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Stomach ulcer clinic treatment prevention. Duodenal ulcer

Peptic ulcer disease (PU) is a fairly common pathology of the digestive tract. According to statistics, up to 10-20% of the adult population encounter it; in large cities the incidence rate is much higher than in rural areas.

This disease is associated with the formation of ulcers on the mucous membrane of the stomach and duodenum, in the absence of proper treatment Peptic ulcer leads to serious complications and even death. The disease may for a long time It is asymptomatic, but it is very dangerous during exacerbations. A correctly selected treatment regimen for stomach and duodenal ulcers ensures healing and prevents complications.

Causes of peptic ulcer

The main reason why the disease occurs is the activity of the bacterium Helicobacter Pylori: it provokes inflammation, which over time leads to the formation of ulcers on the mucous membrane. However, bacterial damage is aggravated by some additional factors:

  • Improper, irregular diet. Snacks on the go, lack of a full breakfast, lunch and dinner, an abundance of spices and over-salted dishes in the diet - all this negatively affects the stomach and creates a favorable environment for the growth of bacteria.
  • Bad habits. Peptic ulcers are especially common in those who smoke on an empty stomach; drinking alcohol also contributes to serious damage to the mucous membranes.
  • Stress and negative emotions. The development of an ulcer and its exacerbation is provoked by constant nervous excitement, as well as constant mental overload.
  • Hereditary factor. It has already been established that if there are cases of ulcers in the family, then the chance of a similar digestive disorder increases significantly.

The ulcer develops over a long period of time: at first the person notices discomfort in the stomach and minor disturbances digestive process, over time they become more and more pronounced.

If measures are not taken in time, an exacerbation with serious complications is possible.

Main symptoms of ulcer

An exacerbation of ulcer occurs suddenly, the duration can reach several weeks.

Various factors can provoke an exacerbation: overeating with a serious violation of the diet, stress, overwork, etc. Symptoms vary depending on the location of the ulcer:

  1. If pain occurs immediately after eating and gradually decreases over the next two hours, this usually indicates that the ulcer is localized in the upper part of the stomach. The pain decreases as food gradually passes into the duodenum during digestion.
  2. If pain, on the contrary, occurs within 2 hours after eating, this indicates an ulcer located in the antrum of the stomach: from it food enters the duodenum, and it is in this area that a large accumulation of Helicobacter pylori is most often observed.
  3. Night pain, which also occurs during long breaks between meals, most often occurs with ulcerative lesions of the duodenum.
  4. In addition to pain of various types in the abdomen, a characteristic symptom of an ulcer is heartburn, which is associated with increased acidity of gastric juice. Heartburn occurs simultaneously with pain or appears before it. With sphincter weakness and reverse peristalsis, patients experience sour belching and nausea; these symptoms often accompany peptic ulcer disease.
  5. Another common symptom is vomiting after eating, and it brings significant relief to the patient. Appetite often decreases, some patients have a fear of eating due to fear of pain - because of this, significant exhaustion is possible.

Methods for diagnosing ulcers

To diagnose stomach and duodenal ulcers, you must consult a gastroenterologist; the sooner the patient comes for help, the higher the chance of recovery or long-term remission without exacerbations.

In case of a sharp exacerbation with bleeding, urgent surgical intervention, in this case it is necessary to urgently call an ambulance.

The main method of examining the stomach is fibrogastroduodenoscopy: it allows the doctor to see the condition of the mucous membrane in order to detect an ulcer and assess the advanced state of the disease. Not only the location of the ulcer is assessed, but also its condition: presence of scars, size.

At the same time, a tissue sample of the mucous membrane is taken to identify Helicobacter pylori and a more accurate diagnosis. A clinical blood test is also carried out, it allows you to evaluate deviations from the norm in the condition of the body.

Although FGDS is a rather unpleasant research method, it is the most informative, so it cannot be abandoned. In some cases, it is supplemented by x-ray examination.

Methods and regimens for treating peptic ulcers

Treatment regimen peptic ulcer is based on taking antibiotics to get rid of Helicobacter Pylori and avoid serious complications.

Three- and four-component treatment regimens are prescribed by a gastroenterologist; only a specialist can select specific drugs in accordance with the individual characteristics of the patient. Several groups of drugs are used to treat ulcers:

  • Antibiotics. Two drugs are prescribed at the same time, the doctor selects the drugs taking into account possible allergic reactions. Self-prescription of antibiotics is unacceptable; they should only be selected by a doctor. The course of treatment takes at least 7-10 days; even if you feel significantly better, you should not stop taking the pills.
  • Drugs that should neutralize the effect of gastric juice. These include Omeprazole, Pantoprazole and other common medications familiar to most patients with digestive disorders.
  • Substances that form a film on the surface of the mucous membrane. It protects it from the aggressive effects of gastric juice, which contributes to faster healing of the ulcer.
  • Antacids, the main purpose of which is to reduce the acidity of gastric juice. They significantly reduce heartburn and improve the well-being of patients; such drugs have an adsorbing effect.
  • Prokinetics (Cerucal, Motilium and others) are drugs designed to normalize the motility of the duodenum and ensure normal movement of food through the intestines. They are prescribed for a feeling of heaviness in the stomach or early satiety.

Complex therapy rarely takes more than two weeks. After this, it is only necessary to help the stomach recover faster; for this, special nutritional plans and additional treatment methods are used.

Diet for gastric ulcer

When diagnosing ulcer, patients are prescribed therapeutic nutrition, designed to provide a gentle regime for the stomach and duodenum with a reduction in load.

For this purpose, diet group No. 1 is used; they are prescribed during the acute phase of the disease. The diet prescribes the following restrictions for patients:

  1. Foods that irritate the stomach are completely excluded from the diet. These are spicy, sour, fatty dishes, pickles, marinades, etc.
  2. You should not eat vegetables containing large amounts of fiber - they can also have a negative effect on digestion during an exacerbation. You can only eat boiled vegetables; in the first days they can only be consumed pureed.
  3. You should not consume sour dairy products and salty cheeses; sour fruits and natural juices are also excluded from the diet.
  4. Alcohol and carbonated drinks are completely excluded; drinking coffee is undesirable.

All these restrictions prevent further negative effects on the digestive tract and prevent the development of complications.

Deviations from the diet can lead to serious complications, including bleeding and perforation of ulcers.

Additional treatments

In addition to drug treatment, methods of physiotherapy and physical therapy in the recovery stage.

They help strengthen the body and minimize the consequences of digestive disorders.

At home, as prescribed by a doctor, you can make warming alcohol compresses– heat helps reduce pain and improve blood circulation.

Patients with peptic ulcer disease are prescribed sanatorium-resort treatment: in addition to health procedures and the climate at the resort, drinking mineral water “Borjomi”, “Smirnovskaya”, “Essentuki” has a beneficial effect.

Physical therapy exercises are aimed at improving blood circulation and preventing congestion, they improve secretory and motor function, and stimulate appetite. A set of therapeutic and health procedures in compliance with medical recommendations gives excellent results and helps eliminate Negative consequences peptic ulcer.

The sooner the patient turns to specialists, the greater the chance of successful healing of the ulcer with normalization of well-being. It is important to take care of yourself in time and go to an appointment with a gastroenterologist at the first negative manifestations.

Complications of peptic ulcer

Peptic ulcer disease is dangerous due to serious complications during exacerbation; they often require urgent surgery to prevent fatal outcome. The following complications are common:

  • Stomach and intestinal bleeding. A characteristic sign is vomit, which is the color of coffee grounds, and black stools.
  • Perforation of the ulcer. A rupture leads to the entry of the contents of the digestive tract into the abdominal cavity, resulting in a condition that threatens the patient’s life. Emergency surgery is required.
  • Penetration is a condition of the so-called hidden breakthrough, in which the contents of the intestine can enter other organs abdominal cavity. Only urgent surgery can save the patient.
  • When healing scars on the mucous membranes, the pylorus may narrow, which leads to disruption of the digestive tract. Treatment is only surgical.
  • Signs of complications from a peptic ulcer and internal bleeding are sudden weakness, fainting, a sharp drop in blood pressure, and severe abdominal pain. In case of vomiting blood and other signs of complications, it is necessary to take the patient to the hospital as soon as possible in order to prevent irreparable consequences.

Peptic ulcer disease is a disease that is largely associated with an incorrect rhythm of life in big city. It is necessary to find time to eat well; taking care of digestion will relieve discomfort and long-term complex treatment. If digestive problems have already arisen, there is no need to postpone a visit to the doctor until later. Timely diagnosis – important factor successful treatment.

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Most often, exacerbation of duodenal ulcers occurs due to gross neglect of diet, abuse of alcohol and junk food that irritates the intestinal mucosa, as well as exposure to stress and fatigue.

Signs of exacerbation are mainly diagnosed in the off-season - spring and autumn. This is due to the deterioration of general immunity during this period. The course of the disease is characterized by cyclicity, when periods of stable remission alternate with exacerbations of the pathology.

Forms of the disease

Exacerbation of duodenal ulcer, its symptoms and treatment depend on the form of the disease.

The disease is classified according to the following criteria:

  • Is it possible to have pea soup during an exacerbation of an ulcer?
  • treatment of duodenal ulcers with propolis
  • symptoms treatment of colon ulcers

By relapse rate:

  • a form that has exacerbations from one to three times a year;
  • a disease that recurs more than three times in a year.

According to the location and depth of the lesion:

  • superficial or deep ulceration;
  • an ulcer located in the area of ​​the bulb or in the post-bulb area.

