Ulcerative defect of the stomach. Prevention of peptic ulcer

Gastric ulcer is a chronic disease in which the formation of ulcerative defects of the gastric mucosa occurs. Most often, stomach ulcers affect men from 20 to 50 years. The disease is characterized by a chronic course with frequent relapses, which usually occur in spring and autumn.

The stomach contains a rather aggressive environment in the form of hydrochloric acid, bile acid, produced by the liver and entering the duodenum, throwing the contents of the duodenum into the stomach. This aggressive environment is neutralized by mucus, which is produced by the cells of the mucous membrane, normal blood circulation, timely restoration of the cells of the mucous membrane.

What it is?

Gastric ulcer - a local defect of the gastric mucosa (sometimes with the capture of the submucosal layer), formed under the action of hydrochloric acid, pepsin and bile. Causing trophic disturbances in this area. Secretion of acid in the stomach usually does not increase.

Peptic ulcer is characterized by a relapsing course, that is, alternating periods of exacerbations (usually in spring or autumn) and periods of remission. Unlike erosion (superficial mucosal defect), the ulcer heals with the formation of a scar.

Causes of an ulcer

What are the types of ulcers, consider in more detail:

Symptoms of a stomach ulcer

Sometimes a stomach ulcer does not manifest itself in any way, which indicates the need for regular examination. As a rule, the course of the ulcerative process without noticeable symptoms is observed in 25 - 28% of cases, and the presence of an ulcer is detected after the death of the patient.

You can suspect a stomach ulcer by the following signs:

1. Increased gas production.
2. Quick feeling of satiety.
3. The appearance of a feeling of heaviness in the abdomen, observed after eating.
4. Decreased appetite in peptic ulcer disease may be associated with a person's fear of experiencing pain or with impaired motility of the gastrointestinal tract.
5. Belching, which is characterized by an uncontrolled reflux of gastric juice into the oral cavity. At the same time, the patient feels.
6. Chair disorders. Most often, patients complain of constipation, and diarrhea is atypical for peptic ulcer. Difficulties with emptying the intestines are experienced by up to 50% of patients, especially during an exacerbation of gastric ulcers.
7. Pain localized in the upper abdomen. This symptom occurs in 75% of cases. Half of the patients complain of sensations of low intensity, in the remaining 50% they are more pronounced and intensify during physical exertion, after ingestion of alcohol or spicy food, during long breaks between meals.
8. Nausea, sometimes accompanied by vomiting. This symptom occurs due to a violation of the motility of the stomach. With an ulcer, vomiting is observed 1.5-2 hours after eating, and as the stomach is released, it brings a feeling of relief. Therefore, often patients cause vomiting on their own.
9. Heartburn. It is expressed in a burning sensation in the epigastric region. It occurs due to the fact that the acidic contents of the stomach, which has an aggressive environment, enters the lumen of the esophagus, irritating its walls. This symptom is observed frequently and occurs in 80% of patients. Heartburn usually appears 1-2 hours after eating.

Among the external signs of a stomach ulcer, it is worth noting the presence of a gray coating on the tongue, which almost always indicates problems with the gastrointestinal tract. The patient may suffer from excessive sweating of the palms and experience pain with pressure on the epigastric region.

Characteristics of pain in stomach ulcers:

1. An ulcer located in the upper curvature of the stomach has a very latent course and can be quickly diagnosed very rarely, and in fact the ulcers of the upper curvature of the stomach are malignant.
2. The defeat of the ulcer of the antrum of the hollow organ is characterized by pain in the evening and at night, may be absolutely not associated with food intake. The pain is constant, aching, accompanied by belching and heartburn.
3. If the ulcer is located in the pyloric part of the stomach, then the pain will be acute, paroxysmal, prolonged (in some cases, one attack lasts more than 40 minutes).
4. With the localization of peptic ulcer in the lesser curvature of the stomach, the pain will be especially intense in the left iliac region. The syndrome occurs 1 hour after eating, the condition stabilizes after the stomach digests the contents. Most often, patients complain of pain in the evening, sometimes they are accompanied by vomiting.
5. If the ulcer is located in the cardinal or subcardinal section of the stomach, then the pain syndrome appears 20 minutes after eating, its localization is very high - almost in the area of ​​the solar plexus. Very often, the pain radiates to the heart, so a heart attack can be misdiagnosed (this happens during self-diagnosis). With such an arrangement of a defective formation, there is never pain after physical exertion, and after drinking even a small amount of milk, the patient's condition stabilizes.

Symptoms of a stomach ulcer during an exacerbation:

1) Dull, cutting, stabbing pain in the upper abdomen, most often in the middle (in the epigastric region), may radiate to the left hypochondrium. The appearance of pain associated with eating, about 0.5-1 hour after eating, stops after about 2 hours, this is due to the emptying of the stomach. The pain appears, as a result of irritation of the ulcerative surface, food, it is stopped by antacids (Almagel). Pain is also characterized by seasonality, i.e. exacerbation occurs in spring and autumn.

2) Dyspeptic disorders:

• heartburn occurs as a result of the reflux of acidic stomach contents into the lower esophagus. It manifests itself simultaneously with the appearance of pain;
• nausea and vomiting also occur at the same time as the pain appears. Vomiting, accompanied by relief for the patient;
• sour eructations, constipation, develop due to increased gastric acidity;

3) Loss of body weight, occurs due to fear of eating, which contributes to the appearance of pain.

perforated ulcer

If the disease is ignored, perforation of the stomach and ulcer penetration occurs. There comes a rupture of its wall and the germination of the ulcer on neighboring organs. The contents and microorganisms enter the abdominal cavity, causing peritonitis.

Chronic discomfort that the patient is accustomed to experiencing suddenly sharply turn into a sharp dagger pain. The person is covered with sweat, the stomach is constrained.

This complication requires the intervention of a surgeon. Within 6 hours, the patient has a chance to escape if they manage to put him on the operating table, wash the damaged tissue and sew it up, thereby stopping the profuse internal bleeding.

Diagnostics

Currently, the diagnosis of gastric ulcer is carried out on the basis of endoscopic examination.

The method is called fibrogastroscopy (FGS), during which a thin flexible instrument is inserted through the esophagus into the stomach, equipped with a light source and a camera that transmits the image to the monitor. This allows you to see the ulcerative defect of the gastric mucosa, determine its location and size. The previously widely used method of contrast fluoroscopy is still used today, but has only an auxiliary value.

Laboratory studies of gastric and intestinal contents for the presence of Helicobacter pylori and occult blood are carried out, general blood and urine tests are prescribed to assess the general condition of the body.

Treatment of stomach ulcer

How to cure a stomach ulcer? - We need complex therapy, which includes not only drug treatment, but also lifestyle correction.

The course of treatment of stomach ulcers consists of:

• elimination of the factors that led to the disease;
• drug therapy;
• medical nutrition;
• physiotherapy, laser therapy, magnetotherapy, etc.

There are several main groups for the treatment of peptic ulcer:

Helicobacter pylori treatment regimen

The destruction of Helicobacter pylori contributes to better scarring of the ulcer. This is the first step in the treatment of peptic ulcer. There are two main antibiotic therapy regimens. They are prescribed step by step, that is, the first-line drugs did not work, then they try the second scheme.

First line eradication (within a week):

• Macrodides (Clarithromycin) 500 mg twice daily.
• Semi-synthetic penicillins (Amoxicillin) 1000 mg twice a day or nitroimidazole derivatives (Metronidazole) 500 mg also twice a day.

In case of failure, a second line of eradication is proposed (1 week):

• Proton pump inhibitors 20 mg twice daily.
• Bismuth subcitrate (De-nol) 120 mg 4 times a day.
• Tetracyclines (Tetracycline) 0.5 g 4 times a day.
• Nitroimidazole derivatives (Metronidazole) 500 mg also three times a day.

Currently, doctors are developing new methods of treating pathology. Helicobacter vaccine is already being tested. For better healing of the mucosal defect, cytokine preparations, trefoil peptides and growth factors are used.

Diet

Special requirements are put forward for food. It should spare the mucous membrane from mechanical and chemical damage and at the same time be complete. Food should be fractional 5-6 times a day. All dishes must be crushed or consumed in liquid form, steamed or boiled, neither cold nor hot.

Pure, easily digestible food is shown, which practically does not increase the secretion of gastric juice:

• soft-boiled eggs, steamed omelet;
• milk and dairy products;
• boiled dishes of beef, chicken, veal, steamed cutlets;
• boiled fish of low-fat varieties;
• white, slightly dried bread;
• milk, chicken, vegetable soups from potatoes, beets;
• boiled vegetables: carrots, potatoes, beets, zucchini, pumpkin;
• buckwheat, semolina, rice, oatmeal, pasta;
• weakly brewed tea;
• sweet kissels, compotes;
• decoctions of wild rose, wheat bran, non-acidic berry juices;
• alkaline mineral water without gas.

