Pathology of gastritis

2021-01-27 12:00 AM

Alcohol is also the cause of acute gastritis bleeding, especially when drinking a lot in a short time, but not before.


Gastritis is a disease where clinical symptoms are sometimes loud but sometimes very gentle and quiet. Diagnosis requires endoscopy and biopsy. Treatment is sometimes simple, but sometimes difficult.

Gastritis is divided into 2 types: acute gastritis and chronic gastritis. The differential diagnosis depends on the cause, the organizational characteristics and the anatomical distribution of gastritis.

Gastritis acute


Alcohol: Acute gastritis sometimes causes bleeding, known as erosive gastritis. Usually occurs when drinking large amounts of alcohol for a short period of time.

Non-steroids (NSAIDs), aspirin.


Ingestion of corrosive substances (usually alkaline).

Virus: CMV, Herpes.

Bacteria: Haemolytic alpha streptococcus, Clostridium septicum

Increased blood urea.


Gastritis forms

Bleeding gastritis or erosive gastritis:

A common cause of high but rarely severe gastrointestinal bleeding. Corrosion is sometimes completely silent. Endoscopy shows multiple-foci erosions, which can spread to the entire gastric mucosa or localized only in the body, cavity or gastric aneurysm. The mucosa becomes red, like scorch, but sometimes almost normal.

Histologically, corrosion only destroys the mucous layer, does not spread to the muscular layer, so does not affect the layers of blood vessels under the mucosa. Lesions are usually completely reversible. This is characteristic of this type of inflammation. At any time, one can find corroded nests that exhibit different stages of progression or recovery. There may be lesions on a flat base or in mucosal folds. Between the erosive foci is the region of epithelial loss and hernasal drainage or diffuse into the submucosal layer (Lamina propria). Corrosion can develop on a mucosa that appears histologically normal or on mucous membranes that show inflammatory stages of the stomach. If progression is prolonged, erosions can spread to the submucosa to form an acute ulcer, where bleeding becomes worse.

The most common cause is the use of non-steroid anti-inflammatory drugs. Especially Aspirin: In acidic environment non-ionized aspirin is easily absorbed by passive diffusion. In the neutral environment of the gastric mucosal epithelium, Aspirin transforms into an ionized form of acid, destroying the cell and opening the door to acid ulcers. When taken with Sodium Bicarbonate, Aspirin does not damage the gastric mucosa because it is not ionized, and therefore is not absorbed in the stomach. When the aspirin is encased in a capsule, it passes through the stomach and is absorbed in the small intestine. In addition, Aspirin and other AINS also prevent Prostaglandin synthesis (which protects the stomach lining as well as stimulates secretion of gastric acid and pepsin), thus damaging the gastric mucosa. Phenylbutazol and Indomethacin are the two drugs most likely to cause gastritis.

Alcohol is also the cause of acute gastritis bleeding, especially when drinking a lot in a short time, but not before.

Portal hypertension is also a factor that facilitates stomach bleeding.

Serious secondary stresses such as burns, infections, trauma, surgery, shock, respiratory failure, kidney failure, and liver failure also often cause acute inflammation or ulcers. The aetiology in these cases is not fully understood, possibly due to changes in blood flow to the gastric mucosa leading to small mucosal necrosis.


Patients may experience mild discomfort in the epigastric region, indigestion, bloating immediately after eating, belching, nausea, vomiting with blood with black stools, sometimes asymptomatic. The best diagnosis is by gastroscopy at the time of bleeding, as otherwise the lesions may heal and disappear. X-rays with a double contrast technique can detect these shallow corrosion traces.

Acute gastritis in combination with H. PYLORI:

The onset of HP infection may result from increased gastric secretion of available acid and lasting for more than 1 year. The patient experiences mild discomfort in the epigastric region. There are many epidemiological features of acute gastritis attributable to HP, but endoscopic and histological features are not evident. Acute HP infection is the premise for active chronic gastritis.

Chronic gastritis


Chronic gastritis due to chemicals: reflux bile, alkaline fluid from the intestine, anti-inflammatory drugs non-steroids.

Specific gastritis: Eosin-increased gastritis (leucocytosis of leukocytes, leukocytic gastroenteritis)

Granulomatous gastritis: Crohn's, tuberculosis, Histoplasmosis, syphilis, sarcoidosis, foreign bodies, parasitic intoxication, idiopathic.

Hypertrophic stomach disease: Ménétrier's disease, pseudo-lymphoma of the stomach, Zollinger-Ellison syndrome.

