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Chronic gastritis (codes C 29.3 - 6)

Definition Chronic gastritis is a clinical morphological concept characterized by a violation of the physiological regeneration of the epithelium with an outcome in atrophy, impaired secretory function of the stomach, its motor and partly incretory activity.

Statistics. Chronic gastritis is the most common digestive system disease, affecting about 50% of the adult population. In the structure of chronic gastritis, a clear predominance of B-gastritis (70-75% of cases) over A-gastritis (15-20% of cases) was noted. C-gastritis accounts for about 5%, “special” forms no more than 0.5-1% of cases.

Etiology. Pathogenesis. Pathological anatomy. The leading cause of A-gastritis is a genetic factor through which atrophy of the gastric mucosa is realized. ? -gastritis is considered an increased risk of developing stomach cancer.

B-gastritis is caused by a pyloric helicobacter. (H. pylori). C-gastritis is caused by reflux of the duodenal contents into the stomach, non-steroidal anti-inflammatory drugs, alcohol, it can develop after gastrectomy. B-gastritis is most affected by antrum, where inflammation is more intense than in the body and bottom of the stomach. The histological main diagnostic criteria for this type of gastritis are:

• severe neutrophilic infiltration in the fossa epithelium with cell damage;

• plasmacytic and lymphocytic infiltration of their own plate;

• N. pylori finds in the form of “short curved rods” on the surface of the mucous membrane and in the lumens of the fossae.

? -gastritis affects the body and the bottom of the stomach. Histologically: lymphoplasmacytic infiltrates, often with the formation of follicles in their own plate, intestinal and "antral" metaplasia.

C-gastritis affects the antrum of the stomach. Its histological characteristics:

• hyperplasia of pit epithelial cells;

• reduction in the number of mucin of the pit cells;

• swelling of your own plate;

• increase in the number of smooth muscle cells in one's own plate;

• eosinophilic infiltration of the deep layers of the mucous membrane.

C. Compton identified gastritis "environment" (metaplastic atrophic gastritis type B). The border region between the antrum and the body of the stomach along the lesser curvature of the stomach (lymphocytic infiltrates, intestinal metaplasia, atrophy of the mucous membrane) is more often involved. The nature of the disease is not specified. A connection with H. pylori or the consumption of toxic substances (nitrates, etc.) with a small amount of cytoprotective nutrients (fresh fruits, vegetables) is not excluded.

Clinically asymptomatic lymphocytic gastritis has characteristic histological signs. It:

• lymphocytic infiltration of the surface and fossa epithelium, “damage” to the epithelium;

• lymphoplasmacytosis of the lamina propria;

• neutrophils, erosion. Lymphocytic gastritis is associated with helicobac

teriosis, spruceliakia, Menetrie disease (phase of development of this disease), stomach lymphoma.

Clinic. Epigastric pain is dull, aching, occurs immediately after eating, monotonous, gradually fading. Dyspeptic syndrome: nausea, belching, regurgitation after eating, heartburn, unpleasant taste in the mouth. Symptoms are clearly related to the quantity and quality of food eaten; it appears after eating spicy, fried, greasy, smoked, and rough foods. The tongue is coated with white plaque, with imprints of teeth. The abdomen is soft, moderately painful in the epigastrium.

Clinical evaluation of gastric secretion. According to gastric pH-metry, at a pH of 1.9-0.9, a conclusion is made about an increased secretory function (strongly acidic stomach), at a pH of 2.0-2.9, the secretory function is preserved (medium acid stomach). Moderately expressed secretory insufficiency is characterized by pH values ​​of 3.0-4.9, pronounced - 6.9-5.0. Achlorhydria corresponds to a pH of 7 or more.

When using probe methods, a judgment on the level of gastric secretion is made on the basis of an assessment of the basal and stimulated phases, the flow rate of free hydrochloric acid. By F.I. Komarov, streets aged 18-19 years, fasting gastric secretion is 20-50 ml with a total acidity of 10-15 UNITS, free hydrochloric acid - 0-40 UNITS; basal - 50-120 ml with a total acidity of 40-60 IU, free hydrochloric acid -30-50 IU, debit per hour of free hydrochloric acid - 50-150 mg; stimulated secretion - 50-130 ml with a total acidity of 40-70 UNITS, free hydrochloric acid - 30-60 UNITS, debit per hour of free hydrochloric acid - 50-200 mg. At the age of 30-50 years, the figures are respectively 5-10% lower.

X-ray examination. In the early stages of antrum gastritis - thickening of the folds, pyloric spasm; in the later stages - smoothed mucosa, sluggish peristalsis.

Gastroscopy: edema, hyperemia, hemorrhage, erosion, contact bleeding of the mucosa.
In mucosal biopsy specimens: superficial, interstitial with glandular lesion without atrophy, atrophic, hypertrophic, granulomatous gastritis. Helicobacter colonization, neutrophil infiltration, atrophy, intestinal metaplasia are semi-quantified. The listed indicators are reflected in the protocol separately for the antrum and body of the stomach. Severe intestinal metaplasia of the 3rd type according to L.I. Aruin belongs to precancerous conditions.

Classification. International Houston Classification of Chronic Gastritis (1996).

Type of gastritis A: (autoimmune); B (helicobacter); C (reflux gastritis); rare forms.

State of gastric secretion: elevated and preserved (normal); secretory insufficiency (moderate and severe, including achlorhydria).

Phase: exacerbations, remissions.

Criteria that make it possible to attribute chronic gastritis to type A (immune, with the development of specific antibodies to parietal cells of the gastric mucosa) are: morphological (localization in the bottom and body of the stomach, mild inflammatory reaction, the development of mucosal atrophy in the early stages of the onset of the disease) ; immunological (the presence of antibodies to parietal cells and internal factor); clinical (severe hypo- and anacidity, gastrinemia, the development of vitamin B12-deficient anemia).

