Symptoms of stomach ulcers, treatment regimens, preparations. Ulcery disease of the stomach and duodenalist what does the ulcer defect of the polygonal form mean

The ulcer of the stomach is a chronic disease at which the formation of ulcerative defects of the stomach mucosa occurs. Most often, the ulcer of the stomach suffer from men from 20 to 50 years. For the disease, a chronic flow with frequent relapses, which are usually spring and autumn are characterized.

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

What it is?

The stomach ulcer is a local defect of the stomach mucosa (sometimes with the capture of the submembraty layer), which is formed under the action of hydrochloric acid, pepsin and bile. Tropical violations in this section. The secretion of acid in the stomach does not usually increase.

The peptic disease is characterized by a recurrent flow, that is, alternating periods of exacerbations (more often in spring or autumn) and periods of remission. Unlike erosion (superficial mucosa), ulcer heals with the formation of a scar.

Causes of ulcers

Cause	Description
Infection Helicobacter Pylori (Helicobacter Pylori)	The main reason for the development of the disease. This spiral bacterium causes 45-75% of all cases of stomach ulcers. The source of infection is a sick person or a bacteria carrier. Microbe can be transmitted through: saliva (with a kiss) dirty dishes food infected water poor sterilized medical instruments (for example, fibrogastroscope) from mother to the fetus
Against the background of receiving medicines	It is the second in frequency causes the development of the stomach ulcers. These include: antihypertensive preparations of central action - "Resern"; preparations of potassium - "Asparkov", "Panagi", "Potassium chloride"; cytostatic - "Formuracyl", "Azatioprin", "Imuran"; corticosteroids - "Betamethasone", "Dexamethasone", "prednisolone"; non-selective non-steroidal anti-inflammatory agents - "butadion", "indomethacin", "diclofenac", acetylsalicylic acid.
As a complication of various chronic diseases	It can be: hyperparathyroidism chronic renal failure diabetes sarcoidosis lungs' cancer chronic viral hepatitis syphilis
Against the background of acute diseases and conditions of the body ("stressful ulcers")	These are certainness: injuries; acute hepatic and renal failure; sepsis; frostbite; extensive burns; all types of shocks
Social reasons	The development of ulcers affect: negative emotions; constant stress; rough errors in nutrition; abuse of alcohol and cigarettes; financial well-being.

What kind of ulcers are, consider it more detailed:

Symptoms of stomach ulcers

Sometimes the stomach ulcer does not show anywhere, which indicates the need for regular survey. As a rule, the course of the ulcer process without noticeable symptoms is observed in 25 - 28% of cases, and the presence of ulcers is detected after the patient's death.

To suspect the ulcerative lesion of the stomach, according to the following signs:

1. Gas formation enhancement.
2. Fast suitable saturation.
3. The appearance of a feeling of gravity in the abdomen area observed after eating.
4. The decline in appetite for ulcerative disease may be associated with the fear of a person to experience pain or with violations of motorcycle gasts.
5. Exterior, which is characterized by uncontrolled cast of gastric juice into the oral cavity. In this case, the patient feels.
6. Stool violations. Most often, patients complain about constipation, and diarrhea is atypical for peptic ulcer. The difficulties with the intestinal emptying are tested up to 50% of patients, especially during the exacerbation of the stomach ulcers.
7. Paints localized in the top of the abdomen. This symptom is manifested in 75% of cases. Half of the patients complain about the sensations of weak intensity, in the remaining 50%, they are more pronounced and amplified during exercise, after adopting inside alcohol or acute food, during the period of long interruptions between food.
8. Feeling nausea, sometimes accompanied by vomit. This symptom occurs due to the violation of the stomach motor. With vomiting ulcers, it is observed 1.5-2 hours after eating and as the stomach is released brings a sense of relief. Therefore, often patients cause vomiting on their own.
9. Heartburn. It is expressed in the feeling of burning in the supred area. It arises due to the fact that the acid content of the stomach having an aggressive medium falls into the lumen of the esophagus, irritating its walls. This symptom is observed often and occurs in 80% of patients. The heartburn appears usually 1-2 hours after eating.

Among the external signs of the stomach ulcers separately, it is worth noting the presence of a gray nail in the language, which almost always indicates problems with the gastrointestinal tract. The patient may suffer from high sweating of palms and experience pain when pressed to the epigastric area.

Characteristics of pain under the stomach ulcer:

1. A ulcer, located in the upper curvature of the stomach, has a very hidden current and it is possible to quickly be diagnosed very rarely, and it is precisely ulcers of the upper curvature of the stomach that is malignant.
2. The defeat of the ulcer of the anthral portion of the hollow organ is distinguished by pain in the evening and night time, can be absolutely not connected with meals. The pain is permanent, which is accompanied by exhaust and heartburn.
3. If the ulcer is located in the pyloric sector of the stomach, the pain will be acute, parotid, long-term (in some cases one attack lasts more than 40 minutes).
4. When localizing a peptic disease in a small curvature of the stomach, pain will be particularly intense in the left iliac region. The syndrome occurs 1 hour after meals, the condition stabilizes after the stomach digest the contents. Most often, complaints from patients on pain come in the evening, sometimes they are accompanied by vomiting.
5. If the ulcer is located in a cardinal or subcardinal stomach department, then painful syndrome appears 20 minutes after eating food, its localization is very high - in almost the field of solar plexus. Very often pain irradiates in the heart, so the heart attack may be mistakenly diagnosed (this is due to self-diagnosis). With this arrangement of defective education, there is never a pain after physical exertion, and after the use of even a small amount of milk, the patient's condition stabilizes.

Symptoms of the stomach ulcers during the exacerbation period:

1) Dupacious, cutting, stitching pain in the upper belly, most often in the middle (in the epigastric area), can give to the left hypochondrium. The appearance of pain is associated with food use, approximately 0.5-1 hours after eating, stops approximately 2 hours, it is associated with the emptying of the stomach. The pain appears, as a result of irritation of the peaked surface, it is food, it is stopped by antacids (Almagel). Also pain is characterized by seasonality, i.e. The exacerbation occurs in spring and autumn.

2) Dyspeptic disorders:

• heartburn, appears as a result of throwing acidic gastric content in the lower departments of the esophagus. It is manifested simultaneously with the appearance of pain;
• nausea and vomiting, also arise at the same time when pain appears. Vomiting, accompanied by relief for the patient;
• acid bumps, constipation, develop due to increased gastric acidity;

3) loss of body weight, due to fear of reception of food, which contributes to the appearance of pain.

True ulcer

If you ignore the disease, the stomach perforation and penetration of ulcers occurs. It comes to break its wall and germination of ulcers to neighboring organs. The contents and microorganisms penetrate the abdominal cavity, causing peritonitis.

Chronic unpleasant sensations that the patient got used to testing, suddenly sharply pass into acute daggie pain. Man is covered later, stomach rolls.

Such a complication requires a surgeon intervention. Within 6 hours, the patient has a chance to escape if it is time to put on the operating table, rinse the damaged tissue and sew it, thereby stopping the abundant inner bleeding.

Diagnostics

Currently, the diagnosis of stomach ulcers is carried out on the basis of endoscopic research.

The method is called fibrogastroscopy (FGS), during it through the esophagus in the stomach, a thin flexible tool is introduced, equipped with a light source and a camera broadcasting the image to the monitor. This allows you to see the ulcerative defect of the stomach mucosa, determine its localization and dimensions. Previously widely used method of contrasting x-ray is used until now, but has only auxiliary value.

Laboratory studies of gastric and intestinal contents are held for the presence of helicobacteria and hidden blood, general blood and urine tests are prescribed to assess the overall condition of the body.

Treatment of stomach ulcers

How to cure a stomach ulce? - Need integrated therapy, which includes not only drug treatment, but also a lifestyle correction.

The course of treatment of the stomach ulcers consists of:

• elimination of factors that led to illness;
• medication therapy;
• medical nutrition;
• physiotherapy, laser and therapy, magnetotherapy, etc.

Several basic groups for the treatment of peptic ulcer:

Group of drugs	Name	Mechanism of action
H2-histamine receptor antagonists	Today, they are mainly used on the basis of two operating components: Ranitidine, Famotidin.	Have a strong antisecretory effect. Reduce the production of hydrochloric acid, stimulate the formation of gastric mucus.
Antibiotics	Clarithromycin, Amoxicillin, Tetracycline.	Preparations are prescribed to reduce the life of Helicobacter Pylori.
Proton pump inhibitors	Omeprazole, Pantoprazole, Rabeprazole, Lansoprazole, Ezomeprazole.	The main group for the treatment of peptic ulcer. When receiving, the final stage of the formation of chloride acid is blocked.
Antacids	Maalox, Renny, Gastal, Almatyel, Phosfalugel.	Used as a supplement to the main methods of treatment. They do not affect the production of hydrochloric acid, they neutralize the already existing acid.
M-cholinolitiki	Gastracepin, Gastromen, Piegexal.	Preparations selectively block the M-Holonoreceptors of the stomach, without affecting the work of other organs. Assigned to strong pains that are not eliminated by antacids.
Preparations of bismuth	De Nol, Ventrisol, Ulkavis.	Have a binding, enveloping and antiseptic effect. When interacting with gastric juice, insoluble salts are precipitated. It protects the mucous meal from hydrochloric acid, eliminates pain.