Congestive stomach disease (portal hypertension): not true gastritis

Nonspecific gastritis:

Non-corrosive group: (type autoimmune gastritis, type B environmental gastritis, HP-related chronic gastritis).

Erosive group: lymphadenitis, chickenpox gastritis.

The invasive inflammatory cells are mainly lymphoid and cytoplasm, a few polymorphonuclear leukocytes, and leukocytes. Lesions in the superficial layer of the secretory region of the gastric mucosa can spread deep, causing dysplasia, decreased production and atrophy of cells.

Chronic gastritis forms

It is divided into two main types of chronic gastritis, in addition to other abnormal symptoms in the stomach, either secondary or non-inflammatory. chronic.

Chronic gastritis type A:

Inflammation of the body and base of the stomach, with an autoimmune factor. Includes superficial gastritis, atrophic gastritis and atrophy of the stomach. This gastritis is often accompanied by malignant anaemia. The appearance of antibodies to parietal cells and antagonistic factors suggests the pathogenesis of the autoimmune mechanism. This type occurs about 20% in people over 60 years old. Poor symptoms, atrophic inflammation with acidosis, anaemia and the risk of stomach cancer. Diagnosed by endoscopy and biopsy.

Chronic gastritis type B:

Gastroenteritis in the gastrointestinal area, Gastritis due to HP accounts for 80%.

Inflammation often occurs in the cavernous region, most commonly seen in young people. Fixed HP on the connective complexes breaks the intercellular bridges and densely secretes neutral mucus. The cells slough off to reveal the submucosa. At the same time, the protease of HP bacteria increases the diffusion of H + ions causing the breakdown of glycoprotein, reducing mucus on the mucous layer. In this body, fasting plasma Gastrin concentration is infrequently high, sometimes normal. This type of gastritis can lead to atrophic gastritis or atrophy of the stomach, stomach lymphatic follicles, and gastric B-cell lymphoma (MALT). The low acidity of gastric juice leads to infection and cancer risk, especially when treated with H2 blockers or H + proton pump inhibitors.

Diagnosed by endoscopy and biopsy, rapid urease test is performed on biopsy of the gastric mucosa or urea breathing test and tests for anti-HP antibodies in the blood (ELISA) or culture for HP.

Clinically only symptoms of epigastric discomfort, indigestion.

The classification above is sometimes not completely clear, people also class AB to refer to lesions involving both the body and gastric cavity.

Gastritis caused by reflux:

It is likely that bile fluid reflux from the duodenum into the stomach causes inflammation of the pyloric gland, inflammation of the pyloric area. Clinical symptoms less blurred, the disease can be associated with gastric ulcer.

Inflammation of portal hypertension:

Stomach congestion.

Not really an inflammatory response, since the infiltration of inflammatory cells was not found in the mucosa as well as in the lower mucosa of the stomach. This is just a complication, a consequence of portal hypertension or cirrhosis. In cases of endoscopic enlargement of the oesophageal vein, often leads to a subsequent reactive gastric congestion.

Through the endoscopy, we can see the stomach lining up, red, bleeding into small clumps in the mucosa, forming a network or mosaic pattern.


Outline of treatment

Gastritis is the common name for gastric conditions resulting from either a specific or nonspecific injury to the gastric mucosa. One classification commonly used by clinicians and pathologists is based on the so-called lesions according to the histopathological, bacterial, and site lesions of the stomach. are more specific and quite accurate.

The purpose of treatment is to protect cells, restore acid secretion back to normal, eliminate the cause, and limit the processing of atrophy of the gastric mucosa, helping to prevent cancer.

Treatment of acute gastritis

Gastritis due to corrosion:

Alcohol gastritis and anti-inflammatory drugs:

This is a common cause of drinking large amounts of alcohol, due to the use of non-steroidal anti-inflammatory drugs and corticoids. Lesions in many places in the form of mucosal wounds, bleeding.

Treatment includes:

Stop the cause as soon as possible.

Ensure effective circulation volume for infusion, fasting and oral feeding.

Gastric lavage to stop bleeding by using cold isotonic saline mixed with Adrenalin.

Anti-secreting drugs: Cimetidine or Ranitidine, or intravenous Omeprazole.

Acid neutralizer.

Mucosa medicine: Sucralfate gel, or Misoprostol (Cytotec 600μg - 800μg / ng can be used).

Infuse vasoconstrictors such as Vasopressin or Sandostatin for heavy bleeding.

