Acute Gastritis

Dwi Rezki Amalia

Medical Faculty of Lambung
Mangkurat University
Anatomy Gaster
Gaster Vascularization
Gaster Vascularization
Innervation of Gaster
Gaster Lymphatic Drainage
 Histology Gaster
The stomach is the site where food is mixed with gastric juice and
reduced to a fluid mass called chyme. This slide shows the structure of
the stomach lining under the light microscope. Begin by identifying the
folds of the stomach wall, or rugae, which are visible in a gross
specimen. The layers of the stomach wall follow the basic plan
described above. The gastric glands are the basic structure of the
stomach wall and can be thought of as tiny pits, or indentations, lined
by epithelial cells. The loose connective tissue of the submucosa
contains some blood vessels that can be discerned upon close
observation. The muscularis externa of the stomach is notable because
it contains an additional muscular layer. It is structured with inner
oblique, middle circular, and outer longitudinal layers. This structure
allows for the churning movements that mix the chyme and expose it
to the acidic gastric juice produced by the stomach glands.
Histology Gaster
 Gastric Glands
Gastric glands are structured as a gastric pit that opens into the lumen,
followed by an isthmus, neck, and base. The mucosal layer appears here with
its columnar epithelial cells, narrow lamina propria, and pink-staining
muscularis mucosa There are several types of cells that are important in
producing stomach secretions:
Mucous-secreting cells produce mucous and bicarbonate ions, which
protect the stomach epithelium from the damaging effects of stomach
acid. They appear pale and contain obvious mucous droplets.
Parietal cells secrete hydrochloric acid and intrinsic factor, which is
important for the absorption of vitamin B12 in the terminal ileum. They
have a characteristic pyramidal shape and are usually found in the isthmus
of the gastric gland.
Chief cells produce pepsinogen, which is stored in large apical secretory
granules. After pepsinogen is secreted, it is converted by the acidic
environment of the stomach to pepsin that is an active protease. Chief
cells are found in the base of the gastric glands.
Enterochromaffin-like (ECL) cells produce histamine, which is important in
the release of stomach acid. They are typically found in the base of the
gastric glands.
G-cells secrete the peptide hormone gastrin into the blood stream.
Gastric Glands
 Physiology of Acid Secretion
The stomach consists of an epithelium made up of pits and
glands.
The two primary functional zones are the oxyntic gland
area, representing approximately 80% of the organ, and the
pyloric gland area representing the remaining 20%.
Parietal cells, which predominate in the oxyntic glands,
secrete hydrochloric acid and intrinsic factor. They are
located in the lower two-thirds of the oxyntic glands and
are largely limited to the fundic region of the stomach.
Chief cells, located at the base of the oxyntic glands, are
responsible for secreting the digestive enzyme precursor
pepsinogen.
Neuroendocrine cells containing hormonal and paracrine
signaling agents that regulate the activity of the parietal
cell reside within the glands. These include D cells,
enterochromaffin-like (ECL) cells, A-like cells and
enterochromaffin (EC) cells.
Regulation gastric acid secretion
 Gastric Mucosal Barrier
The gastric mucosal barrier is the property of the stomach that allows it to
safely contain the gastric acid required for digestion.

If the barrier is broken, as by acetylsalicylic acid (ASA, aspirin) in acid solution,

acid diffuses back into the mucosa where it can cause damage to the stomach
itself.

The barrier consists of three protective components. These provide the

additional resistance for the mucosal surface of the stomach. The three
components include:
A compact epithelial cell lining. Cells in the epithelium of the stomach are
bound by tight junctions that repel harsh fluids that may injure the
stomach lining.
A special mucus covering, derived from mucus secreted by surface
epithelial cells and Foveolar cells. This insoluble mucus forms a protective
gel-like coating over the entire surface of the gastric mucosa. The mucus
protects the gastric mucosa from autodigestion by e.g. pepsin and from
erosion by acids and other caustic materials that are ingested.
Bicarbonate ions, secreted by the surface epithelial cells. The bicarbonate
ions act to neutralize harsh acids.
Gastric Mucosal Barrier
 Factors that can damage the barrier
-Bacterial Infection by Helicobacter pylori

-Alcohol

-NSAIDs
 Helicobacter pylori
Flagellated gram
negative bacilli with
urease activity :
hydrolyzes urea >>
ammonia (NH3) & CO2
(help resist stomatch
acid)

