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GASTRITIS - inflammation of the mucous membrane (sometimes deeper layers) of the stomach wall.

Acute gastritis develops as a result of exposure to the following factors: bacterial infection - foodborne toxicosis ; nutritional factors - excessive overeating, especially when consuming a large amount of unusual spicy, rough foods, as well as alcohol; exposure to chemicals (strong alkalis, acids) and drugs (primarily anti-inflammatory); exposure to allergens - food products (strawberries, eggs, etc.).

The most common is simple gastritis. Suddenly, after 4-8 hours after consuming poor-quality foods, too much food, excessive drinking, nausea appears, combined with a feeling of lightheadedness and severe weakness. Soon, and sometimes at the same time, there is a feeling of fullness, dull pain in the epigastric region, profuse vomiting , which brings some relief. Vomit initially contains freshly eaten foods. Repeated vomiting is accompanied by secretion of mucus, sometimes bile. Vomiting can be very frequent and painful, combined with cramping pain in the epigastric region. There is a complete aversion to food. After vomiting, the patient experiences a sharp weakness, often covered with cold sweat. Sometimes a violation of the digestive function of the stomach is accompanied by diarrhea; repeated vomiting and diarrhea can lead to significant dehydration. Upon examination, the skin is pale, the tongue is dry, usually thickly lined with a grayish-white coating. Bloating in the pit of stomach and splashing noise in the stomach are sometimes determined. Palpation of the epigastric region is moderately painful, but the abdomen always remains soft.

Signs of intoxication are a moderate increase in body temperature, tachycardia , a decrease in blood pressure, and neutrophilic leukocytosis can be detected in the blood .

Diagnosis of acute gastritis usually does not cause difficulties, but it should always be borne in mind that many diseases can also occur with nausea, vomiting, pain in the epigastric region. Acute gastritis must be differentiated from acute appendicitis, acute cholecystitis, myocardial infarction. Vomiting is often observed in infectious diseases (flu, meningitis , hepatitis) and acute cerebrovascular accident. A differential diagnosis is necessarily carried out with salmonellosis and other intestinal infections.

In acute appendicitis, unlike gastritis, maximum pain during palpation is determined in the right iliac region, in the same place - tension of the abdominal muscles and symptoms of peritoneal irritation. Acute cholecystitis begins with an attack of hepatic colic, in the picture of the disease in the initial stages, pain with characteristic irradiation predominates, then pain on palpation and tension of the abdominal muscles in the right upper quadrant of the stomach join; striking along the right costal arch is sharply painful. Sometimes it is possible to palpate a sharply painful enlarged gall bladder, later jaundice appears.

With meningitis, nausea and vomiting are combined with persistent severe headache, high fever. An objective study reveals the symptoms of damage to the meninges.

Myocardial infarction is usually preceded by a period of frequent attacks of angina pectoris, myocardial infarction begins with pain, severe, painful. Even with the gastralgic form of myocardial infarction and the primary localization of pain in the epigastric region, the pain usually extends beyond the sternum, radiating to the scapula, arm. The development of a heart attack is often accompanied by the early onset of symptoms of left ventricular heart failure. A decisive role for making a diagnosis is played by electrocardiographic examination.

Emergency care for the diagnosis of acute gastroenteritis should begin with gastric lavage with 2% sodium bicarbonate solution (1 tbsp. Per 1 liter of water) and alkaline water (Borjomi, Essentuki No. 20). Rinsing is best done with a thick probe - until the stomach is completely cleansed of residues, write, i.e., to clean water. In cases where it is impossible to introduce a probe, the patient is given a glass of water to drink, followed by mechanical irritation with the fingers of the throat until vomiting occurs. After vomiting, a saline laxative should be given (20-30 g of magnesium sulfate in 400-500 ml of water). The patient should be put to bed, put a heating pad on his stomach. For severe pain, antispasmodics are used (atropine 0.5-1 ml of a 0.1% solution or platifillin 1 ml of a 2% solution subcutaneously). The combination of symptoms of intoxication, dehydration with arterial hypotension requires mandatory intravenous drip of fluids (isotonic sodium chloride solution with 5% glucose solution). In cases of severe gastroenterocolitis, with severe intoxication, signs of dehydration, hypotension after emergency care, the patient should be sent to a hospital - an infectious or therapeutic department (depending on the preliminary diagnosis).

The prognosis for timely treatment is favorable, usually the duration of the disease does not exceed 1-4 days.

Corrosive gastritis develops when concentrated acids, alkalis enter the stomach and the development of gastric wall necrosis. The clinical picture depends on the nature of the damaging factor (alkalis damage the esophagus more often, acids - the stomach), its resorptive effect, and also the degree of damage to the gastric mucosa. Severe pains and a burning sensation in the mouth, behind the sternum and in the epigastric region, repeated painful vomiting with an admixture of mucus, blood, sometimes with fragments of the mucous membrane are noted. Complications can be collapse , bleeding and perforation of the hollow organs, in case of secondary infection - peritonitis and mediastinitis , followed by scarring of the esophagus, stomach, and the formation of pyloric stenosis.

The diagnosis is based on the history and clinical picture, during examination pay attention to burn marks on the lips, the mucous membrane of the mouth (gray-white spots occur when burns with hydrochloric and sulfuric acids, yellow, greenish scabs with nitric acid, brownish red with chromic acid) .

