Symptomatic is a complication of various pathological processes that lead to damage to the gastric mucosa and 12 pc severe pathology of the central nervous system myocardial infarction various types of drug endocrine shock. The contingents of HP infection of persons who are in contact with patients with gastric cancer with stomach ulcers and 12pc gastritis HP medical personnel - 68 times more often among endoscopist doctors than in other population groups persons living in unfavorable conditions overcrowding low social status lack of hot water ...

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Stomach ulcer and 12 pc.

Earlier in our country the term "peptic ulcer" was widely used. Currently, in accordance with ICD10, it is recommended to use the term "ulcer" with an indication of the location. It is possible to use both terms.

There are primary chronic lesions of the gastroduodenal region and secondary (symptomatic) ulcers. Symptomatic is a complication of various pathological processes that lead to damage to the gastric mucosa and 12 pc (severe pathology of the central nervous system, myocardial infarction, various types of shock, medicinal, endocrine).

Peptic ulcer- primary (independent) chronic cyclical disease, a characteristic feature of which during the period of exacerbation is the formation of ulcers of the gastroduodenal zone. The prevalence is 5-10% of the population.

Ulcerative defect - a defect in the mucosa, the depth of which reaches the muscular membrane.

Erosion - shallow mucosal defects that heal without scarring. May be large.

Etiology. Pathogenesis. Polyethiological disease.

1. Infection (Н b pylori ) - can cause active inflammation in the mucous membrane.70% of those infected remain healthy, asymptomatic carriers.

Contingents of HP infection

• persons in contact with patients with stomach cancer, gastric ulcer and 12pk, HP gastritis,
• medical staff - 6-8 times more often among endoscopist doctors than in other population groups
• people living in unfavorable conditions (overcrowding, low social status, lack of hot water, hypovitaminosis)
• contingents of closed institutions.

Not all strains are pathogenic. Determination of antibodies in the blood does not always indicate a peptic ulcer. Talk about a possible relationship H b pylori to ischemic heart disease (ischemic heart disease more often in persons with a / t to Helicobacter) and other diseases.

1. Hereditary factors (especially with gastric ulcer).
2. Corticovisceral theory - neuropsychic effects - violation of neurohumoral regulation of the stomach and duodenum 12.
3. Vascular - disorders of the blood supply to the mucous membrane.
4. Alimentary factors (gross errors in nutrition - long-term violation of the diet, irritating food) - are not of leading importance.
5. Bad habits - smoking (stimulation of the parietal cells), abuse of coffee, alcohol.
6. NSAIDs (significantly increase the risk of bleeding, perforation).

As a result of the influence of these reasons, an imbalance develops between the factors of aggression of gastric juice and the factors of protection of the gastric mucosa and 12pc.

V 1910 K. Schwartz emphasized the inviolability of the position: "No acid (hydrochloric) - no ulcer."

Classification.

I. By localization

Stomach ulcer

Ulcer 12pc

Combined gastric and duodenal ulcers

II ... Flow options:

1. Latent.
2. Light (exacerbation less than 1 time per year).
3. Moderate severity (exacerbations 1-2 times during the year).
4. Severe (3 or more times a year)

III ... Endoscopically:

• active (open);
• scarring (a roller is formed);

Red scar stage - just closed - continue therapy;

Stage of the white scar - gradually the vessels empty, their number decreases;

• long-term non-scarring for more than 2 months. continuous treatment - dangerous in terms of rebirth.

IV. Dimensions:

• small up to 0.5 cm;
• average 0.5-1 cm;
• large 1.1-3 cm;
• giant over 3 cm.

V ... Complications (bleeding, perforation, penetration, malignancy, stenosis).

The clinical picture.

The period of exacerbation lasts 3-4 weeks. Ulcer scarring ends in 45-60 days.

1. Pain . Localization. The sooner pain occurs after a meal, the closer the ulcer is to the cardiac part of the stomach.

• with an ulcer of the cardiac region - pain in the epigastrium or under the xiphoid process immediately after eating, sometimes radiating to the region of the heart;
• ulcer of the fundus and body of the stomach pain 20-30 minutes after eating, there may be pain on an empty stomach;
• pyloric ulcer - pain in the epigastrium on the right 2-3 hours after eating, radiating to the back, behind the sternum, to the right hypochondrium;
• duodenal ulcer - pain 3-4 hours after eating, often "hungry" and night pains, calming down after eating.

Character ... Half of the pain is mild, dull, about 30% intense. The pain can be aching, cutting, cramping.

Periodicity. Pain bothers during an exacerbation, during remission, pain does not bother.

Seasonality. Exacerbations of peptic ulcer disease are more often observed in spring and autumn.

1. Dyspeptic phenomena:

• discomfort, heaviness in the epigastric region;
• unpleasant taste in the mouth;
• belching (sour belching is most characteristic);
• heartburn;
• nausea;
• vomiting (occurs at the height of pain, vomit contains acidic stomach contents).
• flatulence;
• stool disorders (in half - constipation due to spastic contraction of the colon, taking antacids).

If a duodenal ulcer near the nipple of Vater m. his swelling and jaundice.

1. Common symptoms - may be weakness, palpitations, pain in the region of the heart - are associated with dysfunction of the autonomic nervous system.

Diagnostics.

Laboratory data.

UAC, OAM. TANK. Stool analysis (Gregersen reaction) - occult blood.

Instrumental research methods.

FEGDS. Biopsy.

For long-term non-healing ulcers, fibrous-thickened and dense edges (callous ulcers) are characteristic. Localization (ulcer of greater curvature, the angle of the stomach is dangerous in terms of degeneration)

Fluoroscopy:

Niche - protrusion of the contours of the stomach outward, filled with a contrast agent.

Studies of acid production in the stomach.(Intragastric pH metry, fractional study of gastric juice).

Ultrasound OBP.

Confirmation of helicobacteriosis.Gastroscopy with biopsy, serological tests (DETERMINATION OF ANTIBODIES IN BLOOD), urease breath test.

Lecture No. 4 TREATMENT of stomach ulcers and 12 pc. Complications.

1. Elimination of factors affecting the development of peptic ulcer disease, exacerbation is better in a hospital, physical. and a psycho rest.
2. Diet. Table n. Food is served boiled. Marinades, smoked meats, canned food, fried meat, hot spices, coffee, alcohol are excluded.
3. Medical treatment.

Ulcer associated with HP

Eradication therapy(destructive therapy), anti-Helicobacter therapy.