Helicobacter Pylori Treatment Scheme

The destruction of Helicobacter Pylori contributes to the best scarring of the ulcer defect. This is the first step of treating ulcerative disease. There are two main antibacterial therapy schemes. They are appointed step by step, that is, the first line drugs did not work, then try the second scheme.

The first line of eradication (within a week):

• Macrodides (clarithromycin) 500 mg twice a day.
• Semi-synthetic penicillins (amoxicillin) 1000 mg twice per day or nitroimidazole derivatives (metronidazole) 500 mg is also twice a day.

In case of failure, the second line of eradication (1 week) is offered:

• Proton pump inhibitors for 20 mg twice a day.
• Bismuth subcitrate (de nol) 120 mg 4 times a day.
• Tetracyclines (tetracycline) 0.5g 4 times a day.
• Nitroimidazole derivatives (metronidazole) 500 mg is also three times a day.

Currently, doctors develop new methods for the treatment of pathology. The testing of the vaccine against Helicobacter is already being tested. For better healing of the defect mucous membrane, cytokine preparations, trefoiley peptides and growth factors are used.

Diet

Special requirements are nominated for food. It should spare the mucous membrane from mechanical and chemical damage and at the same time be full. Power should be fractional 5-6 times a day. All dishes need to be crushed or used in liquid form, in a parenchy or boiled form, not cold and not hot.

The wipe is shown, easily digestible food, practically not increasing the selection of gastric juice:

• eggs sick, omelet for a couple;
• milk and dairy products;
• boiled beef dishes, chicken, veal, cutlets for a couple;
• boiled fish of non-fat varieties;
• white, slightly dried bread;
• dairy soups, chicken, vegetables from potatoes, beets;
• boiled vegetables: carrots, potatoes, beets, zucchini, pumpkin;
• buckwheat, manka, rice, oat groats, pasta;
• weakly brewed tea;
• sweet kisins, compotes;
• ramber, wheat bran, non-acidic berry juices;
• alkaline mineral water without gas.

Symptoms of ulcerative disease exacerbate:

• acute and salty;
• canned, smoked food, sausages;
• bakery products made of dough, pies, rye bread;
• strong tea, coffee;
• foods from oily meat, fat, tanning broths;
• roast;
• all sorts of spices: mustard, pepper, carnation, etc.;
• carbonated drinks.

It is worth abandoning products containing coarse fibers, they are mechanically irritated by the stomach: radish, turnips, radish, beans, bread with bran.

Folk remedies

Fitotherapy does not replace medication treatment. It increases its effectiveness. In the case of a peptic ulcer, the correct use of medicinal plants (as an addition to drug preparations) allows:

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

The anti-inflammatory effect is healing fees, including St. John's wort, yarrow, calendula, etc. In the role of natural antispasmodics, mint, oregano, chamomile can perform, dill. By eliminating the spasm of gastric smooth muscular muscles, these wonderful medicinal plants will bury pain. Enveloping action is inherent in licorice, ninewood, flax seed. The full-fledged scarring of the ulcers contributes cleanly, chicory, Cyprus, the shepherd bag, the root of the burdock. To relax the chair, you can use crash, jox, rhubarb, three-lines, etc.

Mentioned medicinal plants are recommended to use in the form of infusions, decoctions, phytoapplications for the abdominal wall and therapeutic baths. At the same time, it should be not forgotten that phytoapplications are categorically prohibited during bleeding, pregnancy (entire period), fever, any cancer diseases.

Operation

How to treat a stomach ulcery when conservative treatment does not bring the expected results? Unfortunately, there are such cases when it is not necessary to do without surgery. However, surgical intervention should be based on absolute indications, which include:

• sprinkling ulcers;
• the occurrence of bleeding;
• transformation of ulcers in oncology;
• III degree of stenosis.

Operational intervention is not excluded at relative indications, among which II degree of stenosis, the possibility of frequent recurrences, multiple scars, a cellular ulcer, penetration, the impossibility of healing ulceration for a long time.

In the presence of testimony to operation, avoid it is undesirable, even delaying the process is quite dangerous. The reason is that every planned operation is less dangerous than emergency intervention. Plus, the emergency operation is not always effective, but it has a greater risk of postoperative complications.

Stomach ulcer after surgery

After the operation, the patient can proceed to work in about two or three months. It all depends on how the stomach ulcer behaves after the operation, when the seams are removed and discharge from the hospital. It all depends on the flow of recovery and healing of wounds. If everything is in order, the seams take off approximately 7-9 days, but they discharge out of the hospital a few earlier.

It is very important to comply with a diet after surgery. As a rule, it is allowed to eat liquid after two days, half a glass of water per day, dosing a teaspoon. Gradually, every day the water is replaced with soup or broth. Then, after about eight days, allowed to eat with meat, potatoes, porridge, and so on, but only in the scarlet. In order not to harm the postoperative state, it is necessary to observe a strict diet and obey your doctor.

Forecast

The prognosis of the disease is conditionally favorable, with adequate timely treatment, the quality of life does not suffer, the ability to work is completely restored. However, it is possible to develop a number of threatening life of complications, such as bleeding from a ulcerative defect, or sprinkling ulcers, and as a result, the development of peritonitis.

Prevention of pathology

The main preventive measures include:

1. Reducing stress levels. We are needed timely rest, full sleep.
2. Compliance with the rules of healthy nutrition. It is necessary to monitor that there are no constipation, diarrhea, gas formation processes.
3. Refusal of alcohol. Even small doses negatively affect the useful microflora of the gastrointestinal tract. With its violation, the risk of developing ulcerative disease increases several times.

In conclusion, we note that in time the discovered peptic disease in the presence of full-fledged treatment has a favorable forecast. In complications may occur threatening state.

1

The article presents the results of endoscopic studies of the stomach and DPK in patients with ulcerative disease of the surgical profile. The authors of the articles are discussed in detail the mechanisms of pathogenesis of the disease, the role of H.Pylori infection, the requirements for the fulfillment of rapid ureazny test, the principles of classifying the disease of domestic and foreign authors. The most common surgical and therapeutic classifications of the disease are considered. The indications of the completion of the endoscopic study are presented, the features of the endoscopic picture are discussed with a benign course of the disease and in the presence of complications. All the most common complications are illustrated by Endofoto. Separately discussed the stages of the course of the disease, the features of the endoscopic picture, the characteristics of the peptic defects, the perifocal zone, concomitant changes in the gastric mucosa and the DPK are considered. The article is illustrated by endoscopic photographs reflecting the process of process flow.

stages of the flow of ulcerative disease

classification of ulcerative disease

pathogenesis of ulcerative disease

endoscopic study

gastric ulcer and DPK disease

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3. Ivashkin V.T. Sheptulin A.A. Diseases of the esophagus and stomach. Moscow. - 2002.

4. Ivashkin V.T., Komarov F.I., Rapoport S.I., Ed. Quick Guide to Gastroenterology. - M.: LLC Publishing House Moseniya, 2001.

5. Pimanov S.I. Ezophagitis, gastritis, ulcerative disease. - N. Novgorod, 2000.

7. Chernyshev V.N., Belokonev V.I., Alexandrov IK Introduction to the surgery of gastroduodenal ulcers. - Samara: SGMU, 1993. - 214 p.

8. Shapovalian S.G., ChernyaKevich S.A., Mikhalev I.A., Babkova I.V., Storozuk G.N., Malent E.K., ChernyaKevich P.L. The efficiency of Rabeprazole in parenteral administration in patients with sharp ulcerative gastroduodenal bleeding with a high risk of relapse after endoscopic hemostasis // Rzhggg. - 2014. - №3.

9. Shahrokhi N, Keshavarzi Z, Khaksari M. J Pharm Bioallied SCI. 2015 Jan-Mar; 7 (1): 56-9. DOI: 10.4103 / 0975-7406.148739. Ulcer Healing Activity of Mumijo ACETIC ACID INDUCED GASTRIC ULCER IN RATS.

10. Tsukanov VV, Shtygasheva OV, Vasyutin AV, Amel "Chugova OS, Butorin NN, Ageeva ES. Bull Exp Biol Med. 2015 Feb 26. Parameters of Proliferation and Apoptosis of Epithelial Cells in the Gastric Mucosa in Indigenous and Non-Indigenous Residents Of Khakassia with Helicobacter Pylori Positive Duodenal Ulcer Disease.

Ulcery disease of the stomach and DPK (YAB) is a heterogeneous disease with multifactorine etiology and complex pathogenesis. The pathological process is based on the inflammation of the gastroduodenal zone mucosa with the formation of local damage, the morphological equivalent of which is the defect of the mucous membrane and the submucosal layer, designed to the connecting plate.

The YAB is a chronic recurrent disease that flows with alternation of exacerbation and remission periods. In the modern clinic, the duodenal localization of ulcers, meeting 8-10 times more often, dominates localization in the area of \u200b\u200bthe stomach. Typical for Yab are seasonal reinforcement periods of pain and dyspeptic disorders. The possibility of the asymptomatic flow of the YAB should also be taken into account. The frequency of such cases according to the literature can reach 30% (Minskin ON, 1995).

