GASTRITIS (gastritis; grech, gaster stomach + -itis) - a lesion of the gastric mucosa with predominantly inflammatory changes in the acute development of the process and phenomena of dysregeneration, structural restructuring with its progressive atrophy in hron, a course, accompanied by a violation of the functions of the stomach and other body systems.

Ideas about G. changed depending on the level of development of honey. Sciences. References to functional and organic disorders of the stomach can be found in the works of Hippocrates, Galen, Razi, Ibn-Sina, and others. The beginning of G.'s study is associated with the name of the French. physician F. Brusset (1803), who considered G. the most common disease and associated with it the development of diseases of the heart, brain, and lungs. Since introduction to a wedge, practice of a method of sounding of a stomach [Kussmaul (A. Kussmaul), 1867] G. was considered as a functional disease. However, this point of view was revised in the second half of the 19th century. - early 20th century on the basis of new data patol, anatomy, abdominal surgery, rentgenol. method, research by IP Pavlov and his school in the field of physiology of the digestive tract.

Introduction to a wedge, practice of methods of a gastroscopy and especially aspiration gastrobiopsy led to expansion of ideas about G. The Soviet scientists Yu. M. Lazovsky, N. I. Leporsky, O. L. Gordon, I. P made a great contribution to development of the doctrine about G. Razenkov, S. M. Ryss.

Distinguish acute and hron. G.

Acute gastritis

Distinguish the following forms of acute G.: simple (banal, catarrhal), corrosive, fibrinous, phlegmonous.

The pathogenesis of acute gastritis

The pathogenesis of acute gastritis is reduced to the development of an inflammatory process of varying severity - from superficial changes to deep inflammatory-necrotic. The pathogenesis of a wedge, signs is determined, on the one hand, by a violation of the secretory and motor function of the stomach (vomiting, spastic pain, etc.), the depth and severity of inflammatory changes in the stomach (leukocytosis, accelerated ESR, elevated body temperature, pain as a result of irritation of nerve endings in wall of the stomach), on the other - involvement in patol, the process of other organs, body systems and some aspects of metabolism (collapse, dehydration of the body, thickening of the blood, etc.).

Pathological anatomy of acute gastritis

The pathological anatomy of acute gastritis is characterized by inflammatory changes in the gastric mucosa. Distinguish catarrhal, corrosive, phlegmonous and fibrinous G.

Fig.10. The mucous membrane of the stomach with phlegmonous gastritis (a sharp thickening of the folds is expressed); on the cut - purulent infiltration.

At catarrhal G. the mucous membrane is infiltrated with leukocytes (tsvetn, tab. Fig. 1-3), which are also located between the cells of the epithelium, inflammatory hyperemia, dystrophic and necrobiotic changes in the epithelium are noted.

At corrosive G. observed necrotic-inflammatory changes in the wall of the stomach (tsvetn. Fig. 9).

At phlegmonous G. (tsvetn. fig. 10) diffuse leukocyte infiltration all layers of the wall of the stomach, but Ch. arr. submucosal base. Phlegmonous G. is followed by perigastritis (see) and can come to an end with peritonitis.

fibrinous G. is characterized by diphtheritic inflammation of the mucous membrane.

simple gastritis

Simple gastritis (banal, catarrhal)- the most common form. It occurs at all ages and regardless of gender. A common cause of simple G. are inaccuracies in nutrition, infections, especially food poisoning (see. Toxicoinfections food). The irritating effect of certain drugs is known (salicylates, butadione, bromides, iodine, digitalis, antibiotics, sulfonamides, etc.). G.'s development from taking small amounts medicines and under the influence of certain types of food (eggs, strawberries, crabs, etc.) may indicate an allergic mechanism of damage to the gastric mucosa.

Wedge, picture of a simple G.(caused by the most common causes - errors in nutrition and food poisoning) usually develops after 4-8 hours. after influence etiol, a factor. Patients report pain, a feeling of heaviness and fullness in the epigastric region, nausea, weakness, dizziness, vomiting, sometimes diarrhea, salivation, or, conversely, severe dry mouth. The tongue is coated with a grayish-white coating. On palpation of the abdominal wall - pain in the epigastric region. The pulse is usually frequent, blood pressure is somewhat reduced. An increase in body temperature is possible, in the peripheral blood - neutrophilic leukocytosis. In the urine, there may be albuminuria, oliguria, cylindruria, i.e., changes characteristic of toxic kidney damage. There is a lot of mucus in the gastric contents; secretory and acid-forming functions can be suppressed or enhanced. Motor disorders are manifested by pylorospasm (see), hypotension and even atony of the stomach (see). The duration of the acute period of the disease with timely treatment is 2-3 days.

Complications at simple G. are rare. General intoxication, disorders in the cardiovascular system may develop.

Diagnosis simple G. is based on a wedge, a picture. With an increase in temperature and a disorder in the activity of the intestine, gastroenterocolitis can be assumed (see), it is also necessary to differentiate G. with salmonellosis (see). Decisive importance is attached to bacteriol, and serol, to researches.

Treatment simple G., it is necessary to begin with cleansing the stomach and intestines and prescribing antibacterial drugs (enteroseptol 0.25-0.5 g 3 times a day, chloramphenicol up to 2 g per day, etc.) and absorbent substances (activated charcoal, clay, etc. .). In case of severe pain syndrome, atropine (0.5-1 ml 0.1% solution subcutaneously), platyfillin (1 ml 0.2% solution subcutaneously), papaverine (1 ml 2% solution subcutaneously) are administered. With the development of dehydration, fiziol is injected subcutaneously, solution, 5% glucose solution. In acute cardiovascular insufficiency - caffeine, mezaton, norepinephrine. It is necessary to appoint to lay down. nutrition. The first 1 - 2 days should refrain from eating, drinking is allowed in small portions (strong tea, borzhom). On the 2-3rd day - low-fat broth, slimy soup, semolina and mashed rice porridge, jelly. On the 4th day - meat and fish broth, boiled chicken, fish, steam cutlets, mashed potatoes, crackers, dried white bread. Then the patient is assigned table number 1 (see Therapeutic nutrition), and after 6-8 days - the usual diet.

Forecast with simple G. in the case of timely treatment, it is favorable. If action etiol, factors repeats, then acute G. can pass into hron.

Prevention simple G. comes down to a rational diet, observance of a dignity. actions in life and at public catering establishments, a dignity. - a gleam, work.

Corrosive gastritis

The corrosive gastritis develops owing to hit in a stomach of such substances, as strong to - you, alkalis, salts of heavy metals, highly concentrated alcohol.

Wedge, picture of corrosive G. depends on the degree of damage to the mucous membrane of the mouth, esophagus and stomach, the nature and resorptive action of the substances that caused corrosive G. Patients usually complain of pain in the mouth, behind the sternum and in the epigastric region, repeated painful vomiting; in vomit - blood, mucus, sometimes tissue fragments. On the lips, mucous membrane of the mouth, pharynx and larynx, there are traces of burns - edema, hyperemia, ulceration. Sometimes, by the nature of the change in the mucous membranes, it is possible to establish the cause of the burn: from chamois and salt to-t grayish-white spots appear, from nitrogen - yellow and greenish-yellow scabs, from chromium - brownish-red scabs, from carbolic - a bright white coating resembling lime, from acetic - superficial whitish-gray burns. In hard cases the collapse can develop (see). The abdomen is usually swollen, painful on palpation in the epigastric region, sometimes there are signs of peritoneal irritation. In some patients, in the first hours after poisoning, acute perforation of the stomach wall occurs, signs of toxic damage to the kidneys (in the urine - protein, cylinders) are noted, up to the development of acute renal failure.

Complication with corrosive G., it can occur in the first hours from the moment of exposure to etiol, the factor, and is manifested by perforation of the stomach wall with the development of peritonitis (see) and penetration into neighboring organs.

Diagnosis corrosive G. is based on anamnesis data, a wedge, signs (including the nature of changes in the mucous membrane of the mouth, throat and larynx).

Treatment should begin with gastric lavage with plenty of water through a tube lubricated with vegetable oil. Contraindications to the introduction of the probe are collapse and, obviously, severe destruction of the esophagus.

In case of poisoning with to-tami, milk, lime water or burnt magnesia are added to the water; in case of alkali damage - diluted citric and acetic acids, antidotes are administered. With severe pain, morphine, promedol, fentanyl, droperidol are administered; in case of collapse, in addition, caffeine, cordiamine, mezaton, norepinephrine, strophanthin (subcutaneously or intravenously with blood-substituting fluids, glucose, physiol. solution, etc.). During the first days, fasting, parenteral administration of fiziol, solution and 5% glucose solution is necessary. If it is impossible to feed by mouth for several days, parenteral administration of plasma and protein hydrolysates. With perforation of the stomach, urgent surgical treatment is indicated.