With type B gastritis, the inflammatory process is significantly expressed, localized more often in the antrum, erosion is possible. The development of atrophy is secondary, in the later stages of the disease. Helicobacteriosis, antibodies to helicobacteria of the gastric mucosa are detected. Type of secretion any. By P.Ya. Grigoriev should distinguish two forms of gastritis type B - the early stage (antrum gastritis) and late (diffuse atrophic gastritis). Antrum gastritis (non-atrophic, with preserved gastric secretion) is more common in young people, occurs with ulcerative symptoms, edema, hyperemia, erosion of the antrum. Diffuse atrophic gastritis with secretory insufficiency is usually found in the elderly, characterized by dyspeptic syndrome, pale, thinned, smoothed mucous membrane of the antrum and the body of the stomach.

Chemical (C-gastritis) is caused by bile reflux into the stomach, the use of non-steroidal anti-inflammatory drugs, and alimentary chemical irritants. Most often, type C gastritis is diagnosed in patients with a resected stomach; after organ-preserving operations on the stomach; with duodenal ulcers, duodenitis. Radiation gastritis cause radiation damage to the gastric mucosa; lymphocytic gastritis can be associated with cobacter gels at the stage of formation of clinical remission of B-gastritis; eosinophilic gastritis - a symptom of food allergies, other allergoses; non-infectious granulomatous gastritis is diagnosed with Crohn's disease, sarcoidosis, Wegener's granulomatosis, foreign bodies of the stomach.

Diagnosis

• Chronic gastritis type B associated with Helicobacter pylori; exacerbation: erosive pyloritis; medium acid stomach (preserved gastric secretion).

• Chronic gastritis type A: atrophic gastritis of the bottom and body of the stomach; exacerbation, severe secretory insufficiency.

Differential diagnosis

• Stomach cancer. The early signs are unmotivated weakness, fatigue, unclear health concerns and anxiety combined with depression (obsessive-depressive syndrome), aching epigastric pain, decreased appetite. Later symptoms are rapid satiety after eating a small amount of food, weight loss, belching "rotten", black stools, fever. The disease does not occur with periods of exacerbation, but progressively. X-ray diagnostics: “atypical” mucosal relief, filling defect, lack of peristalsis, ulcer with infiltrative edges, flat solitary erosion. Fibrogastroscopy: picture of cancer ulcer; exophytic cancer ("cauliflower"); thickening of the mucosa, a kind of "orange peel" with an infiltrative form.

• Polyposis of the stomach occurs with gastritis-like symptoms, recurrent gastric bleeding, inhibition of gastric secretion up to histamine-resistant achlorhydria. The diagnosis is verified by x-ray and gastroscopic methods. To exclude the malignancy of polyps, a targeted biopsy is necessary.

• Menetrie disease is a serious disease that occurs with severe dyspeptic syndrome, edema, hypoproteinemia, anemia. The diagnosis is verified by the endoscopic method. Wide, high folds of the mucous membrane resembling the human brain are visible, and the stomach is like a “bag of worms”.
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Chronic gastritis (codes C 29.3 - 6)

  1. Chronic gastritis
    CHRONIC GASTRY incremental functions of the stomach.
  2. 66. CHRONIC GASTRITIS
    Pain in the epigastric region is poorly expressed, is not clearly localized, does not affect the general condition of patients • Stomach dyspepsia: bursting in the epigastric region associated with eating; belching, nausea, vomiting, appetite disturbances • Dyspepsia: bloating, rumbling, flatulence, stool instability Asthenovegetative syndrome: weakness, fatigue, irritability and
  3. CHRONIC GASTRITIS
    The most common disease of internal diseases. Chronic gastritis is a clinical anatomical concept. 1. Morphological changes in the mucous membrane are nonspecific, the inflammatory process is focal or diffuse. 2. Structural rearrangement of the mucosa with impaired regeneration and atrophy. 3. Nonspecific clinical manifestations. 4. Violations of the secretory, motor, partially incretory
  4. Chronic gastritis
    - chronic inflammation of the gastric mucosa (diffuse or focal), accompanied by a violation of the physiological regeneration of the epithelium, its atrophy, functional insufficiency of the stomach, upset secretory, motor, and often endocrine functions of the stomach. Main clinical manifestations of chronic gastritis. Local appearance of pain (dull, without radiation), severity and
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  6. Chronic gastritis and gastroduodenitis
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  12. Question 20 GASTRITIS
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  15. Gastritis.
    Gastritis is an inflammation of the gastric mucosa. According to the nature of the course, it is divided into acute and chronic. Acute gastritis is a short-term disease, which, depending on the severity of the course, is most often asymptomatic, less often accompanied by epigastric pain, nausea, vomiting, sometimes with various signs of gastric bleeding. The causes of acute gastritis are diverse:
  16. Gastritis
    - pain cm: localization of pain in the epigastrium, left hypochondrium: provoked by mental, physical exertion, inaccuracies in nutrition, occur after 15-20 minutes. after eating - dyskinetic cm: pain, heartburn, belching, vomiting, diarrhea, constipation - dyspeptic cm: impaired appetite, nausea, vomiting, diarrhea - cm asthenia: weakness, fatigue, headache, sleep disturbance, autonomic
  17. Acute gastritis
    Acute gastritis is an acute inflammatory process of the gastric mucosa in response to its damage. Acute gastritis occurs at any age, and, as a rule, you can trace its relationship with a specific etiological factor. In older children is relatively rare. A feature of this nosological form is a combination of the vulnerability of the gastric mucosa and extremely
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