The factors of aggression include: enhancing the effects of the Acido-peptic factor associated with an increase in hydrochloric acid products and pepsin; Violation of the motor-evacuation function of the stomach and duodenum (delay or acceleration of the evacuation of acidic content from the stomach, duodenogastral reflux).

Protection factors are: the resistance of the mucous membrane to the action of aggressive factors; Gastric mucus products; adequate bicarbonate products; active regeneration of the surface epithelium of the mucous membrane; sufficient blood supply to the mucous The normal content of prostaglandins in the mucous membrane wall; Immune defense.

Of great importance is currently in the pathogenesis of the YAB, especially duodenal ulcers, attached to the infectious agent - Helicobacter Rylori (HP). On the one hand, the microorganism in the process of its livelihoods, forming ammonia from the urea, lars the anthraral department of the stomach, which leads to the hypersecretion of gastrin, constant stimulation of the shell cells and NCL hyperproduction, on the other hand, a number of its strains allocate cytotoxins that damaging the mucous membrane. All this leads to the development of the anthral gastritis, the gastric metaplasia of the duodenal epithelium, the migration of HP in the DPK, the development of duodenitis and, ultimately, can be realized in Yab (Pimanov S.I., 2000).

Along with HP infection, an important role in the pathogenesis of the YAB is given by the hereditary predisposition to the disease and the use of nonsteroidal anti-inflammatory drugs (NSAIDs).

In foreign literature, the term "chronic peptic ulcer of the stomach or DPK" was adopted. This name reflects the main pathogenetic signs of the disease - the appearance of a peptic defect in the stomach or DPK, as a result of the peptic impact on these organs of digestive enzymes. In Russia, the term "ulcerative disease" dominates, and the presence of a detailed classification of the disease is necessary in connection with the traditions of the Russian therapeutic school and the requirements of ability to work (MINUSKIN O.N., 1995).

The most common classification of peptic ulcer is the classification of Johnson.

Classification A.G. Johnson (1990)

• Chronic type I ulcers - small curvature ulcers
• Chronic type II - combined with ulcer DPK, including with a healing duodenal ulcer
• Chronic type III ulcers - prebinor ulcers
• Chronic ulcers IV type - sharp surface ulcers
• Chronic V-type ulcers - due to Zolinger's syndrome - Elisson

Classification of chronic stomach ulcers

(V.N. Chernyshev, V.I. Belokonev, I.K. Aleksandrov, 1993)

I Type - single or multiple ulcers, located from proximal (antral) part of the pyloric stomach station to cardia;

II type - single or multiple ulcers of any gastric department in combination with ulcers or DPK erosions or with a healing dpk ulcer;

III Type - ulcers of a rings of a gatekeeper or an assistant zone (no further 3 cm from the pyloric throat);

IV Type - multiple ulcers, subject to a combination of gatekeeper ulcers and an adreral zone with an ulceration of any overlying stomach department;

V Type - secondary ulcers of any stomach department developed due to various local reasons for ugly ethiology.

Classification of gastroduodenal ulcers on the ICD-10

1. Prank ulcer (ulcerative illness of the stomach) (cipher to 25), including the peptic piping ulcer and other stomach departments.

2. A duodenal ulcer (ulcerative DPK disease), including the peptic ulcer of all duodenal departments (cipher to 26).

3. Gastroinny ulcer, including a peptic ulcer (cipher to 28) anastomosis of the stomach, leading and reducing the loops of the small intestine, fatal with the exception of the primary ulcer of the small intestine.

From the point of view of surgical practice, clinical significance has a complicated course of ulcerative disease - acute gastroduodenal bleeding; penetration of ulcers in neighboring organs; Punching of ulcers; Pyloroduodenal scar stenosis (compensated, subcompensated, decompensated); periviscereitis (perigastrites, perideodenitis); The rebirth of ulcers in cancer.

Fig.5. Bleeding

Endoscopic semiotics of ulcerative disease

In most cases, the ulcers of the stomach are located in its small curvature in the prebilor and pyloric departments. Less often are in the cardiac and subcardial departments. More than 90% of the ulcers of the stomach are located on the border between the zones of gastric and pyloric glands, usually on the side of the pyloric glands. This corresponds to the area of \u200b\u200bthe stomach wall, limited to the front and rear-skewed fibers and the circular layer of the muscular shell of the stomach wall, where with its movements there is the greatest stretching of the wall.

DPK ulcers are usually located in the area of \u200b\u200bthe transition of the stomach mucosa into the DPK mucous membrane in the place where the sphincter of the gatekeeper is separated from the Circular Muscles of the DPK connecting interlayer. It also says the greatest stretching during peristaltic activity. The size of gastroduodenal ulcers can range from several mm to 50-60 mm in diameter and more. The depth of the ulcers can also be different - from 5 to 20 mm. Ulcers may have a rounded, oval or incorrect form. The edge of the ulcers addressed to the entrance to the stomach, as a rule, is bellped, and the mucous membrane hangs over a ulcerative defect. The opposite edge of all appears to be gentle. The folds of the mucous membrane along the periphery of ulcers are thickened and converted to its edges. The serous shell in the ulcer zone sharply thickened.

Testing on Helicobachanty Infection

On the recommendation of the Russian Gastroenterological Association, all patients with a stomach or DPK ulcer, not excluding patients with the presence of an NSAB called, should be examined for HP. The diagnostic test must be carried out before the start of treatment.

When performing FGDS, it is advisable to take a biopsy with a ureaznal test (Kist M., 1996). With its negative values, a morphological study is recommended with a fence of at least two biopsies of the body mucous membrane and one of the anthral stomach. In addition, this test can only be used in patients who do not accept antimicrobial drugs at least four weeks and antisecretory drugs for at least one week.

Characteristics of the ulcerative defect - the size, shape, the depth of the ulcers, the presence and length of infiltration and hyperemia around the defect to a certain extent depends on the stage of development of the ulcer process.

Stages of the development of the ulcer process (Vasilenko V.K. 1987)

I - acute stage. A ulcer into this stage with endoscopic examination is a defect of the mucous membrane of various sizes, shapes and depths. Most often, it has a rounded or oval shape, the edges of it with clear boundaries, hyperemic, edema. In some cases, the edge addressed to the cardiac department is somewhat imposed, and the distal edge is more gently, smoothed (Fig. 6, 7). The mucous membrane of the stomach or bulbs of the DPK Even, hyperemic, the folds are thickened and poorly disappeared by air, often there are small erosion coated with a white bloom and frequently merging into extensive fields. Deep ulcerative defects often have a funnel appearance. The bottom of the ulcers is usually covered with fibrinous overlays of grayish-white and yellowish color, the presence of dark splashes in the bottom of the ulcer points to transferred bleeding.

Figure 6. Endofoto. Ulcer dpk. Acute Stage

II - Stage of the subsoil of inflammatory phenomena. The ulcerative defect in this stage is characterized by a decrease in hyperemia and edema of the mucous membrane and the inflammatory shaft in the periulcous zone, gradually becomes more flat, it may be of the wrong shape due to the appearing convergence of the folds of the mucous membrane to the edges of the defect. The bottom of the defect is gradually cleaned from the fibrinous plaque, while the granulation tissue can be detected, the ulcer becomes a peculiar appearance, which is described as "pepper with salt" or "salami". However, such a picture is observed at the beginning of the formation of ulcers. At various stages of the healing of the ulcer, it changes the shape on a sliding, linear or divided into several fragments.

Fig.7. Endofoto. Ulcer corner of the stomach. Acute Stage

Fig.8. Endofoto. Potable Rubber DPK.

III - the strategy of scarring - ulcers acquires a slight-shaped form with small infiltration and hyperemia around it; On the mucous membrane in the distance from ulcers can be areas of insignificant hyperemia, edema and single erosion.

IV - the stage of the scar. The post-lounged scar has the appearance of a hyperemic section of the mucous membrane with a linear or star-retraser wall (the stage of the Red Rubac). In the future, with an endoscopic study, various disorders of the relief of the mucous membrane are determined at the site of the ex-ulcer: deformations, scars, narrowings. Most often linear and star scars are formed. When healing deep chronic ulcers or, with frequent recurrences, coarse deformations of the organ and stenosis (Fig. 8) can develop. Often healing chronic ulcers can take place without the formation of a visible scar. A mature scar acquires a whispering form due to the replacement of the granulation tissue with a connective tissue and the lack of active inflammation (the "white" stage of the scar). Scars and deformation of the wall of the stomach and DPK, resulting from frequent exacerbations of chronic ulcers, serve as reliable endoscopic yab criteria.

The results of their own studies show that the endoscopic method allows to carry out dynamic observation of the process of scarring the ulcerative defect. On average, healing of the stomach ulcers before the formation of the "red" scar occurs in 6-7 weeks, and duodenal ulcers for 3-4 weeks. The formation of a full-fledged scar is usually ends after 2-3 months (the Phase "White" scar). It should be borne in mind that sharp surface ulcers can be found within 7-14 days without the formation of a visible scar.

