How, when and where is gastritis diagnosed? Instrumental methods for studying chronic gastritis Treatment of autoimmune gastritis
- an unpleasant disease that requires careful diagnosis. Diagnosis of chronic gastritis makes it possible to identify the disease and correctly determine the extent of the disease. There are several different diagnostic methods.
Physical is the simplest test that can be done in a doctor's office. It consists of obtaining information from the patient about the history of his life and illness, visual examination of the skin, tongue, eyes, palpating, tapping and listening with the ear to the entire abdomen.
Clinical laboratory tests(determination of basic indicators) blood, urine, feces:
Additional research methods
Immunological blood test:
- Detects chronic gastritis type A (autoimmune). In the blood, autoantibodies characteristic of this disease are detected to astromucoprotein, parietal cells, and sometimes to vitamin B12.
- At the beginning of inflammatory processes in the stomach, a significant amount of pepsinogen appears - the proenzyme pepsin in the blood. With atrophic processes in the gastric mucosa (), these indicators decrease sharply.
Histological and cytological examination of gastrobiopsy.
Chronic gastritis and its cause - Helicobacter pylori - are confirmed, and the degree of its severity is determined.
Instrumental methods
Diagnosis of Helicobacter pylori bacteria in the stomach
Helicobacter pylori is the main cause of chronic gastritis
- Cytological examination of a smear of the gastric mucosa. Determines the presence of Helicobacter.
- Histological examination of biopsy material. The presence of specific antibodies in the blood serum confirms Helicobacter.
- Urease breath standard test. Bacterial urease is determined in the patient’s exhaled air, which confirms their presence. Aimed not only at diagnosing the disease, but also at correcting treatment.
- Urease express test. A special substance applied to a biopsy of the gastric mucosa changes its color under the influence of Helicobacter urease.
- Bacteriological research method. Bacteria are isolated from gastric biopsy cultures.
- The immunohistochemical method is based on the effect of special antibodies against Helicobacter when applied to biopsy material. In this case, only bacteria change color. Performed in case of resumption of the disease after treatment.
- Molecular biological method. Finds bacterial DNA in gastric biopsy using a special enzyme.
Specific types of examination are prescribed by a gastroenterologist in order to determine an accurate diagnosis and prescribe the correct treatment.
RCHR (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical protocols of the Ministry of Health of the Republic of Kazakhstan - 2017
Gastroduodenitis, unspecified (K29.9), Chronic atrophic gastritis (K29.4), Chronic superficial gastritis (K29.3)
Gastroenterology
general information
Short description
Approved
Joint Commission on Healthcare Quality
Ministry of Health of the Republic of Kazakhstan
dated June 29, 2017
Protocol No. 24
Chronic gastritis- a group of chronic diseases, morphologically characterized by inflammatory and dystrophic processes in the gastric mucosa and a variety of clinical signs.
Inflammation of the gastric mucosa caused by Helicobacter pylori (H. pylori), with disorders of the secretory, motor and endocrine functions of the stomach, histologically manifested by cellular infiltration.
Chronicatrophic gastritis- characterized by functional and structural restructuring with dystrophic processes in the coolant, progressive atrophy with loss of gastric glands and their replacement with metaplastic epithelium and/or fibrous tissue.
There are atrophic gastritis:
autoimmune
multifocal
Non-atrophic (superficial, antral) and atrophic (multifocal) variants of chronic gastritis are considered as stages of one pathological process that occurs as a result of infection of the gastric mucosa with H. pylori infection.
Often combined with other autoimmune diseases, type 1 diabetes mellitus, autoimmune thyroiditis, pernicious anemia.
NB! The diagnosis of any form of gastritis is established only histologically. Endoscopic results are not convincing. During an endoscopic examination, 4-6 biopsies should be taken from different parts of the stomach (according to the modified Sydney system).
INTRODUCTORY PART
ICD-10 code(s):
| ICD-10 | |
| Code | Name |
| K 29.3 | Chronic superficial gastritis |
| K 29.4 | Chronic atrophic gastritis |
| K 29.9 | Chronic autoimmune gastritis |
Date of development of the protocol: 2017
Abbreviations used in the protocol:
| IV | intravenously |
| i/m | intramuscularly |
| PC | subcutaneously |
| r/day | once a day |
| AIG | autoimmune gastritis |
| ALT | alanine aminotransferase |
| ASK | acetylsalicylic acid |
| AST | aspirate aminotransferase |
| AT | antibodies |
| agro-industrial complex | antibodies to parietal cells |
| BHA | biochemical analysis |
| BUT | rapid urease test |
| GDZ | gastroduodenal zone |
| GER | gastroesophageal reflux |
| DGR | duodenogastric reflux |
| DPK | duodenum |
| Housing and communal services | gastrointestinal bleeding |
| Gastrointestinal tract | gastrointestinal tract |
| IPP | proton pump inhibitors |
| KM | intestinal metaplasia |
| UAC | general blood analysis |
| OBP | abdominal organs |
| OAM | general urine analysis |
| PG | pepsinogen |
| RJ | stomach cancer |
| SO GDZ | mucous membrane of the gastroduodenal zone |
| SO DPK | duodenal mucosa |
| coolant | gastric mucosa |
| ESR | erythrocyte sedimentation rate |
| Ultrasound | ultrasonography |
| UD | level of evidence |
| FD | functional dyspepsia |
| FEGDS | fibroesophagogastroduodenoscopy |
| CNS | central nervous system |
| YaBDPC | duodenal ulcer |
| YABZH | stomach ulcer |
| H. pylori | Helicobacter pylori |
Protocol users: GPs, therapists, gastroenterologists.
Level of evidence scale:
| A | A high-quality meta-analysis, systematic review of RCTs or large RCTs with a very low probability (++) of bias, the results of which can be generalized to the relevant population |
| IN | High-quality (++) systematic review of cohort or case-control studies, or high-quality (++) cohort or case-control studies with very low risk of bias, or RCTs with low (+) risk of bias, the results of which can be generalized to an appropriate population |
| WITH | Cohort or case-control study or controlled trial without randomization with a low risk of bias (+), the results of which can be generalized to the relevant population or RCT with a very low or low risk of bias (++ or +), the results of which cannot be directly distributed to the relevant population |
| D | Case series or uncontrolled study or expert opinion |
Classification
Classifications
The generally accepted clinical classification is the Husten modification of gastritis, 1996 (Table 1).