By the number of mucosal lesions:

  • single outbreak;
  • multiple foci.

Acute duodenal ulcer gives a very pronounced clinical picture with vivid symptoms, making it difficult to confuse it with any other disease. Chronic form duodenal ulcers without exacerbation may not produce symptoms at all and proceed hidden.

Causes of duodenal ulcers

The causes of the disease may be due to family history, dietary habits and bad habits. In some cases, the disease is caused Helicobacter bacterium pylori, which affects the lining of the stomach and intestines.

Without adequate and timely treatment, the ulcer may undergo malignant degeneration.

The most likely factors for the occurrence of the disease are the following:

  • abuse of alcohol and tobacco products, which leads to impaired blood circulation in organs, as well as irritation of the mucous membranes of the gastrointestinal tract;
  • irregular meals with long intervals between meals, as well as a predominance in the diet of foods that are fried in fat, too sour, fatty and pickled. Food including canned, smoked foods and sauces;
  • prolonged and uncontrolled use of NSAIDs, which led to inflammation of the intestinal lining;
  • prolonged stress and fatigue can cause duodenal ulcers in people with an unbalanced psyche and mild excitability of the nervous system.

In the first stages, the disease does not always produce noticeable symptoms, so the patient often sees a doctor with an advanced form of the disease. Existing pathologies can also be a trigger for the disease. endocrine system, liver and kidneys, infectious diseases.

Tuberculosis, diabetes, hepatitis, pancreatitis lead to intestinal irritation and can provoke duodenal ulcer. The causes of the disease can also be mechanical damage due to surgery.

Symptoms of relapse of the disease

Clinical symptoms of duodenal pathology do not appear immediately; often, at the very beginning, the disease proceeds latently. An advanced form of peptic ulcer disease can suddenly manifest itself with life-threatening symptoms. In a third of people with this pathology, the presence of the disease is determined after a post-mortem autopsy.

The main diagnostic signs of duodenal ulcers:

The main symptom of the disease is pain in the pit of the stomach or in the upper part of the navel. Relapse often provokes pain in the back and heart area. This is due to the fact that it can radiate from its location to other parts of the body, distorting ideas about the real source of pain. Therefore, gastroenterologists primarily focus on discomfort in the navel area.

All painful sensations occur on an empty stomach, and immediately after eating the abdominal pain subsides. But if the patient overeats or consumes foods prohibited by the nutritionist, the pain may intensify.

Often, the symptoms of exacerbation of a duodenal ulcer exhaust the patient, not allowing him to fully rest at night. This occurs due to excessive production of acid, which irritates the diseased area of ​​the intestinal mucosa.

Even during stable remission stressful situation, poor diet and use of pharmacological drugs (hormones or NSAIDs) can lead to worsening of the condition, pain and nausea.

The second most important sign of duodenal ulcer is gastrointestinal dysfunction, characterized by the ability to bring relief to the patient:

  • constant long-term constipation;
  • bloating, belching and flatulence;
  • dark stool indicating the presence of blood.

The third most important are neurological symptoms. Signs of exacerbation of duodenal ulcer may include: irritability, sleep disturbance, depressed mood, and weight loss.

Diet for exacerbation of duodenal ulcers

Nutrition for gastrointestinal pathologies is of paramount importance. In the first days of the disease, nutrition is limited to a small amount of pureed food. Vegetable and bakery products are excluded.

After 5 days, you are allowed to eat vegetarian soups in which white crackers can be soaked. In addition, puree or soufflé from boiled poultry and fish fillets is allowed; for dessert you can eat fruit jelly.

In the second week, meat dishes are added to the treatment menu, which must be steamed; these can be poultry or fish meatballs. In addition, you should eat eggs in the form of an omelet or boiled, milk porridge with a small amount of butter, as well as mashed carrots or potatoes.

Contraindicated in case of exacerbation of duodenal ulcer:

  • mushroom, meat broth;
  • confectionery and baked goods;
  • dishes that were fried in fat;
  • too fatty foods;
  • fresh fruits and vegetables;
  • fatty sea fish;
  • alcohol-containing products;
  • any lean meat;
  • spices, sauces and marinades.

To neutralize the aggressive effects of hydrochloric acid, you should eat little and often. It is better to treat duodenal ulcers in a hospital setting, and dietary table No. 1-a or 1-b is indicated; such nutrition should last 4 months. After discharge, you can follow diet No. 5.

Pathology therapy

Duodenal ulcers, depending on the severity of clinical manifestations, can be treated conservatively and surgically.

The impact method includes the following set of measures:

  • therapeutic nutrition;
  • pharmacological agents (antibiotics, antacids and antisecretory drugs);
  • herbal decoctions;
  • Surgical treatment is indicated only if conventional methods are ineffective. Most often, the patient needs surgical help after constant exacerbations of the disease, with impaired ulcer healing and severe scarring.

When Helicobacter pylori is detected, treatment should include a complex of several antibiotics with antiprotozoal and bactericidal effects:

  • Amoxicillin;
  • Tetracycline;
  • Clarithromycin;
  • Metronidazole.

In order to neutralize the acidity of gastric juice, antacids are used:

  • Maalox;
  • Rennie;
  • Phosphalugel;
  • Almagel;
  • Gastal.

To improve the healing of the duodenal membrane, antiulcer drugs are prescribed:

  • De-nol;
  • Venter;
  • Misoprostol.

In addition, antisecretory agents are prescribed:

  • Rabeprozole;
  • Omeprazole;
  • Esomeprazole;
  • Lanzoprazole.

When, after taking medications for a long time under the supervision of a doctor, the patient does not feel any improvement, then it is advisable to agree to surgical intervention, which will consist of removing the affected area or suturing the duodenum.

Complications of duodenal ulcers

If duodenal ulcers are treated incorrectly, the pathology can periodically worsen and ultimately cause serious complications.

  • If blood vessels are involved in the process, the disease can be complicated by hemorrhage. Hidden bleeding can be identified by this characteristic feature like anemia. If hemorrhage is profuse, it can be determined by the type of stool (they turn black).
  • Perforation of an ulcer is the appearance of a hole in the wall of the duodenum. This complication can be determined by the occurrence acute pain upon palpation or change in body position.
  • Narrowing of the duodenal lumen occurs as a result of edema or scar. Identified by bloating, uncontrollable vomiting, and lack of stool.
  • Ulcer penetration – penetration into neighboring organs through a defect in the duodenum. The main symptom is pain radiating to the back.

A duodenal ulcer can worsen during the off-season (autumn, spring) and is most often triggered by poor diet or stress. The main symptom is pain in the navel area. To avoid this, you need to remember preventive measures, compliance with all conditions prescribed by a specialist, including strengthening the immune system and following a diet.

Symptoms and manifestations of stomach ulcers

A disease in which lesions of various sizes and shapes form in the human stomach is called chronic gastric ulcer. This disease continues for a long time and has periodic exacerbations, followed by a remission state. What types and signs of the disease exist in adults? How does a stomach ulcer manifest itself and is it treatable?

Characteristic

Peptic ulcer of the stomach and duodenum is a disease that is accompanied by the appearance of ulcers and erosions on the mucous surface layer of the ventricle, which has a unique size and shape (acute flat, giant, chronic, etc.). Frequent exacerbations of the disease occur in the spring or winter, when the functioning of all organs in the body undergoes a restructuring. Particularly common causes of peptic ulcer are multiple nervous tension, eating disorders and bad habits. Due to these reasons, the functioning of the gastrointestinal tract is disrupted; gastric juice does not stimulate the functioning of the ventricle, but causes the exact opposite (destructive) effect on the surface layer of the stomach.

Causes of the disease

Acid-fast bacterium Helicobacter pylori.

The main role in the occurrence of the disease belongs to the acid-fast bacterium Helicobacter, which is the causative agent (Helicobacter pylori infection). It can destroy the mucous membrane of both the ventricle and duodenum. With the help of a diagnostic study, a microbial pathogen is identified, which can be found in the majority of the population of the entire planet, but not everyone suffers from peptic ulcer disease. The situation is that an ulcer of the body of the stomach is formed not only due to the existence of bacteria in the body, but also under the influence of other secondary reasons. So, the causes of stomach ulcers:

  • nervous tension;
  • very bad genetics;
  • there is no diet and mistakes have been made in nutrition: excessive consumption of “junk” food (fast food, fatty, fried, spicy foods);
  • bad habits - excessive alcohol consumption, smoking;
  • appointment self-treatment, which can easily lead to a steroid ulcer - uncontrolled use of medications (treatment with antibiotics, laxatives).

Infection of a person with the bacterium Helicobacter (Helicobacter pylori infection) occurs when people come into close contact with each other (with a handshake, through household objects), when personal hygiene rules are ignored when using shared toilets. When the stomach is damaged, the bacterium, which continues to evolve reproductively and actively in it, secretes organic matter, which contribute to damage to the protective surface layer of the ventricle and small intestine, and also disorganizes the functioning of cells, which can lead to the formation of ulcers and erosions. Only palpation and diagnostic studies will help detect a microbe in the body and understand whether a person is infected with it.

Classification of stomach ulcers

Peptic ulcer of the stomach and duodenum has the following classification:

  • perforated;
  • stressful;
  • peptic;
  • chronic;
  • mirror;
  • callous;
  • lesser and greater curvature of the stomach;
  • medication (steroid);
  • disease of the antrum and cardiac (subcardial) parts of the stomach.