Schemes see chronic gastritis (triple scheme, quadrotherapy scheme)

After the end of the combination therapy, treatment with one of the antisecretory drugs is continued once in the evening for 5-7 weeks.

Ulcer not associated with HP

• basic antisecretory therapy, the purpose of which is to relieve pain and dyspeptic disorders.

In 1990 W. Burget et al. came to the conclusion that ulcers scar in almost all cases if intragastric pH> 3 can be maintained within 24 hours for about 18 hours. None N 2 blockers, neither selective anticholinergics, nor antacids can fulfill this condition. Only proton pump blockers satisfy this requirement; these drugs are currently the most effective in the treatment of peptic ulcer disease.

Proton pump blockers (PPIs) -block the proton deposition of the parietal cells, which ensures the synthesis of hydrochloric acid (Omeprazole, rabeprazole, lansoprazole).

H2 histamine receptor blockers -block receptors through which histamine stimulates gastric secretion (famotidine, ranitidine).

Antacids and adsorbents- neutralize hydrochloric acid in the stomach without affecting its production (soda, Rennie, almagel, gastal, maalox - insoluble, contain aluminum, long-acting - it is not recommended to use more than 2 weeks - damage to bone and muscle tissue, damage to the brain, kidneys. Adsorbents - vikalin, vikair.

M-anticholinergics - reduce the secretion of hydrochloric acid, reduce the tone of smooth muscle organs - non-selective - atropine, platifillin; buscopan.

Selective - do not affect the M-HR of the heart, bronchi (gastrocepin).

For all ulcers,

• Means that normalize motor function (motilium, metoclopramide), spastic phenomena - antispasmodics;
• Reparants: solcoseryl, sea buckthorn oil - improve regeneration in the mucous membrane.
• Centrally acting agents (sedatives, tranquilizers).

1. Herbal medicine (chamomile, St. John's wort)
2. Physiotherapy.
3. Absolute indications for surgical treatment: perforation, profuse bleeding, stenosis, accompanied by severe evacuation disorders, malignancy.

Relative indications: history of multiple profuse gastrointestinal tract infections, penetrating ulcers, ulcers resistant to drug therapy.

1. Endoscopic ulcer therapystomach / duodenal ulcercan be conservative and surgical. Conservative endoscopic therapy includes application or irrigation of the ulcer surface with drugs (sea buckthorn oil, solcoseryl, etc.), injecting the edges of the ulcer with actovegin or solcoseryl through the manipulation channel of the endoscope. Surgical endoscopic treatment is aimed at achieving hemostasis in gastroduodenal bleeding and may include injections of adrenaline into the edges of the ulcer, diathermocoagulation, laser photocoagulation, ligation or clipping of a bleeding vessel.

Prevention: primary and secondary.

1. Continuous (complicated by mal, over 60 years old, ineffective eradication, NSAIDs are required, annual exacerbations) - PPI in ½ dose at night.

1. On demand - taking one of the antisecretory drugs in a full daily dose for 3 days, then in ½ dose for 3 weeks. If pain does not decrease at the full daily dose - FEGDS.

Dispensary observationat a therapist once a year. FEGDS for stomach ulcers 1st year - once a year, then for medical reasons, FEGDS for duodenal ulcers for medical reasons. Analyzes, ultrasound OBP, gastric fluoroscopy according to indications.

Complications of peptic ulcer disease.

Ulcerative bleeding.Bloody vomiting (coffee grounds), black tarry stools, thirst, dry mouth, dizziness, fainting, falling blood pressure, falling Hb.

Put the patient to bed, nat. and a psycho rest.

Eliminate food and liquid intake.

Fill and place an ice pack on the epigastric area.

Hemostatic drugs:aminocaproic acid 5% -100 ml, calcium chloride 10% - 10 ml, vikasol 1% -2 ml, etc.

In case of severe blood loss (1-1.5 l), it is necessary to inject plasma-substituting solutions (polyglucin) IV, FFP, blood. Transfer to x / o.

Perforation. Suddenly, dagger pain, first at the site of perforation, then throughout the abdomen, board-like tension of the abdominal muscles, disappearance of hepatic dullness, dry tongue, decrease in blood pressure, first bradycardia, then tachycardia, forced position with legs brought to the abdomen, uv ESR and leukocyte count. fluoroscopy of the abdominal cavity - gas in the subphrenic space.

Emergency hospitalization in the surgical department, drug administration is contraindicated.

Malignancy - malignant transformation.Referral to an oncologist.

Penetration into the pancreas.Constant pain in the epigastric region with a return to the back, especially intense at night, the appearance of laboratory signs of inflammation (leukocytosis, shift of the leukocyte count to the left, increased ESR). At R - scopy - deepening of a niche, an inflammatory shaft around it, low mobility of the stomach wall.

Treatment in cold-water treatment.

Pylorus stenosis and 12 pc.Organic is due to post-ulcer cicatricial changes, functional - edema and spasm of the pyloroduodenal zone.

Characterized by a feeling of fullness in the epigastric region, vomiting of food eaten the day before, weight loss.

Referral to a surgeon.

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Peptic ulcer is a disease in which defects (ulcers) form in the stomach and (or) the duodenum of a person. Most often, men from 20 to 50 years old suffer from peptic ulcer disease.

The disease is characterized by a chronic course and cyclicity: the disease undermines the health of its owner for years, periods of exacerbation are replaced by deceptive calmness. Most often, the ulcer makes itself felt in the spring and autumn.

Duodenal ulcer is much more common than gastric ulcer.

Causes

The leading role in the development of the disease is played by the helical microbe Helicobacter pylori, which damages the mucous membrane of the stomach and duodenum 12. At the same time, this microorganism can be found in more than 80% of the inhabitants of Russia, but far from all of them suffer from peptic ulcer disease.

The fact is, an ulcer does not develop without a number of additional factors:

• stress, anxiety, depression. In this case, there is a violation of the functions of the autonomic nervous system with a predominance of the tone of the vagus nerve. This, in turn, causes a spasm of the muscles and blood vessels in the stomach. As a result, he remains without adequate nutrition and becomes vulnerable to the action of hydrochloric acid: the walls begin to be digested by caustic gastric juice. An ulcer is formed
• poor heredity;
• unhealthy diet: eating rough and spicy foods. This increases the production of hydrochloric acid.
• alcohol abuse. Alcohol enhances the aggressive properties of gastric juice and reduces the protective properties of the mucous membrane.
• smoking. Nicotine enhances the production of hydrochloric acid, interferes with the normal digestion of food, damages the stomach wall, and also disrupts the production of protective factors for the gastric mucosa in the pancreas .;
• uncontrolled intake of certain medications (reserpine, corticosteroid hormones, aspirin).