Table 1. Sydney classification system for chronic gastritis
| Type of gastritis | Etiological factors | Synonyms (former classifications) | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Non-atrophic |
Helicobacter pylori Other factors |
Surface Chronic antral Gastritis type B Hypersecretory gastritis |
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|
Atrophic autoimmune |
Immune mechanisms |
Gastritis type A Diffuse gastritis of the gastric body associated with B12-deficiency anemia and decreased secretion |
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| Atrophic multifocal |
Helicobacter pylori Eating disorders Environmental factors |
Mixed gastritis type A and B |
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| Special forms | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Chemical |
Chemical irritants: Bile (DGR) Taking NSAIDs |
Reactive gastritis type C Table 2. Classification of atrophic gastritis (OLGA 2007)
Integral indicator of the stage of gastritis in the OLGA system
In each column, atrophy is shown on a four-level scale (0-3) according to the visual analog scale of the modified Sydney Gastritis Classification System . The degree of gastritis refers to the severity of the total inflammatory infiltration (neutrophilic leukocytes and mononuclear cells), and the stage refers to the severity of atrophy. Diagnostics Diagnostic criteria:
List of additional diagnostic measures: · UAC - according to indications; · determination of serum iron in the blood - for anemia; · fecal occult blood test - for anemia; · Ultrasound of the liver, biliary tract and pancreas - according to indications (for chronic autoimmune atrophic gastritis/or for concomitant pathology of the gapatobiliary system); · biochemical blood tests: total bilirubin and its fractions, total protein, albumin, cholesterol, ALT, AST, glucose, amylase - (for chronic autoimmune atrophic gastritis and/or for concomitant pathology of the hapatobiliary system); · Determination of antibodies to parietal cells in chronic autoimmune atrophic gastritis; · Determination of the blood level of gastrin-17 and pepsinogen I (PG I) and pepsinogen II (PG II) - in multifocal atrophic gastritis; · intragastric pH-metry - for severe atrophic gastritis; · X-ray examination of the upper gastrointestinal tract with barium - according to indications (in case of pyloric stenosis, the presence of contraindications to endoscopic examinations and the patient’s refusal to undergo FEGDS). Indications for consultation with specialists:
Diagnostic criteria for various forms of chronic gastritis:
Differential diagnosis
Differential diagnosis of chronic atrophic (multifocal and autoimmune) gastritis
Treatment abroad Get treatment in Korea, Israel, Germany, USAGet advice on medical tourism Treatment Goal of treatment: Main objectives of treatment: Non-drug treatment and general measures include:
Drug treatment. Considering the various etiopathogenetic factors in the development of chronic gastritis, drug therapy differs for different forms of chronic gastritis. Principles of pharmacotherapynon-atrophic gastritis:
Principles of pharmacotherapyatrophic gastritis:
Proton pump inhibitors-PPIs are the most powerful antisecretory drugs. They are prescribed to relieve pain and dyspeptic disorders, as well as to achieve rapid remission. are 2nd line drugs that can be used in cases of intolerance or contraindications to PPIs. Also, histamine H2 receptor blockers can be used as additional therapy in conjunction with PPIs. Antacids capable of maintaining an intragastric pH level > 3 for 4-6 hours during the day, which determines their insufficiently high effectiveness when used as monotherapy. However, patients with hCG take antacids to relieve pain and dyspeptic complaints, which is largely due to their speed of action and over-the-counter availability. Antimicrobials used for chronic hepatitis associated with H. Pylori. For eradication purposes, in combination with PPIs, aminopenicillins (amoxicillin), macrolides (clatrimycin) are used as line drugs and reserve drugs when standard treatment is ineffective: fluoroquinolones (levofloxacin), nitroimidazoles (metronidazole), tetracyclines and bismuth drugs. Drug therapy for hCG associated withH. pylori Recommended eradication regimens (Maastricht-V, 2015)
Second line therapy(10-14 days): The effectiveness of treatment increases with prescribing twice daily higher doses of PPIs (twice the standard dose) (LE B). Eradication therapy for H. pylori may lead to the development of antibiotic-associated diarrhea ( UD S). Adding the probiotic Saccharomycesboulardii to standard triple therapy increases the rate of H. pylori eradication (UDD). List of basic medications used for chronic hepatitis
List of additional medications used for chronic hepatitis
Surgical intervention: No. Preventive actions:
Further management of the patient:
Prognosis for various forms of chronic gastritis
Indicators of treatment effectiveness
Drugs (active ingredients) used in treatmentHospitalization Indications for emergency hospitalization: No InformationSources and literature
InformationORGANIZATIONAL ASPECTS OF THE PROTOCOL List of protocol developers: No. List of reviewers: Review conditions: revision of the protocol 5 years after its publication and from the date of its entry into force or in the presence of new diagnostic and treatment methods with a level of evidence. Disclosure of no conflict of interest: No. Attached filesAttention!
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Currently, world medicine has practically abandoned the clinical diagnosis of “chronic gastritis”. This name now refers to only structural changes in the gastric mucosa observed under a microscope in both patients and healthy people, usually caused by Helicobacter pylori infection. And although in ICD-10 chronic gastritis is still identified as a separate disease and has code K29, its diagnosis does not give the doctor any reason to prescribe treatment to any patient with external signs of the disease, but without complaints.
Currently, if a patient has the corresponding symptoms, it is customary to talk about the presence of functional dyspepsia; if there is a stomach ulcer, pancreatitis, bile reflux and other diseases, we are talking about organic dyspepsia. Modern drug regimens are focused primarily on relieving heartburn, pain, and nausea, and not on eliminating microscopic signs of stomach inflammation.
It would seem, why make a diagnosis of “chronic gastritis”, since it is only morphological and does not in any way affect the treatment of stomach pain? It turned out that diagnosing the disease is very important for identifying precancerous conditions.
Changes in the stomach wall
The cascade of morphological changes in the gastric mucosa begins with the colonization of the bacterium Helicobacter pylori or with the action of another. A superficial pathological process develops, which gradually progresses. In 1–3% of patients, atrophy processes begin within a year, that is, the death of cells in the gastric mucosa. They are replaced by cells resembling intestinal epithelium - intestinal metaplasia develops, and then epithelial dysplasia. This condition is already precancerous.
Out of a hundred patients with an infectious form of the disease, epithelial dysplasia will occur in 10, and stomach cancer will develop in 1–2 people. Up to 90% of all cases of this malignant tumor are associated with changes in the gastric mucosa caused by infection. Eradication (destruction) of Helicobacter makes it possible to stop or even reverse the processes of atrophy and dysplasia and thereby prevent cancer. This is why morphological confirmation of the diagnosis of “chronic gastritis” is so important.
At the same time, we note that the severity of the symptoms of the disease does not depend on the condition of the stomach wall. Therefore, it is the diagnosis of “functional dyspepsia” with an indication of the variant of complaints that helps to correctly select the right medications. Quite often, one person has both of these conditions, different in nature and methods of treatment.
Stages of diagnosing gastritis
First of all, when making a diagnosis, the type of disease is specified (non-atrophic, atrophic autoimmune, atrophic multifocal or special forms of the disease - chemical, radiation, lymphocytic, granulomatous, eosinophilic, other infectious or giant hypertrophic). The type of disease mainly depends on its cause.