Clinical symptoms

The symptoms are:

  1. the appearance of heaviness and discomfort in the abdomen;
  2. belching air or food, heartburn;
  3. gagging;
  4. lack of appetite and complete apathy towards food;
  5. bowel disorder, manifested by diarrhea or constipation;
  6. causeless weight loss;
  7. formation of excess gases (intestinal flatulence);
  8. excessive sweating;
  9. white or yellowish coating on the tongue;
  10. anemia;
  11. pain syndromes in the intestines and other organs.

Symptoms and stages of the disease

Without complications (stage 1 disease)

The main signs of an ulcer are pain and cramps in the stomach.

The main signs of a stomach and duodenal ulcer are pain and spasms, which prompt a person to go to a medical facility. Pain can vary in characteristics and locations. The pain appears unexpectedly, after every snack and full lunch. They are located approximately in the central part of the abdomen, just above the navel.

Pain syndromes characteristic of gastric and duodenal ulcers differ in time and are divided into:

  • early, 40−60 minutes after eating;
  • 3-4 hours after eating, that is, late;
  • less common at night (night pain);
  • on an empty stomach (hunger pains are provoked by long breaks between meals).

The manifestation of pain in all types of ulcers depends on the properties of the food consumed (for example, too spicy or sour food provokes their occurrence); on the state of the nervous system (people suffering from nervous disorders are the most susceptible to pain). Sometimes signs of an ulcer do not appear at all, so people live and do not even suspect the existence of the disease. You can only find out about the presence of the disease and see what a human stomach affected by an ulcer looks like through palpation and diagnostic testing.

Pain in uncomplicated peptic ulcers, as usual, has a slow development and course, periodically increasing and subsiding. Pain that begins to appear is reduced by food, water and various soda solutions. If the pain becomes stronger, the person holds his stomach in a half-bent position, which indicates the “ulcer pose.”

In addition to the pronounced signs, there are also symptoms of a stomach ulcer in adults that occurs without complications, these include: heartburn, belching after eating (accompanied by a sour, putrid odor), vomiting, a feeling of heaviness in the stomach, stool upset (mainly constipation, with in which the release of feces is accompanied by painful sensations in the abdomen), an increase in appetite or, conversely, a complete refusal to eat.

Manifestation of a complicated form (2 stages)

Special forms of ulcers (3 stages)

Special forms of the disease include: pyloric ulcer, giant and postbulbar. Clinical picture With the presented varieties, the ulcer lasts a long time and is expressed as follows: regular painful sensations, heartburn, causeless vomiting. The signs of a stomach ulcer are somewhat mixed - abdominal pain can be bothersome in periods, the appearance of which occurs in the spring or autumn. Spasms and cramps occur early (40 minutes after eating); late (3-4 hours after eating); pain occurs in the left or right corner of the stomach; the pain manifests itself so intensely that it radiates to the back. They are a direct indication for immediate treatment.

Possible complications

If a man or woman is suspected of having gastric ulcers, they should not be ignored under any circumstances - treatment must be carried out, otherwise they will cause a lot of unpleasant complications. Firstly, a stomach ulcer threatens a person with regular painful sensations; secondly, it can provoke bleeding at the most unexpected moment; This is a disease that causes perforation of the stomach walls. It is possible to develop such ailment as gastric outlet stenosis. The biggest and most dangerous problem is degeneration into malignant tumor and possible death. Therefore, it is necessary to carry out treatment in a timely manner, adhere to medical recommendations (diet and proper nutrition), so that the consequences of a stomach ulcer do not cause any trouble and life is healthy and carefree.

Peptic ulcer (PU) - chronic illness with a recurrent course and the development of complications, occurring with alternating periods of exacerbation and remission, the main symptom of which is the formation of an ulcer in the wall of the gastric mucosa. Etiology: Duodenal ulcer is diagnosed 3-4 times more often than gastric ulcer. Among the reasons for the development of peptic ulcer disease are: hereditary predisposition; neuropsychological factors; nutritional factors; bad habits; uncontrolled use of non-steroidal anti-inflammatory drugs; infection (Helicobacter pylori).

Pathogenesis: An ulcer is formed as a result of an imbalance between aggressive and protective factors of the mucous membrane of the stomach and duodenum. Aggressive factors include: hydrochloric acid, pepsin, bile acids (with duodenogastric reflux); protective - the production of mucus, prostaglandins, epithelial renewal, adequate blood supply and innervation.

Clinic: During exacerbation of gastric ulcer, the main complaint is pain in the upper half of the epigastric region. Although the localization of pain is not absolutely important, it is believed that with ulcers of the cardiac part and ulcers on the posterior wall of the stomach, pain is localized behind the sternum and can radiate to left shoulder(resemble the pain of angina pectoris). Ulcers of the lesser curvature of the stomach are characterized by a clear rhythm of pain: they occur 15-60 minutes after eating, especially if the diet is not followed. Immediately after eating, pain occurs if the ulcer is localized in the cardial part or on the posterior wall of the stomach. An ulcer in the antrum of the stomach is indicated by “hungry”, night, late (2-3 hours after eating) pain, reminiscent of pain in duodenal ulcer intestines. With ulcers of the pyloric part, the pain is intense, not associated with eating. The addition of girdling pain or its irradiation to the back, the intense nature of the pain require examination of the pancreas at subsequent stages of the diagnostic search (reactive pancreatitis, penetration into the pancreas). Gastric dyspepsia syndrome expressed to a lesser extent, manifested by belching air, food, regurgitation; nausea and vomiting are often observed with ulcers of the pyloric canal. Vomiting is a common complaint in ulcers; vomit consists mainly of food impurities. Frequent vomiting, intensifying in the evening, containing food eaten a long time ago, combined with a feeling of fullness in the stomach, weight loss, may indicate stenosis of the gastric outlet. Intestinal and asthenovegetative syndromes are less pronounced with gastric ulcer than with duodenal ulcer. Some patients complain of constipation, combined with pain along the colon and bloating. A tendency to bleeding is characteristic of ulcers of the antrum of the stomach in young people; bleeding in elderly patients is alarming regarding malignancy (development of ulcer-gastric cancer). Physical signs of ulcer in an uncomplicated course are few. As a rule, moderate local muscle protection in the epigastrium and point tenderness in various parts of this area are noted. With cardiac ulcers, point tenderness under the xiphoid process is detected; for ulcers of the pyloric part - in the pyloroduodenal zone. Diffuse pain in the epigastrium with simultaneous local pain is a sign of exacerbation of CG (CG accompanies PU) or perigastritis (complication of PU). Physical examination may provide evidence of the development of other complications. Thus, the appearance of a splashing noise 5-6 hours after drinking liquid indicates the development of pyloric stenosis. Pale and wet skin, low-grade body temperature, tachycardia, decreased blood pressure, disappearance of pain in the epigastric region during palpation of the abdomen are signs of ulcerative bleeding.



Diagnostics: X-ray examination of the stomach in approximately 3/4 of patients allows us to detect the main sign of ulcer - a “niche”. Superficial ulcers that are not accompanied by an inflammatory reaction of the surrounding mucous membrane may not be detected radiographically. In the absence of direct radiological sign(“niches”) take into account indirect signs: “finger” retraction, retention of barium sulfate in the stomach for more than 6 hours after its administration, local pain on palpation during the study. X-ray examination can reveal cicatricial narrowing of the pylorus, stomach tumor (polyps, cancer, etc.). The most valuable information about the “niche”, its location, depth, nature (presence of callous ulcer) and to clarify complications (malignancy, penetration , bleeding, etc.) give the results of gastroduodenofibroscopy. Gastroscopy in combination with targeted biopsy facilitates the detection of ulcer malignancy.



Treatment: HP eradication is achieved by conducting a week-long course of a “three-component” regimen (first-line therapy):

omeprazole 20 mg, amoxicillin 1000 mg, clarithromycin

250 mg (2 times a day), or:

omeprazole 20 mg, tinidazole 500 mg, clarithromycin 250 mg

(2 times a day), or: ranitidine bismuth citrate (piloride) 400 mg 2 times a day at the end of meals, clarithromycin 250 mg or tetracycline 500 mg

or amoxicillin 1000 mg (2 times a day), tinidazole 500 mg 2 times a day with meals.

If eradication is ineffective, a backup four-component regimen (second-line therapy) is prescribed for 7 days, consisting of a proton pump inhibitor, a bismuth salt preparation and two antimicrobial drugs: omeprazole 20 mg 2 times a day (morning and evening, not later than 20 hours), colloidal bismuth subcitrate 120 mg 3 times a day 10 minutes before meals and 4 times 2 hours after meals before bedtime, Metronida-30l 250 mg 4 times a day after meals or tinidazole 500 mg 2 times a day after meals, tetracycline or amoxicillin 500 mg 4 times a day after meals.

Peptic ulcer of the stomach and duodenum characterized by classic symptoms. However, there are often cases of atypical course of the disease. The clinical picture and symptoms depend on the characteristics of the ulcerative process (localization, complications), the duration of its existence, the changes that have occurred in other organs and the state of protective reactions of local tissues and the whole body.

Peptic ulcer of the stomach and duodenum occurs cyclically, sometimes for many years, sometimes giving severe exacerbations in the spring and autumn periods, sometimes almost completely relieving the patient of its painful manifestations. IN last years the disappearance of such cyclicality of the disease is noted - it flows like any chronic disease, gradually progressing, sometimes giving exacerbations, which in surgical patients cannot be associated with the change of seasons. The leading and very expressive symptom of peptic ulcer disease is pain associated with eating.