Forecast corrosive G. depends on the severity of inflammatory-destructive changes and therapeutic tactics in the first hours and days of the disease; death may occur from shock, hemorrhage, or peritonitis. The outcome of corrosive G. is usually cicatricial changes in the stomach, more often in the pyloric and cardiac sections.

Fibrinous gastritis

Fibrinous gastritis is rare, develops in severe infectious diseases (smallpox, scarlet fever, sepsis, etc.), as well as poisoning with sublimate, acids, etc., which determines the wedge, picture, treatment and prognosis.

Phlegmonous gastritis

Phlegmonous gastritis occurs, as a rule, primarily due to infection directly in the wall of the stomach. It is caused by streptococcus, more often hemolytic, often in combination with Escherichia coli, less often by staphylococcus, pneumococcus, Proteus, etc. Sometimes it develops as a complication of an ulcer or decaying stomach cancer, with an injury to the abdomen due to damage to the gastric mucosa. Phlegmonous G. can develop a second time with some infections - sepsis, typhoid fever, etc.

Wedge, picture of phlegmonous G. characterized by an acute onset, fever, chills, severe adynamia and pain in the upper abdomen, usually aggravated by palpation, nausea and vomiting. The general condition is deteriorating sharply. Patients refuse to eat and drink; exhaustion sets in quickly. In the peripheral blood - neutrophilic leukocytosis, toxigenic granularity in granulocytes, accelerated erythrocyte sedimentation, changes in the ratio of protein fractions and other reactions.

Complications with phlegmonous G.: purulent diseases chest - mediastinitis (see), purulent pleurisy (see) and abdominal cavity - subdiaphragmatic abscess (see), thrombophlebitis of large vessels (see Thrombophlebitis), liver abscess (see), etc.

Diagnosis phlegmonous G. before surgery is very rare.

It is often recognized on the operating table or at autopsy.

Treatment phlegmonous G. consists mainly in the parenteral administration of broad-spectrum antibiotics in large doses. With the ineffectiveness of conservative treatment, surgical intervention is indicated.

Forecast phlegmonous G. is serious. After treatment, persistent organic changes in the stomach may remain.

Chronic gastritis

Chron. G. makes the most part of diseases of a stomach. Often it is combined with other diseases of the digestive system.

Chron. G. - the concept of a wedge.-morphol., it is manifested by a wedge, signs, functional and morphol, changes in various combinations and can occur with various disorders of secretion, but a decrease in gastric secretion is more characteristic. Function of acid formation at hron. G. is disturbed earlier and more often than enzyme-forming and excretory.

There are many various classifications hron. D. The classification according to Ryss (1966) is given.

I. By etiological grounds

1. Exogenous gastritis: prolonged violations of the diet - the qualitative and quantitative composition of food; abuse of alcohol and nicotine; action of thermal, chemical, fur. and other agents; the influence of occupational hazards - systematic sampling of raw meat seasoned with spices (canning industry), ingestion of alkaline fumes and fatty acids (soap, margarine and candle factories), inhalation of cotton, coal, metal dust, work in hot shops, etc.

2. Endogenous gastritis: neuro-reflex (patol, reflex effect from other affected organs - intestines, gallbladder, pancreas); G., associated with violations in Art. n. with. and endocrine organs; hematogenous G. (hron, infections, metabolic disorders); hypoxemic G. (hron, circulatory failure, pneumosclerosis, pulmonary emphysema, cor pulmonale); allergic G. (allergic diseases).

II. According to morphological features

1. Surface.

2. Gastritis with glandular lesions without atrophy.

3. Atrophic: a) moderate; b) expressed; c) with the phenomena of restructuring of the epithelium; d) atrophic-hyperplastic; other rare forms of atrophic (phenomena of fatty degeneration, lack of submucosa, formation of cysts).

4. Hypertrophic.

5. Antral.

6. Erosive.

III. On a functional basis

1. With normal secretory function.

2. With moderate secretory insufficiency: the absence of free hydrochloric acid on an empty stomach (or a decrease in its concentration after a trial stimulus below 20 titers, units); a decrease in the concentration of pepsin after a trial stimulus to 1 g%, the concentration of mucoprotein is below 23%, positive reaction on the introduction of histamine, the normal content of uropepsinogen.

3. With a pronounced secretory insufficiency: the absence of free hydrochloric acid in all portions gastric juice, decrease in the concentration of pepsin (or its complete absence), absence (or traces) of mucoprotein, histamine-refractory reaction; decrease in the content of uropepsinogen.

IV. By clinical course

1. Compensated (or remission phase): absence of a wedge, symptoms, normal secretory function or moderate secretory insufficiency.

2. Decompensated (or exacerbation phase): the presence of a distinct wedge. symptoms (with a tendency to progression), persistent, difficult to treat, pronounced secretory insufficiency.

V. Special forms of chronic gastritis

1. Rigid.

2. Giant hypertrophic (Menetrier's disease).

3. Polypous.

VI. Chronic gastritis associated with other diseases

1. With Addison-Birmer anemia.

2. With a stomach ulcer.

3. With cancer.

Hron, gastritis is a polyetiological disease, is the result of untimely and insufficient treatment of acute G., as well as prolonged malnutrition, eating foods that irritate the gastric mucosa (spices, onions, garlic, pepper), addiction to hot food and drink, bad chewing food, eating dry food, frequent use of alcoholic beverages, malnutrition, especially with a lack of protein, vitamins and iron. The reason may be the long-term use of certain medications (quinine, atophane, foxglove, salicylates, butadione, prednisolone, sulfanilamide drugs, potassium chloride, antibiotics, etc.), the influence of factors such as inhalation of cotton, metal, coal dust, alkali vapors and k- t. Disorders in the endocrine system (diabetes, gout) can cause the development of structural changes in the gastric mucosa. The release through the gastric mucosa of metabolic products such as acetone, indole, skatole, like toxins in infectious diseases and local foci of infection, causes the development of the so-called. elimination G. Hron, diseases of the digestive system (appendicitis, cholecystitis, colitis, etc.) are especially important in the development of hron. G. Often hron. G. develops in diseases that cause tissue hypoxia (hron, circulatory failure, pneumosclerosis, anemia).

From blood serum of patients hron. G. antibodies were isolated, with the help of which a model of an autoimmune lesion of the stomach was reproduced. However, the pathogenetic nature of circulating gastric antibodies has not yet been elucidated. There are data on a role of genetic factors in developing hron. G. In patients with a severe form of atrophic G., relatives of the first degree of kinship are predisposed to this disease, which is manifested by the early (at a young age) onset of G. and its rapid transformation into a severe form.

The pathogeny is difficult and not identical at various forms hron. G. At hron. G., developed from acute, there is a progression of primary inflammatory changes in the stroma and the development of secondary dystrophic-regenerative changes in the glandular apparatus (atrophy, hyperplasia, metaplasia, etc.). Development mechanism individual forms hron. G., etiologically associated with various malnutrition and neuroreflex effects on the stomach, is reduced to functional secretory-motor disorders of the stomach (see) with subsequent structural changes in its glandular apparatus and the development of an inflammatory process in the stroma. Changes in the secretory activity of the stomach and neuroreflex influences from the affected organ, in turn, cause disruption of the activity of other organs of the digestive apparatus.

On morfol, to signs distinguish superficial G., various stages of an atrophy of a mucous membrane. Ts. G. Masevich (1967) distinguishes G. with lesions of the glands by atrophy of the mucous membrane and G. atrophic. Schindler (R. Schindler, 1968) and Elster (K. Elster, 1970) allocate hypertrophic G.

The results of histochemical, and electron microscopic examination of the biopsy material suggest that the forms hron. G. are phases of disturbance fiziol, regeneration of a mucous membrane of a stomach. According to M. Siurala et al. (1963, 1966), Ts. G. Masevich (1967) and others, superficial G. passes into G. with damage to the glands, and then into atrophic. Surala et al. (1968) believe that this process takes approx. 17 years.