Symptoms of peptic ulcer worsen:

• spicy and salty;
• canned, smoked food, sausages;
• pastry bakery products, pies, rye bread;
• strong tea, coffee;
• fatty meat products, lard, rich broths;
• roast;
• all kinds of spices: mustard, pepper, cloves, etc.;
• carbonated drinks.

It is worth abandoning foods containing coarse fibers, they mechanically irritate the stomach: radishes, turnips, radishes, beans, bran bread.

Folk remedies

Phytotherapy does not replace medical treatment. It increases its effectiveness. In the case of peptic ulcer disease, the correct use of medicinal plants (as a supplement to the medications taken) allows you to:

• reduce the intensity of existing inflammation;
• deal with pain;
• stimulate the healing of ulcers;
• normalize stool;
• protect the gastroduodenal mucosa from aggression factors;
• improve the supply of gastroduodenal mucosa with nutrients.

Healing fees, including St. John's wort, yarrow, calendula, etc., have an anti-inflammatory effect. Mint, oregano, chamomile, dill can act as natural antispasmodics. Eliminating the spasm of the gastric smooth muscle muscles, these wonderful medicinal plants stop the pain. Enveloping action is inherent in licorice, elecampane, flax seed. Celandine, chicory, fireweed, shepherd's purse, burdock root contribute to full-fledged scarring of ulcers. To loosen the stool, you can use buckthorn, joster, rhubarb, three-leaf watch, etc.

Mentioned medicinal plants are recommended to be used in the form of infusions, decoctions, herbal applications on the abdominal wall and therapeutic baths. At the same time, one should not forget that phytoapplications are strictly prohibited for bleeding, pregnancy (the entire period), fever, and any oncological diseases.

Operation

How to treat a stomach ulcer when conservative treatment does not bring the expected results? Unfortunately, there are also cases where surgical intervention is indispensable. However, surgical intervention should be based on absolute indications, which include:

• ulcer perforation;
• the occurrence of bleeding;
• transformation of an ulcer into oncology;
• III degree of stenosis.

Surgical intervention is also possible with relative indications, including grade II stenosis, the possibility of frequent relapses, multiple scars, callous ulcer, penetration, and the impossibility of healing the ulcer for a long time.

If there are indications for surgery, it is undesirable to avoid it, even delaying the process is quite dangerous. The reason is that any planned operation is less dangerous than emergency intervention. Plus, emergency surgery is far from always effective, but it has a greater risk of postoperative complications.

stomach ulcer after surgery

After the operation, the patient can start working in about two to three months. It all depends on how the stomach ulcer behaves after the operation, when the stitches are removed and discharged from the hospital. All this depends on the course of recovery and wound healing. If everything is in order, the stitches are removed after about 7-9 days, but they are discharged from the hospital a little earlier.

It is very important to follow a diet after surgery. As a rule, it is allowed to drink liquid after two days, half a glass of water per day, dosing with a teaspoon. Gradually every day the water is replaced by soup or broth. Then, after about eight days, they are allowed to eat meat, potatoes, cereals, and so on, but only in pureed form. In order not to harm the postoperative condition, it is necessary to follow a strict diet and obey the doctor.

Forecast

The prognosis of the disease is conditionally favorable, with adequate timely treatment, the quality of life does not suffer, working capacity is fully restored. However, it is possible to develop a number of life-threatening complications, such as bleeding from an ulcer, or perforation of the ulcer, and as a result, the development of peritonitis.

Prevention of pathology

The main preventive measures include:

1. Reduced stress levels. Required timely rest, good sleep.
2. Compliance with the rules of healthy eating. It is necessary to ensure that there is no constipation, diarrhea, gas formation processes.
3. Refusal of alcohol. Even small doses adversely affect the beneficial microflora of the gastrointestinal tract. If it is violated, the risk of developing peptic ulcer increases several times.

In conclusion, we note that a timely detected peptic ulcer in the presence of a full-fledged treatment has a favorable prognosis. Complications can lead to life-threatening conditions.

Peptic ulcer of the stomach and duodenum is characterized by the formation of a peptic ulcer in the walls of the stomach or duodenum, which eats through the mucous layer and deeper muscle layers.

A peptic ulcer most commonly presents with pain or discomfort in the upper abdomen (epigastrium). Sometimes the pain can be localized in the upper third of the right and left hypochondrium. Occasionally, pain can radiate to the back, but this is a rare and not very characteristic symptom. If left untreated, symptoms may appear for several weeks and then be replaced by an asymptomatic period, sometimes lasting several months.

Most often, the pain of a duodenal ulcer appears 2 to 5 hours after eating, and also at night (usually between 11 pm and 2 am).

With a stomach ulcer, pain usually occurs during meals. There may be other symptoms: the appearance of belching after eating, the early appearance of a feeling of satiety, heaviness in the epigastrium, intolerance to fatty foods, nausea, and sometimes vomiting.

The asymptomatic course is most typical for the elderly and patients who have been receiving NSAID painkillers for a long time (the most commonly used group of painkillers).

Complications of peptic ulcer develop regardless of whether it is asymptomatic or accompanied by typical complaints.

Main complications:

• Bleeding from a peptic ulcer - is manifested by nausea, vomiting of the color of coffee grounds or chalky (black feces, its staining occurs due to contact of blood with hydrochloric acid in the stomach).
• Pyloric stenosis (reduction of the lumen of the outlet between the stomach and duodenum due to scarring of ulcers) - is manifested by a feeling of early satiety, fullness after a small amount of food, nausea, sometimes vomiting, weight loss.
• Ulcer penetration - penetration, “germination” of an ulcer into other organs (large intestine loops, pancreas, abdominal vessels, etc.). Most often it is manifested by a change in the nature of complaints, an increase in pain, the appearance of an unusual irradiation of pain (for example, in the back). New symptoms depend on which organ was involved. At the same time, antacids (medicines used to relieve pain and get rid of heartburn) stop helping or reduce pain slightly.
• Perforation - an ulcer completely eats through the wall, and the contents of the stomach or duodenum begin to enter the abdominal cavity. It is characterized by the appearance of a sharp, dagger pain in the epigastrium, and then pain throughout the abdomen.
• Malignancy - the degeneration of an ulcer into a malignant tumor - cancer.

Figures and facts

• About 70% of peptic ulcer cases are asymptomatic and are detected with the development of complications - bleeding, perforation or ulcer penetration. Between 43% and 87% of those hospitalized with bleeding ulcers did not report any pain or digestive problems before.
• Up to 60% of ulcers heal on their own.
• Epigastric pain during or after eating is the most common symptom of peptic ulcer disease. Approximately 80% of patients with confirmed peptic ulcer noted epigastric pain associated with eating.
• Helicobacter pylori infection is the most common chronic infection in humans. It infects up to 50% of the population. In some developing countries, this figure reaches 94%.
• Between 5% and 30% of ulcers may recur in the first year after treatment.

When to See a Doctor

• The appearance of black feces. However, you should be aware that the use of certain foods and drugs also causes darkening of the stool, which is in no way associated with bleeding: prunes, pomegranate and black currants, blueberries and dark grapes, liver, beets. Iron preparations, bismuth preparations, activated charcoal and some other drugs also stain the feces dark.
• Pain in the abdomen during or after eating.
• Sudden sharp dagger pain in the epigastrium, then spreading to the entire abdomen, requires an ambulance call and urgent medical attention. In general, the appearance of acute pain in any part of the abdomen is a reason to urgently seek medical help.
• Unexplained weight loss is a formidable symptom, not necessarily associated with peptic ulcer disease. It can be caused by another, no less serious condition.
• The appearance of belching, nausea, feeling of early satiety during meals.
• Vomiting with an admixture of blood also requires an immediate call to an ambulance.

Diagnosis of the disease

For peptic ulcer, a change in laboratory blood parameters is uncharacteristic. Sometimes a decrease in the number of red blood cells and hemoglobin in the general blood test can be determined - anemia. It is also possible to detect occult blood in the stool.

The most accurate method for diagnosing peptic ulcer is EGDS (esophagogastroduodenoscopy) - examination of the esophagus, stomach, duodenum using a special tube with a camera.

In some cases, during the EGDS, a piece of the ulcer (biopsy) is taken to exclude its malignancy - degeneration into a cancerous tumor.