They appear immediately after eating for ulcers of the cardial part of the stomach, after 40-60 minutes for ulcers of the lesser curvature, after 2 hours for ulcers of the pyloric part of the stomach, and hunger pains for ulcers of the duodenum. The nature and intensity of pain is variable. Very often the pain appears in the form of an attack and is very painful. During a painful attack, patients rush around, look for a position that reduces pain: they get on all fours, lower the upper half of the body from the bed and place their elbows on the floor, lean their chest and stomach against the wall and constantly groan in an annoying manner.

These severe pains force the patient to press down abdominal wall with your hands, hold a hot heating pad on your stomach for a long time, causing burns and the formation of age spots. Very often, patients suddenly feel a decrease in pain in some position, freeze in it for a while and stop moaning. But soon another intensification of pain returns to motor restlessness, notes of extreme exhaustion and despair appear in the groans. Such severe pain symptoms occur with large ulcers involving the serous membrane and penetrations.

The pain is localized in the epigastric region near the xiphoid process, but more often below, and when the ulcer is localized in the duodenum, closer to the right hypochondrium. Uncomplicated ulcers in the absence of peri-process do not cause irradiation of pain.

In some patients, an attack of pain begins with drooling, and this sign is well remembered by the suffering person. It happens that after eating, in complete well-being and in a good mood, the patient suddenly becomes wary, and fear appears in his facial expression. A few moments later, he jumps out from behind the table and, with his mouth half-open and filled with saliva, runs to the sink, leans his hands on the wall, bows his head down, and immediately viscous saliva flows through his lower lip in an almost continuous stream. Due to the onset of nausea and in anticipation of approaching pain, the patient moans barely audibly monotonously.

Then the groans intensify, the patient leaves the sink, squeezes his stomach with his hands and, in a half-bent position, grabbing a heating pad on the move or irritably demanding it from frightened relatives, hurries to bed - a pain attack sets in. People caring for the patient quickly place a basin by the bed not only to collect saliva that continues to be released - at the height of a painful attack, vomiting occurs, sometimes repeated and severe. Immediately after vomiting, the pain subsides, the patient’s condition improves, and subsequently he looks forward to vomiting (excruciating in the first period), and sometimes causes it himself by inserting a finger into the pharynx. The pain can be dull, aching, pressing and accompanied by a feeling of fullness in the epigastric region or in the right hypochondrium.

Vomit - This is the second classic symptom of peptic ulcer of the stomach and duodenum. It gives constant relief and this differs from vomiting associated with other pathological processes. Vomit may contain streaks of blood. Vomiting is often preceded by drooling and nausea, which are mild in some patients and completely absent in others.

Peptic ulcer disease is characterized by heartburn. It occurs in 70-75% of patients and indicates hypersecretion and high acidity of gastric juice. Heartburn occurs after eating, before eating, and can appear without any connection with food intake. Heartburn can occur with normal or even low acidity of gastric juice. For many years I observed a patient who had suffered from gastric ulcer for more than 40 years. All the time she complained of periodic attacks of pain, drooling and painful heartburn, which persisted (albeit mildly and inconsistently) for 5 years after Subtotal gastrectomy performed according to about a large cancerous ulcer of the lesser curvature. Therefore, the symptom of heartburn must be assessed carefully.

Repeated attacks of pain, salivation, and vomiting lead to significant neuropsychic changes. Many patients have a distinct clinical picture of neurasthenia and even psychasthenia. They are irritated, hot-tempered, do not react adequately to their surroundings, and are poorly behaved. The characteristic features of patients with gastric and duodenal ulcers are hypersociality, anxiety and irritability (V.P. Belov, 1971).

P. A. Kanishchev (1973) among 186 patients with gastroduodenal ulcers found neurasthenia in 80, hysteria in 24, psychasthenia in 15, neurosis-like syndromes in 27, psychopathy and psychopathic personality in 19; 129 patients had a history of mental trauma (usually chronic). Old authors noting nervously mental disorders in patients, they attached importance to the neuropsychic status and the origin of peptic ulcer disease. Mikulicz (1902) wrote that a stomach ulcer predisposes to hypochondria, neurasthenia and hysteria, but “we must remember that an ulcer can also join neurosis.”

With sometimes preserved increased appetite, patients refuse to eat, fearing attacks of pain, which worsens the condition, increasing emaciation and asthenia.

The clinical picture is complemented by intestinal dysfunction: most patients suffer from constipation, many produce “sheep” feces; but there may also be diarrhea, especially when the pancreas is involved in the process and when sharp decline acidity of gastric juice.

The clinical picture of peptic ulcer disease in elderly people is characterized by weariness and sometimes latent course. Often found atypical forms(up to 46.4% according to Ciorapciu et al.). People over 60 years of age experience severe complications much more often (up to 40-67% - M. F. Kamaev et al., 1963; A. N. Shabanov et al., 1970), among which bleeding ranks first.

Diagnosis consists of a detailed study of complaints, medical history, life history, objective examination and additional methods studies, of which leading value have laboratory and x-ray. Recently, gastroscopy and duodenoscopy have become widely used in practice.

Complaints from patients are characteristic and provide very valuable information about the nature of the patient’s suffering. Studying the anamnesis involves finding out the time of onset of the first complaints, the increase and change of symptoms. We must pay special attention to possible reasons the occurrence of the disease and, if detected, begin treatment of the patient by eliminating them (treatment of carious teeth, dental restoration, diet, diet, etc.).

The condition of patients with uncomplicated peptic ulcer disease is satisfactory, and in some patients outside of an attack it is good. Nutrition, as a rule, is reduced, patients are irritable, and do not always react adequately to their surroundings. The complexion is pale, there are often dark circles under the eyes from sleepless nights and impaired bowel function. The tongue is coated with a whitish coating, and there is often an unpleasant odor from oral cavity. There are pigment spots in the epigastrium from prolonged use of heating pads. Stomach correct form or is somewhat flattened in the epigastrium, and here the abdominal wall lags behind in breathing, especially during an exacerbation.

Active movements cause pain at the site of the pathological process (if the peritoneum is involved in the process - perigastritis, periduodenitis). In these same places, percussion pain is determined. Palpation reveals muscle tension and pain according to the location of the ulcer. During the lull in the process, there may be no pain or muscle tension. Deep palpation must be carried out carefully. At the same time, pain points are identified, making it possible to more accurately determine the localization of the process, as well as the condition of the white line of the abdomen (epigastric hernias can simulate a peptic ulcer). Check for splashing noise.

This symptom will be positive not only with pyloric stenosis, but also with large gastric secretion. Superficial and deep palpation should be carried out taking into account the projection of organs onto the abdominal wall. Shoffard's triangle is of particular importance for a clearer localization of pain and its differentiation from pain associated with the head of the pancreas (Fig. 111). Some clinicians study Zakharyin-Ged hypersthesia zones, as well as Openhovesky, Boas and Herbst pain points. More information from an objective examination is provided by patients with ulcers that have caused a reaction in the visceral and parietal peritoneum.

A thorough analysis of complaints, anamnesis and the results of an objective examination will undoubtedly provide clear guidance for determining the nature of the disease. All manifestations of the disease should be taken into account. For example, lethargy, loss of appetite and fatigue in a patient with a history of ulcers will make you think about the appearance of a cancer process, and irradiation to the right shoulder girdle, which is added to severe pain, will make you think about the penetration of the ulcer into the liver or gall bladder.

Laboratory testing includes a general analysis of blood, urine, feces, gastric juice, determination of the daily amount of urine, electrolytes, liver functions, coagulation and anticoagulation systems. If necessary laboratory test deepen. The study plan must include a consultation with a therapist, an electrocardiogram, and a determination of pulmonary function. The diagnosis of peptic ulcer is completed by X-ray examination methods and gastroscopy. I will dwell only on the methods that are directly related to the diagnosis of the disease.

Thoughtful study required general analysis blood. A decrease in hemoglobin will suggest bleeding, a shift in the white blood count to the left will indicate significant inflammation, and an accelerated ROE will make you pay more attention to the differential diagnosis of cancer and ulcers.

The study of gastric juice involves determining acidity, which, as indicated above, is sharply increased when the ulcer is localized in the duodenum, and when the ulcer is localized in the stomach - normal, decreased or slightly increased. Currently, the fractional method of studying gastric juice according to Kutch, not to mention one-step methods for taking gastric juice with a thick probe, is considered outdated and not adequate modern requirements clinics. To characterize gastric secretion, basal secretion is determined (reflects the state of the glands in the interdigestive period), an insulin test is performed (reflects the sensitivity of the vagal secretory apparatus) and a histamine test (shows the number of functioning parietal cells).

Determination of basal gastric secretion (basal acid output - BAO) is of great diagnostic importance. High basal secretion occurs with duodenal ulcers, normal or reduced - with ulcers and stomach cancer. Very high VAO numbers (above 20 mEq when the norm is 2 mEq) indicate Zollinger-Ellison syndrome. Sparberg and Kirsner (1964) argue that zero acidity of even one sample when determining basal secretion excludes duodenal ulcer. To study basal secretion on an empty stomach, a thin probe is inserted into the stomach and gastric juice is pumped out for 60 minutes.

Immediately after determining the basal secretion, they begin to perform a histamine test (Kau's test, 1953) - the maximum release of hydrochloric acid in an hour (maximal acid output - MAO) after subcutaneous administration histamine at the rate of 0.04 mg per 1 kg of patient weight. Histamine is a stimulant of the second phase of gastric secretion. 30 minutes before the administration of histamine, the patient is given an antihistamine (suprastin 2 ml of a 2% solution intramuscularly).