The second stage in making a diagnosis is determining the endoscopic characteristics of the disease. There are the following types of pathological process:
- surface;
- with flat or raised erosions (superficial damage to the mucous membrane);
- hemorrhagic (with bleeding);
- hyperplastic (with thickening of mucosal areas);
- reflux gastritis with the reflux of the contents of the duodenum into the stomach.
Diagnosis of the atrophic variant is complemented by determining the stage of atrophy using the OLGA system. This classification is based on histological evaluation, that is, studying pieces of tissue obtained during FGDS under a microscope.
Laboratory diagnosis of chronic gastritis
After assessing the patient's complaints and medical history, some laboratory tests are prescribed. Only one of them is mandatory - a rapid urease test of biopsy material of the gastric mucosa. During FGDS, a piece of tissue is taken, then it is placed in a special solution of reagents and it is determined by the color change whether the material contains Helicobacter pylori or not.
A similar diagnosis of gastritis without gastroscopy is possible - analysis of Helicobacter waste products in exhaled air (respiratory urease test).
Breath urease test
Additional methods for diagnosing chronic gastritis depending on its form and concomitant diseases:
Instrumental methods for diagnosing gastritis
The main method for diagnosing chronic gastritis is fibrogastroduodenoscopy (FGDS) with a biopsy and subsequent histological and cytological examination of the obtained material under a microscope.
During an external examination, the doctor can distinguish the main signs that allow differential diagnosis of infectious and atrophic autoimmune gastritis, as well as peptic ulcer:
- redness and hemorrhages in the mucous membrane are a sign of superficial antral inflammation;
- pallor, thinning, translucent vessels are a diagnostic sign of the atrophic process.
On microscopic examination, antral superficial gastritis is characterized by inflammatory infiltration (impregnation with immune cells in the blood), and atrophic gastritis is characterized by intestinal metaplasia with atrophy of the gastric glands.
Additionally, the following may be assigned:
- study of the acidity of gastric juice, or intragastric pH-metry in case of severe atrophic lesions;
- X-ray examination of the stomach with barium - in case of refusal or contraindications to FGDS, as well as in case of stenosis (narrowing) of the pylorus (pyloric stenosis).
In case of multifocal atrophic variant of the disease, consultation with an oncologist is necessary; in case of anemia, a hematologist; in case of neurological symptoms of vitamin B12 deficiency (paresthesia, sensory disturbances, etc.), an examination by a neurologist.
Differential diagnosis of different forms of gastritis
To accurately determine the form of the disease, the patient’s complaints, external signs and additional diagnostic data are used.
Chronic antral gastritis associated with Helicobacter pylori infection
Symptoms:
- heartburn;
- pain on an empty stomach;
- stool disorders.
Patients are characterized by eating dry food, in a hurry, a predominance of spicy, fried, smoked foods, carbonated drinks, as well as a family history of gastritis or ulcers. There is slight bloating and mild pain in the upper abdomen. Blood tests are normal.
FGDS reveals signs of inflammation affecting mainly the antrum; the urease test is positive.
Chronic atrophic multifocal gastritis
Symptoms associated with impaired digestion of food predominate: diarrhea, weight loss, nausea, and sometimes vomiting. Characterized by irritability, a tendency to consider oneself very sick, fear of cancer, sweating, weakness, palpitations. When palpating the abdomen in its upper part, moderate, but quite large in area, pain is determined. The appearance of the tongue changes: it either becomes covered with a thick white coating, or becomes shiny and smooth, as if varnished.
General and biochemical blood tests remain unchanged. The amount of pepsinogen I in the blood decreases.
FGDS reveals a common pathological process affecting not only the antrum, but also the body of the stomach. When measuring intragastric acidity, a reduced amount of hydrochloric acid is detected (hypo- or achlorhydria, what was previously called “low acidity”). The urease test is usually positive. Microscopic examination of the biopsy specimen reveals signs of intestinal metaplasia, atrophy, and Helicobacter colonization.
Chronic autoimmune atrophic gastritis
The main part of the complaints is related to the deficiency of Castle factor that occurs in this form of the disease, a substance that ensures the absorption of vitamin B12. As a result, signs of corresponding hypovitaminosis appear:
- weakness, shortness of breath, palpitations;
- burning tongue;
- loss of appetite, weight loss;
- constant diarrhea;
- numbness and weakness in the limbs;
- irritability and more severe mental disorders, including dementia.
The patient often has an enlarged liver. The analyzes note:
- macrocytic hyperchromic anemia;
- increase in indirect bilirubin;
- antibodies to parietal cells;
- decreased pepsinogen I levels;
- increase in gastrin levels.
FGDS reveals atrophy of the stomach wall and its polyps. Under microscopy, a combination of inflammation, intestinal metaplasia, and absence of parietal cells is noticeable. The acidity of gastric juice is reduced. The urease test is usually negative. Ultrasound reveals an enlarged liver, less often the spleen.
Differential diagnosis of antral gastritis
Diagnosis of hyperacid, erosive and other forms of superficial gastritis should be carried out taking into account the fact that similar symptoms are observed in some common diseases of the gastrointestinal tract. We present the main differential diagnostic signs of these diseases in the table.
| Antral gastritis | Functional dyspepsia | Stomach ulcer | Chronic pancreatitis | |
| Characteristics of pain | The pain is short-term, usually on an empty stomach, often heartburn after eating | Symptoms are similar to those of antral gastritis, less often peptic ulcer | Pain above the navel, at night, “hungry” | Girdle pain, mainly on the left and in the lumbar region |
| Additional diagnostics |
FGDS – signs of inflammation Positive urease test in most patients |
FGDS without pathological changes | FGDS shows an ulcerative defect on the stomach wall | FGDS without pathology, the main changes are noted with ultrasound of the pancreas. |
Differential diagnosis of atrophic gastritis
Diagnosis of hypoacid gastritis is also carried out taking into account other possible diseases, but their list is different than for antral lesions.
| Multifocal option | Autoimmune variant | Stomach ulcer | Stomach cancer | |
| Main symptoms | Nausea, belching, heaviness in the abdomen, pain are uncharacteristic | There are signs of anemia (weakness, dizziness, shortness of breath) and sensory disturbances (“pins and needles” in the lower extremities | Nausea, vomiting, heartburn, pain on an empty stomach and an hour after eating, weight loss, lack of appetite | Nausea, vomiting, weakness; pain is uncharacteristic; aversion to food, especially meat, sudden weight loss to the point of exhaustion |
| Additional diagnostics | FGDS: signs of mucosal atrophy, negative urease test, increased gastrin level in the blood, decreased pepsinogen level - I | Signs of anemia in the blood (decrease in the amount of hemoglobin and red blood cells, macrocytosis), decrease in the number of platelets and leukocytes, increase in indirect bilirubin, alkaline phosphatase and LDH in blood biochemistry; when studying acidity - its pronounced decrease | FGDS: signs of ulcerative defect. Positive reaction to occult blood in the stool. In the blood there are signs of iron deficiency anemia. When examining acidity, it is normal or moderately reduced | There are signs of hypochromic anemia in the blood, ESR increases. FGDS reveals a tumor. Positive reaction to occult blood in the stool. Acidity is significantly reduced. |
Video “Self-diagnosis of chronic gastritis”
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Ministry of Health of the Republic of Buryatia
State Autonomous Educational Institution "Republican Basic Medical College"
them. E.R. Radnaev"
Course work
Subject:Diagnosticschronic gastritis
Ulan - Ude, 2015
Introduction
Gastritis is an inflammation of the gastric mucosa, in which the restoration of the mucous membrane is impaired, the secretion of gastric juice changes and the contractile activity of the stomach is disrupted.