What's happening?

The microbe Helicobacter pylori is transmitted from person to person through close long-term contact, for example, through kissing, through common dishes and towels, as well as by non-compliance with the rules of hygiene in toilets.

Once in the stomach, Helicobacter begins to actively multiply and conduct subversive activities. It produces special enzymes (urease, proteases) that damage the protective layer of the mucous membrane (inner) of the stomach and duodenum, disrupts cell functions, mucus production and metabolic processes and causes ulcers.

How does it manifest?

First of all, the onset and development of peptic ulcer disease is signaled to a person by pain in the upper abdomen. Disturbed by night and "hungry" pains, in which a person needs to eat something in order to "extinguish" the pain.

Pain in peptic ulcer disease has a clear rhythm (time of occurrence and connection with food intake), periodicity (alternation of pain with periods of their absence) and seasonality of exacerbations (in spring and autumn). It is characteristic that pain in peptic ulcer disease decreases or disappears after eating and antacids (almagel, maalox).

One of the common symptoms of peptic ulcer disease is heartburn, which usually occurs 2-3 hours after eating. Nausea, vomiting, "sour" belching, constipation - these nonspecific symptoms can also indicate an ulcer. Appetite in peptic ulcer disease is usually preserved or even increased, the so-called "painful feeling of hunger."

Keep in mind, in some cases, the ulcer may be asymptomatic!

If the disease is left untreated, the ulcer defect extends deep into the stomach wall. This process can end with life-threatening complications: perforation (perforation), in which a through hole forms in the wall of the stomach or intestine, or bleeding.

Peptic ulcer and duodenal ulcer is a fairly common pathology. According to statistics, 5-10% of the population of various countries suffers from it, and men - 3-4 times more often than women. An unpleasant feature of this disease is that it often affects people of a young, working age, for some, and quite a long time, depriving them of their ability to work. In this article, we will look at the symptoms of stomach and duodenal ulcers, the causes of the disease and how to diagnose it.

What is a peptic ulcer?

A peptic ulcer is characterized by the formation of a deep defect in the wall of the stomach or duodenum. Its main cause is the H. pylori bacterium.

This is a recurrent chronic disease of the stomach and duodenum, characterized by the formation of one or more ulcerative defects on the mucous membrane of these organs.

The peak incidence occurs at the age of 25-50 years. In all likelihood, this is due to the fact that it is during this period of life that a person is most susceptible to emotional stress, often leads the wrong lifestyle, and eats irregularly and irrationally.

Causes and mechanism of occurrence

Defects of the mucous membrane of the stomach and duodenum arise under the influence of the so-called factors of aggression (these include hydrochloric acid, the proteolytic enzyme pepsin, bile acids and a bacterium called Helicobacter pylori) if their number prevails over the factors of mucosal protection (local immunity, adequate microcirculation, prostaglandin levels and other factors).

The factors predisposing to the disease are:

• Helicobacter pylori infection (this microbe causes inflammation in the mucous membrane, destroying protective factors and increasing acidity);
• taking certain medications (non-steroidal anti-inflammatory drugs, steroid hormones);
• irregular meals;
• bad habits (smoking, drinking alcohol);
• acute and chronic stress;
• heredity.

Symptoms

Peptic ulcer of the stomach and duodenum is characterized by a chronic, undulating course, that is, from time to time, the period of remission is replaced by an exacerbation (the latter are noted mainly in the spring-autumn period). Patients present complaints during an exacerbation, the duration of which can vary within 4-12 weeks, after which the symptoms regress for a period from several months to several years. Many factors can cause an exacerbation, the main of which are a gross error in the diet, excessive physical activity, stress, infection, and taking certain medications.

In most cases, peptic ulcer disease debuts acutely with the appearance of intense pain in the stomach.

The time of onset of pain depends on which department the ulcer is located in:

• "Early" pains (appear immediately after eating, decrease as the contents of the stomach exit into the duodenum - 2 hours after eating) are characteristic of ulcers located in the upper part of the stomach;
• "Late" pain (occurs about 2 hours after eating) bother people with an ulcer of the antrum;
• "Hungry" or night pain (occurs on an empty stomach, often at night and is relieved after eating) are a sign of duodenal ulcer.

The pains do not have a clear localization and can be of a different - aching, cutting, boring, dull, cramping - character.

Since the acidity of gastric juice and the sensitivity of the gastric mucosa to it in persons suffering from peptic ulcer disease are usually increased. It can occur simultaneously with pain, or precede it.

About half of patients complain of belching. This is a nonspecific symptom, arising from the weakness of the cardiac sphincter of the esophagus, combined with the phenomena of antiperistalsis (movements against the course of food) of the stomach. Belching is often sour, accompanied by salivation and regurgitation.

Frequent symptoms of exacerbation of this disease are nausea and vomiting, and, usually, they are combined with each other. Vomiting often occurs at the height of the pain and brings the patient significant relief - for this reason, many patients themselves try to induce this condition in themselves. Vomit is usually acidic with an admixture of recently eaten food.

As for the appetite, in persons suffering from peptic ulcer disease, it is often unchanged or increased. In some cases - usually with intense pain - there is a decrease in appetite. Often there is a fear of eating food due to the expected subsequent onset of pain syndrome - sitophobia. This symptom can lead to severe weight loss of the patient.

On average, 50% of patients have complaints of defecation disorders, namely constipation... They can be so stubborn that they bother the patient much more than the pain itself.

Diagnostics and treatment of peptic ulcer

The leading method for diagnosing gastric ulcer and duodenal ulcer is fibrogastroduodenoscopy (FGDS).

Complaints and palpation of the patient's abdomen will help the doctor to suspect a disease, and the most accurate method of confirming the diagnosis is esophagogastroduodenoscopy, or EFGDS.

Depends on the degree of its severity and can be either conservative (with optimization of the patient's regimen, adherence to dietary recommendations, the use of antibiotics and antisecretory drugs) or surgical (usually with complicated forms of the disease).

At the stage of rehabilitation, the most important role is played by diet therapy, physiotherapy, psychotherapy.