Then, within an hour, gastric juice secreted under the influence of histamine is collected, and the content of hydrochloric acid in it is determined (in mEq/h). Rune (1966) revealed a correction between the amount of secreted hydrochloric acid and the proteolytic activity of gastric juice, which allows us to consider the Kay test as a method characterizing not only the state of the parietal cells, but also the main cells of the gastric glands (S. M. Ryss, E. S. Ryss) .

Normally, MAO is 17-22.5 meq/h (Vagon, 1963), and according to Segal (1965) - from 1 to 20 meq/h. With a gastric ulcer, MAO is within normal limits or its levels are reduced, with duodenal ulcers - 25-60 mEq/h, and with Zolliger-Ellison disease - 60 mEq/h. The ratio of HLW and MAO is of interest. Normally, VAO accounts for 10-20% of maximum gastric secretion. The same indicators occur in patients with ulcers and stomach cancer. In case of duodenal ulcer, VAO is equal to 20-40% of MAO. Higher numbers of basal secretion in relation to the histamine test indicate a duodenal ulcer or Zollinger-Ellison syndrome.

G. L. Levin (1970) warns against the unconditional use of a histamine test, which can give severe paradoxical reactions and is unsafe for the patient. Kay's test is contraindicated in febrile patients, with high blood pressure, severe atherosclerosis, allergic diseases, bleeding, severe cardiovascular disorders and in the general serious condition of the patient.

To determine the first phase of gastric secretion (sensitivity of the vagal secretory apparatus), the Hollander insulin test is used. This test is based on an increase in gastric secretion under the influence of hypoglycemia, which causes irritation vagus nerves. 10-20 units are administered intravenously. insulin (0.2 units per 1 kg of weight) and examine gastric juice every 15-60 minutes (depending on the method), the acidity of which increases sharply and then gradually returns to normal as hypoglycemia is eliminated.

An insulin test is used to determine the completeness of vagotomy. In some clinics, a single-stage (Maratka, 1964) or sequential (Patel, 1965; V. S. Mayat et al., 1969, etc.) histamine-insulin test is performed.

Recently, most foreign authors and many domestic surgeons, based on the results of the above methods for studying gastric secretion, determine the nature and scope of surgical intervention, which in England, the USA, Canada, France and in many other countries (in 53 countries, according to the III Congress , gastroenterologists in Tokyo) is almost fatally accompanied by truncal or selective vagotomy.

In this regard, the importance of histamine and insulin tests is overestimated. The data of many authors who scrupulously study HLW and MAO, despite firm conclusions about the importance of these samples, do not convince of their high accuracy. Thus, Grossman et al. (1963) performed Kay’s test in 1032 patients with duodenal ulcers and in 1249 healthy people and found that “in almost half of the patients with duodenal ulcers, gastric secretion was higher than in healthy people” (cited from F. F. Kostyuk, 1970).

This means that in more than half of the patients the histamine test had no significance. Levin et al. (1948) studied basal secretion in 560 healthy individuals, in 222 patients with duodenal ulcers, in 50 with gastric ulcers and found the presence of hydrochloric acid on an empty stomach in 55% of healthy men and in 40% healthy women. Goyal et al. (1966) found that the volume of basal secretion in healthy people per hour is 22-115 ml, and in patients with duodenal ulcers - 35-131 ml. The lack of convincingness of the results of the study of basal and stimulated gastric secretion is also evidenced by the table published by Goyal et al. (Table 6).

Gastric secretion can also be judged by uropepsinogen. Gastric ulcers do not cause an increase in the level of uropepsinogen; its content can be normal, decreased and rarely increased. Duodenal ulcers are accompanied by a significant increase in uropepsinogen. Radioisotope studies and determination of the motor function of the stomach (electrogastrography) are included in practice. Great importance give intragastric pH-metry (Hart, Lick, 1963; G. L. Levin, 1970; Yu. M. Pantsyrev et al., 1972; A. A. Shalimov et al., 1973). All patients undergo the Gregersen test (detection of occult blood in the stool), which has not lost its significance to this day.

The most important method in recognizing stomach diseases is x-ray, which, however, cannot be considered absolutely accurate. S.A. Reinberg said that there is no radiological diagnosis, but there is a clinical and radiological diagnosis.

X-ray signs of an ulcer include a niche (Fig. 112) - a persistent barium stain and radial convergence of mucosal folds. A niche is a defect in the stomach wall formed at the site of an ulcer, which is filled during examination with a contrast agent. It can be small (0.5-0.6 cm in diameter) and barely perceptible during fluoroscopy, but it can also be large, reaching a diameter of 4-5 or more centimeters. When localizing a deep niche along the lesser curvature, the liquid level can be detected (Fig. 113). A barium stain occurs in cases where the ulcer is localized on the anterior or posterior wall of the stomach or duodenum. This spot remains on the wall of the organ after the passage of the bulk of the contrast agent, which is only partially retained in the area of ​​the mucosal defect (in the ulcer).

Indirect signs include a painful point on palpation, pyloric spasm, prolonged barium retention (up to 6 hours), circular spasm of the stomach (symptom of the “pointing finger”, or incisura spastica), increased peristalsis, large amounts of gastric juice, deformation of the bulb, “irritated bulb " and some others. Unfortunately, x-rays do not always detect an ulcer.

In cases that are difficult to diagnose, they resort to parietography, X-ray kymography, etc. Errors occur within 5-12% even among very experienced radiologists. It is difficult to overestimate the role of modern devices (fibrogastroscopes, fibroduodenoscopes) in recognizing stomach diseases, which allow you to examine the entire mucous membrane of the stomach and duodenum, if necessary, take a piece of tissue for examination, catheterize the common bile duct or pancreatic duct.

Thoughtful use of the above research methods, of which clinical remains the leading one, recognition of gastric and duodenal ulcers is practically ensured for all patients. This is due, to a certain extent, to the fact that patients with long-term ulcers are admitted to the surgical clinic. However, sometimes extreme difficulties arise when the question of the nature of the disease can only be resolved on the operating table.

Differential diagnosis of gastroduodenal ulcers should be carried out with other diseases of the stomach, with epigastric and diaphragmatic hernias, with hernias of the esophageal opening and white line of the abdomen, with pancreatitis, cholecystitis, hepatitis, chronic appendicitis (with high localization of the cecum), diseases of Meckel's diverticulum.