Over the past 20 years in the Russian Federation there has been an increase in the share of stomach diseases in the structure of diseases of the digestive system, among which chronic gastritis dominates.
Chronic gastritis is a polyetiological disease, characterized by an inflammatory process in the gastric mucosa, accompanied by morphological changes in the latter (atrophy, impaired regeneration), disruption of the motor, secretory and endocrine functions of the stomach and a certain clinical picture. Along with inflammation of the stomach, chronic gastritis also affects other internal organs, that is, the disease is not local, but general, systemic in nature.
Chronic gastritis is one of the most common human diseases. It affects from 30 to 85% of the working population of industrialized countries, and the incidence is high in childhood. The prevalence of chronic gastritis is believed to depend on race, where people live and their age. Chronic gastritis type A is quite rare (about 10% of all atrophic gastritis), mainly in two age groups: in the elderly and in children. Chronic gastritis type B accounts for about 90% of all chronic gastritis, and young and middle-aged men suffer from it much more often than women, but after 60-65 years these differences disappear.
The relevance of the problem is not limited to the widespread prevalence of chronic gastritis. The disease is dangerous due to its etiological connection with stomach cancer and ulcers. And although the prognosis for chronic hepatitis is generally favorable, the disease negatively affects the quality of life of patients, their ability to work and socio-psychological adaptation. In addition, the long course of the disease is accompanied by dysfunction of other digestive organs, as well as the formation of actual psychogenies, persistent inadequate mental reactions to the disease and personality disharmony.
Study the diagnosis of chronic gastritis from literary sources.
1. Study the prevalence
2. Study the etiology and pathogenesis
3. Study the classification according to ICD 10
4. Find out symptoms, diagnosis, complications
PREVALENCE
Chronic gastritis - chronic inflammation of the gastric mucosa - is one of the most “popular” stomach diseases in our country. Almost all patients and a significant part of doctors equate the symptoms of gastric dyspepsia (belching, heartburn, nausea, vomiting, fullness of the stomach after eating and pain in the epigastric region) with the diagnosis of gastritis. Therefore, when asked to the patient: “What diseases do you have or have had before?”, in 8 out of 10 cases “chronic gastritis” is noted. This is partly due to the fact that diagnosis of the disease in most cases is carried out clinically, i.e. based on complaints, without the use of instrumental research methods.
Chronic gastritis is one of the most common human diseases. It affects from 30 to 85% of the working population of industrialized countries, and the incidence is high in childhood. The prevalence of chronic gastritis is believed to depend on race, where people live and their age. Chronic gastritis type A is quite rare (about 10% of all atrophic gastritis), mainly in two age groups: in the elderly and in children. Chronic gastritis type B accounts for about 90% of all chronic gastritis, and young and middle-aged men suffer from it much more often than women, but after 60-65 years these differences disappear. gastritis stomach inflammation
Approximately 50% or even more of the working population of developed countries suffers from this disease, and the incidence increases markedly with age.
ETIOLOGY
According to etiology, chronic gastritis is divided into three main forms:
Type B (bacterial) - antral gastritis associated with contamination of the gastric mucosa by Helicobacter pylori bacteria
Type C (chemical) - develops due to the reflux of bile into the stomach during duodenogastric reflux
Type A (autoimmune) - fundic gastritis; inflammation is caused by antibodies to the lining cells of the stomach.
In addition, there are also mixed - AB, AC and additional (medicinal, alcoholic, etc.) types of chronic gastritis.
Topographically distinguished:
Gastritis of the body of the stomach
Gastritis of the antrum of the stomach
Gastritis of the fundus of the stomach
Pangastrit
In 1990, at the World Congress of Gastroenterology in Sydney (Australia), the following main characteristics of the “Sydney system” of gastritis classification were adopted:
Etiological characteristics:
Autoimmune gastritis type A;
Associated with HP - bacterial gastritis - type B;
Reactive gastritis - type C.
Topographic characteristics:
Antral gastritis;
Fundal gastritis;
Pangastritis.
Chronic gastritis very often occurs in patients with gastroenterological pathology. In this case, it will be expressed by inflammation of the gastric mucosa; associated factors - violation of motor, secretory and some other functions. Very often, chronic gastritis develops against the background of appendicitis, chronic cholecystitis or colitis.
If gastritis occurs in an acute form and is not completely cured, then as a result of further development it can become chronic. But in most cases, the cause of chronic gastritis is external factors such as prolonged poor nutrition (deficiency of vitamins, protein, iron, etc.), consumption of spicy, too hot or rough foods, poor diet, etc.
Chronic gastritis can be caused by certain factors present inside the human body. Some diseases of the internal organs (kidney diseases, gout, etc.) lead to the fact that the gastric mucosa begins to secrete uric acid, urea, indole, skatole, etc. Metabolic disorders, which also lead to the development of chronic gastritis, are triggered by such diseases like diabetes and obesity. Diseases of the gallbladder, pancreas and thyroid glands also lead to various kinds of disorders and changes in the condition of the gastric mucosa.
Long-term exposure to irritating factors leads to functional secretory and motor disorders of the stomach, which, in turn, leads to inflammation, dystrophy, and disruption of the regeneration process in the epithelium of the surface layers of the gastric mucosa. These areas may subsequently atrophy or be completely rebuilt.
PATHOGENESIS
Chronic gastritis most often develops as a result of constantly existing violations of rational nutrition (both in quantitative and qualitative terms): non-compliance with food intake, constant consumption of dry, poorly chewed, too hot or cold, fried, spicy food, etc. Chronic gastritis can develop with long-term use of certain medications (for example, glucocorticoids, NSAIDs, antibiotics, sulfonamides). In recent years, importance has also been attached to hereditary predisposition, since chronic gastritis is more often detected in children with a family history of gastrointestinal diseases. Helicobacter pylori plays a significant role in the development of chronic gastritis. This microorganism is often detected in other family members of a sick child. Helicobacter pylori is capable of breaking down urea (using the enzyme urease), the resulting ammonia affects the surface epithelium of the stomach and destroys the protective barrier, allowing gastric juice access to the tissue, which contributes to the development of gastritis and ulcerative defects of the stomach wall.