Sometimes a barium x-ray is done. The patient drinks a mug of a special contrast agent, and then a series of images is taken to monitor the passage of the contrast agent through the gastrointestinal tract and look for defects in the organ wall.

Also, all patients with peptic ulcer disease are mandatory examined for the presence of the Helicobacter pylori bacterium, which lives in the pyloric section of the stomach and contributes to the destruction of the mucosa and the formation of an ulcer. For the diagnosis of Helicobacter pylori infection, different methods are used: the determination of DNA in feces, the respiratory urease test, the determination of antibodies in the blood, the determination of DNA in a biopsy sample taken during gastroscopy.

In the case of multiple ulcers, an additional examination is performed to rule out other conditions that may be the cause (for example, gastrinoma - a tumor of the pancreas - stimulates the secretion of gastric juice).

Treatment of the disease

Treatment of uncomplicated peptic ulcer disease is conservative, that is, without surgical intervention. Medicines are used that reduce the acidity of gastric juice and reduce the amount of hydrochloric acid. The course of treatment can last up to 12 weeks. You should not interrupt the course of treatment yourself, even if all symptoms have disappeared.

In some cases, for example, if the peptic ulcer is caused by taking NSAIDs and it is necessary to continue taking them, drugs that reduce secretion may be prescribed indefinitely.

If a Helicobacter pylori infection is found that accompanies an ulcer, treatment with antibiotics is prescribed, usually two at the same time. The period of admission is usually two weeks with mandatory control four weeks after the end of treatment - either a urease breath test or a stool test is used for this. The determination of antibodies in the blood is indicative and meaningless for the control of cure.

In addition to medication, patients are advised to limit their intake of alcohol, carbonated drinks, and stop smoking. The doctor also gives recommendations on nutrition during the period of exacerbation and after recovery.

Emergency surgical treatment is indicated for patients with ulcer perforation, with penetration, with gastrointestinal bleeding.

With frequently recurring episodes of peptic ulcer even against the background of drug treatment, or with malignancy of the ulcer, planned surgical treatment is indicated.

Peptic ulcer is a chronic relapsing disease characterized by the formation of a defect in the wall of the stomach or duodenum (duodenum). The prevalence of peptic ulcer among the adult population is quite high: about 10% suffer, mostly males.

At the same time, duodenal ulcer occurs 4 times more often than gastric ulcers. Localization of duodenal ulcers in the vast majority of cases occurs in the male population, stomach ulcers occur with the same frequency in men and women.

The pathogenesis of peptic ulcer

Very often, an ulcerative defect develops against the background of an existing gastritis, which can also occur with the formation of superficial ulcers - erosions. In the pathogenesis of peptic ulcer, the main importance is given to the imbalance between the protective properties of the mucosa and aggressive acid-peptic factors of gastric contents. An important role in the appearance of such an imbalance is given to the bacterium Helicobacter pylori (HP, Helicobacter pylori) discovered in 1983. This microorganism in 85-90% of cases is found in the mucous membrane of the stomach and duodenum. Helicobacter pylori has a direct damaging effect on the cells of the mucosa, producing various enzymes and cytotoxins.

Damage to the protective barrier of the mucous membrane leads to the development of superficial gastritis and duodenitis, the ratio of hormones produced by the antrum of the stomach changes - gastrin synthesis increases, somatostatin secretion is inhibited, which in turn increases wall damage. Under the influence of provoking factors: smoking, stress, errors in the diet, taking NSAIDs, etc., an ulcerative defect is formed, which, unlike erosions in gastritis, captures the submucosal layer.

Classification of peptic ulcer

Symptoms of peptic ulcer

Peptic ulcer of the stomach and duodenum is characterized by seasonality of exacerbations with relapses in the autumn-spring period. The leading symptom of an ulcer is aching, bursting or burning pain in the epigastric (pit of the stomach) region, which can radiate to the back, behind the sternum, to the left supraclavicular region (left-sided phrenicus symptom). According to the localization of pain and the connection of its occurrence with food intake, one can tentatively assume the location of the ulcer in one or another department. Pain immediately after eating occurs under the xiphoid process of the sternum or behind it with an ulcer of the cardia or subcardial region (zone 1 in the figure), 30-50 minutes after eating, to the left of the midline of the abdomen - with an ulcer of the body of the stomach (zone 2). With an ulcer of the pyloric stomach and duodenal bulb, pain is characteristic 2-3 hours after eating, somewhat to the right of the midline of the abdomen (zone 3); hunger pains that appear on an empty stomach and disappear after eating; night pains. Dyspeptic disorders are represented by heartburn, nausea, belching or vomiting of acidic contents. There may be slight bloating, a tendency to constipation. Pain decreases after taking antacids (Almagel-A, Rennie, etc.), taking milk, antispasmodics, a warm heating pad on the epigastric region.

Diagnosis of peptic ulcer

It is based on the collection of complaints, anamnesis of the disease, data from an objective examination, during which pain in the epigastric region, local percussion pain (Mendel's symptom) may be noted.

The main methods of diagnosing ulcers are X-ray and endoscopic. An X-ray examination reveals a symptom of a "niche" - a defect in the mucosa, a circular spasm of the muscles located near the ulcer, cicatricial-ulcerative deformities. Gastroscopy clarifies the localization, size, shape, depth of the ulcer, allows you to take a biopsy to exclude a malignant process, to identify H. pylori in the material. Carry out a study of the acid-forming function of the stomach using PH-metry.

General measures for gastric and duodenal ulcers: smoking cessation, alcohol intake. Walks in the fresh air, enough sleep,diet - table number 1 according to Pevznerduring the period of exacerbation.

There are no fundamental differences in the treatment of ulcers of various localization. A three-component scheme is used, including a proton pump blocker and 2 antibacterial drugs, the purpose of which is the eradication of Helicobacter pylori infection.

An example of a 3-component scheme: pariet (Nexium, omeprazole) 20 mg \ 2 r + metronidazole 500 mg \ 2 r + clarithromycin 250 mg \ 2 r. One of the antibacterial drugs can be replaced with amoxicillin or furazolidone, which has become especially relevant in recent years against the background of increasing resistance of HP strains to clarithromycin and metronidazole.

If the above scheme is ineffective for 7 days, a 4-component scheme is recommended: pariet (nexium, omeprazole) 20 mg \ 2 r + de-nol 120 mg \ 4 r + tetracycline 500 mg \ 4 r + metronidazole 250 mg \ 4 r. The duration of eradication is 7 days.

Alternative scheme: pyloride 400 mg \ 2 r + amoxicillin 500 mg \ 4 r.

- This is a chronic polyetiological pathology that occurs with the formation of ulcerative lesions in the stomach, a tendency to progression and the formation of complications. The main clinical signs of peptic ulcer include pain in the stomach and dyspeptic symptoms. The standard of diagnosis is endoscopic examination with biopsy of pathological areas, radiography of the stomach, detection of H. pylori. The treatment is complex: diet and physiotherapy, eradication of Helicobacter pylori infection, surgical correction of the complications of the disease.

ICD-10

K25 stomach ulcer

General information

Peptic ulcer of the stomach (PU) is a cyclically relapsing chronic disease characterized by ulceration of the stomach wall. PUD is the most common pathology of the gastrointestinal tract: according to various sources, from 5 to 15% of the population suffer from this disease in the world, and among urban residents, the pathology occurs five times more often. Many specialists in the field of gastroenterology combine the concepts of gastric ulcer and duodenal ulcer, which is not entirely correct - ulceration in the duodenum is diagnosed 10-15 times more often than ulcers in the stomach. Nevertheless, GU requires careful study and development of modern methods of diagnosis and treatment, since this disease can lead to the development of fatal complications.

About 80% of cases of primary detection of gastric ulcers occur in working age (up to 40 years). In children and adolescents, stomach ulcers are rarely diagnosed. Among the adult population, there is a predominance of men (women get GU 3-10 times less often); but in old age, gender differences in incidence are smoothed out. In women, the disease is milder, in most cases asymptomatic, rarely complicated by bleeding and perforation.

Peptic ulcer of the stomach ranks second among the causes of disability in the population (after cardiovascular pathology). Despite the long period of study of this nosology (more than a century), therapeutic methods of influence have not yet been found that can stop the progression of the disease and completely cure the patient. The incidence of GU is constantly growing all over the world, requiring the attention of therapists, gastroenterologists, and surgeons.

The reasons

The disease is polyetiological. According to the degree of significance, several groups of reasons are distinguished.