  • Classification
  • 13. Atherosclerosis. Epidemiology, pathogenesis. Classification. Clinical forms, diagnosis. The role of the pediatrician in the prevention of atherosclerosis. Treatment. Modern antilipidemic drugs.
  • 2. Results of an objective examination with the aim of:
  • 3. Results of instrumental studies:
  • 4. Results of laboratory tests.
  • 15. Symptomatic arterial hypertension. Classifications. Features of pathogenesis. Principles of differential diagnosis, classification, clinic, differentiated therapy.
  • 16. Coronary heart disease. Classification. Angina pectoris. Characteristics of functional classes. Diagnostics.
  • 17. Urgent rhythm disturbances. Morgagni-Edams-Stokes syndrome, paroxysmal tachycardia, atrial fibrillation, emergency treatment. Treatment. Vte.
  • 18. Chronic systolic and diastolic heart failure. Etiology, pathogenesis, classification, clinical picture, diagnosis. Treatment. Modern pharmacotherapy of CHF.
  • 19. Pericarditis: classification, etiology, features of hemodynamic disorders, clinical picture, diagnosis, differential diagnosis, treatment, outcomes.
  • II. Etiological treatment.
  • VI. Treatment of edematous-ascitic syndrome.
  • VII. Surgery.
  • 20. Chronic cholecystitis and cholangitis: etiology, clinical picture, diagnostic criteria. Treatment in the phase of exacerbation and remission.
  • 21. Chronic hepatitis: etiology, pathogenesis. Classification. Features of chronic drug-induced viral hepatitis, main clinical and laboratory syndromes.
  • 22. Acute liver failure, emergency therapy. Process activity criteria. Treatment, prognosis. VTE
  • 23. Alcoholic liver disease. Pathogenesis. Options. Features of the clinical course. Diagnostics. Complications. Treatment and prevention.
  • 24. Cirrhosis of the liver. Etiology. Morphological characteristics, main clinical
  • 27. Functional non-ulcer dyspepsia, classification, clinic, Diagnosis, differential diagnosis, treatment.
  • 28. Chronic gastritis: classification, clinical picture, diagnosis. Differential diagnosis with stomach cancer, treatment depending on the form and phase of the disease. Non-drug treatment methods. Vte.
  • 29. Peptic ulcer of the stomach and duodenum
  • 30. Nonspecific ulcerative colitis and Crohn's disease.
  • 31. Irritable bowel syndrome.
  • 32. Glomerulonephritis
  • 33. Nephrotic syndrome: pathogenesis, diagnosis, complications. Kidney amyloidosis: classification, clinical picture, course, diagnosis, treatment.
  • 35. Chronic pyelonephritis, etiology, pathogenesis, clinic, diagnosis (laboratory and instrumental), treatment, prevention. Pyelonephritis and pregnancy.
  • 36. Aplastic anemia: etiology, pathogenesis, classification, clinical picture, diagnosis and differential diagnosis, principles of treatment. Indications for bone marrow transplantation. Outcomes.
  • Differential diagnosis of hemolytic anemia depending on the location of hemolysis
  • 38. Iron deficiency conditions: latent deficiency and iron deficiency anemia. Epidemiology, etiology, pathogenesis, clinical picture, diagnosis, treatment and prevention.
  • 39. B12 deficiency and folate deficiency anemia: classification, etiology, pathogenesis, clinical picture, diagnosis, therapeutic tactics (saturation and maintenance therapy).
  • 41. Malignant non-Hodgkin lymphomas: classification, morphological variants, clinical picture, treatment. Outcomes. Indications for bone marrow transplantation.
  • 42. Acute leukemia: etiology, pathogenesis, classification, the role of immunophenotyping in the diagnosis of ol, clinic. Treatment of lymphoblastic and non-lymphoblastic leukemia, complications, outcomes, VTE.
  • 44. Henoch-Schönlein hemorrhagic vasculitis: etiology, pathogenesis, clinical manifestations, diagnosis, complications. Therapeutic tactics, outcomes, VTE.
  • 45. Autoimmune thrombocytopenia: etiology, pathogenesis, clinical picture, diagnosis, treatment. Therapeutic tactics, outcomes, follow-up.
  • 47. Diffuse toxic goiter: etiology, pathogenesis, clinical picture, diagnostic criteria, differential diagnosis, treatment, prevention, indication for surgical treatment. Endemic goiter.
  • 48. Pheochromocytoma. Classification. Clinic, features of arterial hypertension syndrome. Diagnosis, complications.
  • 49. Obesity. Criteria, classification. Clinic, complications, differential diagnosis. Treatment, prevention. Vte.
  • 50. Chronic adrenal insufficiency: etiology and pathogenesis. Classification, complications, diagnostic criteria, treatment, VTE.
  • I. Primary cnn
  • II. Central forms nn.
  • 51. Hypothyroidism: classification, etiology, pathogenesis, clinical manifestations, therapeutic mask diagnostic criteria, differential diagnosis, treatment, VTE.
  • 52. Diseases of the pituitary gland: acromegaly and Itsenko-Cushing’s disease: etiology, pathogenesis of the main syndromes, clinical picture, diagnosis, treatment, complications and outcomes.
  • 53. Itsenko-Cushing syndrome, diagnosis. Hypoparathyroidism, diagnosis, clinic.
  • 54. Periarteritis nodosa: etiology, pathogenesis, clinical manifestations, diagnosis, complications, features of the course and treatment. VTE, medical examination.
  • 55. Rheumatoid arthritis: etiology, pathogenesis, classification, clinical variant, diagnosis, course and treatment. Complications and outcomes, VTE and medical examination.
  • 56. Dermatomyositis: etiology, pathogenesis, classification, main clinical manifestations, diagnosis and differential diagnosis, treatment, VTE, medical examination.
  • 58. Systemic scleroderma: etiology, pathogenesis, classification, clinical picture, differential diagnosis, treatment. VTE
  • I. According to the course: acute, subacute and chronic.
  • II According to the degree of activity.
  • 1. Maximum (III degree).
  • III. By stages
  • IV. The following main clinical forms of SS are distinguished:
  • 4. Scleroderma without scleroderma.
  • V. Joints and tendons.
  • VII. Muscle lesions.
  • 1. Raynaud's phenomenon.
  • 2. Characteristic skin lesions.
  • 3. Scarring on the fingertips or loss of finger pad substance.
  • 9. Endocrine pathology.
  • 59. Deforming osteoarthritis. Diagnosis criteria, causes, pathogenesis. Clinic, differential diagnosis. Treatment, prevention. Vte.
  • 60. Gout. Etiology, pathogenesis, clinical picture, complications. Differential diagnosis. Treatment, prevention. Vte.
  • 64. Exogenous allergic and toxic alveolitis, etiology, pathogenesis, classification, clinic, diagnosis, treatment, VTE.
  • 65. Occupational bronchial asthma, etiology, pathogenetic variants, classification, clinic, diagnosis, treatment, principles of VTE.
  • 68. Technogenic microelementoses, classification, main clinical syndromes for microelementoses. Principles of diagnosis and detoxification therapy.
  • 69. Modern saturnism, etiology, pathogenesis, mechanism of the effect of lead on porphyrin metabolism. Clinic, diagnosis, treatment. Vte.
  • 70. Chronic intoxication with organic solvents of the aromatic series. Features of damage to the blood system at the present stage. Differential diagnosis, treatment. Vte.
  • 76. Vibration disease from exposure to general vibrations, classification, features of damage to internal organs, principles of diagnosis, therapy, VTE.
  • Objective examination
  • Laboratory data
  • 80. Hypertensive crisis, classification, differential diagnosis, emergency therapy.
  • 81. Acute coronary syndrome. Diagnostics. Emergency treatment.
  • 83. Hyperkalemia. Causes, diagnosis, emergency treatment.
  • 84. Hypokalemia: causes, diagnosis, emergency treatment.
  • 85. Crisis in pheochromacytoma, clinical features, diagnostics, emergency therapy
  • 86. Cardiac arrest. Causes, clinic, emergency measures
  • 87. Morgagni-Edams-Stokes syndrome, causes, clinic, emergency care
  • 88. Acute vascular insufficiency: shock and collapse, diagnosis, emergency care
  • 90. Tela, causes, clinic, diagnosis, emergency treatment.
  • I) by localization:
  • II) according to the volume of damage to the pulmonary bed:
  • III) according to the course of the disease (N.A. Rzaev - 1970)
  • 91. Dissecting aortic aneurysm, diagnosis, therapist tactics.
  • 92. Supraventricular paroxysmal tachycardia: diagnosis, emergency treatment.
  • 93. Ventricular forms of rhythm disturbances, clinical picture, diagnosis, emergency therapy.
  • 94. Complications of the acute period of myocardial infarction, diagnosis, emergency treatment.
  • 95. Complications of the subacute period of myocardial infarction, diagnosis, emergency treatment.
  • Question 96. Sick sinus syndrome, options, diagnosis, emergency measures.
  • Question 97. Atrial fibrillation. Concept. Causes, options, clinical and ECG criteria, diagnosis, therapy.
  • Question 98. Ventricular fibrillation and flutter, causes, diagnosis, emergency therapy.
  • Question 99. Stopping breathing (apnea). Causes, emergency assistance.
  • 102. Infectious-toxic shock, diagnosis, clinic, emergency therapy.
  • 103. Anaphylactic shock. Causes, clinic, diagnosis, emergency care.
  • 105. Poisoning with alcohol and its substitutes. Diagnosis and emergency treatment.
  • 106. Pulmonary edema, causes, clinic, emergency care.
  • 107. Asthmatic status. Diagnosis, emergency treatment depending on the stage.
  • 108. Acute respiratory failure. Diagnostics, emergency therapy.
  • 110. Pulmonary hemorrhage and hemoptysis, causes, diagnosis, emergency treatment.
  • 112. Autoimmune hemolytic crisis, diagnosis and emergency treatment.
  • 113.Hypoglycemic coma. Diagnostics, emergency care.
  • 114.Hyperosmolar coma. Diagnostics, emergency care.
  • 2. Desirable – lactate level (frequent combined presence of lactic acidosis).
  • 115. Ketoacidotic coma. Diagnostics, emergency treatment, prevention.
  • 116. Emergency conditions for hyperthyroidism. Thyrotoxic crisis, diagnosis, therapeutic tactics.
  • 117. Hypothyroid coma. Causes, clinic, emergency treatment.
  • 118. Acute adrenal insufficiency, causes, diagnosis, emergency treatment.
  • 119. Stomach bleeding. Causes, clinical picture, diagnosis, emergency therapy, therapist tactics.
  • 120. Indomitable vomiting, emergency treatment for chloroprivate azotemia.
  • 121) Acute liver failure. Diagnostics, emergency therapy.
  • 122) Acute poisoning with organochlorine compounds. Clinic, emergency therapy.
  • 123) Alcoholic coma, diagnosis, emergency treatment.
  • 124) Poisoning with sleeping pills and tranquilizers. Diagnosis and emergency treatment.
  • Stage I (mild poisoning).
  • Stage II (moderate poisoning).
  • Stage III (severe poisoning).
  • 125. Poisoning with agricultural pesticides. Emergency conditions and first aid. Principles of antidote therapy.
  • 126. Acute poisoning with acids and alkalis. Clinic, emergency care.
  • 127.Acute renal failure. Causes, pathogenesis, clinical picture, diagnosis. Clinical pharmacology of emergency treatment agents and indications for hemodialysis.
  • 128. Physical healing factors: natural and artificial.
  • 129. Galvanization: physical action, indications and contraindications.
  • 131. Diadynamic currents: physiological action, indications and contraindications.
  • 132. Pulse currents of high voltage and high frequency: physiological effects, indications and contraindications.
  • 133. Pulse currents of low voltage and low frequency: physiological effects, indications and contraindications.
  • 134. Magnetic therapy: physiological effect, indications and contraindications.
  • 135. Inductothermy: physiological action, indications and contraindications.
  • 136. Ultra-high frequency electric field: physiological effects, indications and contraindications.
  • 140.Ultraviolet radiation: physiological effects, indications and contraindications.
  • 141.Ultrasound: physiological action, indications and contraindications.
  • 142. Helio- and aerotherapy: physiological effects, indications and contraindications.
  • 143.Water and heat therapy: physiological effects, indications and contraindications.
  • 144. Main resort factors. General indications and contraindications for sanatorium and resort treatment.
  • 145. Climatic resorts. Indications and contraindications
  • 146. Balneological resorts: indications and contraindications.
  • 147. Mud therapy: indications and contraindications.
  • 149. The main tasks and principles of medical and social examination and rehabilitation in the clinic of occupational diseases. Social and legal significance of occupational diseases.
  • 151. Coma: definition, causes of development, classification, complications, disorders of vital functions and methods of supporting them at the stages of medical evacuation.
  • 152. Basic principles of organization, diagnosis and emergency medical care for acute occupational intoxication.
  • 153. Classification of potent toxic substances.
  • 154. Injuries from generally toxic substances: routes of exposure to the body, clinical picture, diagnosis, treatment at the stages of medical evacuation.
  • 156. Occupational diseases as a clinical discipline: content, objectives, grouping according to etiological principle. Organizational principles of occupational pathology service.
  • 157. Acute radiation sickness: etiology, pathogenesis, classification.
  • 158. Military field therapy: definition, tasks, stages of development. Classification and characteristics of modern combat therapeutic pathology.
  • 159. Primary heart damage due to mechanical trauma: types, clinic, treatment at the stages of medical evacuation.
  • 160. Occupational bronchitis (dust, toxic-chemical): etiology, pathogenesis, clinical picture, diagnosis, medical and social examination, prevention.
  • 162. Drowning and its varieties: clinic, treatment at the stages of medical evacuation.
  • 163. Vibration disease: conditions of development, classification, main clinical syndromes, diagnosis, medical and social examination, prevention.
  • 165. Poisoning by combustion products: clinical picture, diagnosis, treatment at the stages of medical evacuation.
  • 166. Acute respiratory failure, causes, classification, diagnosis, emergency care at the stages of medical evacuation.
  • 167. Basic directions and principles of treatment of acute radiation sickness.
  • 168. Primary damage to the digestive organs during mechanical trauma: types, clinic, treatment at the stages of medical evacuation.
  • 169. Principles of organizing and conducting preliminary (upon entry to work) and periodic inspections at work. Medical care for industrial workers.
  • 170. Secondary pathology of internal organs due to mechanical trauma.
  • 171. Fainting, collapse: causes of development, diagnostic algorithm, emergency care.
  • 172. Acute renal failure: causes of development, clinical picture, diagnosis, emergency care at the stages of medical evacuation.
  • 173. Kidney damage due to mechanical trauma: types, clinic, emergency care at the stages of medical evacuation.
  • 174. Radiation injuries: classification, medical and tactical characteristics, organization of medical care.
  • 175. Occupational bronchial asthma: etiological production factors, clinical features, diagnosis, medical and social examination.
  • 176. General cooling: causes, classification, clinic, treatment at the stages of medical evacuation
  • 177. Injuries by toxic substances of asphyxiating effect: ways of exposure to the body, clinic, diagnosis, treatment at the stages of medical evacuation
  • 1.1. Classification of suffocating and suffocating effects. Brief physical and chemical properties of asphyxiants.
  • 1.3. Features of the development of the clinic of poisoning with suffocating substances. Justification of methods of prevention and treatment.
  • 178. Chronic intoxication with aromatic hydrocarbons.
  • 179. Poisoning: classification of toxic substances, features of inhalation, oral and percutaneous poisoning, main clinical syndromes and principles of treatment.
  • 180. Injuries by toxic substances of cytotoxic action: ways of exposure to the body, clinic, diagnosis, treatment at the stages of medical evacuation.
  • 181. Occupational diseases associated with physical overexertion: clinical forms, diagnosis, medical and social examination.
  • 183. Shock: classification, causes of development, basis of pathogenesis, criteria for assessing severity, volume and nature of anti-shock measures at the stages of medical evacuation.
  • Question 184
  • 185. Toxic pulmonary edema: clinical picture, diagnosis, treatment.
  • 186. Primary respiratory injuries due to mechanical trauma: types, clinic, treatment at the stages of medical evacuation.
  • 189. Pneumoconiosis: etiology, pathogenesis, classification, clinical picture, diagnosis, complications.
  • 29. Peptic ulcer of the stomach and duodenum