Chronic superficial gastritis It is characterized by a picture of mucus hypersecretion, sometimes with a predominance of the excretion phase over the secret accumulation phase: there are no neutral mucopolysaccharides in the apical section of the cells, and a large amount of mucus on the cell surface. The presence of PAS-positive granules above the nuclei indicates increased mucus synthesis (see PAS reaction). Occasionally, the epithelium lining the gastric fields and pits appears flattened, with a narrow mucoid band, sparse supranuclear granules, and high RNA content. Granular and vacuolar dystrophy of the epithelium, infiltration by lymphoid and plasma cells of the own membrane of the ridges is revealed (printing, table, Fig. 4). Accessory cells, normally located in the isthmus of the gastric glands, often extend to their middle third.

With chronic gastritis with glandular lesions the surface epithelium of the mucous membrane is flattened, there is a deepening of the gastric pits, additional glandulocytes are hyperplastic.

In the main glandulocytes, vacuoles (Fig. 1) containing neutral mucopolysaccharides are detected (printing table, Fig. 5). In the cytoplasm of these cells, among the granules of the zymogen, shapeless masses are found, sometimes surrounded by a membrane. These masses are similar to "immature" or "mature" mucoid. In the supranuclear zone, a developed lamellar complex (Golgi) with expanded cisterns is revealed (Fig. 2). Thus, elements of both the main (zymogen, RNA, ergastoplasm) and additional glandulocytes (neutral mucopolysaccharides, a well-developed lamellar complex) are found in these cells. These cells are apparently immature chief glandulocytes of the isthmus of the gastric glands. As a result of slowing down their differentiation, they occupy the territory of mature main glandulocytes. Additional glandulocytes are also "immature", with a developed lamellar complex and ergastoplasm; they are found in those parts of the glands where they are not usually observed.

Chronic atrophic gastritis characterized by a decrease (sometimes significant) in the number of main and additional glandulocytes, deepening of the gastric pits (printing. Fig. 7 and coloring, tables. Fig. 6 and 7), which often have a corkscrew-like appearance (Fig. 3), hyperplasia of additional glandulocytes. The epithelium covering the gastric fields and pits is often flattened, contains a lot of RNA and few neutral mucopolysaccharides, in some places it is replaced by intestinal epithelium (printing table Fig. 8) with typical enterocytes, goblet cells and Paneth cells (intestinal metaplasia). The gastric glands are often replaced by mucous glands (pyloric metaplasia). The surviving main glandulocytes are vacuolized; in the parietal glandulocytes, the cytoplasm is rarefied in the perinuclear zone and around the intracellular tubules, as well as a decrease in the number of microvilli and tubulovesicles; reduction of cristae of mitochondria of parietal glandulocytes is noted.

Wolf (G. Wolf, 1968) identifies three stages of atrophy of the gastric mucosa: incipient atrophy, with a cut of the gland is not yet shortened, but looks as if squeezed; partial atrophy (glands), at a cut the groups of glands containing the main and parietal (obkladochny) glandulocytes are kept; total atrophy of the glands (atrophy of the mucous membrane), when the main and parietal (parietal) glandulocytes are not detected, the glands are lined only with mucus-forming epithelium.

Chronic hypertrophic gastritis- thickening of the mucous membrane and increased proliferation of the epithelium (printing. Fig. 6, color. table Fig. 9 and Fig. 7).

There are three forms hron, hypertrophic G.: interstitial, proliferative, glandular. The interstitial form is characterized by abundant lymphoplasmacytic infiltration occurring at the edges of ulcers; for proliferative - proliferation of the surface epithelium, deepening of the dimples, glandular apparatus unchanged; in the glandular form, the mucous membrane is thickened by 2-7 times due to hyperplasia of the glands; this form hron. G. occurs with duodenal ulcer (see. Peptic ulcer), Zollinger-Ellison syndrome (see. Zollinger-Ellison syndrome) and how independent disease. Some authors carry hron to a glandular form. G. and Menetrier's disease, designating it as gastritis hypertrophica gigantea, although Menetrier himself considered this condition of the mucous membrane not as hypertrophic G., but as a "creeping adenoma". Most authors (Yu. N. Sokolov, P. V. Vlasov, etc.) deny the connection of Menetrier's disease with G., considering it as an anomaly in the development of the gastric mucosa.

clinical picture. Depending on a condition of secretory function of a stomach distinguish hron. G. with normal and increased secretion and hron. G. with secretory insufficiency.

Chronic gastritis with normal and increased secretion occurs usually at a young age, more often in men. The main symptoms are dyspeptic disorders and pain, which usually appear during an exacerbation of the disease, after errors in the diet, drinking alcoholic beverages, including table wines and beer. Patients complain of heartburn, sour belching, a feeling of pressure, burning and fullness in the epigastric region, constipation (sometimes diarrhea), and rarely vomiting. The pains are usually dull, aching, without definite irradiation, localized in the epigastric region, their occurrence is usually associated with food intake. But pains can be both “hungry”, and “nightly”, and subside after eating.

Early complications - motor disorders of the intestines and biliary tract (hyper- and hypomotor dyskinesias). Further functional disorders are replaced by organic changes, and then develop hron, cholecystitis (see), hron. pancreatitis (see), hron, enterocolitis with metabolic disorders - hypovitaminosis, Iron-deficiency anemia and others (see Enteritis, enterocolitis).

Massive bleeding from the gastric mucosa is possible, which averages half of non-ulcer bleeding. In this case, they talk about the so-called. hemorrhagic gastritis. Hemorrhagic gastritis - the concept of a wedge.; morfol, its picture can be various. Bleeding at G. is most often connected with development of erosions, but sometimes the mechanism of bleeding remains not clear even after gistol, a research of the resected part of a stomach. A certain importance in the occurrence of gastric bleeding is attached to the acidity of gastric juice (the higher the acidity, the more bleeding). Abundant gastric bleedings develop usually at patients with insignificant wedge, manifestations at which permeability of blood vessels of a stomach is considered to be increased. The cause of massive gastric bleeding may be allergic reactions (see Gastrointestinal bleeding).

Special wedge.-morfol. form hron. G. with normal and increased secretion is gastroduodenitis (synonym: pyloroduodenitis, hypertrophic glandular G., hypertrophic hypersecretory gastropathy), which occurs mainly at a young age. It is similar on a wedge, to displays with a peptic ulcer of a duodenum though is not identical to it. I. M. Flekel (1958) considered gastroduodenitis to be a prestage of peptic ulcer or a form of "peptic ulcer without an ulcer." The frequency of the disease (during the day and year) is less pronounced than with peptic ulcer. From a wedge, symptoms the pains ("painful gastritis") which are localized usually under a xiphoid shoot or to the right of it are most characteristic. Often there is a combination of pain immediately after eating with "hungry" and "night" pain.

The secretory and acid-forming functions of the stomach are usually enhanced, but less than with a duodenal ulcer: the value of basal secretion is up to 10 meq/hour, and the maximum is 35 meq/hour (Yu. I. Fishzon-Ryss, 1972). Often there is abundant gastric secretion at night.

Chronic gastritis with secretory insufficiency more common in adults and the elderly. In patients, weight usually decreases, adynamia appears, symptoms of multivitamin deficiency are detected - dry skin, looseness and bleeding of the gums, changes in the tongue (thickening, redness, smoothness of the papillae, the presence of imprints of teeth), cracks on the lips, in particular in the corners of the mouth. Of the gastric symptoms, there is a violation of appetite and the desire to eat spicy and spicy foods outside the period of exacerbation. Some patients cannot accept solid food without liquid, to-ruyu they drink before meal and in the course of meal. Patients note an unpleasant taste in the mouth, especially in the morning, nausea, a feeling of fullness and fullness in the epigastric region, belching with air. The chair is unstable with a tendency to diarrhea. Dyspeptic phenomena usually occur shortly after eating, especially patients tolerate milk poorly. In some cases, nausea and salivation are persistent and painful for patients, and they seek to alleviate their condition by frequent meals. Sometimes there is pain in the epigastric region.

Complications - hypermotor dysmnesia of the intestine or involvement in patol, the process of the pancreas and gallbladder. Gastric bleeding is rare. At a part of patients allergic reactions to a nek-eye food and medicinal substances are found.

Sometimes (more often in women) iron deficiency anemia develops (see). Often there are changes in the intestines, the exocrine function of the pancreas decreases, dysbacteriosis develops (see), manifested by fermentative or putrefactive dyspepsia.

Special forms hron. G. (rigid, polypous and giant hypertrophic) are distinguished by their originality wedge, manifestations and morphol, features. Some researchers carry these forms to complications hron. G.