1. The main etiological factor in the formation of gastric ulcer is H. pylori infection - more than 80% of patients have positive tests for Helicobacter pylori infection. In 40% of patients with gastric ulcer, infected with the bacterium Helicobacter, anamnestic data indicate a family predisposition to this disease.
2. The second most important cause of gastric ulcer formation is the use of non-steroidal anti-inflammatory drugs.
3. More rare etiological factors of this pathology include Zollinger-Ellison syndrome, HIV infection, connective tissue diseases, liver cirrhosis, heart and lung diseases, kidney damage, exposure to stress factors that lead to the formation of symptomatic ulcers.

Pathogenesis

Of primary importance for the formation of gastric ulcer is the imbalance between the protective mechanisms of the mucous membrane and the impact of aggressive endogenous factors (concentrated hydrochloric acid, pepsin, bile acids) against the background of a disorder in the evacuation function of the gastrointestinal tract (hypokinesia of the stomach, duodeno-gastric reflux, etc.) . Inhibition of protection and slowdown in the recovery of the mucous membrane is possible against the background of atrophic gastritis, with the chronic course of Helicobacter pylori infection, ischemia of the stomach tissues against the background of collagenoses, long-term use of NSAIDs (the synthesis of prostaglandins slows down, which leads to a decrease in mucus production).

The morphological picture in gastric ulcer undergoes a number of changes. The primary substrate for the occurrence of ulcers is erosion - superficial damage to the epithelium of the stomach, which is formed against the background of necrosis of the mucous membrane. Erosions are usually detected on the lesser curvature and in the pyloric part of the stomach; these defects are rarely single. Erosion sizes can vary from 2 millimeters to several centimeters. Visually, erosion is a mucosal defect that does not differ in appearance from the surrounding tissues, the bottom of which is covered with fibrin. Complete epithelialization of erosion with a favorable course of erosive gastritis occurs within 3 days without the formation of scar tissue. With an unfavorable outcome, erosion is transformed into an acute stomach ulcer.

An acute ulcer is formed when the pathological process spreads deep into the mucous membrane (further than its muscular plate). Ulcers are usually single, acquire a rounded shape, on the cut they look like a pyramid. In appearance, the edges of the ulcer also do not differ from the surrounding tissues, the bottom is covered with fibrin overlays. The black color of the bottom of the ulcer is possible with damage to the vessel and the formation of hematin (a chemical substance formed during the oxidation of hemoglobin from destroyed red blood cells). A favorable outcome of an acute ulcer is scarring within two weeks, an unfavorable outcome is marked by the transition of the process to a chronic form.

The progression and intensification of inflammatory processes in the area of ​​the ulcer leads to increased formation of scar tissue. Because of this, the bottom and edges of a chronic ulcer become dense, differ in color from the surrounding healthy tissues. A chronic ulcer has a tendency to increase and deepen during an exacerbation, during remission it decreases in size.

Classification

Until today, scientists and clinicians around the world have not been able to reach agreement on the classification of gastric ulcers. Domestic experts systematize this pathology according to the following features:

• causal factor– H. pylori-associated or non-H. pylori-associated GU, symptomatic ulcers;
• localization- an ulcer of the cardia, antrum or body of the stomach, pylorus; greater or lesser curvature, anterior, posterior wall of the stomach;
• number of defects- solitary ulcer or multiple ulcers;
• defect dimensions- small ulcer (up to 5 mm), medium (up to 20 mm), large (up to 30 mm), giant (more than 30 mm);
• disease stage- exacerbation, remission, scarring (red or white scar), cicatricial deformity of the stomach;
• course of the disease- acute (gastric ulcer was diagnosed for the first time), chronic (periodic exacerbations and remissions are noted);
• complications- gastric bleeding, perforated gastric ulcer, penetration, cicatricial and ulcerative stenosis of the stomach.

Symptoms of stomach ulcer

The clinical course of gastric ulcer is characterized by periods of remission and exacerbation. Exacerbation of GU is characterized by the appearance and increase of pain in the epigastric region and under the xiphoid process of the sternum. With an ulcer of the body of the stomach, the pain is localized to the left of the center line of the body; in the presence of ulceration of the pyloric region - on the right. Possible irradiation of pain in the left half of the chest, shoulder blade, lower back, spine.

For gastric ulcer is characterized by the occurrence of pain immediately after eating with increasing intensity within 30-60 minutes after eating; pyloric ulcer can lead to the development of nighttime, hungry and late pain (3-4 hours after eating). The pain syndrome is stopped by applying a heating pad to the stomach area, taking antacids, antispasmodics, proton pump inhibitors, H2-histamine receptor blockers.

In addition to the pain syndrome, YABZH is characterized by tongue lining, bad breath, dyspeptic symptoms - nausea, vomiting, heartburn, increased flatulence, stool instability. Vomiting mainly occurs at the height of pain in the stomach, brings relief. Some patients tend to induce vomiting to improve their condition, which leads to the progression of the disease and the appearance of complications.

Atypical forms of gastric ulcer can be manifested by pain in the right iliac region (according to the appendicular type), in the region of the heart (cardiac type), and lower back (radiculitis pain). In exceptional cases, the pain syndrome in YABZH may be absent altogether, then the first sign of the disease is bleeding, perforation or cicatricial stenosis of the stomach, due to which the patient seeks medical help.

Diagnostics

If a stomach ulcer is suspected, a standard set of diagnostic measures (instrumental, laboratory) is carried out. It is aimed at visualizing the ulcer, determining the cause of the disease and eliminating complications.

• Esophagogastroduodenoscopy. It is the gold standard for the diagnosis of gastric ulcer. EGDS allows to visualize the ulcer in 95% of patients, to determine the stage of the disease (acute or chronic ulcer). Endoscopic examination makes it possible to timely identify complications of gastric ulcer (bleeding, cicatricial stenosis), conduct endoscopic biopsy, surgical hemostasis.
• gastrography. Radiography of the stomach is of paramount importance in the diagnosis of cicatricial complications and ulcer penetration into adjacent organs and tissues. If endoscopic imaging is not possible, radiography can verify a stomach ulcer in 70% of cases. For a more accurate result, it is recommended to use double contrasting - in this case, the defect is visible in the form of a niche or a persistent contrast spot on the wall of the stomach, to which the mucosal folds converge.
• Diagnosis of Helicobacter pylori infection. Considering the huge role of Helicobacter pylori infection in the development of gastric ulcer, all patients with this pathology undergo mandatory tests for the detection of H. pylori (ELISA, PCR diagnostics, breath test, biopsy examination, etc.).

Auxiliary value in gastric ulcer have:

• Ultrasound of the OBP (reveals concomitant pathology of the liver, pancreas),
• electrogastrography and antroduodenal manometry (makes it possible to assess the motor activity of the stomach and its evacuation capacity),
• intragastric pH-metry (detects aggressive damage factors),
• fecal occult blood test (performed if gastric bleeding is suspected).

If the patient is admitted to the hospital with a clinical picture of "acute abdomen", Diagnostic laparoscopy may be required to rule out gastric perforation. Gastric ulcer should be differentiated from symptomatic ulcers (especially medicinal), Zollinger-Ellison syndrome, hyperparathyroidism, stomach cancer.

Treatment of gastric ulcer

Conservative treatment

The main goals of therapy for GU include repair of the ulcer, prevention of complications of the disease, and achievement of long-term remission. Treatment of gastric ulcer includes non-drug and drug effects, surgical methods.

1. Non-drug treatment YABZH means following a diet, prescribing physiotherapeutic procedures (heat, paraffin therapy, ozocerite, electrophoresis and microwave effects), it is also recommended to avoid stress, lead a healthy lifestyle.
2. Medical treatment should be complex, affect all links in the pathogenesis of GU. Antihelicobacter therapy requires the appointment of several drugs for the eradication of H. pylori, since the use of monoschemes has shown to be ineffective. The attending physician individually selects a combination of the following drugs: proton pump inhibitors, antibiotics (clarithromycin, metronidazole, amoxicillin, furazolidone, levofloxacin, etc.), bismuth preparations.

Surgery

With timely seeking medical help and carrying out a complete scheme of anti-Helicobacter treatment, the risk of complications of gastric ulcer is minimized. Emergency surgical treatment of gastric ulcer (hemostasis by clipping or stitching a bleeding vessel, suturing an ulcer) is usually required only for patients with a complicated pathology: perforation or penetration of an ulcer, bleeding from an ulcer, malignancy, formation of cicatricial changes in the stomach. In elderly patients, with a history of indications of complications of gastric ulcer in the past, experts recommend reducing the time of conservative treatment to one to one and a half months.

Absolute indications for surgery:

• perforation and malignancy of the ulcer,
• massive bleeding
• cicatricial changes in the stomach with a violation of its function,
• gastrojejunostomy ulcer.

