Gastritis is an inflammation of the gastric mucosa in response to its damage. The international classification of gastritis, called the “Sydney system” (1990), is based on histological endoscopic criteria and is the most acceptable. Gastritis is classified by type, location, morphology and etiology. By type, they distinguish:

Acute.
Chronic.
Special forms (Granulomatous, Eosinophilic, Lymphocytic, Hypertrophic, Reactive).

By topography:

Gastritis of an antrum.
Gastritis of the body.
Gastritis of antrum and body (pangastritis).

By morphology:

Inflammation.
Activity.
Atrophy.
Intestinal metaplasia.
Helicobacter pylori.

By etiology:

Microbial: Helicobacter pylori, etc.
Non-microbial: autoimmune, alcoholic, post-resection, non-steroidal anti-inflammatory drugs, chemical agents.
Unknown factors, including microorganisms.

Severity: Light, Moderate, Severe. The criteria for dividing gastritis into mild, moderate, severe form are 5 main signs: 1, Inflammation, 2. Activity, 3. Atrophy, 4. Intestinal metaplasia, 5. Degree of colonization of the mucous membrane (CO) of Helicobacter Pylori (HP). The morphological part of the diagnosis is always attached to the corresponding section of the stomach. In connection with this need biopsy taken precisely at at least 2 bars of CO from antrum (2 cm from the pylorus), and of the body (one piece from the front and rear walls), and necessarily with muscular plate. Superficial and atrophic gastritis are excluded from the modern classification . The following histological conclusions are recommended : “autoimmune chronic pangastritis with a predominance of severe atrophy in the fundus”, “reactive antrum gastritis associated with bile” or “reactive gastritis of the antrum with erosion associated with aspirin”, etc.

ACUTE GASTRITIS.

According to etiological factors, there are: exogenous and endogenous. Exogenous – agents that come from the outside with food or the food itself. Endogenous – blood – brain barrier. Acute gastritis also occurs after overeating. There is an individual intolerance to any food – idiosyncrasy. Exogenous factors – drugs (digitalis, cardiac glycosides, antibiotics, glucocorticoids, sulfonamides) Acute gastritis is caused by infected food (staphylococci, streptococci). Endogenous factors – with infectious diseases (influenza, measles, typhus, typhoid fever, scarlet fever, pneumonia), with acute intoxications (tissue breakdown with burns, acute renal and hepatic insufficiency), while taking medications. Clinical signs of acute gastritis. A vivid manifestation is a stormy beginning, often with exogenous causes. Acute abdominal pains, nausea, salivation, unpleasant taste in the mouth, weakness, headache , dizziness, at the peak of vomiting are possible : food masses are released first , and then mucus, bile, diarrhea is possible (especially with food poisoning). There is dehydration, loss of salts, there may be cramps. Objectively. Pale skin, decreased skin turgor, decreased temperature, tongue overlaid. The abdomen is sometimes swollen, but more often retracted. Acute pains, but nevertheless the abdomen is soft. Since there is dehydration, a small amount of urine is released, there is an increase in the cylinders, there may be protein, blood, increased hemoglobin, leukocytosis. Motility: first hypertonicity, then atony. Forecast: with timely therapy passes without a trace. Exception: infected food. Differential diagnosis. Adnexitis, cholecystitis, pancreatitis, appendicitis (general – pain, vomiting), acute myocardial infarction ( ECG is necessary , if there are lesions, gastric lavage should not be done ). Corrosive gastritis occurs with the intake of acids and alkalis, causing acute destruction of the tissues of the gastric mucosa, which can lead to shock (depending on the acid or alkali taken ). Phlegmanous gastritis occurs against the background of staphylococci, pneumonia, E. coli, more often hemolytic streptococcus.

TREATMENT OF ACUTE GASTRITIS.