Rigid gastritis first described by A. N. Ryzhykh and Yu. N. Sokolov (1947). It is manifested by persistent dyspepsia (see) and achlorhydria (see). The diagnosis is established at rentgenol. research and on the basis of gastroscopy data. The outlet section of the stomach is mainly affected, which, due to hypertrophic changes, edema and spastic contraction of the muscles, is deformed, turning into a narrow tubular canal with dense rigid walls.

Polypous gastritis(tsvetn. fig. 8) usually develops against the background of atrophic G. with histamine-refractory achlorhydria, it can be considered as a further progression hron. G. (dysregenerative hyperplasia of the mucous membrane).

Giant hypertrophic gastritis or, more precisely, the excessive development of the mucous membrane described by Menetrier (P. Menetrier, 1886) is a relatively rare disease manifested by metabolic disorders (often protein) and very rarely by the development of iron deficiency anemia. The change in the acid-forming function of the stomach is different (see also the table).

The diagnosis is based on the analysis of the wedge, the manifestations of the disease, the results of the study gastric secretion(see Stomach, research methods), rentgenol, research, gastroscopy data (see) and gastrobiopsy.

In an assessment morfol, pictures of a mucous membrane of a stomach it is necessary to give preference to data of a gastrobiopsy. Exfoliative cytodiagnosis, determination of the absorption and excretory functions of the stomach are of secondary importance.

Certain difficulties arise in the differential diagnosis with functional disorders of the stomach, stomach cancer (see Stomach, tumors) and peptic ulcer (see).

At functional disturbances of a stomach usually there are no sharp morfol, changes. In addition, they have a relatively short-term (up to 1 year) course, less dependence of the occurrence of pain on food intake, greater wedge variability. manifestations, which is associated with neuropsychic influences, atypical localization of pain on palpation of the abdomen, and, finally, a sharp fluctuation in acidity in separate studies.

Radiodiagnosis is based on careful rentgenol, a research of a stomach. At the same time, restructuring of the relief of the gastric mucosa and other radio-functional and morfol symptoms are determined. These include: excessive secretion on an empty stomach, a rapid increase in secretory fluid, changes in tone, persistent deformation of the pyloric part of the stomach, impaired peristalsis, etc. The most constant symptom of increased secretion on an empty stomach, sometimes manifested by a horizontal level of fluid against the background of the gastric bladder before taking barium suspension. The first one or two sips of barium suspension confirm the presence of excess liquid. By the nature of the mixing of barium with a liquid, one can to a certain extent judge the amount of mucus contained in it: slow mixing with the formation of shapeless flakes indicates the presence of mucus. Another symptom of the presence of mucus (mucus phenomenon) is small-point enlightenment in the barium suspension layer - the smallest droplets of mucus suspended in the barium suspension. The mucus phenomenon is indistinguishable by transillumination and can only be ascertained on images with compression. Chron. G. is more often accompanied by a decrease in the tone of the stomach. An increase in tone often has a local character; at antral G. it is shown by spastic states or motive excitation of an output part of a stomach. Violation of peristaltic function is not always detected. Approximately in a half of cases hron. G. observed superficial and rare peristalsis. Severe disorders of peristalsis up to the appearance of an aperistaltic zone are observed with the so-called. rigid antral G. The evacuation of barium from the stomach usually occurs at normal times, although occasionally it can be delayed.

Forms hron. G. radiologically differ hl. arr. according to the nature of the relief of the mucous membrane. According to Schindler-Gutzeit's classification, hypertrophic G., atrophic G., mixed G., superficial hron, mucous catarrh are distinguished. In turn, hypertrophic G. has subspecies: polypous, warty, ulcerative, or erosive. However, this classification is outdated and needs to be revised, since the inaccuracy rentgenol is proven. criteria for hypertrophy and atrophy of the mucous membrane; besides, at hron. G., as a rule, atrophic processes progress.

On the basis of opportunities rentgenol. of a method distinguish: hron, universal G., hron, antral G. and its wedge, and rentgenol, versions (including rigid antral G.); hron, polypous (warty) G.; hron, granular G.; erosive G.; so-called accompanying gastritis (concomitant), for example, with peptic ulcer.

Rentgenol, data hron. G. can be taken into account only with an appropriate wedge, picture, anamnesis, etc. Numerous facts are known when severe rentgenol, G.'s symptomatology was not confirmed by biopsy data and, conversely, morphologically proven G. was not manifested radiographically.

At hron, universal G. the area of ​​the reconstructed relief is usually very extensive (also the body of a stomach is captured). As a result of edema, hyperemia and inflammatory cell infiltration, mainly of the submucosal layer and connective tissue stroma, the mucosal folds swell unevenly (Fig. 4 and 5), sometimes so significantly that their number decreases. In some places, the folds form polyp-like thickenings and have a distinct appearance (Fig. 6). Along the greater curvature, oblique and transversely located bridges between the folds thicken, therefore the contour of the greater curvature, ch. arr. the lower half of the body of the stomach and sinus, becomes serrated and fringed. With severe edema, the mucous membrane loses its plasticity, which is accompanied by a symptom of relief rigidity. Inflammatory reorganization of a relief of a mucous membrane at hron. G. is sometimes so disorderly and chaotic that it is difficult to distinguish it from an atypical relief at stomach cancer. Series only sighting shots relief of the mucous membrane help to establish the still remaining variability of its pattern. In difficult cases it is useful to resort to pharmacol, stimulation of peristalsis (morphine).

The described changes in the relief of the mucous membrane are not specific for G. Similar pictures can occur with allergic edema of the mucous membrane, with systemic diseases, etc. An important help in the X-ray diagnosis of hron, universal G. is a symptom of hypersecretion, as well as signs of the presence of mucus in the gastric contents on an empty stomach.

Hron, antral G. carry to the most often found varieties hron. D. It has a bright, diverse, and most importantly, the most convincing X-ray semiotics. Rentgenol, the picture is characterized by signs of hypersecretion, the phenomenon of mucus, patol, restructuring of the relief of the mucous membrane. In addition, deformation of the antrum and a violation of its peristalsis are detected. The relief pattern varies: often sharply swollen, widened folds, but retaining the usual longitudinal direction, their number is reduced. With pronounced edema, they form shapeless, pillow-shaped relief defects, the grooves between the folds disappear, the relief is smoothed out. A classical example of a relief at hron. G. of the antrum are quite persistent thickened transverse folds of the mucous membrane (Fig. 7), along the greater curvature of the stomach - an uneven contour in the form of uniform serrations. At it is long proceeding hron. G. with secretory insufficiency, the relief is disordered and consists of shapeless bulges (defects) and spots and barium strips randomly located between them. In some cases, relief atypia occurs due to increased mobility of the swollen mucosa relative to the loose, inflammatory submucosa. With a wide pyloric canal, partial prolapse of the mucous membrane into the duodenal bulb is possible. With a normal pyloric lumen, the gastric mucosa does not fall out. However, the periodically “sliding” mucous membrane, accumulating in front of the pylorus, forms a kind of defect here, resembling a tumor lesion (Fig. 8). This “creeping phenomenon” of the mucous membrane was first explained and described by Yu. N. Sokolov and V. K. Gasmaeva (1969).

Due to the thickening of the circular and longitudinal muscles, the antrum of the stomach is deformed: it narrows and shortens, in contrast to the deformation in infiltrating cancer, with Krom, the lumen of the pyloric part of the stomach only narrows, but does not shorten. As the process progresses, the walls of the antrum become thicker, lose their elasticity, and the deformation becomes persistent. As a result of an inflammatory submucosal sclerosis (so-called sclerosing G.) the peristalsis disappears and there is a rigid antral G. which, undoubtedly, is a late stage hron, antral G. with secretory insufficiency. At these patients quite often on the basis a wedge, data suspect a cancer of a stomach that is often difficult to refute at rentgenol, a research. Deformation of the antrum is very pronounced and has a persistent character. Attention is drawn to the circular narrowing of the pyloric part of the stomach, with Krom its simultaneous shortening often goes unnoticed (Fig. 9). On palpation, a feeling of a dense and painful tumor is created. The presence of cancer is indicated by a symptom of the aperistaltic zone, usually involving the entire antrum. Observation of at least short-term peristalsis testifies against cancer, edges can be caused also by means of morphine.

At polypous (warty) G. patol, changes are often localized in antrum. They are multiple homogeneous in size, rounded, unsharply outlined defects dia. 3-5 mm, sometimes in the form of elevations on the ridges of the folds, but more often forming a disordered or honeycomb pattern (Fig. 10). With true polyps, even multiple ones, the relief of the gastric mucosa is usually not changed. At polypous G., as a rule, also other rentgenol, symptoms are found. With smaller growths, G. is called warty, or verrucous; small defects are usually recognized only on targeted images with compression.