Conditionally absolute indications include:

• ulcer penetration,
• giant callous ulcers,
• recurrent gastric bleeding against the background of ongoing conservative therapy,
• lack of repair of the ulcer after its suturing.

A relative indication is the absence of a clear effect from drug therapy for 2-3 years. For decades, surgeons have been discussing the effectiveness and safety of various types of surgery for gastric ulcers. To date, gastric resection, gastroenterostomy, various types of vagotomies are recognized as the most effective. Excision and suturing of a stomach ulcer is used only in extreme cases.

Forecast and prevention

The prognosis for gastric ulcer largely depends on the timeliness of seeking medical help and the effectiveness of anti-Helicobacter therapy. PUD is complicated by gastric bleeding in every fifth patient, from 5 to 15% of patients suffer perforation or penetration of the ulcer, 2% develop cicatricial stenosis of the stomach. In children, the incidence of complications of gastric ulcer is lower - no more than 4%. The likelihood of developing gastric cancer in patients with GU is 3-6 times greater than among people who do not suffer from this pathology.

Primary prevention of gastric ulcer includes the prevention of infection with Helicobacter pylori infection, the exclusion of risk factors for the development of this pathology (smoking, cramped living conditions, low standard of living). Secondary prevention is aimed at preventing relapses and includes dieting, avoiding stress, prescribing an anti-Helicobacter drug regimen when the first symptoms of PUD appear. Patients with gastric ulcer require lifelong follow-up, endoscopic examination with obligatory testing for H. pylori once every six months.

22839 -1

Peptic ulcer of the stomach and duodenum is a chronic and recurrent disease. It is manifested by the formation of a defect (ulcer) on the wall of the stomach or duodenum. The frequency of detection of gastric and duodenal ulcers in adults averages 10-12%. More than 80% of ulcers are localized in the duodenum. The disease occurs more often (70-80%) at the age of 30-40, however, about 1% of duodenal ulcers and 0.7% of gastric ulcers occur in childhood and adolescence.

Duodenal ulcer occurs at a younger age, and gastric ulcer in the elderly and senile. In both groups of patients, there is a clear prevalence of males (4:1), which is even more significant for duodenal ulcers. Duodenal ulcer is 6 times more common in men than in women, and the ratio of gastric ulcer is 27:1. A duodenal ulcer in 94% of patients is localized in the bowel bulb. There can be two ulcers at the same time - on the anterior and posterior walls ("kissing ulcers"). The diameter of ulcers here usually does not exceed 1.5 cm. Various stages of chronic duodenitis are found in duodenal mucosa. This ulcer often penetrates into the head of the pancreas, into the hepatoduodenal ligament. Scarring of the ulcer causes deformation of the bulb, the formation of diverticulum-like protrusions of its walls, narrowing of the lumen.

Etiology and pathogenesis PUDs remain understudied. Currently, there is no generally accepted theory of its etiopathogenesis. PU is a polyetiological disease, its pathogenesis is multifactorial.

In the modern view, in its etiology, a number of basic and predisposing factors are accepted, which, obviously, contribute to the development of the disease and its exacerbation:

1) long-term or often recurring neuro-emotional overstrain (stress), negative emotions that disrupt the nervous and hormonal mechanisms of regulation of the function of the stomach, its trophism and duodenum. As a result, blood circulation and oxygen supply to the stomach and duodenum are disturbed, leading to the formation of an ulcer. In connection with circulatory disorders, the wall of the stomach and duodenum becomes sensitive and unstable to rich in pepsin and hydrochloric acid ZhS;
2) genetic predisposition, including a persistent increase in the acidity of ZhS, of a constitutional nature;
3) local disorders of the digestive process and changes in the trophism of the gastroduodenal system;
4) the presence of chronic gastritis, duodenitis, functional disorders of the stomach and duodenum (pre-ulcerative condition);
5) violation of the diet;
6) smoking;
7) long-term use of strong alcoholic beverages, certain medications (aspirin, butadnon, indomstacin, reserpine, glucocorticoids, etc.).

These drugs have an adverse effect on the protective barriers of the gastric mucosa, suppress the formation of mucus and change its qualitative composition, cause a violation of capillary circulation, etc.

Local factors include a violation of the protective mechanisms of the mucous barrier, circulatory disorders and structural changes in the CO. The development of gastric ulcers is associated mainly with the weakening of CO resistance, the development of the so-called antral stasis and duodenogastric reflux. The occurrence of duodenal ulcers is realized by acid-peptic aggression. Normal gastric and duodenal mucosa stably withstands, is protected from aggressive factors (hydrochloric acid, pepsin, lysolecigin and bile acids) of the stomach and duodenum.

Protection factors include blood flow through CO, secretion of mucus and pancreatic juice, regeneration of the surface epithelium, local synthesis of prostaglandins, etc. Damage to CO with the formation of ulcers, erosions and inflammation is associated with the predominance of aggression factors (hydrochloric acid, pepsin, nutritional factors, dysmotility, trauma mucosa) over protective factors (CO resistance, antroduodenal acid "brake", alkaline secretion, food).

The features of NS reactivity, genetic predisposition (increase in the mass of parietal cells), age-related neuroendocrine changes in the body (peculiarities of puberty, menopause), violations of regulatory processes due to various diseases, increased acid-peptic secretion, intestinal metaplasia of the gastric mucosa, antroduodenal dysmotility, endocrine influence, etc.

Chronic liver disease (violation of histamine and gastrin inactivation, stagnation in the portal vein - a violation of microcirculation), kidney disease, acute and chronic circulatory disorders, stressful situations. An ulcer can form in elderly patients ("senile ulcer"), with lesions of the central nervous system, with extensive burns and severe purulent diseases.

Local mechanisms of ulceration also include slowing down and irregular evacuation of intestinal contents, prolonged antral stasis of food chyme, gaping of the gatekeeper, duodenogastric reflux with regurgitation of bile acids and lysolecithins, which destroy the mucous barrier and cause retrodiffusion of H-ions and the formation of an ulcer under the influence of pepsin (P. Ya. Grigoriev and E.P. Yakovenko, 1993).

As separate pathogenetic factors, an increase in the release of hydrochloric acid and pepsin, a decrease in the active release of bicarbonates and the process of mucus formation can serve.

Ulceration in the pyloroduodenal mucosa is also affected by prolonged hyperchlorhydria with peptic proteolysis caused by hypervagotonia, hypergastrinemia and hyperplasia of the main gastric glands, ineffective neutralization of SF by mucoid substances and the alkaline component of the duodenum, and prolonged local acidification of the pyloroduodenal environment. The main aggressive and damaging factors are SA and pepsin. The old statement: "No acid - no ulcer" remains, in fact, correct at the present time, despite the fact that the boundaries of acid production in patients with ulcer fluctuate widely.

In the regulation of acid secretion, among other factors, prostaglandins also play an important role, which are able to inhibit this process. In addition, they have a cytoprotective effect due to the stimulation of mucus secretion. The most important mechanisms of protection of CO from the stomach and duodenum from the action of damaging agents are the normal regulation of secretory function, resistance of CO from the protective barrier, its microcirculation, and high regenerative capacity of the surface epithelium.

Of great importance in providing resistance to CO is mucin, which is secreted by cells of the integumentary epithelium, additional cells of the cervical part of the gastric glands, pyloric glands, and in the duodenum - Brunner's glands and goblet cells. Having a large buffer capacity, mucin neutralizes both acids and alkalis, it absorbs pepsin, and is resistant to various physiological and chemical agents. Mucus covers the surface of the GI tract with a layer in the form of a film 1-1.5 mm thick and serves as a protective barrier.

With a decrease in the resistance of CO due to damage to its protective barrier, the reverse diffusion of H-ions increases. The resulting tissue acidosis promotes the release of histamine from CO cells and acetylcholine from intramural nerve plexuses. As a result, the secretion of hydrochloric acid and pepsin is stimulated, microcirculation and capillary permeability are disturbed, stasis and edema develop, hemorrhage in the CO. Such CO is easily damaged by hydrochloric acid, pepsin and other agents.
The gastric mucosa is damaged and as a result of duodenogastric reflux, bile changes the properties of mucin, dissolves the surface layer of mucus.

Bile acids in the presence of hydrochloric acid acquire the ability to penetrate cell membranes and damage cells of the surface epithelium. The resistance of CO decreases with inflammatory and degenerative changes in CO, accompanied by a decrease in mucin release and a change in its properties. The resistance of CO depends on the organ blood flow, hypoxia as a result of impaired blood flow from spastic contractions of the muscles of the stomach, etc.