Transmission : fecal-oral,
oral-oral and most
infection acquired in
childhood

Natural habit :
gastric mucosa of the
antrum, if found in
duodenum, associated
with metaplastic gastric
epithelium
 Definition
Gastritis is inflammation of the gastric
mucosa, submucosa, or muscularis.
Acute gastritis refers to a sudden onset of
inflammation of the stomach lining, called the
gastric mucosa.
 Classification
Acute gastritis can be broken down into 2
categories:
erosive (eg, superficial erosions
deep erosions (hemorrhagic erosions)
Non erosive (generally caused by Helicobacter
pylori).
Acute gastritis with superficial erosions. Mucosal erythema and edema
consistent with acute gastritis.
 Etiology
Acute gastritis has a number of causes, note the following:
Drugs - NSAIDs, such as aspirin, ibuprofen, and naproxen; cocaine; iron; colchicine, when
at toxic levels, as in patients with failing renal or hepatic function; kayexalate;
chemotherapeutic agents, such as mitomycin C, 5-fluoro-2-deoxyuridine, and floxuridine
Potent alcoholic beverages, such as whisky, vodka, and gin
Bacterial infections - H pylori (most frequent), H heilmanii (rare), streptococci (rare),
staphylococci (rare), Proteus species (rare), Clostridium species (rare), E coli (rare),
tuberculosis (rare), secondary syphilis (rare)
Viral infections (eg, CMV)
Fungal infections - Candidiasis, histoplasmosis, phycomycosis
Parasitic infection (eg, anisakidosis)
Acute stress (shock)
Radiation
Allergy and food poisoning
Bile: The reflux of bile (an alkaline medium is important for the activation of digestive
enzymes in the small intestine) from the small intestine to the stomach can induce
gastritis.
Ischemia: This term is used to refer to damage induced by decreased blood supply to the
stomach. This rare etiology is due to the rich blood supply to the stomach.
Direct trauma
 Pathophysiology
Acute gastritis has a number of causes, including
certain drugs; alcohol; bile; ischemia; bacterial,
viral, and fungal infections; acute stress (shock);
radiation; allergy and food poisoning; and direct
trauma. The common mechanism of injury is an
imbalance between the aggressive and the
defensive factors that maintain the integrity of
the gastric lining (mucosa).
 Epidemiology
Data from a national administrative database
(2009-2011) revealed standardized estimated
prevalence rates of 6.3 per 100,000
population for eosinophilic gastritis and 3.3
per 100,000 population for eosinophilic colitis;
women were affected more often.
Gastritis affects all age groups. The incidence
of H pylori infection increases with age.
 Sign and Symptom
Patients may experience gnawing or burning epigastric distress,
occasionally accompanied by nausea and/or vomiting. The pain may
improve or worsen with eating.

Obtain the following information, if available:

Presence of a previous mucosal injury (eg, gastritis, peptic ulcer
disease, endoscopic injury caused by polypectomy, injury caused by
any surgery)
History of eating raw fish
Exposure to potentially noxious drugs or chemical agents. This
includes corticosteroids or other prescription medications that can
cause gastritis.
Routine use of aspirin or nonsteroidal anti-inflammatory drugs
(NSAIDs), especially at high doses
 Physical Examination
The physical examination findings are often
normal with occasional mild epigastric
tenderness. The examination tends to exhibit
more abnormalities as the patient develops
complications in relation to gastritis.
 Differential Diagnosis
Also consider the following in the differential
diagnosis of patients with suspected gastritis:
Hyperplastic gastropathy/Menetrier disease
Granulomatous gastropathy
Pregnancy
 Laboratory Studies
A number of laboratory tests are usually ordered,
including the following:
Complete blood cell (CBC) count to assess for
anemia, as acute gastritis can cause
gastrointestinal bleeding
Liver and kidney function tests
Gallbladder and pancreatic function tests
Pregnancy test
Stool for blood
 Imaging Studies
Plain photo-BNO
Maag-Duodenography (MD) atau
Oesophago-Maag-Duodenography (OMD)
USG
CT scan abdomen
MRI
 Other Test
A number of H pylori tests are available. They are classified as either
nonendoscopy based or endoscopy based.

Three nonendoscopy-based H pylori tests are available.