    Peptic ulcer of the stomach and duodenum- a chronic relapsing disease in which, as a result of disturbances in the nervous and humoral mechanisms that regulate secretory-trophic processes in the gastroduodenal zone, an ulcer (less often two or more ulcers) forms in the stomach or duodenum.

    Etiology, pathogenesis. Peptic ulcer disease is associated with a violation of the nervous and then humoral mechanisms that regulate the secretory and motor functions of the stomach and duodenum, blood circulation in them, and trophism of the mucous membranes. The formation of ulcers in the stomach or duodenum is only a consequence of disorders of the above functions.

    Negative emotions, prolonged mental stress, pathological impulses from the affected internal organs in chronic appendicitis, chronic cholecystitis, cholelithiasis, etc., they are often the cause of the development of peptic ulcers.

    Among hormonal factors, disturbances in the activity of the pituitary-adrenal system and the function of sex hormones are important, as well as disturbances in the production of digestive hormones (gastrin, secretin, enterogastron, cholicystokinin - pancreozymin, etc.), disturbances in the metabolism of histamine and serotonin, under the influence of which acid activity increases sharply. -peptic factor. Hereditary constitutional factors play a certain role (hereditary predisposition occurs among patients with peptic ulcer disease in 15–40% of cases).

    The direct formation of an ulcer occurs as a result of a violation of the physiological balance between “aggressive” (proteolytically active gastric juice, bile reflux) and “protective” factors (gastric and duodenal mucus, cellular regeneration, the normal state of local blood flow, the protective effect of some intestinal hormones, such as secretin, enterogastron, as well as the alkaline reaction of saliva and pancreatic juice). In the formation of ulcers in the stomach, the greatest importance is the decrease in the resistance of the mucous membrane, the weakening of its resistance to the damaging effects of acidic gastric juice. In the mechanism of development of ulcers in the outlet of the stomach and especially in the duodenum, on the contrary, the decisive factor is the increased aggressiveness of the acid-peptic factor. The formation of ulcers is preceded by ultrastructural changes and disturbances in the tissue metabolism of the gastric mucosa.

    Once having arisen, the ulcer becomes a pathological focus that, through afferent pathways, supports the development and deepening of the disease in general and dystrophic changes in the mucous membrane of the gastroduodenal zone in particular, contributes to the chronic course of the disease and the involvement of other organs and systems of the body in the pathological process. Predisposing factors are eating disorders, abuse of spicy, rough, irritating foods, constantly fast, hasty eating, consumption of strong alcoholic drinks and their surrogates, smoking.

    RoleHelicobacter pylori

    Helicobacter settles only in the epithelium of the stomach - in the lower sections of the mucus and on the surface of epithelial cells, as well as in areas of gastric metaplasia in the duodenum.

    An important virulent property of this microorganism is adhesion. Primary adhesion occurs through interaction with specific glycoproteins and glycolipids, phospholipids and high molecular weight sulfates on the surface of mucus-producing cells. After damage to epithelial cells by aluminum ions and toxins, Helicobacter can penetrate intracellularly and colonize the extracellular matrix.

    This microorganism is capable of stimulating the production of various inflammatory cytokines, the infiltration of neutrophils, the activity of T- and B-lymphocytes, leading to the formation lymphoid follicles in the gastric mucosa.

    Neutrophil infiltration, activated by bacterial factors, becomes the main mediator of mucosal damage.

    Helicobacter produces urease, which causes the hydrolysis of urea into ammonium ion and carboxylic acid.

    The formation of ammonium hydroxide performs a protective function - creating an alkaline barrier around the bacterial cell.

    In addition, ammonium ions have a damaging effect on the gastric mucosa due to disruption of the protective properties of the epithelium.

    Helicobacter contains a whole complex of enzymes that provide the main functions of this microorganism (cellular metabolism, colonization, epithelial damage). Its proteolytic enzymes lead to a decrease in the thickness and hydrophobicity of the protective mucus gel covering the surface of the mucosa.

    Helicobacter is not only the cause of ulcerogenesis, it also contributes to the development of chronic atrophic gastritis and even metaplasia. Many diseases of the gastrointestinal tract can be associated with it.

    Helicobacter settles in the actual part of the stomach, causing chronic inflammation. As a result, the motility of the pyloroduodenal zone is impaired, leading to the early discharge of acidic gastric contents into the duodenum. Its hyperacidity promotes metaplasia of the mucous membrane into the gastric epithelium: the intestinal epithelium, which is not resistant to hydrochloric acid, is replaced by a more resistant gastric epithelium. Helicobacter settles on these islands, causing inflammation of the duodenum - a relapse of peptic ulcer disease.

    The microorganism produces urease and proteases that damage the protective layer, disrupts cell functions, mucus production and metabolic processes, and potentiates the formation of ulcers under the influence of NSAIDs.

    Symptoms, course. Characterized by pain, heartburn, and often vomiting of acidic gastric contents soon after eating at the height of pain. During the period of exacerbation, the pain is daily, occurs on an empty stomach, after eating, it temporarily decreases or disappears and appears again (with a stomach ulcer after 0.5-1 hour, duodenal ulcer - 1.5-2.5 hours). Night pain is common. The pain is relieved with antacids, anticholinergics, and thermal procedures on the epigastric region. Often duodenal ulcer is accompanied by constipation. Palpation reveals pain in the epigastric region, sometimes some resistance of the abdominal muscles. A scatological examination determines hidden bleeding. When the ulcer is localized in the stomach, the acidity of the gastric juice is normal or slightly reduced, while with a duodenal ulcer it is increased. The presence of persistent histamine-resistant achlorhydria excludes peptic ulcer disease (cancerous, trophic, tuberculous and other nature of ulceration is possible).