Food as a result of mechanical and chemical effects on CO can cause increased rejection of cells of the integumentary epithelium. The insufficiency of the regenerative capacity of SO creates conditions for an increase in the reverse diffusion of H-ions, depletion of the intracellular buffer system, the appearance of hemorrhages, erosions and ulcerations of the SO (V.T. Perederni et al., 1997).

Nutritional factors, in addition to the ability to aggravate shifts in the secretory and motor activity of the stomach and duodenum, can also be a protective factor due to the dilution and neutralization of hydrochloric acid, the binding of pepsin to protein components.

In recent years, the interest of scientists to a new factor in the occurrence of Helicobacter pylori. The latter is detected in PU with localization of the ulcer in the antropyloroduodenal zone in almost 100% of cases, which makes one think about its significant role in the pathogenesis of this disease and consider it one of its most important factors (P.Ya. Grigoriev et al., 1993; M. G. Gonchar et al., 1999).

PU has different pathogenetic mechanisms at different localizations (stomach, duodenum, stomach bodies, prepyloric and pyloric ulcers, combined gastric and duodenal ulcers).

YaB duodenum has some features, which are as follows:

1. In patients with duodenal ulcer, hypersecretion with increased acidity of the SF is often observed, which is due to a high tone of the vagus nerve, an increase in the number of parietal cells, an increased release of G-cell gastrin, a weakening of the antroduodenal mechanism of autoregulation of inhibition of acid production, a decrease in the acid-neutralizing ability of the stomach associated with a decrease in secretion of pyloric alkali glands.

2. Gastroduodenal dysmotility is more pronounced, which is manifested by accelerated evacuation from the stomach, resulting in a decrease in the buffer role of food and an increase in acidity in the duodenum.

3. In duodenal ulcer, the effect of the physiological depressor mechanism on the release of hydrochloric acid is less pronounced, and the release of the alkaline secretion of the pancreas is markedly reduced.

4. As a result of a decrease in the resistance of the SO of the duodenum to the effects of JS and the violation of its protective barrier, the reverse diffusion of H-ions increases.

5. Psychosomatic factors are relatively more important, leading to a disorder of the secretory and motor functions of the stomach and duodenum.

6. The relationship between duodenal ulcer and CP increases the incidence of duodenal ulcer among patients with CP. This is due to a decrease in the buffering capacity of duodenal contents due to a decrease in the concentration of bicarbonate in pancreatic juice.

Thus, if the peptic factor is important in the pathogenesis of the formation of a duodenal ulcer, then in many cases with a stomach ulcer, not only the peptic factor is important, but also the weakening of the protective abilities of the gastric mucosa (impaired mucus formation, worsening blood circulation, etc.).

Pathological anatomy. A peptic ulcer is defined as a defect in the mucosa of the stomach and duodenum that spreads through the tun. musc, mucosae. The ulcer can penetrate to different depths, up to the serous cover, or, when the latter is destroyed, communicate with the free cavity of the peritoneum (perforation) or the surface of one of the adjacent organs (penetration) can serve as its bottom.

Pathologically distinguish:

1) acute ulcers (OYA);
2) chronic ulcers (CH);
3) penetrating ulcers;
4) cicatricial changes caused by an ulcer (M.Yu. Pantsyrev, V.I. Sidorenko, 1988).

OA have a round or oval shape with clearly defined edges that have penetrated through the submucosal layer up to the serous one. The development of OT is based not on an inflammatory process, but on necrosis with distinct changes in the vessels and connective tissue of the stomach. During the healing of the OT, linear or star-shaped scars are formed.

A distinctive feature of the CN is the progressive compaction of its edges and bottom (callous ulcer) due to the abundant development of scar connective tissue. Over time, the development of connective tissue becomes more and more pronounced, it becomes sclerotic, the edges of the ulcer become more and more dense and turn into a callous (causal) ulcer (M.Yu. Pantsyrev, V.I. Sidorenko, 1988; V.N. Chernov and et al., 1993), which makes the ulcer look like a tumor (ulcus tumor).

This ulcer penetrates to different depths of the organ wall and beyond (penetrating ulcer). The diameter of the ulcer is from 0.3 to 6 cm. Various stages of chronic gastritis and chronic duodenitis are revealed in the CO. Cicatricial changes tighten CO in the form of folds, converging to the edges of the ulcer. Around the ulcer, the vessels have thickened walls, their lumen is narrowed or obliterated due to endovasculitis, proliferation of connective tissue. Nerve fibers and ganglion cells undergo dystrophic changes and decay.

A callous ulcer does not tend to heal, often accompanied by destruction of the wall of one of the adjacent vessels. After healing of the CN, star-shaped scars remain with a characteristic retraction in the center. Scars can be accompanied by a significant deformation of the stomach (stomach in the form of a "snail", "hourglass") or narrowing of its outlet (pyloric stenosis). Deep-penetrating ulcers, as a rule, are complicated by the development of peritoneal adhesions (perigastritis, periduodenitis), which also deform the stomach and duodenum.

A penetrating ulcer is understood as a form in which the ulcerative process passes through all layers of the wall of the stomach or duodenum, but does not perforate into the free abdominal cavity. With this variant of PU, the destructive process is slow and the bottom of the ulcer communicates with neighboring organs. Therefore, when the serous membrane of the stomach and duodenum is destroyed, the ulcer, as it were, penetrates into the corresponding organ, the tissues of which form the bottom of the crater.

Classification. There is currently no generally accepted classification of PU. The classification proposed by CM is the most widespread. Ryss (1968).

According to this classification, the following are distinguished:

- localization of the ulcer; the body of the stomach; small curvature; cardiac department; big curvature; bulb duodenum;
- concomitant changes in the gastric and duodenal mucosa: normal gastric mucosa (parietal cells hyperplasia), duodenum; XP, superficial, with glandular lesions without atrophy; atrophic; chronic duodenitis, superficial, diffuse, atrophic;
- gastric secretion: normal, decreased, increased, true achlorhydria;
- course: periodically relapsing, often relapsing, latent; juvenile ulcer, ulcer in the elderly, senile age; benign, malignant malignancy of the ulcer, the consistent development of cancer outside the ulcer;
- special forms: pyloric ulcer, giant ulcer, postbulbatory ulcer;
— complications: bleeding, penetration, perforation, cicatricial changes.

In practical surgery, the IL classification proposed by Johnson is used: type I - ulcers of lesser curvature - mediagastric ulcer (above 3 cm from the pylorus); Type II - quilted ulcers of the stomach and duodenum; Type III - ulcers of the prepyloric stomach (up to 3 cm from the pylorus).

Clinical picture and diagnosis. The course of PU is long, with alternating periods of exacerbation and prolonged remissions. Exacerbations are associated with an error in the diet, overwork, emotional and nervous strain. For YaB typical "seasonal". Exacerbations most often occur in spring and autumn. The most typical is the presence in history and on physical examination of the "triad" of symptoms: pain, vomiting and bleeding.

The seasonality of the disease is explained by a change in the state at different times of the year, the neuroendocrine system that regulates the secretory and motor functions of the stomach and duodenum.

One of the main subjective manifestations of PU is pain. Being the main complaint of patients, it is usually noted in the epigastric region. Pain can also be localized to the right of the midline of the abdomen. Pain usually occurs after eating. The time of its onset (after eating) can help determine the location of the ulcer. There are early, late, nocturnal and hungry pain. If the ulcer is localized in the area of ​​​​the entrance and body of the stomach, early pain occurs (the first 30 minutes). Arising immediately after taking food, it stops after emptying the stomach.

With the localization of the ulcer in the region of the outlet part of the stomach or duodenum, late pain is noted. The latter occurs after some time (1.5-2 hours after eating), on an empty stomach, hungry pains or at night (night pains). Pain can radiate to the left half of the chest, the area of ​​the xiphoid process, the left shoulder blade, the difficult part of the spine. Hunger pains are associated with the fact that a duodenal ulcer is often accompanied by a constant secretion, which continues even outside the meal and during sleep. This violation is due to a sharp increase in the tone of BN, and for an ulcer localized in the stomach, an increase in gastrin secretion.

The genesis of hunger pains that occur during a long break in food intake is due to hypoglycemia, which causes an increase in the tone of the BN and, as a result, an increase in the secretory and motor activity of the stomach.

Night pains occur between about 24-3 o'clock in the morning, subside after taking food (milk) or after profuse vomiting of acidic stomach contents. The appearance of pain is associated with an increase in the tone of BN at night. Night pains to a certain extent can also be hunger pains.