Which doctor to contact

Treatment of gastric ulcer and 12 duodenal ulcer is carried out by a gastroenterologist, and in case of complications (for example, bleeding or perforation of the ulcer), surgical intervention is necessary. An important stage in the diagnosis is FGDS, which is carried out by an endoscopist. It is also helpful to visit a nutritionist, undergo a course of physiotherapy, consult a psychologist and learn how to properly cope with stressful situations.

MINISTRY OF HEALTH OF THE CHELYABINSK REGION STATE BUDGET EDUCATIONAL INSTITUTION OF SECONDARY VOCATIONAL EDUCATION

"SATKINSKY MEDICAL TECHNICUM"

COURSE WORK

Ulcerative disease of the stomach and duodenum

Specialty: 060501 Nursing

Full-time form of education

Student: Akhunov Ilgiz Gigantovich

Introduction

1. Peptic ulcer and 12 persistent ulcer

1.1 Etiology and pathogenesis

1.2 Classification of gastric ulcer and 12 duodenal ulcer

1.3 Manifestations of gastric ulcer

1.4 Causes of peptic ulcer and 12 - duodenal ulcer

1.5 Dispensary observation of patients with gastric ulcer and duodenal ulcer

2. Prevention of the development of peptic ulcer and 12 - duodenal ulcer

2.1 Prevention of peptic ulcer

2.2 Prevention of exacerbations of peptic ulcer disease

2.3 Data processing

Conclusion

List of sources used

Application

Introduction

The relevance of discussing the current state of the problem of peptic ulcer disease is due to its widespread prevalence among the adult population, which in different countries of the world ranges from 5 to 15%. Duodenal ulcers occur 4 times more often than stomach ulcers. Among patients with duodenal ulcers there are more men than women.

Peptic ulcer of the stomach and duodenum is a chronic disease prone to recurrence, characterized by the formation of ulcerative defects in the mucous membrane of the stomach and duodenum. This disease is one of the most common lesions of the gastrointestinal tract.

Up to 5% of the adult population suffers from peptic ulcer disease (during mass preventive examinations, ulcers and cicatricial changes in the wall of the stomach and duodenum are found in 10-20% of those examined).

The peak incidence is observed at the age of 40-60 years.

The incidence is higher in urban than in rural areas.

In men, peptic ulcer disease develops more often, mainly before the age of 50.

Duodenal ulcers prevail over gastric ulcers in a ratio of 3: 1 (at a young age - 10: 1).

At the age of 6 years, an ulcer is found with equal frequency in girls and boys (with the same localization in the duodenum and stomach). In children over 6 years of age, ulcers are more often recorded in boys with a predominant localization in the duodenum.

Recurrence occurs in about 60% of patients within the first year after the duodenal ulcer has healed and in 80-90% within two years.

Mortality is mainly due to bleeding (it occurs in 20-25% of patients) and perforation of the wall of the stomach or duodenum with the development of peritonitis. Mortality in perforation of the stomach wall is approximately 3 times higher than in perforation of the duodenal wall.

Purpose: To study the clinical examination of gastric ulcer and duodenal ulcer.

To study the prevalence of gastric ulcer and duodenal ulcer and the structure of morbidity in general.

To study the etiology and pathogenesis of gastric ulcer and duodenal ulcer.

Object: patients on dispensary registration with gastric ulcer and duodenal ulcer

Subject: Prevention of gastric ulcer and 12 duodenal ulcer.

1. Peptic ulcer and 12 persistent ulcer

1.1 Etiology and pathogenesis

The disease is polyetiological in nature. Hereditary disposition, a violation of the diet (overeating, the same food, dry food, non-observance of the rhythm of food, burning food, etc.) matter. Disorder of neuro-endocrine influences on the digestive tract (stressful situations, the rhythm of corticosteroid secretion), impaired secretion of sex hormones, thyroid gland, gastrointestinal tract hormones, allergy to food and medicinal products, changes in local immunity. Violation of microcirculation in the mucous membrane and hypoxia create conditions for ulceration. An increase in the level of acidity and activation of the digestive ability of stomach enzymes contribute to the formation of an ulcerative process.

The data on the prevalence of peptic ulcer disease are diverse, which is associated not only with regional and ethnic characteristics, but also with the diagnostic methods that are used.

Up to 6-10 years old, peptic ulcer disease affects boys and girls with approximately the same frequency, and after 10 years, boys get sick much more often. This fact may be explained by the antiulcerogenic effect of estrogens. It should be noted that recently there has been a significant rejuvenation of peptic ulcer disease. Often this disease is diagnosed at the age of 5-6 years.

Over the past decades, we can follow the radical changes in the point of view on the etiology and pathogenesis of peptic ulcer disease. The paradigm “no acid, no ulcer” was replaced by the belief “no Helicobacterpylori (HP), no ulcer”. It should be considered proven that the absolute majority of cases of ulcer fighting are Helicobacter-associated. At the same time, of course, the ulcerogenicity of HP depends on a significant number of endogenous and exogenous risk factors. Taking into account the high level of infection of individual HP populations, one would expect significantly higher characteristics of the incidence of peptic ulcer disease.

Thus, peptic ulcer disease is a polyetiological, genetically and pathogenetically heterogeneous disease. Among the unfavorable factors that increase the risk of developing peptic ulcer disease, heredity takes a fundamental place. Perhaps, not the disease itself is inherited, but only a tendency to it. Without a certain hereditary tendency, it is difficult to imagine the occurrence of peptic ulcer disease. Moreover, it should be noted that the so-called anticipatory syndrome is inherent in children with a burdened heredity: that is, they, as a rule, begin to get sick with peptic ulcer disease earlier than their parents and close relatives.

According to modern concepts, the mechanism of ulceration both in the stomach and in the duodenum is reduced to a violation of the interaction between the factors of anger in the gastric juice and protection (resistance) of the mucous membrane of the gastroduodenal zone, which is manifested by a shift towards strengthening the first link of the said ratio and weakening the second.

1.2 Classification of gastric ulcer and 12 duodenal ulcer

Type I. Most ulcers of the first type occur in the body of the stomach, namely in the area called the place of least resistance (locusminorisresistentiae), the so-called transition zone located between the body of the stomach and the antrum.

Type II. Stomach ulcers arising with duodenal ulcers.

Type III. Pyloric canal ulcers. In their course and manifestations, they are more similar to duodenal ulcers than stomach ulcers.

Type IV. High ulcers located near the esophageal-gastric junction on the lesser curvature of the stomach. Despite the fact that they proceed like type I ulcers, they are separated into a separate group, since they are prone to malignancy.