The erosion of the mucous membrane (the surface defect that extends not to the deeper muscle layer of the mucous membrane and heating without the formation of a scar) is often found at the Yab and only endoscopically diagnosed.

The erosion of the distal ventricular and bulbous DPK is found in 30-50% of patients with saworoduodenal ulcers, and approximately 75% of patients with exacerbation of the Yab detect only erosive lesions of this zone.

Reviewers:

A.G. Korothevich, D.M., Professor of the Department of Surgery, Urology and Endoscopy GBOU DPO NHYUZ, Novokuznetsk;

S.E. Schemers, D.N., Professor of the Department of Surgery Nome Vpo Caliiz, Head of the Endoscopy Department of the State University "SGKB No. 8", Saratov.

Bibliographic reference

Blashentseva S.A., Supilnikov A.A., Ilina E.A. Endoscopic aspects of the diagnosis of gastric ulcer and DPK disease in patients of surgical profile // Modern problems of science and education. - 2015. - № 3;
URL: http://science-education.ru/ru/article/view?id\u003d18709 (Date of handling: 27.01.2020). We bring to your attention the magazines publishing in the publishing house "Academy of Natural Science"

22839 -1

Yab stomach and DPK It is a chronic and periodically recurrent disease. It is manifested by the formation of a defect (ulcer) on the wall of the stomach or DPK. The detection frequency of the stomach and DPK ulcers in adults on average is 10-12%. More than 80% of the ulcers are localized in the DPK. The disease of the bowl (70-80%) is found in 30-40 years old, but about 1% of the DPK ulcers and 0.7% of the stomach ulcers fall on children's and youthful age.

DPK ulcers occurs in a younger age, and the ulcer of the stomach in the elderly and senile. In both groups of patients, there is a clear prevailing of the male (4: 1), even more significant for the DPK ulcers. The DPK ulcers in men are 6 times more often than in women, and the ratio of the stomach ulcers is 27: 1. DPK ulcers in 94% of patients are localized in the bowl. At the same time, there may be two ulcers - on the front and rear walls ("kissing ulcers"). The diameter of the ulcers here usually does not exceed 1.5 cm. In the CCP, various stages of chronic duodenitis are detected. This ulcer often penetrates into the head of the PJ, into the hepatic-duodenal bundle. The scarring of ulcers causes the deformation of the bulbs, the formation of diverticopod-like protruding of its walls, the narrowing of the lumen.

Etiology and pathogenesis Yab remains not sufficiently studied. Currently, there is no generally accepted theory of its etiopathogenesis. Yab is a polyethic disease, its pathogenesis is multifactorious.

In modern presentation, its etiology takes a number of major and predisposing factors, which obviously contribute to the development of the disease and its exacerbation:

1) Long or frequently repeated neuro-emotional overvoltages (stress), negative emotions that break the nerve and hormonal mechanisms for regulating the function of the stomach, the trophics of it and the DPK. As a result, blood circulation and ensuring the oxygen of the stomach and DPK leading to the formation of a ulcerative defect is disturbed. In connection with the circulatory impairment, the wall of the stomach and DPK becomes sensitive and unstable to a rich pepsin and hydrochloric acid ZHS;
2) genetic predisposition, including a persistent increase in the acidity of the ZHS, constitutional nature;
3) local violations of the process of digestion and changes in the trophic of the gastroduodenal system;
4) the presence of chronic gastritis, duodenitis, functional disorders of the stomach and DPK (prevailing state);
5) disruption of the power mode;
6) smoking;
7) Long use of strong alcoholic beverages, some drugs (aspirin, butadnon, indomistacin, reserpine, glucocorticoids, etc.).

These drugs have an adverse effect on the protective barriers with the stomach, suppress the formation of mucus and change its qualitative composition, cause a disturbance of capillary blood circulation, etc.

Local factors include a violation of the protective mechanisms of the mucous barrier, circulatory disorder and structural changes of CO. The development of the ulcer of the stomach is associated mainly with the weakening of the resistance of the CO, the development of the so-called anthral state and duodenogastric reflux. The occurrence of duodenal ulcers is realized by acidic peptic aggression. Normal with stomach and DPK stably maintains, protected from the effects of aggressive factors (hydrochloric acid, pepsin, lysolecigin and bile acids) of the stomach and DPK.

The factors are sewn include blood flow through CO, secretion of mucus and pancreatic juice, regeneration of the cover epithelium, local synthesis of foremeal structons, etc. Damage with ulcers, erosion and inflammation are associated with the predominance of aggression factors (hydrochloric acid, pepsin, power factors, dysmotorics, injury mucous) over protection factors (CO resistance, anthrodugenic acid "brake", alkaline secretion, food).

The features of the reactivity of the NA, genetic predisposition (increase in the mass of parietal cells), age-related neuroendocrine changes in the body (features of puberty, climax), violation of regulatory processes due to various diseases, increased acid-peptic secretion, intestinal metaplasia with stomach, anthroduoden dyotloxy, endocrine Effects and others.

Chronic liver disease (violation of the inactivation of histamine, gastrin, stagnation in a carrier vein - a disturbance of microcirculation), kidneys, acute and chronic circulatory disorders, stressful situations. A ulcer can form in patients of senile age ("senile ulcer"), with damage to the central nervous system, with extensive burns and severe purulent diseases.

Also, the slowdown and irregularity of the evacuation of the intestinal content of the intestines are also referred to local mechanisms of ulcerative formation, long-term anthraral stasis of food chimus, the gaping of the gatekeeper, duodenogastral reflux with the regurgitation of bile acids and lysolecitins that destroy the mucosa barrier and the resulting retrofusion of H-ions and the formation of a peptic defect under the influence of pepsin (P. Ya. Grigoriev and E.P. Yakovenko, 1993).

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

A long-term hyperchlorogide with peptic proteolysis, due to hypervagotone, hypergastrine and hyperplasia of the main gastric glands, ineffective neutralization of ZHS mucoid substances and an alkaline component of the DPK, long-term acidic acidification of the saworoduodenal medium. The main aggressive and damaging factors are SC and pepsin. Old statement: "No acid - no ulcers" remains, in fact, right and currently, despite the fact that the borders of acid products in patients with Yab fluctuate widely.

In the regulation of acid secretion, in addition to other factors, the foreguide is also played, which are able to inhibit this process. In addition, they provide cytoprotective effect due to stimulation of secretion of mucus. The most important protection mechanisms for the stomach and DPK on the action of damaging agents are the normal regulation of the secretory function, the resistance of the CO from the protective barrier, its microcirculation, the high regenerative ability of the surface epithelium.

Of great importance in ensuring the CO resistance is Muzin, which secretes the cells of the cover epithelium, the addition cells of the cervical gastric glands, the pylorical glands, and in the DPK - Brunner gland and glazing cells. Possessing a large buffer capacity, Muzin neutralizes both acids and alkali, it absorbs pepsin, resistant to the effects of various physiological and chemical agents. The mucus covers the surface with a gastrointestinal layer in the form of a film with a thickness of 1-1.5 mm and serves as a protective barrier.

With a decrease in resistance content, due to damage to its protective barrier, the inverse diffusion of H-ions increases. The resulting tissue acidosis contributes to the release of histamine from CO cells and acetylcholine from intramural nervous plexuses. As a result, the secretion of hydrochloric acid and pepsin is stimulated, microcirculation and permeability of capillaries is disturbed, stasis and edema, hemorrhage in CO. Such with is easily damaged by hydrochloric acid, pepsin and other agents.
The stomach is damaged and as a result of a duodenogastral 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 the cell membranes and damage the cells of the surface epithelium. System resistance decreases with inflammatory and degenerative changes of CO, accompanied by a decrease in the release of mucin and changes in its properties. Resistance to CO depends on organ blood flow, hypoxia as a result of blood flow from spastic abbreviations of the gastric muscles, etc.

Food as a result of mechanical and chemical effects on CO can cause increased rejection of the cells of the coating epithelium. The lack of regenerative ability CO creates conditions for increasing the inverse diffusion of H-ions, the depletion of the intracellular buffer system, the appearance of hemorrhages, erosion and ulcerations of CO (V.T. Peremernie et al., 1997).

Food factors In addition to the ability to exacerbate shifts in secretory and motor activities, the stomach and DPK may be a protective factor due to the dilution and neutralization of hydrochloric acid, the binding of pepsin protein components.

In recent years, the interest of scientists for the new factor in the emergence has increased dramatically Helicobacter pylori.. The latter is detected at the Yab with the localization of ulcers in the anthropyloro-duodenal zone in almost 100% of cases, which makes thinking about its meaningful role in the pathogenesis of this disease and consider it one of its most important factors (P.Ya. Grigoriev et al., 1993; M. G. Potter and Sow., 1999).

Yab has different pathogenetic mechanisms with different localizations (stomach, DPK, gastric bodies, preparatory and pylorical ulcers, combined stomach and DPK ulcers).

