CC BY
0«шиитешим-лшшаи» 2024 / medical sciences
37
УДК 616.33-002-036.1-071-08
Dorogokupets A. V.,
6th year student of 14 group Bukovinian State Medical University Honcharuk L.M. PhD in Medical Sciences, Associate Professor Department of Internal Medicine;
Andrushchak M.O.
PhD in Medical Sciences, Associate Professor of Department of Infectious Diseases and Epidemiology Bukovinian State Medical University Antonyuk Yu.Yu., 6th year student of 14 group Bukovinian State Medical University
Tkachuk N.V., 6th year student of 14 group Bukovinian State Medical University
Zumer V.V. 6th year student of 14 group Bukovinian State Medical University DOI: 10.24412/2520-6990-2024-3196-37-39 GASTRITIS AS A MODERN DISEASE. CLINICAL SYMPTOMS, DIAGNOSIS AND TREATMENT
Abstract.
Gastritis is one of the most common diseases of the gastrointestinal tract, which affects about 50% of the population of our country. Diseases of the digestive system have been on the rise for the past few years. In the structure of general morbidity, diseases of the digestive organs take third place after diseases ofthe cardiovascular system and respiratory organs.
Keywords: digestive system, gastritis, nausea, vomiting, gastrointestinal tract, Helicobacter pylori.
The purpose of the work is to study the peculiarities of the course of gastritis, the main causes ofits occurrence and progression, as well as to get acquainted with the tactics of its diagnosis and treatment.
Gastritis is a collective term used to describe inflammatory and dystrophic changes of the gastric mucosa of different origin and course. Depending on the intensity and duration of the affecting factors, the pathological process can be acute, occurring mainly with inflammatory changes, or chronic, accompanied by structural restructuring and progressive atrophy of the mucous membrane[1].
Accordingly, two main forms are distinguished: acute and chronic gastritis. In many countries of the world, chronic gastritis is recorded in 80-90% of the population, while the most dangerous form of gastritis, which belongs to the so-called "precancerous conditions", is atrophic gastritis, which is found in patients younger than 30 years old in 5% of cases, in patients aged from 31 to 50 years old - in 30% of cases, in patients over 50 years old - in 50-70% of cases [2].
Acute gastritis (OG) is an acute inflammation of the gastric mucosa caused by a single exposure to strong irritants. Acute gastritis often develops as a result of irritant chemicals entering the stomach, taking certain medications, eating poor-quality food contaminated with pathogenic microorganisms. Depending on the clinical manifestations and nature of damage to the gastric mucosa, the following types of acute gastritis are considered: catarrhal, fibrinous, corrosive and phlegmonous [3].
Catarrhal gastritis is most often the result of food poisoning and improper nutrition.
Fibrinous gastritis occurs with acid poisoning, sulema or severe infectious diseases.
Corrosive gastritis occurs due to the entry into the stomach of concentrated acids or alkalis, salts of heavy metals[4]. Corrosive gastritis is characterized by ne-crotic changes in the stomach tissues.
The causes of phlegmonous gastritis are injuries and complications after peptic ulcer or stomach cancer, some infectious diseases. It is characterized by purulent melting of the stomach wall and spread of pus in the submuco s al lay er.
The main thing in the treatment of acute gastritis is to eliminate the causes of its occurrence. To clean the stomach, the patient is given 2-3 glasses of warm water and induces vomiting. In the case of toxic-infectious or chemical poisoning, the stomach is washed with warm water in the first hours, using a thick gastric probe for this. Rinsing is carried out to clean water[5]. During the first day, no food is taken, the patient is given warm water to drink in small amounts or a water-tea diet is also possible. Then the ration is gradually expanded, observing the principle of mechanical, thermal and chemical sparing. Gradually include slimy soups, liquid pureed porridges, pickles, fruit jellies, boiled eggs, white flour crackers in the diet [6].
Antispasmodics, cholinolytics, and antacids are taken to eliminate pain. It is recommended to take en-terosorbents (smekta and others). Prokinetics are prescribed for vomiting. With acute toxic-infectious
38
MEDICAL SCIENCES / «©0LL®@UWm-J0y©MaL» 2024
gastritis - antibiotics (aminoglycosides, fluoroquinolones, biseptol and others). In case of severe acute gastritis, glucose solution, physiological solution, and potassiumpreparations are administered parenterally to correct water and electrolyte disturbances.
Chronic gastritis (CG) is a long-term recurrent inflammatory lesion of the gastric mucosa, which occurs with its structural rearrangement and disruption of gastric functions [7].