Ulcerative duodenal ulcer:

Most of the duodenal ulcers are located in its initial part (in the bulb); their frequency is the same both on the front and on the back. About 5% of duodenal ulcers are located postbulbar. Pyloric canal ulcers should be treated as duodenal, although anatomically they are located in the stomach. Often these ulcers do not respond to drug therapy and require surgical treatment (mainly for developing stenosis of the gastric outlet).

1.3 Manifestations of gastric ulcer

Pain in the epigastric region.

With ulcers of the cardiac region and the posterior wall of the stomach, it appears immediately after eating, localized behind the sternum, and can radiate to the left shoulder. With ulcers of lesser curvature occurs 15-60 minutes after eating.

Dyspeptic phenomena - belching with air, food, nausea, heartburn, constipation.

Asthenovegetative manifestations in the form of decreased performance, weakness, tachycardia, arterial hypotension.

Moderate local pain and muscle protection in the epigastric region.

peptic ulcer stomach dispensary

NSAID-induced ulcers are often asymptomatic; they may debut with perforation or bleeding.

Manifestations of duodenal ulcer Pain is the predominant symptom in 75% of patients.

Pain occurs 1.5-3 hours after eating (late), on an empty stomach (hungry) and at night (night). Subjectively, pain is perceived as a burning sensation in the epigastric region. Eating improves the condition.

Vomiting at the height of the pain, bringing relief (pain relief).

Uncertain dyspeptic complaints - belching, heartburn (the earliest and most frequent manifestation), bloating, food intolerance - in 40 - 70%, frequent constipation.

On palpation, pain in the epigastric region is determined, sometimes some resistance of the abdominal muscles.

Asthenovegetative manifestations.

Periods of remission and exacerbation are noted, the latter lasting for several weeks.

There is a seasonality of the disease (spring and autumn).

1.4 Causes of peptic ulcer and 12 - duodenal ulcer

The reasons are divided into:

Predisposing, which form the conditions for the development of the disease - realizing, which directly cause the development of ulcers.

Predisposing reasons include:

Features of the neuropsychic development of a person. More often, peptic ulcer disease occurs in people with dysfunction of the autonomic nervous system under the influence of negative emotions, mental overload, stressful situations.

Food factor. This is a violation of the rhythm of eating. Eating rough, too hot or too cold food, abuse of spices, etc. However, to date, the impact of the food factor on the occurrence of gastric ulcer is not considered proven.

Taking certain medications can contribute to the development of stomach ulcers. These are non-steroidal anti-inflammatory drugs, aspirin, reserpine, synthetic adrenal cortex hormones. These drugs can both directly damage the mucous membrane of the stomach and duodenum, and reduce the function of the protective barrier of the stomach, and activate the factors of aggression of gastric juice. It is now believed that drugs do not cause chronic peptic ulcer disease, but an acute ulcer, which heals after drug withdrawal. In chronic peptic ulcer disease, these drugs can exacerbate the ulcerative process.

Bad habits. Strong alcoholic beverages can also directly damage the mucous membrane. In addition, alcohol increases gastric secretion, increases the content of hydrochloric acid in the stomach, and chronic gastritis occurs with prolonged use of alcoholic beverages. Smoking and the nicotine in tobacco smoke stimulates gastric secretion, thereby disrupting the blood supply to the stomach. However, the role of smoking and drinking alcohol is also considered unproven.

Often, not one factor leads to the occurrence of peptic ulcer, but the effect of many of them in combination.

Helicobacter pylori infection is currently considered the realizing cause of gastric ulcer and duodenal ulcer.

1.5 Dispensary observation of patients with gastric ulcer and duodenal ulcer

Peptic ulcer disease has a chronic course with periods of exacerbation and remission. If left untreated, it can cause serious complications. Possible development of gastrointestinal bleeding, pyloric stenosis, intestinal obstruction, perforation (release of the contents of the stomach or duodenum into the abdominal cavity), penetration (release of the contents of the stomach or duodenum into a nearby organ). An ulcerative defect can also degenerate into an oncological process.

Therefore, it is so important to be under constant medical supervision. With frequent relapses and the presence of complications, it is necessary to be examined by a therapist or gastroenterologist 4 times a year, and in the stage of stable remission - 2 times a year.

Every year and with exacerbations, patients should undergo an esophagogastroduodenal study. Analysis of feces for occult blood (Gregersen reaction) and analysis of gastric or duodenal secretion should be performed once every 2 years with frequent exacerbations, and with persistent remission - once every 5 years. Since peptic ulcer disease can lead to anemia, it is recommended to take a complete blood count 2-3 times a year in case of a frequently recurrent form and once a year in case of persistent remission.

2. Prevention of the development of peptic ulcer and 12 - duodenal ulcer

2.1 Prevention of peptic ulcer

The prevention of peptic ulcer disease in general includes the prevention of any diseases of the digestive system. Prevention of recurrence of peptic ulcer disease consists in dynamic (dispensary) observation of patients with mandatory examination and clinical and endoscopic examination 2 times a year.

As a prophylaxis of exacerbations, alternation of work and rest, normalization of sleep, rejection of bad habits, rational five meals a day and the use of two- or three-component therapy for a week every 3 months are recommended

Primary prevention of peptic ulcer disease

Primary prevention of gastric ulcer or duodenal ulcer includes:

Helicobacter pylori infection prevention . If there are patients with an ulcer or carriers of this microbe in the family, it is recommended to strictly carry out anti-epidemic measures. These include individual crockery and cutlery, personal towels, and sharp limitation of kissing to reduce the risk of transmission of the pathogen to healthy people, especially children.

2. Timely treatment and oral hygiene.

Refusal from strong alcoholic drinks and smoking.

Organization of proper nutrition . In terms of the composition and regularity of food intake, it should correspond to the age and needs of the body. Gentle cooking is essential, with a sharp restriction of spicy, smoked and annoying dishes. Do not consume excessively hot or very cold foods, caffeine and carbonated drinks.

Prevention and active treatment of hormonal disorders, acute and chronic diseases is especially important for the prevention of duodenal or stomach ulcers.

Avoiding frequent or haphazard use of medications , causing the formation of ulcers.

Rational organization of work and rest, sports . It is imperative to adhere to the daily regimen and sleep at least 6 hours a day (and for children - adhere to the age norm).

Timely psychological assistance . Calm family and school relationships and quick resolution of conflict situations during adolescence are especially important.