CLASSIFICATION ACCORDING TO ICD 10
K29.0 Acute hemorrhagic gastritis
Acute (erosive) gastritis with bleeding Excludes: erosion (acute) of the stomach (K25.-)
K29.1 Other acute gastritis
K29.2 Alcoholic gastritis
K29.3 Chronic superficial gastritis
K29.4 Chronic atrophic gastritis
Mucosal atrophy
K29.5 Chronic gastritis, unspecified
Chronic gastritis: antral. fundamental
K29.6 Other gastritis
Hypertrophic giant gastritis Granulomatous gastritis Menetrier's disease
K29.7 Gastritis, unspecified
K29.8 Duodenitis
K29.9 Gastroduodenitis, unspecified
The most widespread in our country is the classification of chronic gastritis proposed by S.M. Ryssom (1966). According to this classification, chronic gastritis is divided into:
1. According to etiology:
a) primary (exogenous):
b) secondary (endogenous);
2. According to morphological characteristics:
a) superficial gastritis;
b) gastritis with damage to the glands without atrophy;
c) atrophic gastritis (moderate and severe, with intestinal type restructuring):
d) hypertrophic gastritis;
3. By localization:
a) widespread (pangastritis);
b) limited (antral or fundic);
4. Based on functionality:
a) with normal (or increased) secretion;
b) with secretory insufficiency (moderate or severe);
5. According to clinical signs:
a) exacerbation phase;
b) remission phase.
Special forms of chronic gastritis: rigid, giant hypertrophic (Menetrier's disease), polypous, erosive (hemorrhagic), eosinophilic (allergic).
The development of chronic gastritis is based on a genetically determined defect in the restoration of the gastric mucosa damaged by the action of irritants.
There are two main forms of chronic disease: superficial and atrophic gastritis. These terms, based on the results of endoscopic studies of the gastric mucosa, were first proposed in 1948 by the German surgeon R. Schindler. These terms have received universal recognition and are reflected in the classification of gastritis according to ICD-10. The division is based on the factor of preservation or loss of normal glands, which has obvious functional and prognostic significance.
CLINICAL PICTURE
Many gastroenterologists believe that chronic gastritis is not accompanied by a typical clinical picture. However, a carefully collected anamnesis (medical history, its manifestations) in many cases makes it possible to identify, perhaps not very bright, but characteristic signs of this disease (for all forms). The clinical picture of chronic gastritis is often manifested by pain and gastric dyspepsia, but can be asymptomatic. In most cases, the general condition of the patient with chronic gastritis does not suffer.
This is a fairly characteristic sign of chronic gastritis. Pains are observed after eating, and are associated with a certain type of food, less often appear on an empty stomach, at night, or regardless of food, they are dull, aching in nature, do not radiate, and intensify when walking and standing. Acute paroxysmal pain is not characteristic of chronic gastritis; their appearance should alert you to the development of any complications (peptic ulcer, etc.). Sometimes patients, even after eating a small amount of food, experience a feeling of pressure in the stomach, a feeling of fullness in the stomach. In rare cases, the pain may be more intense (with erosive gastritis). In a few cases, pain in children is mild. Sometimes the pain has the nature of a crisis - acute and severe pain in the epigastric region, which is preceded by profuse, uncontrollable vomiting. In a number of patients, the pain syndrome resembles an ulcer (pain occurs 1 1/2-2 hours after eating, on an empty stomach and at night). Half of patients with chronic gastritis have no pain syndrome. An asymptomatic course is especially characteristic of secondary forms of the disease.
GASTRIC DYSPEPSIA SYNDROME
It includes decreased appetite, a feeling of unpleasant taste in the mouth, belching, nausea, bloating, rumbling and fullness in the stomach. This syndrome is caused by impaired gastric digestion and absorption due to insufficient secretion of gastric juice, enzymes and hormones formed in the gastric mucosa. Constipation and a tendency to it are more often observed in patients with Helicobacter gastritis and with high or normal gastric secretion, and flatulence, rumbling and a tendency to loose stools, periodic diarrhea after drinking milk or fats - in patients with reduced secretion. Often the tongue of patients with chronic gastritis is covered with a white or yellow-white coating with tooth marks on its side surface.
HYPOVITAMINOSIS SYNDROME
It is a consequence of insufficient digestion and absorption and is manifested by signs of deficiency of various vitamins, most often group B (cracks and seizures in the corners of the mouth, increased peeling of the skin, premature hair loss, brittle nails).
ASTHEN-NEUROTIC SYNDROME
Often determined in patients with chronic gastritis. It is characterized by increased irritability, suspiciousness, sweating, paresthesia (impaired skin sensitivity, “crawling”), chilliness of the limbs, neurogenic pain in the heart, etc.
ELECTROLYTE DISTRIBUTION SYNDROME
It is observed mainly in atrophic gastritis with reduced secretory function of the stomach. Depending on the specific characteristics, a deficiency of potassium (accompanied by impaired nutrition of the heart muscle and changes in the ECG), calcium (characterized by osteoporosis, brittle bones), and iron (iron deficiency anemia) may be observed.
ENDOCRINE INSUFFICIENCY SYNDROME
It is not so common with gastritis, it is very variable, often mildly expressed. Sometimes it manifests itself as sexual dysfunction, especially in men.
FEATURES OF SOME FORMS OF GASTRITIS
CHRONIC SUPERFICIAL GASTRITIS WITH NORMAL OR INCREASED GASTRIC SECRETION
It is more often found in young and middle age, mainly in men. It is characterized by intense pain in the epigastric region that occurs on an empty stomach, heartburn, sometimes sour belching, and a feeling of heaviness in the epigastric region after eating. Constipation is often observed in patients with this form of gastritis.
CHRONIC EROSIVE GASTRITIS
It is characterized by the presence of numerous superficial ulcerations of the gastric mucosa with frequent hidden gastric bleeding, which leads to moderate anemia. Epigastric pain, heartburn, belching may be present, but sometimes absent. Of primary importance in the diagnosis of this form of gastritis is an endoscopic examination of the stomach (gastroscopy) and a clinical blood test (decreased hemoglobin and the number of red blood cells).
CHRONIC ATROPHIC GASTRITIS WITH LOW ACIDITY
This is the most common form of gastritis. It usually diffusely affects the entire gastric mucosa. The main clinical symptoms: unpleasant taste in the mouth, loss of appetite, nausea, especially in the morning, belching of air, a feeling of rumbling and transfusion in the stomach after eating, bowel irregularities, more often diarrhea, sometimes constipation. With a long course in severe cases of the disease, weight loss, polyhypovitaminosis (insufficient absorption of various vitamins), dysfunction of the endocrine glands (general weakness, hypotension, sexual dysfunction), hypochromic anemia, etc. can be observed.