Granular gastritis is recognized by the symptom of "granularity" of the relief (Fig. 11). This symptom was studied by Frick (W. Frik) with the help of relief images of a sharp-focus X-ray tube at short exposures (no more than 0.1 sec.). This creates the impression of a granular surface of the mucous membrane with the smallest elevations - the so-called. gastric fields. Comparison of data from the "thin relief" study with the results of gastrobiopsy revealed a parallelism between the picture of gastric fields and the presence of inflammatory changes in the mucous membrane. If under normal conditions the diameters of the fields are 0.5-1.5 mm, then with hron. G. gastric fields become more convex - "granular" type, and in advanced cases - and larger (3 mm in diameter or more), uneven, resembling a warty surface. Along with this symptom it is necessary to find also other above rentgenol, G.'s signs.

Erosive G. is seldom recognized radiographically since opportunities of detection of erosions rentgenol, a research method are very limited.

So called. the accompanying (accompanying) G. is constantly found radiologically at a peptic ulcer (an exception make so-called senile ulcers of a stomach) and is more rare at a cancer of a stomach.

The expressed pictures of the accompanying G. are observed at an ulcer of a duodenum, after operation of a gastroenterostomy. At the accompanying G. the output part of a stomach is more often surprised. All above described rentgenol are observed also. symptoms G. Often there is a rough pattern of the relief of the mucous membrane, disorder and swelling of the folds. Dynamic klin. - rentgenol, supervision over the accompanying G.'s course at a peptic ulcer show that if under the influence of conservative treatment the ulcerative "niche" disappears, and other rentgenol, G.'s symptoms remain without changes, then, as a rule, patients do not note improvement.

At rentgenol, a research known difficulties can represent recognition of polyposis G. which should be differentiated from true polyps of a stomach. At diagnosis hron. antral G. it is necessary to mean also pernicious anemia, at a cut polymorphic changes of a relief of a mucous membrane of a pyloric part of a stomach can be observed.

In addition to rigid antral gastritis, it is necessary to take into account other types of antral gastritis with a sharp restructuring of the relief of the mucous membrane, which is sometimes indistinguishable from the atypical relief in cancer. Of particular importance in this sense is the above-described "phenomenon of the creeping of the mucous membrane." In case of difficulties, a series of photographs or X-ray cinematography, fibroscopy and gastrobiopsy are used. With the so-called system diseases only careful analysis of all a wedge, pictures allows to come to the correct diagnosis.

See also Stomach, X-ray diagnostics.

Treatment complex and differentiated. Treatment is usually done on an outpatient basis; patients are hospitalized with exacerbations, especially those with complications and severe general disorders.

Health food in G.'s complex therapy has a leading value. During an exacerbation hron. G., regardless of the nature of secretory disorders, observe the principle of sparing the gastric mucosa and its functions. Food should be well cooked and chopped. Foods and dishes that have a strong juice effect, as well as causing mechanical, thermal and chemical reactions, are excluded from the diet. irritation of the gastric mucosa. Assign a diet 1A (see Therapeutic nutrition). Food is fractional, 5-6 times a day. As the exacerbation subsides, diet therapy is carried out in accordance with secretory disorders.

With secretory insufficiency of the stomach (without exacerbations), the diet should be complete with a sufficient amount of proteins (110-115 g), fats (80-90 g), carbohydrates, vitamins; it should correspond to the calorie content of labor activity and the patient's lifestyle. Assign diet number 2. Food must be taken 4-5 times a day. The diet includes a normal amount of salt and extractives. With a stable remission, you can prescribe extended nutrition. Fresh bread and other fresh dough products, fried (including breaded) meat and fish, fatty meats and fish, spicy, salty dishes, canned fish, cold drinks, ice cream are prohibited.

With normal and increased secretion, they begin with the appointment of table 1A, after 7-10 days they go to table 1B, and after the next 7-10 days - to diet No. 1. The diet should be complete, but with restriction of salt, carbohydrates and extractives, especially with high acidity. At night, milk laxatives are recommended (fresh kefir, yogurt). Shchi, borscht, fatty meat, fried fish, pickles, smoked meats, marinades, raw vegetables are prohibited. Alcohol, beer, carbonated water, fruit water are strictly contraindicated.

Medical treatment of patients hron. G. provides influence on pathogenetic links patol, process. For normalization of a functional state of the higher departments of c. n. with. recommend preparations of valerian, small tranquilizers, sleeping pills.

With increased secretory and motor-evacuation function of the stomach, anticholinergic drugs (atropine, platifillin, spasmolytin, benzohexonium) should be prescribed in combination with antacids (vikalin, almagel, etc.) and agents that stimulate regenerative processes (methyluracil, pentoxyl, licorice preparations, etc. ).

With secretory insufficiency, anticholinergic drugs are prescribed, similar to quateron and gangleron, which cause a pronounced antispasmodic effect, but have relatively little effect on the secretory function of the stomach. A good wedge, the effect is achieved with the use of Caucasian Dioscorea, plantain juice, plantaglucid, which cause a slight increase in secretion, enhance the motor function of the stomach and have anti-inflammatory and antispasmodic effects. In order to influence the secretory function of the stomach, vitamins PP, C, B 6 and B 12 are also prescribed.

Outside the period of exacerbation, substitution therapy is used - gastric juice, abomin, betacid, pancreatin, etc.

Physical methods of treatment are also included in the complex to lay down. activities: heating pads, mud therapy, diathermy, electro- and hydrotherapy.

Sanatorium-and-spa treatment of patients with chronic gastritis is carried out without exacerbation of the disease. The resorts with mineral waters for drinking treatment are shown: Arzni, Arshan, Berezovsky mineral waters, Borjomi, Izhevsk, Jalal-Abad, Jermuk, Druskininkai, Essentuki, Zheleznovodsk, Pyatigorsk, Sairme, Feodosia, Shira, etc. Mineral waters can also be used in non-resort conditions: in case of secretory insufficiency, it is preferable to use chloride, chloride-bicarbonate waters for 15-20 minutes. before meals, and with normal and increased secretory function - bicarbonate water 1 hour before meals.

Treatment hron. G. is possible in local sanatoriums, as well as under the usual regimen under the conditions of diet.

The prognosis for life is favorable. Under the influence of treatment, the well-being of patients improves relatively quickly. But the main morfol, the changes characteristic of hron. G., as well as the secretory function of the stomach, are not normalized under the influence of treatment. At massive bleeding at patients hron. G. with normal and increased secretion, the prognosis is more serious, as well as in patients with insufficient secretory function when they develop anemia, gastritis enterocolitis with impaired absorption processes and involvement in patol, the process of other organs of the digestive apparatus (hron, pancreatitis, hron, cholecystitis, etc.). At special forms hron. G. (rigid, polypous, giant hypertrophic) there is a danger of malignancy.

Prevention hron. G. consists in a rational diet and compliance with the rules of food hygiene, as well as in the fight against the use of alcoholic beverages and smoking. It is necessary to monitor the condition of the oral cavity, timely treat diseases of other abdominal organs, eliminate occupational hazards and helminthic-protozoal invasions. Clinical examination of patients with G. is of great importance.

Gastritis in children

Acute gastritis in children occurs due to infection, consumption of infected, indigestible food, overeating, and as a manifestation of allergies. Its etiology, clinic and treatment methods are similar to acute gastritis in adults.

Chronic gastritis occurs mainly in preschool and school age; its prevalence in school-age children is higher.

Causes of occurrence hron. G. are irrational nutrition and regimen, various diseases of the digestive and other systems, infection, allergies, as well as congenital features of the neuro-endocrine system and impaired synthesis of hydrochloric acid, which is confirmed by the presence of persistent achylia (in practically healthy and sick G. children), to -ruyu cannot be explained either by previous diseases or by malnutrition.

At children with long diseases and disturbances went. - kish. path hron. G. as an independent disease is rarely observed. At the same time, the study of the gastric mucosa by gastrobiopsy changed the idea of ​​the prevalence of G. in children: a wedge, G.'s diagnosis is confirmed only in half of the cases. At children of the senior school age and teenagers hron. G. becomes quite a frequent disease.

Morphologically, superficial gastritis and gastritis with glandular lesions without atrophy predominate in children; atrophic gastritis is less commonly observed (some authors do not find it in children).