The first test is the H pylori stool antigen test (HpSA). This test is based on
the detection of the H pylori antigen in the stool. It has sensitivity and
specificity of greater than 90%. It can be used for both the diagnosis of H
pylori and the confirmation of eradication after therapy.
The second test is the urea breath test. It uses 13C- or 14C-labeled urea
taken orally. H pylori metabolizes the urea and liberates labeled carbon
dioxide that is exhaled. This, in turn, can be quantified in breath samples.
The sensitivity and specificity of the urea breath test is greater than 90%.
This is considered the noninvasive diagnostic method of choice in
situations where endoscopy is not indicated. It can also be used to confirm
eradication after therapy
The third test depends on the presence of antibodies to H pylori in the
serum. The major drawback to this test is that serologic assays may
remain positive for as long as 3 years after eradication of the bacteria.
Therefore, serologic assays are often unreliable to document eradication
of H pylori. This test can be used for the diagnosis of H pylori, provided
that the patient has not received any prior therapy for it.
 Other Test
Three endoscopy-based H pylori tests are available.

The first test is the rapid urease test (RUT). It is performed by placing a
gastric biopsy specimen, obtained at endoscopy, onto a gel- or membrane-
containing urea and a pH-sensitive indicator. If H pylori is present, the
bacterial urease hydrolyzes urea and changes the color of the media. The
sensitivity and specificity of this test is greater than 90%.
Another test is bacterial culture H pylori. It is highly specific but is not
widely used because of the degree of expertise required. It is used when
antibiotic susceptibilities are necessary.
Histologic detection of H pylori in the biopsy specimen is another
endoscopy-based test. Appropriate staining is achieved using such stains
as hematoxylin and eosin, Warthin-Starry, Giemsa, or Genta.

American Society for Gastrointestinal Endoscopy guidelines suggest

endoscopic evaluation for patients older than 50 years who have alarm
features such as weight loss and anemia. For patients younger than 50 years
with no alarm features who are H pylori negative, endoscopic evaluation
may be considered
 Endoscopic Findings
Endoscopy may reveal a thickened,
edematous, nonpliable wall with erosions and
reddened gastric folds. The edema can be
severe resulting in gastric outlet obstruction.
Ulcers and frank bleeding might be present.
 Histologic Findings
Histologic examination of a biopsy specimen can help in establishing the
etiologic agent of gastritis.
H heilmanii is better diagnosed on smears using Giemsa or Warthin-Starry
silver stains than by gastric biopsy specimens via observation of distinct
morphology. A culture of H heilmanii has not been established yet, and
the diagnosis of this bacterial infection is based on morphological
identification by histologic examination and tissue smear cytology.
As mentioned earlier, H pylori can be found by histologic staining of a
gastric mucosal biopsy specimen. It has a sensitivity and specificity of
greater than 90%.
The main histologic feature of CMV infection is cytomegalic cells with
intranuclear inclusions. Viral cultures, immunocytochemistry, and in situ
hybridization can further aid in establishing the diagnosis.
The main histologic feature of C albicans infection is yeast forms in a
biopsy specimen.
The main histologic feature of tuberculosis is necrotizing granulomas.
The main histologic feature of histoplasmosis is presence of
nonnecrotizing granulomas containing the organisms. The diagnosis of
histoplasmosis requires a positive culture result from the gastric mucosal
biopsy specimen.
 Histologic Findings
In ulcero-hemorrhagic gastritis, the epithelium appears eroded with edema and
hemorrhage with typically little inflammation. In severe cases, the lumen of the
stomach may be coated with fibropurulent exudates and the lamina propria may
be replaced by eosinophilic hyaline material.
In iron-induced gastritis, erosions, foveolar hyperplasia, or even hyperplastic-type
polyps can be detected. Iron has been associated with infarctlike necrosis given its
corrosive properties. Iron stains can highlight the golden brown pigment in tissue
samples, but these are often easily visible. Of note, such findings should be
differentiated from glandular siderosis seen in systemic iron overload or
hemochromatosis.
Histologic features of chemotherapy-induced gastritis may include atypical
epithelial cells with bizarre features at the base of the glands, limited mitoses, and
pleomorphic nuclei. These characteristics may make it difficult to differentiate
from an adenocarcinoma.
The findings at histology of radiation-induced gastritis include nuclear karyorrhexis
and cytoplasmic eosinophilia of the gastric pit epithelium during the first 10 days
following treatment, followed by mucosal edema, congestion, submucosal
collagen bundle swelling, fibrin deposition, and telangiectasia. If extensive,
hemorrhage and ulceration may be evident.
In eosinophilic gastritis, a prominent eosinophilic infiltrate is present in the gastric
wall or epithelium. Distribution can be patchy, so multiple biopsy specimens
should be obtained during endoscopy.
 Treatment
Surgical intervention is not necessary, except
in the case of phlegmonous gastritis. With this
entity, surgical intervention with resection of
the affected area may be the most effective
form of treatment.
Consult a gastroenterologist in complicated
cases.
 Medication
No specific therapy exists for acute gastritis, except for
cases caused by H pylori.
For patients who need eradication of H pylori, this
should not be a concern. In patients with persistent H
pylori infection despite appropriate initial treatment,
combination therapy with a a proton pump inhibitor
(PPI), levofloxacin, and amoxicillin for 10 days appears
to be more effective and better tolerated than a PPI,
bismuth, tetracycline, and metronidazole.
Administer fluids and electrolytes as required,
particularly if the patient is vomiting.
Discontinue the use of drugs known to cause gastritis
(eg, NSAIDs, alcohol).
 Medication
Specific treatment is dependent on the etiology of gastritis.
According to the Centers for Disease Control and Prevention (CDC),
the treatment of tuberculosis consists of a 2-month course of daily
isoniazid, rifampin, and pyrazinamide, followed by 4 months of daily
isoniazid along with rifampin.
Medical management generally is ineffective in treating
phlegmonous gastritis. No effective antiviral therapy exists for the
treatment of human cytomegalovirus (HCMV) infection, though 2
agents (ie, ganciclovir, foscarnet) have been shown to be virostatic.
The treatment of C albicans includes a variety of agents, including
nystatin, oral clotrimazole, itraconazole, fluconazole, amphotericin
B, and ketoconazole.
The treatment of disseminated histoplasmosis includes a variety of
agents, including amphotericin B, itraconazole, and fluconazole.
They have all been determined to be effective.
No drugs are available to treat anisakidosis. Endoscopic removal
may be necessary.
 General Medication
Antacid : Used for general prophylaxis. Antacids containing
aluminum and magnesium can help relieve symptoms of gastritis by
neutralizing gastric acids. These agents are inexpensive and safe.
H2 Blocker : This class includes drugs whose mechanism of action is
competitive inhibition of histamine at the histamine 2 (H2) receptor.
Histamine plays an important role in gastric acid secretion, thereby
making H2 blockers effective suppressors of basal gastric acid
output and acid output stimulated by food and the neurological
system. There are different drugs with different potencies and half-
lives (eg, cimetidine, ranitidine, famotidine, nizatidine).
Proton Pump Inhibitor : Proton pump inhibitors are potent
inhibitors of the proton (acid) pump (ie, the enzyme H+,K+-ATPase),
located in the apical secretory membrane of the gastric acid
secretory cells (parietal cell). Proton pump inhibitors can completely
inhibit acid secretion and have a long duration of action. They are
the most effective gastric acid blockers.
 Antibiotic Use
Duplet therapy
Proton pump inhibitor + amoxicillin (no longer recommended
because eradication rates are only 30-80%)
Proton pump inhibitor + clarithromycin 3 x 500 mg (eradication
rate of roughly 71%)