Chronic atrophic gastritis with secretory deficiency is often accompanied by enteritis, colitis (inflammation of the small and large intestines), pancreatitis, cholecystitis and other chronic inflammatory diseases of the digestive organs. The occurrence of these concomitant intestinal dyskinesias and inflammatory lesions of other organs of the digestive system is explained, on the one hand, by a disorder of gastric digestion, the accelerated entry of insufficiently digested food masses into the intestines and pathological reflexes of its mucous membrane, and on the other hand, by a violation of the production of special hormones (which are synthesized in mucous membrane of the stomach and intestines), regulating the functions of the digestive system.
CHRONIC HYPERTROPHIC GASTRITIS
Complaints with this form of gastritis are not of any specific nature and may coincide with complaints with other forms of gastritis (pain, belching, nausea, etc.). The main criterion for making such a diagnosis is a gastroscopic examination, which reveals a sharp thickening and increase in the folds of the gastric mucosa and hypertrophy of the glands.
CHRONIC HELICOBACTER GASTRITIS
This form of gastritis, as we have already noted, is caused by the microbial pathogen Helicobacter pylori. The clinical picture of this form is dominated by the following complaints: general weakness, feeling of heaviness, fullness of the stomach, dull pain in the epigastric region, unpleasant taste in the mouth, loss of appetite, belching of air, unstable stool. The onset of Helicobacter pylori gastritis can sometimes manifest itself as ulcer-like symptoms: moderate hunger pain, night pain, nausea and even vomiting after eating, sour belching and heartburn. These symptoms are caused by increased gastric secretion and motor-evacuation disorders that occur immediately after infection with this type of bacteria.
COMPLICATIONS
The complications that can arise as a result of the development of chronic gastritis are worth mentioning separately, since they can be quite serious and lead to death. Although, with timely, systematic and correct treatment, many undesirable and destructive consequences can be avoided and even a complete recovery can be achieved.
The following possible complications caused by the development of the disease are identified:
1. Increased atrophy and achylia.
2. Transformation into peptic ulcer disease.
3. Transformation into cancer.
Among the possible complications, five most likely groups are noted:
1. Anemia. Develops with erosive and atrophic gastritis.
2. Bleeding. Occurs with erosive gastritis.
3. Pancreatitis, cholecystitis, hepatitis, enterocolitis. These diseases may occur due to exacerbation or development of certain forms of chronic gastritis.
4. Pre-ulcerative condition and ulcer. Especially likely with piluroduodenitis.
5. stomach cancer. Any form of advanced chronic gastritis can lead to this disease. It has already been proven that cancer tumors primarily appear in patients with primary lesions of the antrum and antrocardial expansion (at the border between healthy and diseased cardiac expansion, as well as at the border between healthy and diseased tissue). In addition, if there have already been cases of cancer in the family, the risk of this complication increases 4 times. The first signs of the development of a cancerous tumor are the following: causeless weakness, rapid satiety with food, deterioration of appetite, a change in the nature of a pre-existing symptom, the appearance of minor signs syndrome. The absence of an immunological reaction and Rh+ blood group II can also serve as signs of early cancer.
DIAGNOSTIC METHODS
There are several main types of examination for gastritis:
1. Objective.
2. Non-invasive diagnostics (clinical blood test, stool test for Gregersen’s reaction, etc.).
3. Invasive diagnostics (histological method, rapid urease and enzyme immunoassay tests, phase contrast microscopy and bacteriological method).
4. X-ray.
5. Probe diagnostics (histamine test).
6. Fibrogastroscopy (FGS) and fibroesophagogastroduodenoscopy (FEGDS).
7. Thermography.
Objective diagnosis
Objective diagnosis provides little information, since it relies only on the external symptoms of gastritis - such as severe weight loss, pale skin, etc. With chronic autoimmune gastritis with poor digestion and absorption syndrome, bleeding gums, premature baldness, brittle nails, dry skin are observed ( especially in the corners of the mouth), hyperkeratosis, white or yellow coating on the tongue. With Helicobacter pylori gastritis, painful sensations occur during palpation.
Increased drowsiness and fatigue are observed with autoimmune gastritis. In this case, the patient quickly loses weight, appetite decreases sharply, and symmetrical paresthesia appears in the extremities. In addition, pale skin, plaque on the tongue and palate, and some neurological symptoms are observed. In some cases, vision problems occur, and there is often a burning sensation in the tongue and mouth.
A more accurate diagnosis can be made only after a thorough examination using additional diagnostic methods.
Non-invasive diagnostics.
This method is based on the study of analyzes of feces, blood, and exhaled serum. This type of examination includes a urease breath test using labeled urea and an enzyme-linked immunosorbent test (Read-Fast Test).
The enzyme immunoassay test is indirect and refers to rapid tests. This examination method allows you to detect antibodies to the bacterium Helicobacter pylory (Hp) in the patient’s blood. Test results are established very quickly; this does not require laboratory conditions or complex equipment for special processing. However, the presence of antibodies in the body cannot serve as absolute proof of the development of infection in the human stomach. In addition, in the early stages of infection, tests do not give any results. These tests are usually used during mass research (during the outbreak of epidemics, etc.).
Invasive diagnostics.
The histological method, such as bacteriological and fast urease, as well as phase-contrast microscopy, is an invasive diagnostic method. These tests are based on the study of the mucous membrane and gastroduodenal zone of the stomach with the identification of Hp bacteria in the human stomach. A biopsy of the gastric mucosa is examined.
The histological method is considered the most effective in diagnosing Helicobacter bacilli infection and at the same time simple to carry out. The test does not deteriorate during transportation or storage, and studies of the results obtained can be carried out under normal conditions without any special laboratory equipment.
The quick urease test method involves introducing a substance into the stomach that leads to an increase in the pH environment; certain results affect the color change. The test can last several minutes, and sometimes a day. Effective results are obtained only if the patient is infected and the bacteria are actively spreading. The test is very easy to perform and has a high guarantee of detecting Hp bacteria.
In practice, several types of rapid urease test are used: CLOtest (Delta West Ltd, Bentley, Australia); Denol-test (Yamanauchi); Pyloritek (Serin Research Corporation, Elkhart, India); HPfast (GI Supply, Philadelphia, USA).
In case of severe infection of the gastric mucosa, the test results are ready in 1 hour (+++). For moderate infection after 2 hours (++). For minor infections, the test will give results after 2 hours or a day (+). To ensure a negative (-) test result, you must wait more than 24 hours for the color change to appear.