The disease usually occurs gradually, has relatively little effect on the development of the child, has a milder course than in adults, and is easier to treat; sometimes there is a persistent flow.

Distinguish two forms hron. G. in children - oligosymptomatic and a form with severe symptoms, often similar to peptic ulcer. The asymptomatic course of G.

An oligosymptomatic form hron. G. is less common than the form with severe symptoms; often occurs in children of an earlier age: the pain usually appears after eating, is of low intensity, localized in the epigastrium or spilled. Dyspeptic phenomena in some children are absent. The acid-forming function of the stomach is reduced or histamine reflex achylia is determined.

At hron. G. with severe symptoms, the pain symptom is intense, it can occur immediately after eating, after 1 to 2 hours or at night. Dyspeptic symptoms are constant. The acid-forming function in most sick children is increased during long-term follow-up. In some children, peptic ulcer disease is further detected, in this case G. is essentially a pre-ulcerative condition.

G.'s diagnosis is established on the basis of a combination of anamnesis data, a wedge, manifestations and laboratory tests.

Differential diagnosis hron. G. in children is carried out with peptic ulcer (see), diseases of the liver (see), bile ducts (see Bile ducts) and diseases of the nervous system. Taking into account an exclusive rarity of malignant new growths of a stomach at children and easier, than at adults, a current hron. G., there are no sufficient grounds for widespread use in pediatric practice of the method of gastrobiopsy for diagnostic purposes. It is used only under strict indications and always in a specialized clinic in order to exclude possible complications.

Treatment of gastritis in children is basically the same as in adults (taking into account the age and form of the disease).

At G., similar on clinic to a peptic ulcer, treatment is carried out as antiulcer, including seasonal prophylactic courses.

Prevention hron. G. in children has the same principles as in adults.

The special attention is demanded by the constitutionally weakened children with signs of dysfunction went. - kish. tract (increased acid-forming function, achilia, etc.), with residual effects after past illnesses digestive and other systems.

Sick hron. D. children are subject to supervision by a pediatrician in order to prevent exacerbations of the disease, conduct preventive anti-relapse courses of treatment and recreational activities.

Gastritis in the elderly and senile age

Features of the course of G. are due to age-related changes in the digestive organs and a decrease in overall reactivity. A wedge, manifestations of G. at patients of advanced and senile age are less expressed, than at young. Dyspepsia and pain are relatively mild, and there is rarely a decrease in appetite. The digestive capacity of gastric juice and the content of gastromucoproteins in it is reduced, as well as the acid-forming function of the stomach. The electropherogram of gastric juice proteins compared to the electropherogram of young patients has a more “compressed” appearance, the debit of the protein component is lower in both fractions of gastric mucus, and the carbohydrate component is increased in insoluble mucus. A vitreous basal secret is often found - a jelly-like mass with a large number of desquamated mucosal cells. Atrophic changes in the gastric mucosa (according to aspiration biopsy) and secretory insufficiency occur in patients hron. G. over the age of 60 years is 2-3 times more common than in 30-40-year-olds. After 60 years, atrophic G. is more often observed in women, while at a younger age it is more often in men. The big prevalence of atrophic G. at advanced age is connected, apparently, with frequent development at this age hron, the diseases of a liver, pancreas, intestines promoting development hron. G.

Treatment and prevention are under construction taking into account accompanying hron, diseases and features of reaction of an elderly organism to introduction of medicinal substances. When determining the prognosis, one should keep in mind the possibility of cancer on the background of hron, atrophic G.

experimental gastritis

In order to study the patterns of activity and mechanisms of regulation of the digestive system in pathological conditions, as well as the development of questions of G.'s therapy on animals, G.'s model is reproduced.

There are two groups of models of experimental G., which are used depending on the objectives of the study: a) G., caused by local impact various damaging agents on the gastric mucosa; b) G., caused by unusual conditions of contact of normal acidopeptic factors with the gastric mucosa.

To damage the gastric mucosa of animals, hot and cold water is used, as well as chemical. substances (1 - 10% solutions of silver nitrate, 1% acetic and 10% hydrochloric acid, solutions of alcohol, infusion of mustard, red pepper, etc.), which are once or repeatedly injected into the stomach cavity. With such exposure to a damaging agent, it cannot be excluded that it enters the initial section of the duodenum, which complicates the picture of functional and morphol disorders and cannot always be taken into account. There are methods of limited damage to the gastric mucosa, reproducing focal G., usually acute. At repeated damages experimental acute G. can pass into hron, a form. Of practical interest in the models of this group is experimental gastritis caused by the introduction of various volumes of alcohol of different concentrations into the stomach.

IP Pavlov created models of experimental G., directly damaging the stomach and observing the work of an isolated ventricle. He established the compensatory ability of the preserved mucous membrane, analyzed in detail the complex complex of intra-systemic and extra-systemic reactions in the body in response to damage to the stomach. IP Pavlov initiated the classification of types of disorders of gastric secretion, which is used in the clinic.

G.'s model caused by creation nefiziol. conditions of contact of normal secretion products of the gastric glands (acidopeptic factors) with the mucous membrane, is achieved by prolonged repeated imaginary feeding (gastric juice remains in the stomach cavity), the addition of hydrochloric acid or gastric juice to food in excess. Experimental violation fiziol. the ratio between free and bound hydrochloric acid in the stomach also has a damaging effect on the mucous membrane.

Experimental G. can also be caused by a change in the spectrum of proteolytic enzymes or by the introduction of histamine or pilocarpine. This G.'s model develops gradually against the background of disturbances of microcirculation and trophic processes in a mucous membrane, has hron, a current.

Clinical and diagnostic characteristics of some clinical forms of chronic gastritis