Rinse with warm water. If acid poisoning, then add soda, milk, egg white to the water . If alkali, then you need to add lemon juice.
Enter in / in a cap. – Phys. solution, glucose + vitamin C + vitamin B
In case of pain, anticholinergic drugs (atropine, platyphyllinum hydrotartrate s / c), antispasmodics (papaverine hydrochloride, baralgin). With severe pain shock – drugs.
In infectious gastritis – appropriate antibacterial drugs are prescribed (see acute gastroenterocolitis) and absorbent substances (activated charcoal, kaolin, etc.).
In acute allergic gastritis , Antihistamines are also indicated.
Bismuth-containing drugs.
Then – olive oil, milk, butter.
The first 1-2 days it is better not to eat, but only drink – mineral water, weak tea in small portions. In the future, you must follow the appropriate diet (see diets).
Acute gastritis with hemorrhage of erosions should be treated using Blockers H2-receptors of histamine (w / w 100 mg of Zantac mono- and inwardly of 150 mg 2 times a day, or in / 40 mg kvamatel mono- and inwardly of 20 mg 2 times a day or Loseka / w 40 mg once and inwardly to 20 mg 2 times a day) and simultaneously inside Sucralfate in an initial dose of 6.0 g with continuing bleeding designate additional 4.0 g of product from possible adjusting daily to 15.0 g .

CHRONIC GASTRITIS.

Chronic gastritis (CG) is a chronic inflammation of the gastric mucosa (coolant), manifested by its cellular infiltration, a violation of physiological regeneration and, as a result , atrophy of the glandular epithelium, intestinal metaplasia, a disorder of the secretory, motor and often endocrine function of the stomach. Approximately 50% of the working age population of developed countries suffers from chronic hepatitis.

Most chronic hepatitis C occurs as a result of infection of the coolant HP (Helicobacter pylori), less often they are caused by an autoimmune process. Often, chronic antral gastritis associated with HP proceeds latently, without pronounced symptoms. However, with a careful study of the anamnesis and complaints, as a rule, a number of symptoms are detected . However , they still have infection with the coolant HP, and a histological examination of gastrobiopaths confirms the presence of chronic hepatitis C. With prolonged infection with HP, the pathological process from the antrum extends to the body of the stomach, while atrophic changes begin to prevail over inflammatory ones and the disease transforms into pangastritis.

FORMS OF CHRONIC GASTRITIS.

Antral Neatrophic gastritis (early stage).

It is more common at a young age. Clinic. With an exacerbation, they often complain of ulcer-like dyspepsia: periodic pain, including hungry, heartburn, sometimes sour belching, constipation. When abdominal palpation determined local stress in the abdominal wall piloroduodenalnoy zone. Endoscopically. Against the background of hyperemia and edema of the CO of the antrum , submucous hemorrhages and erosion (flat, elevated), fold hyperplasia, exudation, antral stasis, pyloric spasm are often visible . The results of a histological examination show pronounced ative antral gastritis (infiltration of the own plate of CO and epithelium with lymphocytes, plasmocytes, neutrophils). Foci of intestinal metaplasia. Many HP on the surface and in the depths of the pits. Diffuse Pangastritis with atrophy (late stage).

More common in the elderly.
Clinic.
During an exacerbation, they complain of “gastric” dyspepsia, a feeling of heaviness, fullness, dull pain in the epigastric region, an unpleasant taste in the mouth, a decrease in appetite, nausea, belching of the air, and unstable stool. Palpation determined diffuse stress anterior abdominal wall in epigastrium.

Endoscopically. Determined pallor, smoothness, thinning, sometimes spotty congestion in the body and antrum of the stomach, translucence vessels, increased vulnerability. Hypotension, hypokinesia, bile reflux. Histological examination shows atrophy of the glandular epithelium, intestinal metaplasia, a small amount of NP in the antrum CO and in the body of the stomach, minimal activity of inflammation. CG with significant activity is characterized not only by neutrophilic CO infiltration, but also by the formation of “intracavitary” and “intraepithelial” abscesses and erosion. Detection of such changes in coolant and often and duodenal intestine is an indication for the biopsy of antral CO and other parts of the stomach (3-4 biopsy), and sometimes from dvenadatsatiperstnoy guts for cytological, histological and bacteriological studies. Chronic Active Gastroduodenitis and Antropylorobulbit.