Haemostasis with laser, heat or photolysis.

Preventive treatment for cases requiring anti-inflammatory drugs: Use anti-H2 or proton pump inhibitors H +.

Chemical gastritis:

Inflammatory agents can be strong alkalis like KCl, or iron, or Cocaine. Treatment in these cases is:

Pain relief, fasting, intravenous feeding.

Cardiopulmonary and respiratory resuscitation.

If there is fibrosis causing stenosis, surgery to connect the gastrointestinal tract is indicated.

Gastritis due to physical trauma:

After insertion of gastrostomy tube, after treatment of gastric haemostasis with endoscopy, laser, thermostats

Treatment with fasting, infusion, gastric mucosa and anti-secretory.

Gastritis caused by radiation therapy:

Gastroenteritis, pre-pyloric inflammation. Lesions can be deeply punctured, bleeding, or narrow.

Treatment with mucosal, anti-secretory and radiotherapy drugs.

Gastritis caused by anaemia:

Is a manifestation of systemic disease such as Scholein - Henoch disease, Cytomegalovirus infection?

Treatment with mucosal and anti-secretory drugs, antiviral drugs.

Stomach congestion:

Met in portal hypertension of cirrhosis.

Treatment is mainly with sympathomimetic β blockers such as Propranolol, or Nadrolol 60mg- 80 mg/ng so that the pulse is 3/4 compared to before using in combination with anti-acid secretion.

Gastritis caused by infection:

Common causes are tuberculosis, CMV, Candida Albicans, Histoplasmosis, Crohn's disease. Specific treatment with antibiotics, antifungal, antiviral drugs. In severe cases, surgery can be done.

Acute non-erosive gastritis combined with acute or chronic Helicobacter pylori (HP) infection:

Treatment of HP killers includes Omeprazole (40mg / ng) with Amoxicillin (1.5 g / ng), Clarithromycin (500mg / ng) for 7- 10 days.

Treatment of chronic gastritis

Chronic gastritis not caused by corrosion:

Chronic gastritis type A :

This is gastroenteritis in the trunk, usually atrophic mucosal inflammation, associated with malignant anaemia, due to present in the blood antibodies to parietal cells, antibodies to intrinsic factor, often in association with diseases. Other autoimmune such as autoimmune thyroiditis, adrenal insufficiency, primary biliary fibrosis.

Treatment: no specific treatment: often use neutralizing drugs acid, vitamin C, iron, vitamin B12, corticoids. Need to monitor progress leading to stomach cancer.

Chronic gastritis type B:

Lesions in the gastric cavity are found in 80% of cases and very importantly, it is also known as HP gastritis.

Anti-secretory therapy combined with antibiotics to kill HP.

Gastritis type AB:

Combined gastritis Damage to both the stomach and stomach.

Treatment includes anti-secretory drugs, antibiotics, mucous membranes, Vitamin B12, iron to improve anaemia.

Gastritis caused by reflux:

Pyloric gastritis occurs after 2/3 of the gastric bypass. Treatment includes drugs that change the bile component such as Cholestyramine with the combination of sucralfate and Cizapride or Metoclopropramide to accelerate food out of the stomach.

Hypertrophic gastritis: (Ménétrier's disease)

Also known as lymphocytic gastritis, the damage spreads throughout the stomach mainly on the large curvature.

Treatment with anticholinergic drugs, anti-secretory, Tranexamic acid (Frenolyse), corticoids and Ortreotide with antibiotics if there is additional HP infection, or with an antiviral agent if CMV infection is present.

In severe cases, a complete gastric bypass may be required.

Chronic erosive gastritis:

Uncommon, lesions of the gastric mucosa in the form of chickenpox with central erosive small streaks are found in the cavernous and gastric stem, also known as lymphoid gastritis. This disease has an increase in blood IgE suggestive of immunological aetiology. The disease responds to Cromoglycate 80- 160 mg/ng.

Lymphoma pseudo-gastritis:

Often combined ulcerative lesions. The disease is usually benign, possibly an allergic inflammatory reaction or possibly a mucous Associated limphome Tissues (MALT) in HP infection.

Treatment: If there is evidence of HP, it must be eradicated by anti-secreting and antibiotic resistance

Eosinophilic gastritis:

Rarely, because the eosinophils form small polyps in the cavernous region also known as peri-capillary cell tumours.

Treatment with Prednisolone is a drug of selective dose 10-15 mg/ng, the lesions will regress after three days.