Yab DPK has some features that are as follows:

1. In patients with hypertension of the DPK, hypersecrate with increased acidity ZS is often observed, which is due to the high tone of the wandering nerve, an increase in the amount of parietal cells, an increased release of gastroelectric g-cells, with the weakening of the anthroduoden mechanism for the deceleration of acid production, the decrease in the acid-meterailizing ability of the stomach associated with a decrease in the secretion of pyloric Iron alkaline juice.

2. The gastroduodenal dyotility is more pronounced, which is manifested by accelerated evacuation from the stomach, decreased as a result of this buffer role of food and increasing acidity in the DPK.

3. At the Yab DPD, the effect of the physiological depressor mechanism on the release of hydrochloric acid is expressed to a lesser extent, and the selection of the alkaline secretary of the PJ is noticeably reduced.

4. As a result of a decrease in DPK resistance to the effects of ZHS and disorders, its protective barrier increases the inverse diffusion of H-ions.

5. A relatively more important is the importance of psychosomatic factors leading to the disorder of the secretory and motor functions of the stomach and DPK.

6. The existing bond between the duodenal ulcer and CP increases the incidence of duodenal ulcer among patients with HP. This is due to a decrease in the buffer capacity of duodenal content due to a decrease in bicarbonate concentration in pancreatic juice.

Thus, if in the pathogenesis of the formation of DPK ulcers is important, the peptic factor is important, then with a stomach ulcer in many cases, not only the peptic factor is important, but also the weakening of the protective abilities from the stomach (mucus formation, the deterioration of blood circulation, etc.).

Pathological anatomy. The peptic ulcer is defined as a defect with the stomach and DPK, propagating through Tun. Musc, Mucosae. A ulcer can penetrate into various depths, up to the serous cover, or, in the destruction of the latter, communicated with the free cavity of the peritoneum (perforation) or the bottom of it can be the surface of one of the adjacent organs (penetration).

Pathoanatomyically distinguish:

1) sharp ulcers (OA);
2) chronic ulcers (he);
3) penetrating ulcers;
4) scar changes caused by ulcers (M.Yu. Pantsarev, V.I. Sidorenko, 1988).

OA have a round or oval shape with clearly bounded edges that penetrate through the submool layer up to the serous. The basis of the development of the OA is not an inflammatory process, but necrosis with distinct changes in the vessels and connective tissue of the stomach. When healing the OA, linear or star scars are formed.

A distinctive feature of HA is the progressive seal of its edges and the bottom (CALLESS OF AZH) due to the abundant development of scar connective tissue. Over time, the development of connective tissue is becoming more pronounced, it is scarring, the edges of the ulcers are becoming increasingly dense and turn into a molds (corn) ulcer (M.Yu. Pantsurev, V.I. Sidorenko, 1988; V.N. Chernov and Sovat, 1993), which gives ulcers similarity to the tumor (ULCUS TUMOR).

This ulcer penetrates the different depth of the organ wall and beyond its limits (penetrating ulcer). The diameter of the ulcers from 0.3 to 6 cm. In CO, detect various stages of chronic gastritis and chronic duodenitis. Scar changes are tightened with collaps, converging to the edges of ulcers. Around the ulcers of the vessels have thickened walls, their lumen is narrowed or refrused by endovasculitis, the growth of the connective tissue. Nervous fibers and ganglion cells are subjected to dystrophic changes and decay.

A canometric ulcer does not have a tendency to be healing, often accompanied by the destruction of the wall of one of the adjacent vessels. After healing, he remains star scars with characteristic retractions in the center. The scars may be accompanied by a significant deformation of the stomach (the stomach in the form of "snail", "hourglass") or narrowing its weekend (stenosis of the gatekeeper). Deep-rotating ulcers are usually complicated by the development of peritoneous adhesions (perigastite, peridodenitis), also deforming the stomach and DPK.

Under the penetrating ulcer, the forms are understood under which the peptic process passes through all the layers of the stomach wall or DPK, but does not give perforations into a free abdominal cavity. With this version of the YAB, the destructive process goes slowly and the bottom of the ulcers is reported to neighboring bodies. Therefore, in the destruction of the serous shell of the stomach and the PCP of the ulcer, it seems to penetrate into the appropriate organ, the tissue of which form the bottom of the crater.

Classification. The generally accepted classification of the YAB currently does not exist. The classification proposed by see was the greatest distribution. Ryss (1968).

According to this classification, the following distinguish:

- Localization of ulcers; body of the stomach; Small curvature; cardiac department; big curvature; DPK bulb;
- related changes in the stomach and DPK: normal with stomach (head-eyed hyperplasia), DPK; Xp, superficial, with lesions of glands without atrophy; atrophic; chronic duodenitis, superficial, diffuse, atrophic;
- Gastric secretion: normal, reduced, increased, true ahlorohydria;
- Current: periodically recurrent, often recurrent, latent; juvenile ulcer, ulcer in the elderly, senile age; benign, malignant malignancy ulcers, consistent development of cancer outside ulcers;
- Special forms: gatekeeper ulcers, giant ulcer, postbulbatory ulcer;
- Complications: bleeding, penetration, perforation, scar changes.

In practical surgery, the classification of the LA proposed by Johnson is used: I type - small curvature ulcers - mediagastric ulcer (above 3 cm from the gatekeeper); II type - stamped stomach and DPK III type - ulcers of the prebillar stomach (up to 3 cm from the gatekeeper).

Clinical picture and diagnostics. The course of the YAB is long, with alternating periods of exacerbation and long-term remission. The exacerbations are associated with the error in diet, overwork, emotional-nerve overvoltage. For the Yab typical "seasonality". The exacerbations of the bowl of all occur in spring and autumn. The most typical is the presence of a history and with an objective examination of the "Triads" of symptoms: pain, vomiting and bleeding.

Seasonality of the disease is explained by the change in the state at different times of the year, the neuroendocrine system, which regulates the secretory and motor functions of the stomach and DPK.

One of the main subjective manifestations of the Yab is pain. Being the main complaint of patients, it is usually noted in the epigastric area. The pain can be localized and to the right of the middle line of the abdomen. Pains usually occur after meals. The time of its occurrence (after receiving write) can help in determining the localization of ulcers. There are early, late, night and hungry pain. If the ulcer is localized in the field of entrance and body of the stomach, an early pain occurs (the first 30 minutes). Winds immediately after receiving write, it stops after the gastric emptying.

When localizing ulcers in the area of \u200b\u200bthe output part of the stomach or DPK, the late pain is marked. The latter occurs after a while (1.5-2 hours after reception of writing), on an empty stomach, hungry pain or at night (night pain). Pains can be irradiating to the left half of the chest, the region of the sword-shaped process, the left blade, the difficult spine department. Hungry pains are connected with the fact that the PCK ulcer is often accompanied by a constant secretion, which is continuing even outside the reception of writing and during sleep. This violation is due to a sharp increase in the BN tone, and for ulcers, localized in the stomach, is an increase in garbage release.

The genesis of the hungry pain arising from a long break in food reception is due to hypoglycemia that causes an increase in the BN tone and the strengthening in connection with this secretory and engine activity of the stomach.

Night pain arise around between 24-3 hours, poke after taking write (milk) or after abundant vomiting with an acidic stomach content. The appearance of pain is associated with an increase in the BN tone at night. Night pain can be in a certain extent and hungry pains.

With a cardia of pains, pain is localized in the field of a sword-shaped process and the left half of the epigastric region with irradiation into the left shoulder and the blade, with pyloroantral and duodenal ulcers, the pain is most noted on the right in the mesog wrist, the right hypochondrium, irradiages in the back. Under the defeat of the small curvature of pain marks on the white line in the epigastric area.

The irradiation of pain can be in the lower back of the XII rib - the point of Boas and the spine, respectively, the location of the ulcers is the point of Openhovsky. However, it should be noted that the pain at the YB is often not clearly a clear rhythm. The intensity, localization, irradiation and rhythm of pain depends on the depths of the ulcer process, its prevalence and severity in the gastroduodenal CO.

With surface ulcers, pain may be absent or being expressed so insignificant that it is practically not to attract the patient's attention. Pain occurs or enhanced with the penetration of ulcers or periulicosis inflammation in the deep layers (muscular, subserosic) wall of the organ. These layers are innervated with sensitive fibers of sympathetic nerves that react to spasm.

Pain may cause hypersection of acid ZHS, enhancing the engine function of the stomach, pylorospasm, an increase in intragastric pressure. With the penetration of ulcers and the periulcous inflammatory process, the pain is enhanced, becomes almost constant, stubborn, at times very acute. At the height of the pain, the irradiation of the left under ulcers of the upper sections of the stomach and in the right hypochondrium - with ulcers of the weekend of the stomach and the Bulb of the DPK are manifested.

The pain under penetration of ulcers is due to the involvement in the pathological process of tissues innervated by the sensitive fibers of intercostal nerves. When wearing ulcers, there is a sharp constant pain of a "quinge nature". In the origin of pain, the condition of organ blood circulation, venous stasis in the vessels of the small curvature of the stomach in the vessels.