Along with chronic active antral gastritis and pangastritom in patients infected with Helicobacter Pilory (HP) , developed chronic active gastroduodenitis , often antropilorobulbit. Clinic. In patients with chronic active antropilorobulbitom, the association of Helicobacter Pilory (HP) 20% indicated the formation of peptic ulcer disease with localized recurrent ulcers in the bulb duodenal ulcer , or (ii) in the outlet of the stomach, and in patients with chronic active H. pylori pangastritom with intestinal metaplasia and progressive atrophy in in some patients (about 3%) , stomach cancer occurs in the long term . In patients with chronic pangastritis , antibodies to parietal cells are detected in 10% of cases, and some of them subsequently develop B12-deficient anemia, mainly in patients with an antibody titer exceeding 1:40.

Autoimmune gastritis.

Morphological changes are mainly localized in the bottom and body of the stomach . The inflammatory reaction is mild. Primary atrophy of the epithelium. Rarely there may be erosion. Immunologically infectious factor (HP) is not detected, there are no antibodies to HP . There are antibodies to parietal cells and to an internal factor. Clinic. Severe gastrinemia, pronounced hypoacidity. B12 deficiency anemia develops . A combination with peptic ulcer has not been identified. Malignancy is extremely rare.

Helicobacter pylori gastritis.

Morphological changes are mainly localized in the antrum. Inflammatory reaction is pronounced. Secondary atrophy of the epithelium develops . Often erosion appears. Infection with HP is immunologically determined; there are antibodies to HP. There are no antibodies to parietal cells and to an internal factor. Clinic. There is no pronounced gastrinemia. Any type of acidity occurs , except achlorhydria. B12 deficiency anemia does not develop. This type of gastritis is often combined with peptic ulcer , and also leads to malignancy. Patients with B12-deficient (megaloblastic) anemia complain of fatigue, drowsiness, pain in the tongue, paresthesia. In most untreated patients, a lacquered tongue is found, in the case of more severe anemia, pallor of the skin and yellowness of the sclera. Hematological parameters are completely normalized after treatment with B12 alone.

SPECIAL FORMS OF GASTRITIS.

Granulomatous gastritis is a rare sign of sarcoidosis, Crohn’s disease , mycoses, with foreign bodies and tuberculosis. The diagnosis is based on the results of a histological examination of targeted biopsy samples of CO.

Eosinophilic gastritis is extremely rare and is usually associated with vasculitis, some of them have a history of allergies, eczema, and others. It is characterized by severe infiltration by eosinophils, not only CO, but also other layers of the stomach wall . Along with infiltration , edema and plethora are noted .

Hypertrophic gastritis (Menetrier’s disease) may lead to the loss of body weight due to the loss of protein as a result of diarrhea accompanied with pains in epigastrium, nausea. Hypertrophic mucous fields detected by contrast x-ray examination should be differentiated from lymphoma. The main morphological trait is giant folds resembling meanders of the brain, abundant viscous mucus covering the folds.

Lymphocytic (chronic erosive) gastritis is characterized by severe selective lymphocytic infiltration of the gastric CO epithelium . An endoscopic examination reveals nodules, thickened folds and erosion mainly in the body of the stomach.

Reflux gastritis , or reactive gastritis , associated with bile or drugs. Gastritis associated with bile has been previously described as reflux gastritis (type C gastritis ), which develops in patients who have undergone a gastrectomy. This form of gastritis often has to be differentiated from Helicobacter pylori gastritis.

Polypous gastritis or polyposis of the stomach. 1 or more polyps on the gastric mucosa. Blastomatous changes — precancer. Diagnosis: radiologically, mobility is lost , the contours of the stomach are uneven, the contours of polyps are also uneven. Need endoscopy with a biopsy.

TREATMENT OF CHRONIC GASTRITIS.

Gastritis that occurs latently does not need treatment. In these cases, it is recommended to limit yourself to general events: exclude strong alcoholic beverages, taking non-steroidal anti-inflammatory drugs, and smoking.

1. In chronic active gastritis (gastroduodenitis) , associated with Helicobacter pylori (HP) treatment must be complex, but in the presence helikobakterioza, must be included and antibacterial therapy. Proved development of resistant strains of bacteria to antibiotics, such as metronidazole, Applied scheme triple therapy (bismuth drug and an antibiotic 2) , to minimize NO resistance to an antibacterial treatment.