Emergency care includes washing the stomach with plenty of cold water through a thin soft rubber probe, pre-oiled, parenteral administration of antispasmodics (1 ml of a 0.1% solution of atropine, 2 ml of a 2% solution of papaverine or no-shpa), narcotic analgesics (morphine, promedol , fentanyl), transfusion of an isotonic sodium chloride solution and 5% glucose solution during collapse. Full treatment is possible only in a hospital, where the patient should be hospitalized immediately after first aid.

Phlegmonous gastritis develops when the stomach wall is infected with bacteria (usually streptococci) against a background of severe infection (sepsis, typhoid fever), stomach ulcer or cancer, a stomach injury by a foreign body (including gastroscopy), stomach injury, poisoning with strong acids and alkalis.

It is clinically characterized by an acute onset with the development of fever, intense pain in the epigastric region, nausea, vomiting, the appearance of signs of peritonitis, toxic changes in peripheral blood (neutrophilic leukocytosis , an increase in ESR).

The differential diagnosis is carried out with acute pancreatitis, accompanied by girdle pain in the abdomen, repeated painful vomiting, collapse, increased serum amylase; with a perforated gastric ulcer, which is characterized by the sudden appearance of dagger pain in the abdomen, board-like muscle tension in the anterior abdominal wall and the patient's stationary position.

With phlegmonous gastritis, in addition to broad-spectrum antibiotic therapy, surgical treatment is necessary - resection or drainage of the stomach, so a patient with suspected phlegmonous gastritis should be hospitalized immediately.

Chronic gastritis is a common disease resulting from the formation of antibodies to the lining cells of the stomach (autoimmune fundus gastritis is more common in the elderly and adulthood), due to infection of the gastric mucosa, more often Helicobacter pylori (bacterial antrum gastritis is more common in young patients), when throwing into the stomach of the duodenal contents (for example, after operations on the stomach and duodenum - reflux gastritis), as well as for unknown reasons (idiopathic gastritis). Predisposing factors include long-term systematic violation of the regime and nature of nutrition, alcohol abuse, smoking , the use of drugs (primarily non-narcotic analgesics), chronic infections and diseases of the digestive system (cholecystitis, enterocolitis), metabolic disorders in diabetes, gout, etc. In the pathogenesis of the disease, a violation of the secretory and motor functions of the stomach plays a role, later inflammatory and dystrophic changes, atrophy of the ventricle develop glands.

Often, gastritis is asymptomatic. With normal or increased secretory function (in patients with infectious gastritis), heartburn , acid burping, sometimes vomiting , a feeling of fullness or pain in the epigastric region after eating can be observed; with exacerbation of gastritis, slight soreness in the epigastric region can be detected. With an increase in atrophy of the mucous membrane and a decrease in the secretory function of patients, the unpleasant taste in the mouth, nausea , salivation, belching of air are more often disturbed; pain is not pronounced. With severe atrophy of the gastric glands, Castle's internal factor is not produced. This can lead to the development of B12-deficient anemia , manifested by pallor, glossitis, neurological disorders, etc. Violation of the secretory and motor functions of the stomach leads to symptoms of intestinal dyspepsia, manifested by flatulence, stool instability; against the background of chronic gastritis, signs of asthenoneurotic syndrome (weakness, irritability, etc.) may also be remembered.

The diagnosis of chronic gastritis can only be established by gastroscopy and morphological examination of biopsy specimens with an assessment of the severity of inflammation (superficial, deep gastritis), degree of atrophy of the glands (absent, partial, complete), metaplasia - transformation of the gastric mucosa; using special tests in biopsies determines the presence of Helicobacter pylori.

With an uncomplicated course of chronic gastritis in most cases, treatment is not required; when Helicobacter pylori is detected, ampicillin , trichopolum or de-nol are prescribed; with severe signs of inflammation - sucralfate (venter); hospitalization is indicated only with severe exacerbation of the disease and, if necessary, differential diagnosis of chronic gastritis and gastric cancer.

The prognosis is favorable (chronic gastritis in itself practically does not affect the duration and quality of life), but gastritis with pronounced signs of atrophy and metaplasia of the mucous membrane is considered as a precancerous condition.

Erosive gastritis - a common cause of bleeding from the upper digestive tract - can also be acute and chronic. Acute erosive gastritis occurs against the background of extensive trauma, head injuries, extensive burns, blood loss, shock, sepsis, renal or liver failure. Typically, the patient is in serious condition, and it is not possible to identify any dyspeptic manifestations; the first sign of acute erosive gastritis is bloody vomiting (hemathemesis) or tarry stool (melena). The diagnosis is established endoscopically, during the manipulation, electrocoagulation of erosion is immediately carried out. Further treatment includes antacids and H2-histamine receptor blockers (cimetidine, ranitidine).

Chronic erosive gastritis often develops while taking non-steroidal anti-inflammatory drugs, as well as with Crohn’s disease or viral infection, or with no apparent cause (idiopathic erosive gastritis). Symptoms may be absent. Sometimes patients note nausea, discomfort in the epigastrium; most often, patients seek medical help with the appearance of symptoms of gastrointestinal bleeding.

The diagnosis is made by gastroscopy; treatment includes antacids, H2-histamine receptor blockers. With gastritis, which occurred during therapy with anti-inflammatory drugs (suppressing the production of prostaglandin E in the stomach), therapy with misoprostol, a synthetic analogue of prostaglandin E with cytoprotective properties, is advisable.