The penetration of ulcers to the surrounding organs and tissues is accompanied by the development of inflammatory processes in the affected organs and the formation of extensive adhesions (periviscererite). Pain syndrome in penetration becomes more intense, permanent polymorphic, pain appear peculiar to diseases of related bodies involved in the pathological process. The pain is mainly dependent on the organ in which an ulcer penetrates. In case of penetration of ulcers in a small gland, the pain irradiates into the right hypochondrium, sometimes into the right blade, with penetration into the gastrointestinal ligament - up and left, with a typical "farian syndrome" (left or right), with penetration of ulcers appears to the diaphragm The mesentery of transverse ok occurs pain in the umbilical area.

Duodenal and pyloric ulcers are more often penetrated into the PJ. Large sizes are accompanied by stronger pain than chronic, and have dense edges.

For Yab typical cyclic pain, calm after rest and treatment. A symptom characteristic of YAB is a heartburn, a feeling of burning in the epigastric area and beast. After receiving food, heartburn antacides decreases or disappears. The emergence of heartburn is associated with a violation of motor skills, secretory activities of the stomach and reflux of its contents as a result of the insufficiency of the circular function of the esophageal and gastric transition, increase the tone of the muscles of the stomach and spasm of the gatekeeper. The insufficiency of "physiological cardia" can be due to the hernia under, often combined with the YAB.

Sometimes an acid exterior is observed due to the regurgitation of gastric content in the esophagus due to cardius failure and an increase in intragastric pressure. Acosite belching is often at the Yab DPK. With a stomach ulcer, it is empty or containing food residues. Nausea, flickering fucked and vomiting in the uncomplicated form of the YAB is rare. These symptoms indicate a violation of the evacuation of the contents of the stomach due to a long spasm and a pronounced inflammatory swelling edema or DPK bulbs, and maintain them in the Remissions phase - about the scar stenosis of the gatekeeper.

Being a less permanent symptom than pain, vomiting when Yaz occurs a few more than a cup (68%) than with the PCK ulcers (53%). The lots of the masses contain acidic gastric content, remnants of undigested food and an abundance of mucus. In complications of the YAB (stenosis of the gatekeeper, bleeding), the nature of vomiting and the vomit varies accordingly. Vomiting with an uncomplicated Yab occurs at the height of pain. She can be early or late. Vomiting is due to the irritation of inflamed CO and, apparently, is reflexive.

Most patients, especially with DPK ulcers, in the exacerbation phase there are constipation, Based by spastic dyskinesia colon. In some patients, the latency of the chair may be a precursor of the exacerbation of the YAB.

Appetite With the uncomplicated form of the YAB, it is usually not reduced, and often even increasing, especially with duodenal ulcers ("painful feeling of hunger").

Patients gradually lose weight, Lose weight, because, despite the good appetite, they consciously avoid meals because of the fear of exacerbation of pain. The exacerbation phase usually lasts 4-5 days, and in some cases up to 6-8 weeks, and then a period of more or less prosperous well-being, which can last for several years. The general condition of the sick yab is usually satisfactory.

In the aggravation phase, it worsens, increased fatigue, weakness, sweating, disability, is observed or, on the contrary, increased excitability. Various neurological reactions due to violations of vegetative NA may be observed. Patients often adhere to normal or even increased nutrition, but more often than reduced. This is due to a number of reasons: self-restriction in a diet, durability, sleep impairment during night pain, with nausea and vomiting.

Clinical manifestations of the Yab in terms of recurrence also depend on the localization of ulcers. Pilrory ulcers are characterized by a resistant recycling flow, short unstable remissions, frequent complications with bleeding and stenosis. The pain syndrome is extremely intense, repeatedly renewed during the day, due to the involvement in the pathological process of a very sensitive neuromuscular apparatus of the gatekeeper.

The ulcer of the top of the stomach clinically often does not fit into the description of the classical forms of the disease, concealed by manifestations of angina, cholecystitis, pleurrites, etc. due to the difficulties of clinical, x-ray and even endoscopic assessment of the ulcers of this localization are often not diagnosed.

Outlukovical ulcers proceed with frequent exacerbations, recurrent bleeding, accompanied by stubborn pain, heartburn, bitterness in the mouth, relatively rare vomiting. One of the signs of an extravukovical ulcers may be jaundice due to a periulcerous inflammatory process that propagates on the Sphinteer of a large duodenal papilla (BDS), penetration of ulcers in the PJ with the development of reactive inflammation in it, squeezing the OGP. Reactive pancreatitis that occurs in patients with postbulbar ulcers is accompanied by an intense constant pain in the left half of the abdomen, which is enhanced during the physical exertion and when palpation. After receiving write, the feeling of cutting in the stomach and gravity is joined.

When palpation, you can define moderate pain in the epigastric region, a slight muscle tension. Of great importance belongs to the detection of spherical pain areas (K. Mendel): for the PCK ulcers - in the right half of the epigastria with the distribution to the right hypochondrium; for stomach ulcers - middle line and somewhat left from it; With a cardiac ulcer - a sword-shaped process.

Is diagnostic importance to identifying hidden blood in feces and reticulocytes in peripheral blood, confirming the bleeding ulcer, but, of course, not excluding other gastrointestinal diseases with bleeding. The diagnosis of YAB is based primarily on the objective study of the stomach and DPK.

Of the special diagnostic methods up to the present, RF is common. This method is safe, objective and allows you to identify not only morphological changes, but also accurate localization of ulcers, value, to evaluate secondary changes in the body under study, deformation, connection with neighboring bodies, etc. This method is becoming more informative due to the improvement of X-ray diagnostic devices equipped with electron-optical brightness amplifiers, a television system, computers and video recordings. All this makes it possible to more accurately assess the morphological changes and quite fully study the motor function of the stomach and DPK.

The reliability of the establishment of x-ray Yab filed by X-ray population comparisons is 95-97% (Yu.M. Pantsurev, V.I. Sidorenko, 1988). Ri is priority if the patient suspects stenosis, violation of the gastric emptying, anomaly of the situation, a hernia under, fistulus, diverticulosis, and also in patients with a so-called elevated endoscopic risk.

The main and direct x-ray sign, allowing to diagnose ulcers with confidence, is a symptom of "niche" surrounding its inflammatory shaft, convergence of folds of the CO. The ulcerative "niche" (Symptom of Gaudek) is the structureless depot of the barium suspension, the added shadow ("plus the shadow"), protruding the contours of the stomach, and is the most reliable sign of ulcers decisive when diagnosis. The periulhesive ring-shaped roller, protruding over the level of CO, is formed as a result of inflammatory infiltration of tissues and functional spastic changes in the muscles of the submembraty layer around ulcers. The ulcerative "niche" usually happens the right form with clear contours.

There is also a scar deformation of the DPK bulbs (in the form of a tribal, tube narrowing). Around the ulcerative "niche" with a thorough and methodologically correct study, the rim of the enlightenment of a greater or less width is visible - the inflammatory shaft to which the folds of the CO are converted. Based on this feature, it is possible to judge the periulcous inflammatory shaft. Surface sharp ulcers without an inflammatory shaft do not give a characteristic symptom of "Niche". Rarely accompanied by a radiological symptom of "niche" bleeding ulcers, since their crater is filled with thrombotic masses, and the inflammatory shaft decreases dramatically, the CO is impeded surface.

It is easier to recognize deep ulcerative niches in the body of the stomach and the Lukovice of the DPK. Identification of ulcers "niche" in the cardiac and subcardial departments, as well as in the pyloric sector of the stomach and an outlukovical ulcers, requires special methodical 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 occur during their localization in the zone of pronounced scar deformations of the stomach and DPK (MA Filipkin, 1977, etc.). Street ulcers are relatively easily recognized (A.S. Loginov, V.M. Majorov, 1979). In order to increase the informativeness of the X-ray method, it is carried out a positional examination of the Relief of CO, along the course of the study makes overview and aiming pictures. The direct radiological symptoms of the YAB include scarsing deformation of the stomach or DPK (reduction of the bulb, diverticopod-like protrusion, stomach in the form of "hourglass", cascade ulitskogo stomach, etc.).

Indirect signs that are indicators of functional disorders, little significant in the diagnosis of ulcers. The auxiliary radiological features include reinforced motor skills, the strengthening of the tone, the convergence of the folds of the CO, hypersecretion and disruption of the evacuator function, local spasm, the deformation of the organ wall, the accelerated evacuation of the barium mass from the stomach and the rapid passage of it on the DPK to the top hinges of the TC and others deserve special attention A sharp expansion of the stomach due to the scar changes in the saworoduodenal department, the lack of cardia, the SBR, the deformation of the Lukovitsa DPK.

Currently, the double contrast method is successfully used, which allows you to identify small parts of the CO structure and in pathological conditions. This method makes it possible to more often diagnose surface ulcers, which in the usual method are detected extremely rarely.

The diagnosis of old, kallese ulcers of the stomach is based on the incorrect form of "niche" and the exhaustion of the barium depot beyond the shadow of the stomach in different positions of the patient. To recognize the HA with a linear or sliding crater and other atypical ulcers, double contrasts and simultaneous premedication are required. The use of cholinolitical and antispasmodic drugs during the study allows you to achieve better conversion of CO and, therefore, to obtain better information about the state of the authority.