De-nol (bismuth colloidal subcitrate, 120m g) – 1 tablet 30 minutes before breakfast, lunch and dinner, and the 4th time in the evening on an empty stomach before bedtime.
Tetracycline (500 mg) – 3 times a day,
Metronidazole (400 mg) – 3 times a day for 2 weeks.

With Active gastritis and Gastroduodenitis, De-nol is prescribed for 3-4 weeks , Tetracycline can be replaced with Oxacillin and Amoxacillin, or Clarithromycin (clacid). Elimination of infection is observed in more than 90% of patients. With triple therapy, some patients experience transient side effects (nausea, abdominal discomfort). Do not use antacids with de nol at the same time !!

2. In case of Chronic Active Antral Gastritis ( Gastroduodenitis ) with Ulcer-like dyspepsia , Denol should be combined with Gastrocepin (25 mg 3-4 times a day).

3. In chronic active antral gastritis (gastroduodenitis) erosion and severe pain in an alternative triple therapy using other combinations:

Omeprazole or Lanzoprazole 20mg at 8 o’clock in the morning and at 20 o’clock in the evening and
Antibiotic (oxacillin or amoksatsillin or tetratsikllin of 0,5 g 4 times a day or clarithromycin by 0.5g 2 times a day ) , the treatment for 7 days.

4. Treatment of Autoimmune HCG.

Tools Replacement Therapy (natural gastric juice, Acid-pepsin, Pepcid, etc.)
Drugs that stimulate the secretory function of the stomach (insulin, aminophylline, calcium preparations),
Affecting tissue metabolism, trophism and CO regeneration processes (sodium nucleate, vitamins, combined enzymes).

From the 1st day of treatment, natural gastric juice is prescribed for 1 table. spoon in 1/2 cup of water in small sips with meals. Acidin-pepsin or pepsidil or betacid, or other tablet preparations are prescribed only after the acute symptoms of inflammation subside . In the presence of megaloblastic anemia, vitamin B12 is prescribed . The course of treatment consists in daily intramuscular administration of 1 ml of 0.1% oxycobalamin solution for 6 days. Then, within a month, the drug is administered 1 time per week, and subsequently 1 time in 2 months. Cycobalamin can be used instead of oxycobalamin . After 3-6 months, a small number of patients develop iron deficiency. In such cases, a short course of oral iron supplementation is indicated.

5. Treatment of Hypertrophic Gastritis (Menetrie disease).

Ingestion 25 mg of gastrocepine 4 times or 15 mg of probantin 4 times, or 2 mg of metacin 4 times a day until the symptoms of the disease are relieved . In the presence of intestinal metaplasia in the coolant, annual control endoscopic examinations with a biopsy are indicated.

6. Treatment of dyspepsia. With many diseases of the upper digestive tract, especially with gastritis, there are various manifestations of dyspepsia. The most common symptoms are severity or discomfort in the epigastric region, rapid satiety with food, retrosternal or upper abdominal discomfort associated with eating, taking certain foods, hunger or time of day. Often, such complaints of patients are combined with heartburn, rumbling, transfusion, bloating (flatulence). In these cases, antacids are prescribed for several days . The most neutralizing ability is possessed by preparations consisting of magnesium oxide and (or) aluminum hydroxide. You can prescribe one of these drug.

Maalox (aluminum hydroxide and magnesium hydroxide), which has an antacid, enveloping and adsorbing effect.
Phospholugel (a colloidal gel containing aluminum phosphate, pepsin gel and agar-agar), which has an enveloping, antacid, cytoprotective effect.
Gastal (aluminum hydroxide, magnesium carbonate, magnesium hydroxide), has an antacid and enveloping property.
Gasterin-gel, Actal , etc.

Liquid antacids have a faster effect than tablets, but they are more convenient. Aluminum-containing antacids bind bile acids. They can cause constipation. Magnesium-containing antacids can cause diarrhea.

7. With nausea and vomiting. Prescribe drugs that regulate the motor function of the gastrointestinal tract:

Metoclopramide ( raglan, cerucal and other synonyms). Side effects include: drowsiness, tinnitus, dry mouth.
Domperidone ( Motilium and other synonyms). They do not cross the blood-brain barrier and therefore do not cause extrapyramidal disorders, is a more preferred drug, especially in the elderly.