2.2 Prevention of exacerbations of peptic ulcer disease

Secondary prevention of peptic ulcer or duodenal ulcer includes mandatory clinical examination:

Regularly conducted courses of anti-relapse treatment , especially in autumn and spring. They should consist of drugs prescribed by a gastroenterologist, physiotherapeutic procedures, herbal medicine, and the intake of mineral water.

2. Sanatorium-and-spa prophylactic treatment of ulcers in specialized institutions.

Remediation of chronic foci of infection and any diseases that can provoke an exacerbation of an ulcer.

Long-term and strict adherence to the anti-ulcer diet.

Continuous laboratory and instrumental monitoring of the ulcer for early detection of symptoms of exacerbation and early initiation of active treatment.

Secondary prevention of ulcers also includes a full range of measures for its primary prevention .

2.3 Data processing

Were taken statistical data from the medical institution Satka Central Regional Hospital No. 1

Conclusion

Thus, in modern medicine, drugs and their combinations are used to treat and alleviate the course of peptic ulcer disease, which are highly effective and have little side effect. However, in more severe cases, surgical methods of treatment are used.

The incidence rates of peptic ulcer disease are quite high, so there is a question about further research of the disease and the prevention of morbidity among the younger generation.

In order to prevent peptic ulcer disease, it is recommended to eliminate nervous tension, negative emotions, intoxication; smoking cessation, alcohol abuse; normalization of nutrition, active drug therapy of Helicobacter pylori infection in patients with chronic gastritis.

List of sources used

1. Khavkin A.I. Modern principles of peptic ulcer therapy / A.I. Khavkin, N.S. Zhikhareva, N.S. Rachkova // Russian medical journal M .: Volga-Media, 2005. - T.13 №3. - S.153-155

Fisenko, V.P. Helicobakterpylori pathogenesis of diseases of the gastrointestinal tract and the possibility of pharmacological effects / V.P. Fisenko. // Doctor: Monthly scientific, practical and journalistic journal / Moscow Medical Academy named after M.V. THEM. Sechenov (M.). - M .: Russian doctor, 2006. - №3. - p. 46-50

Kucheryavyy Yu.A. Bismuth tricalium dicitrate in treatment regimens for erosive and ulcerative lesions of the mucous membrane of the gastroduodenal zone / Yu.A. Kucheryavy, M.G. Gadzhieva // Russian journal of gastroenterology, hepatology, coloproctology: scientific and practical journal. - M .: B. and., 2005. - Volume 15 N1. - P.71-75

Burakov, I.I. Peptic ulcer associated with Helicobakterpylori (pathogenesis, diagnosis, treatment) / I.I. Burakov; V.T. Ivashkin; V.M. Semenov, 2002 .-- 142 p.

Bronovets I.N. Modern principles and methods of treatment of gastric ulcer and duodenal ulcer: collection of I.N. Bronovets // Theory and practice of medicine: Sat. scientific. Tr. - Minsk, 1999. - Issue 1. - S.83-85

Isaev G.B. The role of Helicobakterpylori in the clinic of peptic ulcer / G.B. Isaev // Surgery. - 2004. - No: 4. - P.64-68

Pharmaceutical Chemistry Journal. M .: "Folium", Vol. 40, No. 2, 2006, P.5

Mashkovsky M.D. Medicines. - 15th ed. - M: - RIA "New Wave" -Moscow, 2007

Fundamentals of organic chemistry of medicinal substances / A.T. Soldatenkov, N.M. Kolyadina, I. V. Shendrick. M .: "Mir", Moscow, 2003

Recommendations for the diagnosis and treatment of Helicobacterpylori infection in adults with gastric ulcer and duodenal ulcer // Russian Journal of Gastroenterology, Hepatology, Coloproctology -. - M .: B. and., 1998. - No. 1. - S.105-107.

A. A. Sheptulin, D. R. Khakimova Algorithm for the treatment of patients with peptic ulcer // BC. - 2003. - T.11. # 2. - S. 59-65

Application

Appendix # 1

Helicobakterpylori Helicobacterpylori is a spiral-shaped gram-negative bacterium that infects various areas of the stomach and duodenum. Many cases of gastric and duodenal ulcers, gastritis, duodenitis, and possibly some cases of gastric lymphomas and gastric cancer are etiologically associated with Helicobacterpylori infection. However, many infected carriers of Helicobacterpylori show no symptoms of the disease. Helicobacterpylori is a bacterium, about 3 microns in length, with a diameter of about 0.5 microns. It has 4-6 flagella and the ability to move extremely quickly even in thick mucus or agar. It is microaerophilic, that is, it requires the presence of oxygen for its development, but in much lower concentrations than those contained in the atmosphere.

History In 1875, German scientists discovered a spiral-shaped bacterium in the mucous membrane of the human stomach. This bacterium did not grow in culture (on artificial culture media known at that time), and this accidental discovery was eventually forgotten.

In 1893, Italian researcher Giulio Bizocero described a similar, spiral-shaped bacterium that lives in the acidic stomach contents of dogs.

In 1899, the Polish professor Valery Jaworski from the Jagiellonian University in Krakow, while examining the sediment from the washing waters of the human stomach, discovered, in addition to bacteria resembling twigs in shape, a number of bacteria with a characteristic spiral shape. He named the bacterium he discovered Vibriorugula. He was the first to suggest the possible etiological role of this microorganism in the pathogenesis of stomach diseases. In 2005, the pioneers of the medical importance of bacteria, Robin Warren and Barry Marshall, were awarded the Nobel Prize in Medicine.

Before the role of Helicobacterpylori infection in the development of gastric ulcer and duodenal ulcer and gastritis was understood, ulcers and gastritis were usually treated with drugs that neutralize acid (antacids) or reduce its production in the stomach (proton pump inhibitors, H2-histamine receptor blockers, M-anticholinergics, etc.). Although such treatment has been effective in a number of cases, ulcers and gastritis very often recurred after treatment was discontinued. A very frequently used drug for the treatment of gastritis and gastric ulcer and duodenal ulcer was bismuth subsalicylate (peptobismol). It was often effective, but fell out of use because its mechanism of action remained unclear. Today it became clear that the effect of pepto-bismol was due to the fact that bismuth salts act on Helicobacterpylori as an antibiotic. To date, most cases of gastric and duodenal ulcers, gastritis and duodenitis with laboratory-proven Helicobacter pylori etiology, especially in developed countries, are treated with antibiotics effective against Helicobacterpylori.

Although Helicobacterpylori remains the most medically significant bacterium capable of dwelling in the human stomach, other members of the Helicobacter genus have been found in other mammals and some birds. Some of them are capable of infecting humans as well. Species of the genus Helicobacter have also been found in the liver of some mammals, and they can cause liver damage and disease.