Triplet (recommended as first line therapy)

Lansoprazole 30 mg, omeprazole 20 mg, or ranitidine bismuth
citrate 400 mg orally twice daily + Clarithromycin 500 mg orally
twice daily + Amoxicillin 1000 mg or metronidazole 500 mg orally
twice daily (7-14 days)

Quadruple (recommended as second line therapy)

PPI (lansoprazole 30 mg or omeprazole 20 mg) orally twice daily +
Tetracycline HCl 500 mg orally 4 times daily + Bismuth subsalicylate
120 mg orally 4 times daily + Metronidazole 500 mg orally 3 times
daily (10-14 days)
 Patient Education
Explain the disease to the patient.
Encourage cessation of smoking and alcohol
consumption, and warn patients of the
potential effects of noxious drugs and
chemical agents.
 Complication
Complications of acute gastritis include the
following:
Bleeding from an erosion or ulcer
Gastric outlet obstruction due to edema
limiting the adequate transfer of food from
the stomach to the small intestine
Dehydration from vomiting
Renal insufficiency as a result of dehydration
 Prognosis
Gastritis generally clears spontaneously. With
treatment, the mortality rate of phlegmonous
gastritis is 65%.

Mortality/morbidity
The mortality/morbidity is dependent on the
etiology of the gastritis. Generally, most cases of
gastritis are treatable once the etiology is
determined. The exception to this is
phlegmonous gastritis, which has a mortality rate
of 65%, even with treatment.
 Follow up
H pylori eradication testing can be performed 4
weeks after completing therapy. It is carried out
using either rapid urease breath testing or stool
antigen testing. However, it is not cost effective
and is not always done. The current
recommendation is that patients with ulcers from
H pylori, MALT lymphoma, history of gastric
cancer, and those with no improvement of
symptoms despite treatment must be checked for
resolution of H pylori infection