Radiological recognition of scarcered ulcers from the stomach and DPK, especially the post-free scar, is based on indirect signs (convergence of folds to the contour of the gastric wall, accumulation of the barium suspension with clear uneven contours and the convergence of the stuffing of the gastric wall).

In addition to identifying a ulcerative defect in the stomach and DPK, the X-ray method is valuable in suspected stenosis, the hernia under, diverticulosis, during subblystal formations, as well as in patients with increased endoscopic risk. Ri is determined by the motility of the stomach. With ulcerative damage to the stomach of Motorika, it is often not different from normal even during the period of exacerbation and with pain syndrome. Sometimes it is reduced. In case of ulcers, the DPK occurs to strengthen the stomach motility, especially its anthral department. Most patients have a periodic activity of the stomach: abbreviations of the authority of the empty stomach are continuous or the elongation of the period of operation and the shortening of rest periods is observed.

Reliable method, allowing, with rare exception, confirm or reject the diagnosis of the YAB, is esophagogastrodumoscopy. It makes it possible not only to identify the ulcerative defect, but also ensure control over its scarring, and gi material obtained by the aiming biopsy makes it possible to estimate CO changes, reliably guarantee the accuracy of the diagnosis on the morphological and even morphofunctional level. The endoscopic picture in chronic ulcers depends on the localization of the process, the stages of healing or exacerbation.

For the endoscopic pattern of aggravation of the ulcer process, a peptic defect of a round or oval shape and inflammation of CO was characterized. Sizes, shapes, depth, bottom, edges, degree of severity of periulcous inflammation and infiltration are different. Differentiations contribute to gi bioptats of CO obtained from the edges of the ulcers and the periulicosis zone.

With the help of duodenoscopy, the diagnosis and postbulbar ulcers have significantly improved, which constitute at least 1% of all duodenal ulcers. These ulcers can also be both solid and multiple. When the inflammatory process is subsided, hyperemia is reduced around ulcers surrounding it shaft smoothes, is compact. The ulcer becomes less coarse, both as a result of a decrease in the height of the inflammatory shaft and as a result of the development of granulation at the bottom. Ulcers in the healing process can acquire a different shape, fragmented. With full healing at the site of ulcers, gentle pink scars of a linear or star form are visible. As a rule, the scarring of ulcers leads to more or less pronounced deformation from the organ.

It is very important to use endoscopy for differential diagnosis of benign and malignant stomach ulcers. In obscure cases, multiple (six pieces of edges and bottom of ulcers) is essential, targeted gastrobills with histologically studied biopsy. The morphological diagnosis of the YAB is important not only for the differential diagnosis of the disease, but also to determine adequate therapy.

The endoscopic method is used to determine the acid-forming zone of the stomach (Yu.M. Pantsierev et al., 1978). This method is successfully used to marking the intermediate zone in the preoperative period. Endoscopic study (EI) is also used to explore the nature and localization of the mucous microflora, as well as to determine its sensitivity to antibiotics. Endoscopy allows you to recognize the disorders of the motor and evacuation functions of these organs (cardius failure, gastroesophageal and duodenogastral reflux, etc.).

One of the most important achievements was the use of EI to diagnose the causes of bleeding from the upper gastrointestinal departments.

The patients with gastric secretion are important in patients, especially to identify the functional disorders of the stomach. Learn the volume of the ZHS, the acid composition of the content, the flow rate of the National Assembly and pepsin. In the assessment of the acid and enzyme production function of the stomach, the RF LSL and pepsin in basal and stimulated secretion phases are taken into account.
Gastric secretion at Yab differs significantly depending on localization. In case of boulevard and pylorial ulcers, acidic products are most often increasing both in basal (empty stomach) and in the stimulated phase.

In the majority of patients with pylorobulbar ulcers there are continuous acid formation with a sharp and constant acidification of the stomach and the DPK bulbs. High ventricular secretion indicators are installed and the combined lesion of the stomach and DPK. With a stomach ulcer, the acid-forming function is usually normal or significantly lower if the ulcer is located closer to the cardiac ventilator. Only individual patients detected moderate hypersection.

Differential diagnosis. The YAB is differentiated with gastritis, rzh, diseases of the biliary tract, coronary vessels, disorders of duodenal patency, pancreatitis, appendicitis, pathology of the right kidney and ureter, colon, etc. The diagnosis of the Yab DPK in typical clinical manifestations does not represent difficulties. For this disease, seasonality of the course of the disease, the daily rhythm of pain associated with meals, etc. In each case, the final diagnosis can guarantee only RI and EI with aiming gastrobiopsy.

When the location of the parietal pain in the right hypochondrium can resemble the HCB, XX. However, the observed seasonality of the exacerbation of the disease lasting 3-4 weeks, daily daily rhythm of pain, the disappearance of pain after vomiting they speak of a YAB, and not about hepatic colic, which occurs episodically after taking oily roasted food and in which pains disappear after vomiting. In case of hepatic colic, patients are restless, looking for a comfortable position, attacks are short-lived, when applying spasmolytic pains sneeze, etc.

In case of diseases of the Farm Palpation of the abdomen causes pain in the right hypochondrium (duck from the edge of the right-handed muscle), and with the DPK ulcers in the area of \u200b\u200bthe right-handed muscle (in the zone of the DPK projection on the abdominal wall). Differential diagnostics helps Ri, in which the functional changes in the biliary tract or combination with the HCR are detected. The similarity with the Yab DPK can have a HP, in which the strengthening of pain in the upper half of the abdomen is connected with the reception of writing. However, when HP, the pain often takes a sinking character, does not disappear after receiving antacids, it may increase after vomiting.

In the diagnosis of CP, it is necessary to take into account the role of alcoholism in history. HP may accompany the Yab DPK, more often in cases of penetrate ulcers in PJ. The use of ultrasound scanning of the PJ, the LDP provides information used to conduct a differential diagnosis of the Yab DPK with PZH and LP diseases.

Grigoryan R.A.

Fibrogastroduodenoscopy is the main method of diagnosing peptic ulcer. During the need to establish the fact of peptic ulcer as such. From the research protocol, the attending must receive information that will allow you to put a detailed clinical diagnosis.

The endoscopic picture of the stomach ulcers and the duodenum depends on the stage of ulcers. It is proposed to allocate the following stages of the development of a ulcer defect:

In the activity stage, the ulcers endoscopically has a rounded or oval shape (from 1-2 mm to gigantic sizes in 8-10 cm) with a pronounced inflammatory shaft around and a bottom covered with a gray rode. The edges of the ulcers are smooth, clear. The proximal edge of the ulcers is higher and craterly silent over the ulcer, and its distal edge is flat. Crater ulcers most often cone, and its depth depends on the height of the surrounding inflammatory shaft and the depths of the ulcer itself. Fresh epithelium is not visible.

In the A2 activity stage, the size of the ulcers remains the same, the inflammatory shaft is slightly less, the edges of the ulcers are clean and a small cut of fresh epithelium is adjacent to them, and a hyperemic mucosa is visible to the periphery. Sometimes there are minor folds, radially directed to the ulcer.

In the healing stage 31, the shape of the ulcers can be round or oval, but sometimes it changes to a linear, polygonal or slital. Flip, covering bottom of ulcers, becomes thin, whitish. Compared to the active stage, the size of the ulcers decreases, the inflammatory shaft is very poorly expressed, as a result of which the edges of the ulcers become flat, the fresh epithelium spreads to 2/3 of the surface of the ulcers and only its center is not covered by it. The surrounding mucosa moderately hypereated.

The healing step 32 is characterized by a further decrease in the size of the ulcer. Fresh epithelium covers the entire surface of the ulcers, and only in the center there is a small plot with a white thin hoist. The surrounding mucosa is normal, there is no angle of inclination between the edge of the ulcers and its bottom.

In the scarring stage of P1 ("Fresh" scar) the bottom of the ulcers is completely covered with fresh pink-colored epithelium, there is no plaque. With close inspection in the fresh epithelium, many blood vessels can be seen. This is the stage of the red scar.

Stage of scarring P2, or the stage of the white scar ("old" scar), is formed in a few weeks or months and is characterized by full elimination

the inflammatory process in the mucous membrane, and the slurry of the scar acquires a blessed color.

When developing complications, the endoscopist should give their detailed characteristics:

bleeding: establishing a fact and source of bleeding, its characteristic, type of hemostasis;
Perforation: diagnosis of complication, localization and size of ulcers and perforation hole, the presence of related complications (bleeding, stenosis) and ulcerative defects;
Penetration: depth, dimensions and localization of the ulcerative defect;

about stenosis: The degree of stenosis and the presence of a ulcerative defect, the size of the stomach, the nature and amount of stagnant content, the tone of the wall.

In the Study Protocol, it is necessary to indicate the presence of direct or indirect signs of motor-evacuator disorders (duodenogastric or gastroesophageal reflux, distal reflux-esophagitis, anthral reflux-gastritis, bile in the lumen and on the walls of the stomach and esophagus, food residues). When describing the ulcerative defect, the value, shape, depth of ulcers, the result characteristics, bottom, localization should be reflected.