chronic gastritis	Main Clinical signs	Data from the study of gastric secretion	X-ray research	Gastroscopy data	Biopsy data
Antral	Pain in the epigastric region hungry, nocturnal, sometimes subsiding after eating; heartburn, belching sour, often vomiting at the height of pain. Tendency to constipation	Increased	The relief of the mucous membrane in the antrum is changed: thickening of the longitudinal folds, patol. restructuring, granular formations, the presence of the phenomenon of mucus. Increased tone and weakening of the peristalsis of the antrum. Signs of hypersecretion. Often deformity of the antrum	In the pyloric part of the stomach, redness of the mucous membrane, swelling of the folds, erosion and hemorrhages in the submucosal layer are found. The tone of the pyloric part is increased, sometimes there is a prolonged pylorospasm. Signs of hypersecretion	Gistol, the picture of a mucous membrane is normal or has signs hron, gastritis of various degree of manifestation. In the antrum - signs of hyperplasia, often a rare location of the pyloric glands, pronounced cellular infiltration of its own layer, areas of intestinal metaplasia
Giant hypertrophic gastritis (Menetrier's disease)	Weight loss, signs of hypoproteinemia, iron deficiency anemia. Persistent gastric dyspepsia. Patients note a feeling of spasm and pressure in the epigastric region. Pains sometimes remind pains at a peptic ulcer; vomiting may be bloody	Decreased, normal or elevated	Pronounced changes in the relief of the mucous membrane along the greater curvature (in the region of the sinus and the lower half or third of the body of the stomach) in the form of excessively located, elastic thickened folds hanging into the lumen of the stomach, and sometimes into the duodenum	The mucous membrane is swollen, with wide sinuous folds covered with mucus, sometimes with warty, polypoid growths.	Hyperplasia of all elements of the mucous membrane
Gastritis with normal and increased secretory function	The general state does not change. Pain in the epigastric region occurs immediately after eating, combined with a feeling of heaviness, fullness. The pains are diffuse, dull, aching, usually moderate, rarely intense, last 1 - 11/2 hours. Heartburn, often belching, intermittent vomiting	Basal secretion increases up to 10 meq/hour, maximum histamine secretion - up to 35 meq/hour. There is often profuse gastric secretion at night.	Widespread restructuring of the relief of the mucous membrane with thickening of the folds (sometimes their cushion-like bulging) until the grooves disappear; smoothness of the relief in the antrum. Violation of tone and peristalsis. Signs of hypersecretion	Redness, hypertrophy of folds, edema, presence of mucus, single erosions and hemorrhages in the submucosa, signs of hypersecretion. With severe hypertrophy, the mucous membrane has a velvety appearance without the usual sheen.	Flattening of the mucous membrane due to hyperplasia of the surface epithelium, less often of the interstitial tissue. The epithelium is often flattened, with a basal arrangement of nuclei of various sizes; flour hypersecretion yes, signs of granular and vacuolar dystrophy; profuse cellular infiltration of the own layer
polyposis	Reminds clinic hron, gastritis with secretory insufficiency; may be asymptomatic. Prolapse of polyps into the duodenum and their infringement is clinically manifested by a pronounced pain syndrome. There may be bleeding	More often reduced	Characteristic changes are more often localized in the antrum - typical small homogeneous rounded filling defects, sometimes on the ridges of the folds, but usually they form a disordered or honeycomb pattern. With true polyps, even multiple ones, the relief of the mucous membrane is usually not changed	Multiple polyps are found, identical or different in shape and size, which are more often located in the pyloric part. The mucous membrane is pale, thinned, its folds are smoothed out, blood vessels are translucent (atrophic gastritis)	Outside the localization of the polyp, the picture of atrophic gastritis
Rigid	Prolonged persistent dyspepsia. In the epigastric region, patients note diffuse moderate pain, often a feeling of heaviness and pressure. A tendency to diarrhea and the development of anemia is revealed	Dramatically reduced	Deformation (narrowing, shortening) of the antrum, restructuring of its internal relief; weakening or disappearance of peristalsis	Deformation, rigidity and narrowing of the pyloric part of the stomach, swelling of the mucous membrane	In output department a picture of atrophic and hyperplastic hron, gastritis. In other departments, atrophy of the glandular apparatus of varying severity
Gastritis with secretory insufficiency	Loss of weight and loss of appetite, feeling of heaviness and pressure in the epigastric region after eating. Pain is moderate and intermittent, nausea, rarely vomiting. Tendency to diarrhea, flatulence; poor milk tolerance, without exacerbation - addiction to sour and salty foods. Often anemia	Basal secretion approx. 0.8 meq/hour, maximum histamine secretion up to 10 meq/hour	The relief of the mucous membrane is smoothed, the tone and peristalsis are often weakened, the evacuation of the contents of the stomach is accelerated	Diffuse or focal thinning of the mucous membrane, its color is pale, dilated blood vessels of the submucosa are clearly visible. The folds of the mucous membrane are small, sometimes covered with mucus, when the stomach is inflated with air, the folds are easily smoothed out. Erosions and petechial hemorrhages are sometimes observed	Various degrees of atrophy of the glands (decrease in the main and parietal glandulocytes), flattening of the mucosal epithelium, deepening of the pits, intestinal and pyloric metaplasia
Erosive gastritis(hemorrhagic)	Pain in the epigastric region: early, on an empty stomach and late; acid heartburn, sometimes vomiting mixed with blood (from traces to clots). The higher the acidity, the more bleeding Tendency to constipation	Normal or elevated	The relief of the mucous membrane is changed more often in the pyloric part of the stomach. The ability to detect erosion is very limited.	Multiple erosions of a rounded or stellate shape are determined, mainly in the outlet section of the stomach, against the background of superficial gastritis phenomena - edema, infiltration, hyperemia of the mucous membrane	Gistol, the picture of a mucous membrane is more often similar to a picture hron, gastritis with the increased secretion. Erosions are more often detected with targeted biopsy

Bibliography: Aruin L. I. Morphological study of biopsies of the gastric mucosa, Arkh. patol., t. 31, No. 3, p. I, 1969; AruinL. I. and Sh and -r about in VG To a question of a morphogenesis of chronic gastritis, in the same place, t. 21, 1971; Belousov A. S. Essays on the functional diagnosis of diseases of the esophagus and stomach, M., 1969, bibliogr.; Gordon OL Chronic gastritis and so-called functional diseases of the stomach, M., 1959, bibliogr.; Gubar VL Physiology and experimental pathology of the stomach and duodenum, M., 1970; Kanishchev P. A. Methods for diagnosing diseases of the stomach, L., 1964; Lazovsky Yu. M. Functional morphology of a stomach in norm and pathology, M., 1947; Levin G. L. Essays on gastric pathology, M., 1968; L and s o ch to and B. G. N, Ultrastructure of the glands of the stomach and its change in conditions of chronic gastritis, Arkh. patol., t. 34, No. 10, p. 11, 1972; Masevich Ts. G. Aspiration biopsy of the mucous membranes of the stomach, duodenum and small intestine, L., 1967; about N e, Pretumor diseases of a stomach, L., 1969, bibliogr.; Menshikov F. K. Diet therapy, M., 1972, bibliogr.; Pavlov I.P. Complete works, vol. 2, book. 2, M.-L., 1951; PeleshchukA. P. Diseases of the system and digestive organs, in the book: Fundamentals of gerontol., ed. D. F. Chebotareva and others, p. 322, M., 1969; Rachvelishvi-l and B. X. Gastrobiopsy in clinical practice, Tbilisi, 1969; P s with S. M. Diseases of the digestive system, L., 1966; Tugolukov VN Modern methods of functional diagnostics of the state of the gastric mucosa and their clinical significance, L., 1965; F and sh-z about N-P s with Yu. I. Modern methods of research of gastric secretion, L., 1972, bibliogr.; about N e, Gastritis, L., 1974, bibliogr.; In about with k u s H. Gastroenterology, at. 1-3, Philadelphia-L.* 1963-1965; Gastritis, hrsg. v. G. Clemenson, Basel, 1973; HafterE. Praktische Gastroenterologie, Stuttgart, 1962, Bibliogr.; M o r s o n B. C. a. Davson, I. M. P. Gastrointestinal pathology, p. 80, Oxford, 1972, bibliogr.; Peleschtschuk A. P. u. a. Funktionelle und morpholo-gische Veranderungen des Magens bei Patienten mil umunischer Gastritis im hoheren Lebensalter, Z. Alternsforsch., Bd 25, S. 271, 1972; Schindler R. Gastritis, N. Y., 1947, bibliogr.; Spiro H. M. Clinical gastroenterology, p. 155, L., 1970; Wolff G. Chronische Gastritis, Lpz., 197 4.

X-ray diagnosis G.- Ryzhykh A. N. and Sokolov Yu. H. Rigid antral gastritis as a precancerous disease of the stomach, Surgery, No. 4, p. 34, 1947; Saghatelyan G. M. X-ray diagnostics of diseases of the esophagus, stomach and gastroscopy, Yerevan, 1966, bibliogr.; Smirnova N.V. Diagnosis of gastritis of the distal stomach, Klin, medical, t. 49, No. 1, p. 69, 1971; With about to about l about in Yu. N. and In l and with about in P. V. Relief of a gastric mucosa in norm and pathology, M., 1968, bibliogr.; Sokolov Yu. N. and Gasmaev V. K. About the phenomenon of "crawling" of the gastric mucosa, Vestn, rentgenol, and radiol., No. 2, p. 66, 1969; Sokolov Yu. N. id river. Our experience in studying the thin relief of the stomach in chronic gastritis, ibid., No. 5, p. 3, 19 73, bibliography; Tikhonov K. B. and Pruchansky V. S. Microrelief of the gastric mucosa and its significance in the diagnosis of chronic gastritis, ibid., No. 2, p. 82, 1970, bibliogr.; F and N and r d-sh I am V. A N. X-ray diagnostics of diseases of a digestive tract, t. 1, Yerevan, 1961; Sh l and fer I. G. Relief of the mucous membrane of the stomach and duodenum, Gastritis, ulcer, carcinoma, b. M., 1935, bibliogr.; Cummack D.H. Gastrointestinal X-ray diagnosis, Edinburgh - L., 1969; Pr£v6t R. u. L a s s r i c h M. Rontgendiagnostik des Magen-Darmka-nals, Stuttgart, 1959, Bibliogr.

G. in children- Balashova T. F. Enzyme-forming function of the stomach in chronic gastritis in children, Pediatrics, No. 5, p. 14, 1971; And in all about in S. M., etc. Endocrine cells of the gastric mucosa in children, in the same place, No. 3, p. 12, 1975, bibliogr.; Koroleva R. I. and Bialik V. L. About the diagnostic value of aspiration biopsy of the gastric mucosa in chronic gastritis in children, ibid., JNft 12, p. 22, 1966; KossyuraM. B. Diseases of the stomach in children, M., 1968, bibliogr.; Lukyanova E. M., Korole-z in a R. I. and Sh ly to about in I. A. Endoscopic studies of the stomach in chronic gastritis in children, Pediatrics, No. 3, p. 17, 1975; Multivolume Guide to Pediatrics, ed. Yu. F. Dombrovskaya, vol. 4, p. 191 and others, M., 1963; Ostr about p about lets S. S. and others Morphological day-n1st hroshchnogo gastritis with normal i shdvshtsenoy secretory func- tion of the duct in children, Ped1at., obstetrician. i gshek., No. 4, p. 3, 1975; Samarina G. Ya. Clinical features of antral gastritis in children, Vopr. och. mat. and children, vol. 18, no. 6, p. 23, 1973; Smirnov H. M. Chronic gastritis in children, Minsk, 1967, bibliogr.; Sandberg D. N. Hypertrophic gastropathy (Menetrier's disease) in childhood, J. Pediat., v. 78, p. 866, 1971; Sedl&ckov& M. a. Bedn£r B. Chronic gastritis in childhood, Gastroenterologia (Basel), v. 107, p. 251, 1967.