With an ulcer of the cardia, pain is localized in the region of the xiphoid process and the left half of the epigastric region with irradiation to the left shoulder and scapula, with pyloroanthral and duodenal ulcers, pain is most noted on the right in the mesogastric, right hypochondrium, radiating to the back. When the lesser curvature is affected, pain is noted along the white line in the epigastric region.

Irradiation of pain can be in the lower back to the left of the XII rib - the point of Boas and the spine, according to the location of the ulcer - the point of Openhovsky. However, it should be noted that the pain in PU quite often does not have a clear rhythm. The intensity, localization, irradiation and rhythm of pain depend on the depth of the ulcerative process, its prevalence and severity in the gastroduodenal mucosa.

With superficial ulcers, pain may be absent or be expressed so slightly that it practically does not attract the attention of the patient. Pain occurs or intensifies when an ulcer or periulcerous inflammation penetrates into the deep layers (muscular, subserous) of the organ wall. These layers are innervated by sensitive fibers of the sympathetic nerves that respond to spasm.

Pain can be caused by hypersecretion of acidic fatty acid, increased motor function of the stomach, pylorospasm, and increased intragastric pressure. With the penetration of the ulcer and the periulcerous inflammatory process, the pain intensifies, becomes almost constant, persistent, at times very acute. At the height of the pain, irradiation to the left appears with ulcers of the upper sections of the stomach and to the right hypochondrium - with ulcers of the output section of the stomach and duodenal bulb.

Pain during ulcer penetration is due to the involvement in the pathological process of tissues innervated by sensory fibers of the intercostal nerves. When the ulcer is perforated, there is a sharp constant pain of a “dagger character”. The state of organ circulation, venous stasis in the vessels of the lesser curvature of the stomach also matters in the origin of pain.

The penetration of the ulcer into the surrounding organs and tissues is accompanied by the development of inflammatory processes in the affected organs and the formation of extensive adhesive processes (perivisceritis). The pain syndrome during penetration becomes more intense, permanent polymorphic, pains appear that are characteristic of diseases of adjacent organs involved in the pathological process. Pain in this case mainly depends on the organ into which the ulcer penetrates. When the ulcer penetrates into the lesser omentum, the pain radiates to the right hypochondrium, sometimes to the right shoulder blade, when it penetrates into the gastrosplenic ligament - up and to the left, when the ulcers penetrate to the diaphragm, a typical “phrenicus syndrome” appears (left or right), when the ulcer penetrates into mesentery of the transverse OK there is pain in the umbilical region.

Duodenal and pyloric ulcers often penetrate into the pancreas. Ulcers of large sizes are accompanied by more severe pain than chronic ones, and have dense edges.

For PU, cyclical pain, calm after rest and treatment are typical. A characteristic symptom of PU is heartburn, a burning sensation in the epigastric region and behind the sternum. After eating, antacids heartburn decreases or disappears. The occurrence of heartburn is associated with impaired motility, secretory activity of the stomach and reflux of its contents as a result of insufficiency of the closing function of the esophageal-gastric junction, increased tone of the muscles of the stomach and spasm of the pylorus. The insufficiency of the "physiological cardia" can also be due to a hernia of the POD, often combined with PUD.

Sometimes there is an acid eructation due to regurgitation of gastric contents into the esophagus due to cardia insufficiency and increased intragastric pressure. Sour belching often occurs with duodenal ulcer. With a stomach ulcer, it is empty or contains food debris. Nausea, rotten belching, and vomiting are rare in uncomplicated PU. These symptoms indicate a violation of the evacuation of the contents of the stomach due to prolonged spasm and severe inflammatory edema of the pylorus or duodenal bulb, and their persistence in the remission phase indicates cicatricial pyloric stenosis.

Being a less constant symptom than pain, vomiting in GU occurs somewhat more frequently (68%) than in duodenal ulcer (53%). The vomit contains acidic gastric contents, undigested food residues and an abundance of mucus. With complications of PU (pyloric stenosis, bleeding), the nature of vomiting and vomit changes accordingly. Vomiting in uncomplicated PU occurs at the height of pain. It may be early or late. Vomiting is caused by irritation of the inflamed SO and, apparently, is of a reflex nature.

In most patients, especially with duodenal ulcers, in the acute phase there are constipation, often caused by spastic dyskinesia of the colon. In some patients, stool retention may be a harbinger of an exacerbation of PU.

Appetite with an uncomplicated form of PU, it usually does not decrease, and often even increases, especially with duodenal ulcers (“painful hunger”).

sick gradually lose weight, lose weight, because, despite a good appetite, they deliberately avoid eating due to fear of exacerbation of pain. The exacerbation phase usually lasts 4-5 days, and in some cases up to 6-8 weeks, and then follows a period of more or less well-being, which can last several years. The general condition of patients with PU is usually satisfactory.

In the phase of exacerbation of the disease, it worsens, there is increased fatigue, weakness, sweating, disability, depression is observed or, on the contrary, increased excitability. There may be various neurological reactions due to disorders of the autonomic nervous system. Patients often adhere to normal or even increased nutrition, but more often reduced. This is due to a number of reasons: self-restriction in the diet, duration, sleep disturbance during night pain, persistent nausea and vomiting.

Clinical manifestations of PU in terms of recurrence also depend on the localization of the ulcer. Pyloric ulcers are characterized by a persistent relapsing course, short unstable remissions, frequent complications of bleeding and stenosis. The pain syndrome can be extremely intense, repeatedly renewing during the day, which is due to the involvement of a very sensitive neuromuscular apparatus of the pylorus in the pathological process.

An ulcer of the upper stomach clinically often does not fit into the description of the classical forms of the disease, masked by manifestations of angina pectoris, cholecystitis, pleurisy, etc. Due to the difficulties of clinical, radiological and even endoscopic evaluation of an ulcer of this localization, it is often not diagnosed for a long time.

Extra-bulbous ulcers occur with frequent exacerbations, recurrent bleeding, accompanied by persistent pain, heartburn, bitterness in the mouth, and relatively rare vomiting. One of the signs of extra-bulbous ulcers may be jaundice caused by a periulcerous inflammatory process that spreads to the sphincter of the major duodenal papilla (MDP), penetration of the ulcer into the pancreas with the development of reactive inflammation in it, compressing the CBD. Reactive pancreatitis, which occurs in patients with postbulbar ulcers, is accompanied by intense constant pain in the left side of the abdomen, which increases during exercise and palpation. After taking food, a feeling of fullness in the stomach and heaviness joins.

On palpation, you can determine moderate pain in the epigastric region, slight muscle tension. Of great importance is the identification of zones of percussion soreness (K. Mendel): for duodenal ulcers - in the right half of the epigastrium with spread to the right hypochondrium; for stomach ulcers - along the midline and somewhat to the left of it; with a cardiac ulcer - at the xiphoid process.

Of the LI, detection of occult blood in the feces and reticulocytes in the peripheral blood is of diagnostic importance, confirming a bleeding ulcer, but, of course, not excluding other gastrointestinal diseases with bleeding. Diagnosis of PU is based primarily on the data of an objective study of the stomach and duodenum.

Of the special diagnostic methods, RI is still common. This method is safe, objective and allows you to identify not only morphological changes, but also the exact localization of the ulcer, size, evaluate secondary changes in the organ under study, deformation, connection with neighboring organs, etc. This method is becoming more and more informative in connection with the improvement of X-ray diagnostic devices equipped with image intensifiers, television systems, computers and video recorders. All this makes it possible to more accurately assess morphological changes and to study the motor function of the stomach and duodenum quite fully.

The reliability of the establishment of radiographically PU given by X-ray surgical comparisons is 95-97% (Yu.M. Pantsyrev, V.I. Sidorenko, 1988). RI is a priority if the patient is suspected of stenosis, impaired gastric emptying, anomaly in position, hernia of the POD, fistula, diverticulosis, as well as in patients with the so-called increased endoscopic risk.

The main and direct radiological sign, which allows diagnosing an ulcer with confidence, is a symptom of a “niche” surrounding its inflammatory shaft, convergence of CO folds. The ulcerative "niche" (Gaudeck's symptom) is an unstructured depot of barium suspension, an added shadow ("plus shadow"), protruding beyond the contours of the stomach, and is the most reliable sign of an ulcer, decisive in making a diagnosis. Periulcerous annular ridge, protruding above the CO level, is formed as a result of inflammatory tissue infiltration and functional spastic changes in the muscles of the submucosal layer around the ulcer. Ulcerative "niche" is usually the correct form, with clear contours.