According to our data, patients with complicated flow are characterized by large sizes of ulcers exceeding 1.0 cm in diameter, having a pronounced periulcous inflammatory shaft, rigid edges, a significant depth in some cases of ulcers are multiple, double localization; The frequency and severity of the deformation of the stomach and / or the bulbs of the duodenum and duodenogastral reflux are high.

The fibrin raid with hemosiderin indicates a tendency to bleeding or can be considered as stigma of suffering bleeding. A deep ulcer on the rear or medial wall, more often penetrates into the pancreas, which is accompanied by concomitant inflammation of the gland. In addition, such localization is dangerous by the development of heavy bleeding due to the proximity of large vessels.

Control studies make it possible to estimate the dynamics of the scarring of the ulcerative defect.

The degree of severity of scar deformation objectively can be judged according to X-ray research in hypotension. Nevertheless, the endoscopist should reflect the presence and severity of the strain of the stomach and / or duodenum in the study protocol.

Moderate batch deformation of the duodenal bulb is characterized by a change in the shape of the bulbs in the form of a minor decrease in its size, shortening one of the walls, the balcony folds of the mucous membrane, which is completely dissolved during air insufflation. A more significant decrease in the dimensions of the duodenal bulb, the appearance of pseudodivekuli (divertic-like "pockets") on the walls listed from the main cavity of the bulb with comb-like or semi-short folds that do not disappear even with hyperinsoff of air, the mixing of the BULBODENAL zone characterizes the pronounced scarsing deformation. With severely pronounced scar deformation, there is a significant narrowing of the cavity and shortening of the bulbs, pseudodivecals are formed, the bullboduen boundary is shifted to the area of \u200b\u200bthe upper or front wall (less often of the bottom), it is detected with difficulty. The folds are coarse, anastomosen among themselves. Often there is a varying degree of severity by stenovation in the Bhulbodenal border and the suprasical failure of the gatekeeper. With this type of disease, the diagnostic possibilities of endoscopy are limited due to the impossibility of a detailed inspection of the bulb of the duodenum. Only the presence and level of stenosis (gatekeeper, a bulb, a lowry department), the size of the narrowing, the nature and volume of gastric content (semi-resistant), the increase in the size of the organ, the condition of the gastric mucosa (, inflammation, hypertrophy or atrophy, etc. can be appreciated. ), folds, rigidity or elasticity of walls, accompanying damage, the nature of changes in the peristaltic (hypo-, normo or hypermotoric). The dynamics of these changes in the treatment is also subject to evaluation. It is reliably to assess the degree of stenosis and disorders of the evacuator function, to carry out a detailed description of the ulcerative defect (except for the establishment of the very fact of the presence of ulcers) and the accompanying duodenal lesions are usually possible.

Exododent deformations are more often associated with the pathology of the pancreas and are observed in the downward department of the medial wall.

The article has prepared and edited: a surgeon doctor

Ulcerative disease This is a chronic recurrent disease, the main sign of which is the presence of a long non-prominent and recurrent ulcer, which can be located both in the stomach and in duodenalistician. This disease differs from acutely developing ulcerative defects, for example, such as erosion and sharp ulcers. Acute ulcerative defects may arise due to operations, anesthesia, infection, intoxication, circulatory disorders, situation of situations, hepatic and other pathologies; may be accompanied by abundant bleeding, but should be considered as complications.

This pathology is more likely to suffer young people and middle-aged people. Moreover, there is a tendency, both to the growth of the total number of diseases and to the incidence shift in the "young" groups (adolescents 12-14 years old). This disease occurs in the city 2 times more often than in rural areas and 4 times more often in men than women. There is a link between the frequency of occurrence and unfavorable stressful situation.

Morphology of chronic peptic disease

The topographically peptic defect is most often located in the food track zone. Localization is different, but more often: the small curvature of the stomach (high, mediocastral ulcer), then the piloroantral zone, and, finally, the upper part of the duodenum. The defect in most cases is a single (very rarely double), rounded-oval shape (ULCUS Rotundum), deep (bottom of ulcers goes into the muscular shell). The top edge hangs, the bottom is smoothed; The edges of the ulcers are dense (caloric ulcer). Thus, when describing ulcers, its localization, form, shape, depth, edge and diameter should be taken into account.

The histological structure is described, estimating the layers of ulcers in the context. It depends on the period of the flow (the period of acute flow, the period of the regression and the period of healing of ulcers).

Histology of ulcers during the period of acute flow is presented in the bottom - necrotic substrates impregnated with exudate (the bottom is uneven, rough, covered with a raid). For necrosis, a layer of granulation tissue (rich-seeking, rich-milk, low-fiber), in which fibrinoid necrosis of vessels may cause bleeding. The lowest layer is represented by a ripening cloth (dense, rich-fed, small-cell). The vessels in this zone are usually scruvied sharply. Sometimes at the bottom of the ulcers, formations are formed by the type of traumatic neuro (traumatic restructuring of the endings of nerve trunks). On the edge of the ulcers (where the mucous membrane survived) is usually the signs of inflammation (gastritis) and the hyperplasia of ferrous cells and cells of the coupling epithelium. As a rule, the malignation of ulcers occurs in this hyperplastic zone (irritation zone).

Characteristics of ulcers during regression. The bottom is cleaned of necrosis (seen when endoscopy). From the side of the stored mucous membrane, i.e. From the edges, the epithelial lumber begins to the ulcerative defect. It should be noted that the epithelium of the stomach is quite quickly regenerating (about 3 days). Ideally, this epithelium must completely close the peptic defect (complete epithelialization). First, the so-called red scar is formed (through the epithelium shone the vessels of the granulation tissue). Then it acquires a whiten shade, because, as the granulation tissue ripens, the number of vessels in it decreases. In the end, the epithelium is being promed, and a normal mucous membrane is formed, and the synchronization of epithelium growth at the ripening rate of granulation tissue is important. It should be noted that the ulcer of the stomach heals in about 8 weeks, the duodenum - for 6 weeks. Scar tissue remains long, because little is absorbed, so the area of \u200b\u200bthe ulcerative defect is noticeable for a long time. The healing ulcerative defect is Locus Minoris, where there may be recurrence and aggravation.

Recurrement marks the necrotic process, the death of the epithelium and exudation. During the exacerbation, the ulcerative defect can expand, or due to the necrosis of the edges and their slides, or by the merger of small erosions around the perimeter with a ulcerative defect. Thus, microscopically aggravation is represented by necrosis and exudation, and macroscopically - the expansion of the ulcer crater.

The mechanism of the occurrence of peptic ulcer of the stomach and duodenum

It is believed that the ulcerative defect is formed stadium. The first stage of erosion is small, always acute, superficial (not lower than Tunica Muscularis Mucosae) A peeled defect containing pathological hemoglobinogenic pigment is a salty hematin. The second stage of formation of chronic ulcers is the formation of acute ulcers (has an oval shape, soft edges and a greater depth, but the top of the funnel does not fit the muscular layer). With the further action of negative factors, the defect is aggravated, and the ulcer takes a chronic current.

It has about 12 etio-pathogenetic concepts of ulcerative disease. In the XIX century, it was believed that this is an inflammatory process; Virhov believed that these are vascular changes; taught the activation of peptic factors and mechanical damage; And also suspected the defeats of infectious nature. The last hypothesis was confirmed in our days: in 100% of cases of chronic ulcers, Helicobacter pylori can be allocated. One dispute is not solved, since there are cases of healthy carrier of this microorganism. In our age began to consider the hereditary-constitutional moments. The cortic-visceral theory of Bykov - Kurcina was very popular: ulcers develop due to vectors of vertical bonds and changes in the functions of the chipboard of the hypothalamic-pituitary zone, which affects the acid-peptic factor. However, this theory was not ideal, therefore the theory of reflux appeared, the immunological theory, the theory of the return of hydrogen ions (the defect of the mucous barrier is the so-called phenomenon of the flowing roof). Thus, it is not possible to explain this pathology of some one theory, therefore it is believed that, most likely it is a multifactorial, polyethological disease.

However, the pathogenesis of the medigastral ulcers differs from the development of pyloroantral and duodenal ulcers (both in the central mechanisms and local).

The voltage factor of the hypothalamic-pituitary system and irritation of the center N. Vagus is active at "low ulcers"; It also activates the acid-peptic factor. With overlying ulcers, the emphasis is not made on the increased activity of the feeder and pepsin, but to reduce the protective properties of the mucous membrane.

The emission of adrenocorticotropic hormone (ACTH) is also increased at low ulcers.

Motorika: either a fast evacuation of the contents of the stomach, or its delay in the duodenum has an influence in pyloroantral and duodenal ulcers (the damaging effect of the content saturated with hydrochloric acid). Motoric does not matter with mediobascular ulcers.

Complications:

Groups of complications for Samsonov:

1. Georns and destructive complications:

1.1 Arrocya of blood vessels (arrosive bleeding, vomiting of coffee grounding).

1.2 Penetraration of ulcers.

1.3 Perforation of ulcers.

2. Georns and inflammatory complications (perigastites, the spread of inflammation to other organs, etc.)

3. Ulcerative-scar complications (stricture leading to disruption of evacuation):

4. Maligination (about 3%).

5. Combined complications.