The phase-contrast microscopy method makes it possible to detect the presence of the Hp bacterium in the human body in a matter of minutes. This test is highly accurate, since the results are examined in a laboratory setting in an endoscopy room using a phase-contrast microscope. The fresh biopsy obtained during the study is placed on a special glass and covered with another glass moistened with immersion oil. Further studies are carried out using the phase contrast method. A hundredfold magnification makes it possible to detect the presence or absence of Hp bacteria, which are spiral-shaped, curved microorganisms. If there are any, then an indisputable diagnosis of gastritis can be made. Processing of test results can only be carried out in laboratory conditions and with the help of special equipment, which excludes the possibility of using this method under normal conditions.
The bacteriological research method is considered one of the most complex and therefore quite expensive. It consists of determining the sensitivity of the human body to various drugs for the presence of infection.
This examination method is necessary for differentiation from peptic ulcer disease and cancer, but the development of gastritis cannot be detected in this way. If peptic ulcers or tumors are not detected by X-ray results, then other methods are used to further diagnose gastritis.
Probe diagnostics.
Probing has been practiced in our country for quite some time in diagnosing gastritis, although recently this method has become a little outdated. However, with its help you can study the condition of the stomach in sufficient detail. The probe is a thin tube equipped with a micro-chamber and sensors. The patient swallows this tube, so the probe enters the stomach and the doctor is able to examine his condition.
Probing includes three phases. The first phase is carried out on an empty stomach, when the patient does not eat for 6-8 hours before the start of the session. The second phase begins an hour after insertion of the probe: basal secretion is established, that is, the reaction of the intestinal organs to mechanical stress. The third phase takes place after artificial stimulation. Parenteral secretagogues are used to stimulate the stomach, although in the recent past various doses of food were given to the patient as stimulants. Parenteral secretion agents - special drugs (pentagastrin, histamine, in some cases aminophylline or insulin).
Histamine is administered in an amount of 0.008 mg per kilogram of the patient’s weight; with an average weight, the amount of the drug administered is approximately 0.4-0.5 mg. Taking histamine allows the doctor to determine the condition of the stomach according to the following parameters:
General acidity;
The total amount of gastric juice secreted in 2 hours (the norm is 150-200 ml);
Increasing the pepsin content in gastric juice produced in 1 hour, or, in scientific terms, pepsin debit hour;
The amount of acid produced in 1 hour, or the production hour of hydrochloric acid.
A method using histamine to probe the stomach is called a submaximal histamine test. This method will allow you to accurately establish the diagnosis in 97 cases out of 100.
There is also a method using daily monitoring. Its essence lies in the fact that several probes are placed into the patient’s abdominal cavity at once, which are much smaller in size than those used when conducting a histamine test. Daily monitoring lasts much longer than a histamine test and allows you to thoroughly examine the condition of the internal organs of the abdominal cavity.
Probe diagnostics makes it possible to make a very accurate diagnosis, which is why it is widely used in most clinics in our country.
FGS and FEGDS
Fibrogastroscopy with biopsy is one of the main methods in diagnosing gastritis, as well as in examining the stomach for the possible development of a malignant tumor. Using this method, it is possible to thoroughly examine 45 sections of the stomach with a full guarantee of identifying possible precancerous signs.
Fibroesophagogastro-duodenoscopy is one of the effective methods for examining the condition of the stomach, esophagus, and duodenum. It is used in many clinics, although it is believed that this method is somewhat outdated. Examination of the internal organs of the abdominal cavity is carried out using flexible liquid crystal endoscopes with fiber optics, which is a kind of camera. FEGDS is used mainly as a starting test in the initial stages of disease development and at the first complaints of the patient. Indications for this method can be emergency or planned.
conclusions
Chronic gastritis is sometimes the result of the further development of acute gastritis, but more often develops under the influence of various factors (repeated and prolonged eating disorders, consumption of spicy and rough foods, addiction to hot foods, poor chewing, dry food, consumption of strong alcoholic beverages). The cause of chronic gastritis can be qualitatively poor nutrition (especially deficiency of protein, iron and vitamins); long-term uncontrolled use of medications that have an irritating effect on the gastric mucosa (salicylates, butadione, prednisolone, some antibiotics, sulfonamides, etc.); industrial hazards (lead compounds, coal, metal dust, etc.); diseases that cause oxygen starvation of tissues (chronic circulatory failure, anemia); intoxication due to kidney diseases, gout (in which the gastric mucosa secretes urea, uric acid, indole, skatole, etc.); action of toxins in infectious diseases. In 75% of cases, chronic gastritis is combined with chronic cholecystitis, appendicitis, colitis and other diseases of the digestive system.
The most common symptoms of chronic gastritis are a feeling of pressure and fullness in the epigastric region after eating, heartburn, nausea, sometimes dull pain, loss of appetite, and an unpleasant taste in the mouth. Most often, the acidity of gastric juice decreases. At a young age, predominantly in men, the acidity of gastric juice can be normal or even increased. Characterized by pain, often heartburn, sour belching, a feeling of heaviness in the epigastric region after eating, and sometimes constipation.
By collecting theoretical material and studying all the intricacies of the topic of chronic gastritis, I gained knowledge that will undoubtedly be useful to me in my profession.
While doing all the work, I relied on my knowledge gained during my studies. I experienced slight difficulties when working with the information of the course work, and yet I managed to present the material, as it seems to me, in full.
Having completed my coursework, I can say that I have mastered all the skills and abilities I need when working with patients.
Bibliography
1. Aruin L.I., Kapuller L.L., Isakov V.A. Morphological diagnosis of diseases of the stomach and intestines. - M.: "Triad-X", 1998. - 483 p.
2. Aruin L.I. New international classification of dysplasia of the gastric mucosa // Ross, journal of gastroenterol., hepatol., coloproctology. - 2002, No. 3. - pp. 15-17.
3. Encyclopedic Dictionary of Medical Terms. - ed. B.V. Petrovsky. - M.: Soviet Encyclopedia, 1982. - T. 1. - 464 p.
4. . Aruin L.I., Grigoriev P.L., Isakov V.A., Yakovenko E.P. Chronic gastritis. Amsterdam, 1493. 362 pp.
5. Minushkin O.N., Zverkov I.V. Chronic gastritis. / Attending doctor. - 2003, No. 5, p. 24--31.
6. Ivashkin V.T. Lapina T.L. Chronic gastritis, principles of diagnosis and treatment. //R.M. J. - 2001; 2; 54-61.
7. Osadchuk M.A., Pakhomov A.L. Kvetnoy I.M. Chronic gastritis with functional dyspepsia: pathological features of clinical manifestations. //Rus. J.G.G. K. - 2002; 5; 35-39.
8. Pajares-Garcia H. Helicobacter gastritis with and without dyspepsia: morphological or clinical unit. //Rus. J.G.G. K. - 2002; 6; 76-80.
9. Livzan M.A., Kononov A.V., Mozgovoy S.N. EX-Helicobacter gastritis: neologism or clinical reality. /Experimental and clinical gastroenterology. - 2004; 5; 55-59.