Influence

The bacterium contains hydrogenase, which can be used to generate energy by oxidizing molecular hydrogen produced by other gut bacteria. The bacterium also produces oxidase, catalase and urease. It has the ability to form biofilms that make the bacteria immune to antibiotic therapy and protect the bacterial cells from the host's immune response. It is believed that this increases its survival in the acidic and corrosive environment of the stomach.

In unfavorable conditions, as well as in "mature" or old cultures, Helicobacterpylori has the ability to transform from a spiral to a round or spherical coccoid shape. This favors its survival and may be an important factor in the epidemiology and spread of the bacterium. The coccoid form of the bacterium does not lend itself to cultivation on artificial nutrient media (although it can spontaneously arise as crops "age"), but has been found in water sources in the United States and other countries. The coccal form of the bacterium also has the ability to adhere to epithelial cells of the stomach in vitro.

Coccoid cells differ in the details of the structure of the cell wall (the predominance of N-acetyl-D-glucosaminyl-β (1,4) - N-acetylmuramyl-L-Ala-D-Glu motif in the peptidoglycan of the cell wall (GM-dipeptide)), changes in the structure of the cell wall leads to the unrecognition of the bacteria by the host's immune system (bacterial mimicry). enters the stomach with saliva, contaminated food, insufficiently sterilized medical instruments.

A small amount of urea is always present in the stomach, which is excreted from the blood through the stomach and intestines. From urea, with the help of its own enzyme, ureaselikobacter forms ammonia, which, having an alkaline reaction, neutralizes hydrochloric acid and creates favorable conditions for the microorganism. Another enzyme produced by the bacteria, mucinase, breaks down the mucin protein in gastric mucus and loosens the mucus. Thanks to this, Helicobakterpylori penetrates the protective mucus layer and attaches to the epithelial cells of the mucous membrane in the antrum of the stomach.

Helicobacter can only attach to mucus-forming cells of the columnar epithelium. The epithelial cell is damaged, its function is reduced. Further, Helicobacteria multiply rapidly and populate the entire mucous membrane in the antrum of the stomach. An inflammatory process occurs in the mucous membrane due to the fact that a large number of other enzymes produced by the microorganism lead to the destruction of cell membranes, alkalization of the normal acidic environment of the stomach. Ammonia acts on the endocrine cells of the stomach, enhancing the production of the hormonal substance gastrin and reducing the production of somatotropin, resulting in increased secretion of hydrochloric acid. The inflammatory reaction of the gastric mucosa gradually arises and intensifies. It produces substances called cytotoxins. These substances cause damage to the cells of the mucous membrane and can lead to the development of erosion and stomach ulcers. If Helicobacter pylori do not secrete these substances, then the ulcer does not form and the process stops at the stage of chronic gastritis.

Appendix # 2

How to treat symptoms of a duodenal ulcer

1. Quitting smoking significantly speeds up the healing process of ulcers and reduces the number of exacerbations.

2. Compliance with a diet (excluding spicy, smoked, fried foods), diet (meals six times a day in small portions) promotes scarring of duodenal ulcers and reduces the risk of new mucosal defects.

Drug treatment consists in prescribing a course of antibacterial agents and drugs that lower the acidity of gastric juice.

Surgical treatment is performed in the event of life-threatening complications (acute bleeding, ulcer perforation).

From folk remedies, decoctions and infusions of chamomile, St. John's wort, mint, yarrow, plantain, cabbage, potato juices, sea buckthorn oil are used.

Proper nutrition, giving up bad habits, increasing resistance to stress through the conduct of psychological trainings will reduce the symptoms of duodenal ulcer, prevent the exacerbation of the disease and the emergence of formidable complications.

Peptic ulcer and duodenal ulcer is the most common pathology of the gastrointestinal tract, which has a chronic, most often recurrent course. It is observed mainly in spring and autumn. The male population is 4 to 5 times more at risk of the disease than the female population. Young patients are characterized mainly by duodenal lesions; in people over forty, as a rule, a stomach ulcer is diagnosed.

Causes of occurrence

Peptic ulcer disease, or peptic ulcer of the stomach and duodenum, is a pathological process, during which a combination of aggressive factors, prevailing over the protection of weakened factors of the mucous layer, forms an ulcerative defect in it.

Numerous studies have proven that infection with Helicobacter pylori bacteria is the cornerstone of the disease. They cause 96 - 98% of duodenal peptic ulcers and share their priority with the effects of corticosteroids, NSAIDs and cytostatics for stomach ulcers. The further development of the disease is facilitated by an unfavorable background from the so-called risk factors:

• unbalanced diet;
• persistent bad habits such as nicotine and alcohol addiction;
• neuropsychiatric disorders;
• genetic predisposition.

Classification

According to ICD-10, peptic ulcers are distinguished:

• sharp;
• chronic;
• unspecified;
• perforated;
• bleeding.

Symptoms of stomach and duodenal ulcers

The clinical manifestations of the disease depend on the location and extent of the ulcer. The first signs of the disease are pain:

• with stomach ulcers, they disturb during the day, mainly after eating;
• duodenal ulcers are characterized by night and "hungry pains".

More often the pain is localized in the epigastric region, occurs in attacks, can be bursting, burning, pulling or baking in nature. Pain syndrome is accompanied by heartburn and belching. At the peak of the disease, nausea joins, and soon after it - vomiting. Vomiting brings the patient a characteristic relief in the form of the disappearance or weakening of pain. Many patients have either diarrhea or constipation with bloating. The chronic recurrent course of the disease leads to the development of common asthenic signs:

• to weakness, malaise;
• to insomnia, emotional lability;
• to weight loss.