There is also cicatricial deformity of the duodenal bulb (in the form of a trefoil, tubular narrowing). Around the ulcerative "niche", with a thorough and methodically correct study, a rim of enlightenment of a greater or lesser width is visible - an inflammatory shaft, to which the CO folds converge. On the basis of this sign, it is possible to judge a periulcerous inflammatory shaft. Superficial acute ulcers without an inflammatory shaft do not give a characteristic symptom of a "niche". Bleeding ulcers are rarely accompanied by an x-ray symptom of a “niche”, since their crater is filled with thrombotic masses, and the inflammatory shaft decreases sharply, the CO defect appears superficial.

Deep ulcerative niches in the body of the stomach and duodenal bulb are more easily recognized. Identification of ulcerative "niches" in the cardiac and subcardial regions, as well as in the pyloric region of the stomach and extra-bulbous ulcers requires special methodological techniques. The complexity of identifying such ulcers is due to the anatomical and functional features of these departments.

Difficulties in the diagnosis of ulcerative defects also arise when they are localized in the zone of pronounced cicatricial deformities of the stomach and duodenum (MA Filipkin, 1977, etc.). Senile ulcers are relatively easy to recognize (A.S. Loginov, V.M. Mayorov, 1979). In order to increase the information content of the X-ray method, a positional examination of the CO relief is carried out, and general and sighting pictures are taken in the course of the study. Direct radiographic symptoms of PU include cicatricial deformity of the stomach or duodenum (a decrease in the volume of the bulb, diverticulum-like protrusions, an hourglass-shaped stomach, a cascade cochlear stomach, etc.).

Indirect signs, which are indicators of functional disorders, are of little significance in the diagnosis of ulcers. Auxiliary radiological signs include increased motility, increased tone, convergence of CO folds, hypersecretion and impaired evacuation function, local spasm, deformity of the organ wall, accelerated evacuation of the barium mass from the stomach and its rapid passage through the duodenum to the upper loops of the TC, etc. Deserve special attention a sharp expansion of the stomach due to cicatricial changes in the pyloroduodenal section, cardia insufficiency, gastrointestinal tract, deformation of the duodenal bulb.

Currently, the method of double contrasting is successfully used, which makes it possible to reveal fine details of the SO structure in normal and pathological conditions. This method makes it possible to more often diagnose superficial ulcers, which are extremely rare with the usual method.

Diagnosis of old, callous ulcers of the stomach is based on the irregular shape of the "niche" and the exit of the barium depot beyond the shadow of the stomach in different positions of the patient. For recognition of CN with a linear or slit-like crater and other atypical ulcers, double contrasting and simultaneous premedication are required. The use of anticholinergic and antispasmodic drugs during the study allows to achieve a better distribution of CO and, therefore, to obtain better information about the state of the organ.

X-ray recognition of a scarring ulcer of the gastric mucosa and duodenum, especially a post-ulcer scar, is often based on indirect signs (convergence of folds to the contour of the gastric wall, accumulation of barium suspension with clear uneven contours and convergence of the folds of the gastric wall to it).

In addition to identifying an ulcerative defect in the stomach and duodenum, the X-ray method is valuable in case of suspected stenosis, hernia of the submucosa, diverticulosis, with submucosal formations, as well as in patients with an increased endoscopic risk. RI is also determined by the motility of the stomach. With ulcerative lesions of the stomach, its motility often does not differ from normal even during an exacerbation and with pain. Sometimes it is reduced. With a duodenal ulcer, there is an increase in the motility of the stomach, especially its antrum. In most patients, the periodic activity of the stomach is disturbed: the contractions of the organ on an empty stomach are continuous or there is an increase in the period of work and a shortening of periods of rest.

A reliable method that allows, with rare exceptions, to confirm or reject the diagnosis of PU is esophagogastroduodemoscopy. It makes it possible not only to identify an ulcerative defect, but also to ensure control over its scarring, and the GI of the material obtained by targeted biopsy allows assessing changes in SO, reliably guaranteeing the accuracy of the diagnosis at the morphological and even morphofunctional level. The endoscopic picture in chronic ulcers depends on the localization of the process, the stage of healing or exacerbation.

The endoscopic picture of exacerbation of the ulcer process is characterized by a round or oval ulcer and inflammation of the mucous membrane. Sizes, shapes, depth, bottom, edges, severity of periulcerous inflammation and CO infiltration are different. Differentiation is facilitated by the GI of SO biopsy samples obtained from the edges of the ulcer and the periulcerous zone.

With the help of duodenoscopy, the diagnosis of postbulbar ulcers, which account for at least 1% of all duodenal ulcers, has significantly improved. These ulcers can also be either single or multiple. When the inflammatory process subsides, the hyperemia around the ulcer decreases, the shaft surrounding it is smoothed out, flattened. The ulcer becomes less rough, both as a result of a decrease in the height of the inflammatory shaft, and due to the development of granulations at the bottom. Ulcers in the healing process can take on a different shape, fragment. With complete healing, tender pink scars of a linear or star shape are visible at the site of the ulcer. As a rule, scarring of the ulcer leads to a more or less pronounced deformation of the SO of the organ.

The use of endoscopy for the differential diagnosis of benign and malignant gastric ulcers is very important. In unclear cases, multiple (six pieces from the edges and bottom of the ulcer) targeted gastrobiopsy from histologically examined biopsy specimens becomes essential. Morphological diagnosis of PU is important not only for the differential diagnosis of the disease, but also for determining adequate therapy.

The endoscopic method is also used to determine the acid-forming zone of the stomach (Yu.M. Pantsyrev et al., 1978). This method has been successfully used for marking the intermedial zone in the preoperative period. Endoscopic examination (EI) is also used to study the nature and localization of the mucosal microflora, as well as to determine its sensitivity to antibiotics. Endoscopy allows you to recognize violations of the motor and evacuation functions of these organs (insufficiency of the cardia, gastroesophageal and duodenogastric reflux, etc.).

One of the most important achievements has been the use of EI to diagnose the causes of bleeding from the upper gastrointestinal tract.

In patients with PU, the study of gastric secretion is important, especially for the detection of functional disorders of the stomach. The volume of LS, the acid composition of the content, the debit of NS and pepsin are studied. In assessing the acid- and enzyme-producing function of the stomach, the debit-hour of HCl and pepsin in the basal and stimulated phases of secretion is taken into account.
Gastric secretion in PU varies significantly depending on the localization. With bulbar and pyloric ulcers, acid production most often increases both in the basal (fasting) and in the stimulated phase.

Most patients with pylorobulbar ulcers have continuous acid formation with a sharp and constant acidification of the stomach and duodenal bulb. High levels of gastric secretion are also established with combined lesions of the stomach and duodenum. In gastric ulcers, acid-forming function is usually normal or significantly lower if the ulcer is located closer to the cardia of the stomach. Moderate hypersecretion is found only in some patients.

differential diagnosis. PU is differentiated from gastritis, gastric cancer, diseases of the biliary tract, coronary vessels, duodenal obstruction, pancreatitis, appendicitis, pathology of the right kidney and ureter, colon, etc. The diagnosis of duodenal ulcer with typical clinical manifestations is not difficult. This disease is characterized by the seasonality of the course of the disease, the daily rhythm of pain associated with food intake, etc. In each case, the final diagnosis can only be guaranteed by RI and EI with targeted gastrobiopsy.

When localized paroxysmal pain in the right hypochondrium may resemble cholelithiasis, XX. However, the observed seasonality of exacerbations of the disease lasting 3-4 weeks, the daily rhythm of pain, the disappearance of pain after vomiting speak of a ulcer, and not of hepatic colic, which occurs sporadically after taking fatty fried foods and in which pain disappears after vomiting. With hepatic colic, patients are restless, looking for a comfortable position, the attacks are short-lived, with the use of antispasmodics, the pain subsides, etc.

In diseases of the gallbladder, palpation of the abdomen causes pain in the right hypochondrium (outside of the edge of the right rectus muscle), and in case of a duodenal ulcer, in the region of the right rectus muscle (in the area of ​​the projection of the duodenum on the abdominal wall). Differential diagnosis is helped by RI, which reveals functional changes in the biliary tract associated with duodenal ulcer or their combination with cholelithiasis. CP may have similarities with duodenal ulcer, in which increased pain in the upper abdomen is associated with food intake. However, in chronic pancreatitis, pain often takes on a girdle character, does not disappear after taking antacids, and may increase after vomiting.

When diagnosing CP, it is necessary to take into account the role of alcoholism in the anamnesis. CP may accompany duodenal ulcer, more often in cases of ulcer penetration into the pancreas. The use of ultrasound scanning of the pancreas, gallbladder provides information used for differential diagnosis of duodenal ulcer with diseases of the pancreas and gallbladder.

Grigoryan R.A.