10. Clinical lectures on gastroenterology and heptology / Edited by A.V. Kalinina, A.I. Khazanov, in 3 volumes. Volume
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Any inflammatory disease first occurs in an acute form. To become chronic, the process requires time and lack of treatment.
Diagnosis of chronic gastritis - inflammation of the gastric mucosa, is based on the receipt and analysis of cumulative data from a conversation with the patient, external examination and internal clinical, instrumental, laboratory, bacteriological and biochemical studies.
Chronication of acute inflammation of the stomach occurs over a period of time. This could be a year or a year and a half, or several months - the speed of development of the disease and its transition to the chronic stage directly depends on a combination of a number of factors:
- lifestyle;
- nature of nutrition;
- presence of bad habits;
- occupational hazards of a chemical, physical or psychological nature;
- individual characteristics of the patient;
- genetic predisposition;
- presence of cases of familial disease.
You can suspect a diagnosis of “chronic gastritis” if you feel sick after eating for several months, sometimes before vomiting. Patients may also indicate a decrease in general tone, fatigue, drowsiness, irritability, and dyspeptic symptoms. Among them, the most common are appetite disturbances, belching with an unpleasant odor, and problems with stool: constipation or diarrhea.
Particular attention should be paid to the connection between such symptoms and the nature of the food taken. Consumption of sour, salty, fried foods, carbonated drinks, and alcohol leads to a significant deterioration of the condition.
Diagnosis of chronic gastritis
If you observe the above changes in general health in yourself or your loved ones, you should immediately seek help from a doctor. Usually, this is a general practitioner who, after examining and talking with the patient, will decide what additional examinations and highly professional consultations are needed.
Despite the apparent simplicity and frequency of occurrence of gastritis, including chronic gastritis, the diagnosis of this disease is a process that requires time, special tests and research methods. To successfully get rid of the pathology or significantly improve the condition and achieve long-term remission, it is necessary to conduct a full examination to accurately establish the etiology (cause) of inflammation of the gastric wall.
Patient examination plan
A gastroenterologist acts according to a specific plan in order to collect as much objective data as possible in favor of a particular cause of inflammation. The pathogenesis of the disease depends on the trigger mechanism. Therefore, chronic gastritis is usually classified according to several parameters. Depending on the cause, the disease is divided into mechanical, physical, chemical, bacterial or combined inflammation.
Atrophic and hypertrophic gastritis are classified according to the degree of pathological changes in the gastric mucosa. The nature of the inflammatory changes is manifested by the appearance of a diffuse lesion of the inner lining of the stomach - catarrhal gastritis. Foci of local deep lesions are characteristic of the ulcerative form of the pathology.
The degree of severity of subjective symptoms, objective signs of digestive disorders, and deterioration in general condition characterizes the stage of development of gastritis: exacerbation or remission. The totality of data from all patient examination tests leads to the establishment of a final diagnosis, which is coded in the ICD.
Examination of a patient with suspected chronic gastritis includes diagnostics with collection of anamnesis, examination of the patient, and the appointment of instrumental methods for studying the state of internal homeostasis, digestion and secretion.
Objective patient examination data
After examination, the doctor can confirm his opinion about the presence of gastritis if:
- When palpating the abdomen, pain in the epigastric region is noted;
- pallor of the skin is noted;
- the tongue has signs of being coated with a whitish or yellowish coating;
- bad breath;
- upon palpation of the lower third of the abdomen, rumbling is felt, there are signs of excessive gas formation in the intestines;
- There may be ulcerations in the corners of the mouth - jams.
It is imperative to prescribe an instrumental examination, which includes several important, informative methods.
FGDS – fibrogastroduodenoscopy
A rather painful procedure, during which a special probe with a video camera is inserted into the patient’s esophagus into the stomach cavity. The doctor sees the image of the mucous membrane of the stomach, esophagus and duodenum on the monitor screen and can objectively determine the presence of inflammatory changes, their nature, and the amount of gastric juice.
During the procedure, the following diagnostic procedures may additionally be performed:
- sampling material for biopsy;
- measuring the pH value of gastric juice;
- taking a sample for bacteriological analysis for the presence of Helicobacter pylori.
Biopsy
A tiny piece of the stomach lining is pinched off with a special instrument to be examined in the laboratory. This will make it possible to judge the presence or absence of oncological changes in tissues, the depth of the process, differentiate the localization of proliferation of cell layers, and preliminarily establish the presence of a bacterial pathogen.
pH-metry
During an internal examination of the stomach, it is possible to check the level of acidity of gastric juice - conduct pH measurements. The results of pH measurements make it possible to differentiate gastritis by the level of hydrochloric acid production and its effect on the nature of the disease: hyperacid or hypoacid gastritis.
Useful video
How the disease is detected can be found in this video.
Diagnosis of Helicobacter pylori
This is a set of measures to identify a microbe in the stomach. This includes the results of a biopsy examination, pH measurement, seeding of material in a bacteriological laboratory in order to obtain a pure culture of the microorganism and establish its species, and the results of a breath test.
Breath test
The patient is asked to exhale air twice into a disposable container: the first time before taking a special drug, the second time after taking urea. This makes it possible to establish the presence and degree of activity of Helicobacter pylori in the stomach.
An obligatory step for a complete diagnosis of chronic gastritis is the assessment of the results of a clinical examination of feces, blood and urine.
Blood analysis
The level of hemoglobin, color index, leukocytes - all this data must be assessed for a final diagnosis. Severe disturbances in the digestion and absorption of nutrients in the stomach can lead to pernicious anemia and an increase in the number of white blood cells.
Stool and urine analysis
The results of these studies help to assess the degree of pathological changes in internal homeostasis: the development of inflammation, anemia, dysbiosis, disturbances in food digestion, metabolism and excretion of bile pigments
X-ray method
Should be used at the stage of differential diagnosis. The patient is asked to swallow a radiopaque substance - barium compounds. It fills the cavity, and all changes in the relief of the gastric and duodenal mucosa become visible on the x-ray. This method is especially valuable for diagnosing peptic ulcers and oncological pathologies.
Differential diagnosis
At the final stage of diagnosis, it is necessary to conduct a comparative analysis of symptoms and the results of an objective study in order not to be mistaken with the diagnosis of “chronic gastritis”.
This disease should be distinguished from peptic ulcer of the stomach and duodenum, pancreatitis, dyskinesia of the gallbladder and bile ducts, and pathological neoplasms of these organs. Symptoms of chronic gastritis may be similar to those of an ulcer of the antrum or fundus of the stomach or duodenal portion of the gastrointestinal tract.
Pancreatitis with localization of inflammation in the head part, adjacent to the entrance to the duodenum, can also be characterized by subjective symptoms similar to gastritis. In combination with gallbladder dyskinesia, dietary errors, and occupational hazards, such inflammations can be multilocal in nature and masquerade as chronic gastritis.