    X-ray examination in most cases (60–80%) reveals limited flow of barium suspension beyond the contour of the mucous membrane - an ulcerative niche. In the stomach, ulcers are usually localized along the lesser curvature, in the duodenum - in the bulb. Pyloric ulcers and extra-bulbous duodenal ulcers are rare and difficult to diagnose.

    The most reliable diagnostic method is gastroduodenoscopy, which allows you to detect an ulcer, determine its nature, and take a biopsy (for stomach ulcers).

    Differential diagnosis carried out with symptomatic gastric ulcers, ulcerated tumor (including primary ulcerative cancer), tuberculous, syphilitic ulcers; ulcerations due to collagenosis, amyloidosis. A feature of peptic ulcer disease is the nature of the pain (hungry, after eating after a certain period of time, at night), a long history of the disease with periodic exacerbations in the spring and autumn, the presence of hydrochloric acid in the gastric juice during the study.

    Flow usually long-term with exacerbations in the spring-autumn period and under the influence of unfavorable factors (stressful situations, dietary errors, consumption of strong alcoholic beverages, etc.).

    Complications: bleeding, perforation, penetration, deformation and stenosis, degeneration of ulcers into cancer, vegetative-vascular dystonia, spastic dyskinesia of the gallbladder, chronic cholecystitis, fatty hepatosis, reactive pancreatitis.

    In the treatment of patients with peptic ulcer there are two main period (two tasks):

    Treatment of the active phase of the disease (newly diagnosed peptic ulcer or its exacerbation);

    Prevention of relapse (preventative treatment).

    Treatment methods (in the active phase)

    Activities aimed at changing lifestyle

        Quitting smoking reduces the duration of scarring and the frequency of exacerbations.

        Stopping or reducing alcohol consumption.

        According to WHO recommendations, it is possible to consume no more than 14 alcoholic units per week for women and 20 for men (1 serving or 1 alcoholic unit is equal to: 330 ml of beer, 150 ml of wine, 40 ml of strong alcohol).

    Stop taking non-steroidal anti-inflammatory drugs and steroids if possible, or reduce the dose.

        Non-pharmacological measures Diet therapy

        Diet does not significantly affect the course of peptic ulcer disease, however, patients should be given advice on rational nutrition with the exclusion from the diet of food that increases the symptomatic manifestations of the disease. Regular meals can help the symptoms of the disease disappear more quickly. The use of mechanically and chemically gentle anti-ulcer diets is justified only in case of symptomatic manifestations of exacerbation of peptic ulcer disease.

    There are mandatory 5 meals a day, food is steamed.

        Physiotherapy

        • For peptic ulcers, the following types of physiotherapeutic treatment have found their application: UHF therapy, mud therapy, paraffin and ozokerite applications.

          Drug treatment

        Antisecretory antiulcer agents

        H2-histamine receptor blockers

        • Proton pump inhibitors

          Antacids

          Gastroprotective agents. Gastroprotective drugs include drugs that can protect the mucous membrane of the upper digestive tract from the aggressive effects of digestive juices.

        Enveloping and astringent preparations of bismuth

        Sucralfate (Venter)

        Prostaglandins

    Anti-Helicobacter drugs

    Prokinetics - drugs regulating gastrointestinal motility

    Enzyme preparations

        Surgery

        Used only for complicated forms of the disease. In this case, minimally invasive techniques are mainly used (endoscopic bleeding control, laparoscopic operations).

        Indications for surgical treatment:

        Exacerbation with relapse of an ulcer after a complication, despite continuous use of antisecretory drugs in a maintenance dose and courses of 7 or 10 days of anti-Helicobacter therapy.

        A benign gastric ulcer that does not scar for 6 months or 12pc.

    Standard regimens for eradication of helicobacteriosis (one of the regimens is used)

    Seven-day regimens (first line of therapy)

    All of the listed drugs are prescribed simultaneously, in a course of 7 days, taken 2 times a day. Proton pump inhibitor ( Omeprazole 20 mg ( Losek MAPS, Ultop, Omez) or Lanzoprazole 30 mg ( Lanzoptol) or Rabeprazole 20 mg ( Pariet) or Esomeprazole 20 mg ( Nexium)) or ranitidine bismuth citrate in a standard dose. Clarithromycin 500 mg ( Klacid, Fromilid). Amoxicillin 1000 mg ( Flemoxin solutab, Amoxiclav).

    Ten- and fourteen-day regimens (second line of therapy)

    Course duration is 10-14 days. Proton pump inhibitor ( Omeprazole 20 mg ( Losek MAPS, Ultop, Omez) or Lanzoprazole 30 mg ( Lanzoptol) or Rabeprazole 20 mg ( Pariet) or Esomeprazole 20 mg ( Nexium)) - 2 times a day; Bismuth subcitrate 120 mg ( De-nol) 4 times a day; Metronidazole 500 mg ( Trichopolum) 3 times a day; Tetracycline 500 mg ( Tetracycline hydrochloride) 4 times a day.

    Continuation of treatment after completion of one of the regimens

    After the end of eradication therapy, it is necessary to continue treatment for another 5 weeks for duodenal and 7 weeks for gastric localization of the ulcer. Therapy is carried out using one of the proton pump inhibitors ( Omeprazole 20 mg ( Losek MAPS, Ultop, Omez) or Lanzoprazole 30 mg ( Lanzoptol) or Rabeprazole 20 mg ( Pariet) or Esomeprazole 20 mg ( Nexium)) - 1-2 times a day or histamine H2 receptor blockers ( Ranitidine 150 mg ( Ranitidine, Ranisan) or Famotidine 20 mg ( Kvamatel, Gastrosidin, Famotidine)) - 2 times a day.

    Stomach bleeding emergency therapy

    Among acute gastric ulcers, there are unique, rare ulcerations, accompanied by massive bleeding from large arrosive vessels - the so-called simple erosions, or simple ulcerations. They are located outside the zone of primary localization of chronic gastric ulcers - 3-4 cm parallel to the lesser and greater curvature. In this zone (1-2 cm wide), often the primary branches of the gastric artery pass, without dividing, through the muscularis propria into the submucosal layer, bend in the form of an arc and form a choroid plexus, from which branches feeding the muscular layer extend retrogradely. When acute erosion or ulceration occurs in this area, arrosion of a large arterial vessel occurs, leading to massive bleeding, which is an indication for emergency surgical intervention.

    Agents with hemostatic and angioprotective properties: - Dicinone is administered intravenously in 2-4 ml of 12.5% ​​solution, then 2 ml every 4-6 hours. Can be administered intravenously, adding to regular infusion solutions. - 5% solution of epsilon-aminocaproic acid, 100 ml every 4 hours; 5-10% ascorbic acid solution, 1-2 ml IV. - 10% calcium chloride solution up to 50-60 ml/day i.v. - 1% or 0.3% vikasol solution, 1-2 and 3-5 ml, respectively. - Intravenous administration of histamine H2 blockers (ranitidine) 50 mg 3-4 times a day, famotidine (quamatel) 20 mg 2 times a day, proton pump inhibitors (omeprozole 40 mg 1-2 times a day).

    Prevention

    Continuous maintenance therapy. Conducted over months or years.

    Indications

          Ineffectiveness of eradication therapy.

          Complicated course of peptic ulcer.

          The need for long-term or continuous use of NSAIDs.

          Concomitant erosive-ulcerative esophagitis.

          Peptic ulcer with a frequently relapsing course, not associated with helicobacteriosis.

          Age over 60 years, with annual relapses of peptic ulcer.

    Appointments. The following medications are recommended: Proton pump inhibitor ( omeprazole 20 mg or lansoprazole 30 mg or rabeprazole 20 mg or esomeprazole 20 mg) - 1 time per day or Histamine H2 receptor blocker inhibitor ( famotidine 20 mg or ranitidine 150 mg) 1 time per day.

    Preventive therapy, on-demand prophylaxis

        Indications The appearance of symptoms of peptic ulcer after successful eradication therapy.

        Appointments Recommended: Proton pump inhibitors (omeprazole 20 mg or lansoprazole 30 mg or rabeprazole 20 mg or esomeprazole 20 mg) 2 times a day or Histamine H2 receptor blockers (famotidine 20 mg or ranitidine 150 mg) 2 times a day. These drugs are prescribed in the indicated dose for 2-3-5 days, and then the administration continues at half the dose for 2 weeks.

    Medical examination of patients with peptic ulcer disease

    Nosological form

    Frequency of therapist observations

    Examinations by doctors of other specialties

    Diagnostic tests

    Basic therapeutic and health measures

    Peptic ulcer, severe course

    4 times a year

    Surgeon 1-2 times a year, dentist 2 times a year

    Diet, regime, anti-relapse treatment - 2 times a year, dispensary, employment - according to indications, inpatient treatment during an exacerbation, sanatorium treatment - according to indications

    Peptic ulcer, moderate to severe course.

    2 times per year

    Surgeon - according to indications, dentist once a year

    Clinical blood test 2 times a year, general urine test, stool test occult blood, examination of gastric contents, x-ray examination stomach (gastroduodenofibroscopy) – according to indications

    Diet, regime, anti-relapse treatment - 2 times a year, sanatorium-resort treatment, dispensary, employment.

    Peptic ulcer, mild course

    1 time per year

    Dentist once a year

    Clinical blood test 2 times a year, general urine test, feces for occult blood, examination of gastric contents, X-ray examination of the stomach (gastroduodenofibroscopy) - according to indications

    Diet, regimen, anti-relapse treatment - 2 times a year, sanatorium-resort treatment, dispensary, employment



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