Chronic gastritis often develops asymptomati-
cally.
There are two main forms of the chronic course of the disease: superficial and atrophic gastritis.
In addition to the two main forms, there are also special forms of chronic gastritis: atrophic-hyperplastic gastritis, hypertrophic gastritis, giant hypertrophic gastritis, lymphocytic, granulomatous, collagenous, eosinophilic (synonymous with allergic), radiation, infec-tious[8].
The appearance and development of chronic gastritis is determined by the influence of many factors on the stomach tissues. The most significant external etio-logical factors that contribute to the occurrence of HCV are infection of the stomach by Helicobacter pylori and, to a lesser extent, other bacteria or fungi, nutritional disorders, bad habits such as alcoholism and smoking, long-term use of drugs that irritate the gastric mucosa and the effect on the mucous membrane of radiation and chemicals, parasitic infestations[9]. Today, chronic stress is almost second among the factors after Helicobacter pylori, which has not decreased in our country recently[10].
There are also internal factors that contribute to the occurrence of CG: genetic predisposition, duode-nogastric reflux, autoimmune processes that damage stomach cells, endogenous intoxications, hypoxemia, chronic infectious diseases, metabolic disorders, endocrine dysfunctions, hypovitaminosis, reflex effects on the stomach from other affected organs [11] .
According to the etiology, chronic gastritis is divided into three main forms: type A, B, C and mixed forms.
Chronic gastritis is clinically manifested by both local and general disorders, which, as a rule, appear during periods of exacerbation. Local disorders are characterized by symptoms of dyspepsia (heaviness and a feeling of fullness in the epigastric region that appear or intensify during or after eating, belching, nausea, unpleasant taste in the mouth, often heartburn, which indicates a violation of evacuation from the stomach and throwing up of the gastric contents into the esophagus) [12].
General disorders can be manifested by the following syndromes:
- weakness, irritability, disorders of the cardiovascular system - cardiac pain, arrhythmia, arterial instability;
- patients with atrophic chronic gastritis may develop a symptom complex similar to the dumping syndrome (sudden weakness, pallor, sweating, drowsiness that occur shortly after eating), which are sometimes combined with intestinal disorders, with imperative urges to stool;
- patients with chronic gastritis of the body of the stomach and the development of B12-deficiency anemia develop weakness, increased fatigue, drowsiness, a decrease in vitality and loss of interest in life, pain and burning in the mouth and tongue.
- patients with Helicobacter pylori associated antral chronic gastritis with increased acidity may develop ulcer-like symptoms, indicating a possible pre-ulcer condition.
Establishing a clinical diagnosis is based on determining the type of chronic gastritis, assessing the degree of prevalence of morphological signs of the disease, the presence and severity of gastric function disorders^].
Stages of diagnosis of chronic gastritis:
Clinical diagnosis - the patient's complaints, medical history, patient examination data are analyzed, a probable diagnosis is expressed and a rational plan of instrumental examination is drawn up.
Endoscopic diagnosis with a mandatory biopsy -the presence of Helicobacter pylori, the nature and localization of changes in the gastric mucosa, and the presence of precancerous changes in the gastric mucosa are clarified. At least 5 points are taken for biopsy (2 -from the antrum, 2 - from the body of the stomach, 1 -from the angle of the stomach).
Laboratory diagnostics - clinical blood analysis, biochemical blood analysis, clinical urine analysis, clinical analysis of feces, analysis of feces for occult blood, detection of Helicobacter pylori infection[14].
Ultrasound examination ofthe liver, pancreas, gall bladder - to detect concomitant diseases of the gastrointestinal tract.
Intragastric pH-metry - determination of the state of secretion and diagnosis of disorders in acid-dependent diseases ofthe gastrointestinal tract.
Electrogastroenterography - study of the motor-evacuatory function of the gastrointestinal tract with the aim of determining duodenogastric reflux
Manometry of the upper parts of the gastrointestinal tract, which determines the presence or absence of reflux gastritis[15].
Treatment of chronic gastritis is carried out on an outpatient basis, the course of treatment, including diagnostics, is designed for 14 days. Proton pump inhibitors, H2-histamine receptor blockers, prokinetics, selective M-cholinergics, and antacids are used for the treatment of chronic gastritis. Eradication therapy is recommended for Helicobacter pylori associated gastritis. It is conducted according to the modern recommendations of the Maastricht Consensus, the last of which was held in 2023.
