in a subset of patients chronic gastritis progresses
to complications.
However, over 80 percent of individuals infected with the bacterium are asymptomatic and it
has been postulated that it may play an important role in the natural stomach ecology.
Diagnosis Often, a diagnosis can be made based on the
patient's description of their symptoms, but other methods which may be used to verify
gastritis include: Blood tests:
Blood cell count Presence of H. pylori
Liver, kidney, gallbladder, or pancreas functions
Urinalysis Stool sample, to look for blood in the stool
X-rays ECGs
Endoscopy, to check for stomach lining inflammation and mucous erosion
Stomach biopsy, to test for gastritis and other conditions
Treatment Over-the-counter antacids in liquid or tablet
form are a common treatment for mild gastritis.
Antacids neutralize stomach acid and can provide fast pain relief.
When antacids do not provide enough relief, medications such as cimetidine, ranitidine,
nizatidine or famotidine that help reduce the amount of acid the stomach produces are
often prescribed.
An even more effective way to limit stomach acid production is to shut down the acid "pumps"
within acid-secreting stomach cells.
Proton pump inhibitors reduce acid by blocking the action of these small pumps.
This class of medications includes omeprazole, lansoprazole, rabeprazole, and esomeprazole.
Proton pump inhibitors also appear to inhibit H. pylori activity.
Cytoprotective agents are designed to help protect the tissues that line the stomach
and small intestine.
They include the medications sucralfate and misoprostol.
If NSAIDs are being taken regularly, one of these medications to protect the stomach may
also be taken.
Another cytoprotective agent is bismuth subsalicylate.
Many people also drink milk to relieve symptoms, however the high calcium levels actually stimulate
release of gastric acid from parietal cells, ultimately worsening symptoms.
In addition to protecting the lining of stomach and intestines, bismuth preparations appear
to inhibit H. pylori activity as well.
Several regimens are used to treat H. pylori infection.
Most use a combination of two antibiotics and a proton pump inhibitor.
Sometimes bismuth is also added to the regimen.
The antibiotic aids in destroying the bacteria, and the acid blocker or proton pump inhibitor
relieves pain and nausea, heals inflammation, and may increase the antibiotic's effectiveness.
See also Gastroenteritis
Infection Esophagitis
peptic ulcers References