Unfortunately, in the 21st century, the recognition of peptic ulcer disease is hampered by the appearance of many atypical forms. Pain syndrome sometimes loses its characteristic epigastric localization. The pain can be localized in the liver, move to the lumbar region, as with pyelonephritis or ICD. Often, patients feel a burning sensation in the region of the heart and behind the sternum, as with angina pectoris or myocardial infarction. Increasingly, peptic ulcers let the patient know about themselves only with heartburn. As a result, in 10% of cases, patients go to medical institutions at the stage of complications. Complications:

• Rough scarring of prepyloric ulcers leads to pyloric stenosis, which are manifested by a feeling of fullness and fullness of the stomach, pain in the epigastric region. Typical symptoms are vomiting of food eaten the day before and a sharp weight loss.
• Deep ulceration can lead to destruction of the walls of the blood supplying vessels. The resulting bleeding manifests itself as severe weakness and pallor, vomiting of "coffee grounds" and black, tarry feces, the so-called "melena", dizziness and a drop in blood pressure and, finally, loss of consciousness.
• A perforated ulcer is ulceration through the walls of hollow organs, leading to the outflow of their contents into the abdominal cavity. A perforated ulcer is manifested by a sudden onset of acute "dagger pain", which is initially localized in the epigastrium, and then, as peritonitis develops, spreads throughout the abdomen. Symptoms of "board-like" anterior abdominal muscles and a sharp decrease in blood pressure, characteristic of peritonitis, join.
• Penetration occurs when ulceration through the walls, closely adjacent to other organs. With penetration into the pancreas, liver, colon or omentum, intense pain of a constant nature occurs, localized mainly in the upper abdomen. The pain can radiate to the lower back, collarbone, shoulder blade, shoulder. It has no relationship with food intake and is not removed by taking antacids.
• Malignancy of an ulcer is a degeneration into cancer. She is characterized by increasing weakness and lack of appetite, a clear aversion to meat products, a sharp unreasonable weight loss, constant pains throughout the abdomen without clear localization, often aching.

Diagnostics

A clinical blood test reveals:

• hyperhemoglobinemia or anemia, indicating the presence of latent blood loss;
• leukocytosis, increased ESR are reliable signs of an inflammatory process;
• a coagulogram study may indicate a decrease in blood coagulation factors;
• scatology reveals "latent" blood - a sign of latent blood loss.

EGDS - fibroscopy - allows you to reliably determine the shape, size and depth of the ulcer, to clarify the characteristics of its bottom and edges, to identify possible violations of organ motility.

A targeted biopsy concomitant with the EGD, followed by the study of the resulting biopsy allows:

• conduct an express search for Helicobacter pylori using the urease rapid test;
• conduct morphological detection of Helicobacter pylori;
• to clarify the particulars of the morphological state of the mucosa;
• exclude the presence of signs of malignancy;
• to exclude rare possible causes of ulcerative defects;
• biopsy is also used for cultures to determine the sensitivity of Helicobacter pylori to antibacterial drugs.

Helicobacter pylori tests are mandatory when examining patients with peptic ulcers:

• thanks to the "13C respiratory urease test", especially when used as a control at the stages of treatment, it is possible to quickly and almost permanently get rid of Helicobacter pylori;
• stool-test - detection of Helicobacter pylori antigens in stool samples by immunochromatography.

Intragastric daily pH monitoring examines the secretory function of the gastric mucosa. The data obtained are of great importance when choosing an individual patient's treatment regimen.

Rg survey:

• reveals the presence of an ulcerative tissue defect, the so-called "niche symptom";
• it is carried out to exclude perforation and to confirm the absence of free gas in the abdomen, in the presence of which "sickle symptoms" appear under the diaphragm;
• contrast Rg-graphy is reliably effective in detecting pyloric stenosis.

Ultrasound control of the gastrointestinal tract is carried out on suspicion of the presence of concomitant pathology, aggravating the course of peptic ulcer disease, and to exclude or confirm its complications.

Treatment of stomach and duodenal ulcers

Modern treatment of peptic ulcers is a combination of equivalent measures:

• complete eradication of Helicobacter pylori;
• preventing the development of complications;
• normalization of the digestion process;
• protection of the gastrointestinal tract from the aggressive effects of urbanized food products;
• decrease in gastric acid secretion;
• protecting the mucous membrane from irritation by digestive juices;
• stimulation of the regeneration process of peptic ulcers;
• treating concomitant aggravating diseases;
• treatment of complications that have arisen.

The treatment regimen for peptic ulcers caused by Helicobacter pylori includes two stages and is aimed at the complete destruction of the bacterial population, the so-called eradication. It must combine several types of medicines:

• antibiotics: groups of semi-synthetic penicillins (Amoxiclav, Amoxicillin), macrolide groups (Clarithromycin), Metronidazole from the nitroimidazole group or Tetracycline;
• acid secretion inhibitors: proton pump inhibitors Omeprazole, Lansoprazole, Rabeprazole, or antihistamines such as Ranitidine;
• gastroprotective agents, for example, bismuth subcitrate.

The first stage of eradication therapy requires the prescription of a mandatory drug that inhibits the proton pump or an antihistamine in combination with Clarithromycin and Metronidazole. If necessary, it is possible to replace these drugs with similar ones. But how to treat, the doses of drugs and the final scheme are prescribed only by the attending doctor, focusing on the individual information obtained during the examination of the patient.

The first stage of treatment usually takes a week. This is usually enough to complete a complete eradication. According to statistics, a complete cure occurs in 95% of patients, while relapses occur in only 3.5% of patients.

In rare cases of failure of stage I of therapy, they proceed to stage II. Prescribed tablets of Bismuth subcitrate, Tetracycline, Metronidazole and proton pump inhibitor. The course lasts two weeks.

Methyluracil, Solcoseryl, anabolic steroids and vitamins are used as stimulators of regeneration processes - pantothenic acid and vitamin U are prescribed. Such drugs as Almagel, De-Nol and Sucralfat, in addition to stimulating regeneration, also help to successfully relieve pain.

Treatment of complications - stenosis, penetration, perforation, bleeding - is carried out in the surgical and intensive care units.

The diet for peptic ulcers requires the patient to strictly refrain from coarse raw food, fried foods, smoked meats, pickles, pickles, spices, saturated broths, coffee and cocoa. The patient's diet should consist of boiled and steamed dishes, cereals, vegetable, berry and fruit purees. It is very useful to include fermented milk products in the diet, the most preferred of which are low-fat kefir, yogurt and yogurt. Traditional medicine recipes recommend using propolis, aloe extract, honey, sea buckthorn oil, medicinal herbs - chamomile, licorice, fennel fruits.

Prophylaxis

Effective preventive measures are:

• adequate work and rest regimes;
• elimination of ulcerogenic habits - nicotine and alcohol addiction;
• controlled intake of cytostatics, NSAIDs, corticosteroids, implying observation and, if necessary, the appointment of drugs that inhibit the proton pump;
• clinical examination of patients with a history of stomach ulcers or atrophic gastritis;
• EGDS monitoring with targeted biopsy every two years in patients with atrophic gastric mucosa to control recurrence and malignancy of the ulcer.