Conclusion: Summarizing the above, we understand that gastritis is a complex problem and a multi-disciplinary approach is necessary for the treatment of this disease. Taking into account the variety of factors that can cause it, it is necessary to meticulously understand its causes, qualitatively collect the anamnesis of patients and not neglect the peculiarities of the patient's working conditions or place of residence.
«@®ii®@yjum-j®urnal» 2024 / medical sciences
39
^iTepaTypa.
1. Watari J, Chen N, Amenta PS, Fukui H, Oshima T, Tomita T, Miwa H, Lim KJ, Das KM. Helicobacter pylori associated chronic gastritis, clinical syndromes precancerous lesions, and pathogenesis of gastric cancer development. World J Gastroenterol. 2014 May 14;20(18):5461-73. doi: 10.3748/wjg.v20.i18.5461
2. Kulnigg-Dabsch S. Autoimmune gastritis. Wien Med Wochenschr. 2016 Oct; 166(13-14):424-430. Epub 2016 Sep 26.
3. Sugano K, Tack J, Kuipers EJ, Graham DY, El-Omar EM, Miura S, Haruma K, Asaka M, Uemura N, Malfertheiner P; faculty members of Kyoto Global Consensus Conference. Kyoto global consensus report on Helicobacter pylori gastritis Gut. 2015 Sep:64(9):1353-67. doi: 10.1136/ /gutjnl-2015-309252. Epub 2015 Jul 17. Review.
4. Kamimura K, Kobayashi M, Sato Y, Aoyagi Y, Terai S. Collagenous gastritis: Review. World J Gas-trointest Endosc. 2015 Mar 16;7(3):265-73. doi: 10.4253/wjge.v7.i3.265.
5. Nayak VH, Engin NY, Burns JJ', Ameta P". Hypereosinophilic Syndrome With Eosinophilic Gastritis. Glob Pediatr Health. 2017 Apr 24;4:2333794X17705239 doi: 10.1177/2333794X17705239. eCollection 2017.
6. Lambrecht NW. Menetrier's disease of the stomach: a clinical challenge. Curr Gastroenterol Rep. 2011 Dec;13(6):513-7. doi: 10.1007/s11894-01 1-0222
7. Watari J, Chen N, Amenta PS, Fukui H, Oshima T, Tomita T, Miwa H, Lim KJ, Das KM. Helicobacter pylori associated chronic gastritis, clinical syndromes precancerous lesions, and pathogenesis of gastric cancer development. World J Gastroenterol. 2014 May 14;20(18):5461-73. doi: 10.3748/wjg.v20.i18.5461
8. Kulnigg-Dabsch S. Autoimmune gastritis. Wien Med Wochenschr. 2016 Oct; 166(13- 14):424-430. Epub 2016 Sep 26.
9. Sugano K, Tack J, Kuipers EJ, Graham DY, El-Omar EM, Miura S, Haruma K, Asaka M, Uemura N, Malfertheiner P; faculty members of Kyoto Global Consensus Conference. Kyoto global consensus report on Helicobacter pylori gastritis Gut. 2015 Sep:64(9):1353-67. doi: 10.1136/ /gutjnl-2015-309252. Epub 2015 Jul 17.
10. Review. Kamimura K, Kobayashi M, Sato Y, Aoyagi Y, Terai S. Collagenous gastritis: Review. World J Gastrointest Endosc. 2015 Mar 16;7(3):265-73. doi: 10.4253/wjge.v7. i3.265.
11. Nayak VH, Engin NY, Burns JJ', Ameta P". Hypereosinophilic Syndrome
With Eosinophilic Gastritis. Glob Pediatr Health. 2017 Apr 24;4:2333794X17705239 doi: 10.1177/2333794X17705239. eCollection 2017.
12. Lambrecht NW. Menetrier's disease of the stomach: a clinical challenge. Curr Gastroenterol Rep. 2011 Dec;13(6):513-7. doi: 10.1007/s11894-01 10222-8. Review
13. Coati I, Fassan M, Farinati F', Graham DY', Genta RM', Rugge M". Autoimmune gastritis: Pathologist's viewpoint. World J Gastroenterol. 2015 Nov 14;21(42): 12179- 89. doi: 10.3748/wjg.v21.i42.12179
14. Carmel R. Prevalence of undiagnosed pernicious anemia in the elderly. Arch Intern Med. 1996 May 27;156(10):1097-100.
15.Sipponen P, Maaroos HI. Chronic gastritis. Scand J Gastroentero1. 2015 Jun;50(6):657-67. doi: 10.3109/00365521.2015.1019918. Epub 2015 Apr 22. Review.