F. I. Komarov; L. I. Aruin (path. An.), M. B. Kossyura (ped.), H. N. Lebedev (path. physical.), A. P. Peleshchuk (geront.), Yu. N. Sokolov ( rent.), compiler of the table F. I. Komarov.

1. lung tissue

   lobar pneumonia

1. stained with hematoxylin and eosin

   stomach wall

   chronic stomach ulcer

1. stained with hematoxylin and eosin

2. metastasis of mucosal cancer in the LU

   with tumor progression

1. coloring Sudan Sh

1. coloring Congo red

   kidney tissue

   kidney amyloidosis

1. stained with hematoxylin and eosin

   section of LU tissue

   tuberculosis

1. stained with hematoxylin and eosin

2. septic myocarditis

   causes - sepsis

1. stained with hematoxylin and eosin

   cause is damage

1. brain tissue

   local hemosiderosis

1. stained with hematoxylin and eosin

   cut of skin

   causes are polyetiological

1. stained with hematoxylin and eosin

   gastric mucosa

   gastric adenocarcinoma

   causes are polyetiological

1. stained with hematoxylin and eosin

   aortic section

   In the wall of the aorta, in its middle shell, where the vasavasorum is located, there is an inflammatory infiltrate consisting of lymphocytes, plasma cells, fibroblasts, and single giant cells of the Pirogov-Langhans type. There are also small foci of necrosis.

   syphilitic mesaortitis

1. stained with hematoxylin and eosin

2. myocardial hypertrophy

1. stained with hematoxylin and eosin

   brain tissue

   purulent leptomeningitis

   meningococcal infection

MICROPRODUCTION No. 58. Fibromyoma ()

1. stained with picrofuchsin according to Van Gieson

   fibromyoma

   causes are polyetiological

1. stained with hematoxylin and eosin

   kidney tissue

   ischemic infarction of the kidney

MICRO PREPARATION No. 62.

1. stained with hematoxylin and eosin

   lung tissue

   hemorrhagic pulmonary infarction

   thrombosis, embolism

1. stained with hematoxylin and eosin

   brain tissue

   hemorrhage in the brain

1. coloring Sudan Sh

   lung tissue

   pulmonary fat embolism

MICRO PREPARATION No. 80.

1. Glandular hyperplasia of the endometrium

1. stained with hematoxylin and eosin

   LU in lymphogranulomatosis

   causes are polyetiological

MICRO PREPARATION No. 87.

1. stained with hematoxylin and eosin

   papillary cancer thyroid gland

   causes are polyetiological

1. stained with hematoxylin and eosin

   section of the ovary

   actinomycosis

1. stained with picrofuchsin according to Van Gieson

2. cardiosclerosis

1. stained with hematoxylin and eosin

   kidney tissue

   causes are polyetiological

1. stained with hematoxylin and eosin

2. acute myocardial infarction

1. Perls reaction

   lung tissue

   brown induration of the lung

1. stained with picrofuchsin according to Van Gieson

   liver tissue

1. stained with hematoxylin and eosin

   slice of liver tissue

   nutmeg liver

1. stained with hematoxylin and eosin

   lung tissue

   focal influenza pneumonia

1. stained with hematoxylin and eosin

   cross section of a vessel

1. stained with hematoxylin and eosin

   lung tissue

   miliary pulmonary tuberculosis

1. stained with hematoxylin and eosin

   thyroid tissue

1. stained with hematoxylin and eosin

   section of tumor tissue (skin)

   skin melanoma

1. stained with hematoxylin and eosin

   lung tissue

   bronchopneumonia

1. stained with hematoxylin and eosin

   lung tissue

   emphysema

1. stained with hematoxylin and eosin

   lung tissue, pleura

   hyalinosis of the pleura

1. stained with hematoxylin and eosin

   lung tissue

   healed tuberculosis affect

1. stained with hematoxylin and eosin

   skin tissue

   skin papilloma

   causes are polyetiological

1. stained with hematoxylin and eosin

   uterine tissue

   hydatidiform mole

   causes are polyetiological

1. coloring Sudan Sh

   cross section of an artery

   artery atherosclerosis

1. stained with hematoxylin and eosin

   fallopian tube cut

   tubal pregnancy

1. stained with hematoxylin and eosin

   breast tissue

   causes are polyetiological

1. stained with hematoxylin and eosin

   liver tissue

   cavernous hemangioma of the liver

   causes are polyetiological

1. stained with hematoxylin and eosin

   section of the small intestine

   causes - salmonellosis

1. stained with hematoxylin and eosin

   uterine tumor tissue

   chorionepithelioma

   causes are polyetiological

MICRO PREPARATION No. 185.

1. stained with hematoxylin and eosin

   subarachnoid hemorrhage

MICRO PREPARATION No. 187.

1. stained with hematoxylin and eosin

   pancreatic tissue

   pancreatic atrophy in diabetes

   causes - SD

1. stained with hematoxylin and eosin

   tracheal tissue

1. stained with hematoxylin and eosin

   transverse section of the appendix

1. stained with hematoxylin and eosin

   kidney tissue

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MICRO PREPARATIONS (to lay down)

MICROPROGRAM No. 2. Croupous pneumonia

stained with hematoxylin and eosin

lung tissue

almost all alveoli are filled with fibrinous exudate, septa are thickened, full-blooded vessels. Pink exudate in the lumen of the alveoli. It contains fibrin threads (homogeneous in the form of a network or grains) and polymorphonuclear leukocytes. A characteristic pathognomonic symptom is the presence of Kohn's bridges (fibrin strands from one alveolus pass into another). The capillaries of the interalveolar septa are empty, differ from the

lobar pneumonia

infectious agents - pneumococci, streptococci, staphylococci

MICROPRODUCTION No. 8. Chronic gastric ulcer

stained with hematoxylin and eosin

stomach wall

ulcerative defect in the wall of the stomach. The bottom of the ulcer is filled with necrotic masses. The defect extends to the mucous and muscular membranes. Muscle fibers in the bottom of the ulcer are not defined. In the bottom, 4 layers can be distinguished: fibrinous-purulent exudate, fibrinoid necrosis, granulation and scar tissue

chronic stomach ulcer

causes are polyetiological: stress, nutritional factors, bad habits, helicobacter pylori

MICROPREP No. 9. Metastasis of mucosal cancer in the LU

stained with hematoxylin and eosin

on the preparation, the LU pattern is erased due to the growth of atypical cells containing a large amount of mucus. Among the tumor cells there are cricoid (the nucleus is pushed to the periphery by the mucous mass)

metastasis of mucosal cancer in the LU

with tumor progression

MICROSLOPE No. 14. Fatty degeneration of the liver (staining Sudan III)

coloring Sudan Sh

liver tissue (peripheral cells)

on the preparation in the cytoplasm of hepatocytes there are accumulations of large drops of fat, painted in yellow-orange color. Larger fat droplets are contained in the cytoplasm of hepatocytes of the peripheral (periportal) sections of the hepatic lobules, smaller ones - in the cells of the central zone of the lobule

large droplet fatty degeneration of the liver

causes - chronic alcoholism, intoxication, protein starvation, beriberi, anemia, transfusion of incompatible blood

MICROSLOPE No. 15. Kidney amyloidosis (Congo red stain)

coloring Congo red

kidney tissue

in the capillary loops of the renal glomeruli, in the walls of the arterioles and under the basement membrane of the renal tubules, there are red amyloid deposits. Amyloid deposited along the reticular fibers

kidney amyloidosis

causes - chronic infections (tuberculosis), purulent-destructive processes, malignant neoplasms, rheumatoid diseases

MICROpreparation No. 16. Caseous necrosis of lymph nodes in tuberculosis

stained with hematoxylin and eosin

section of LU tissue

the focus is a homogeneous substance, in a healthy tissue - lymphocytes, at the border - a macrophage productive reaction

caseous necrosis of lymph nodes in tuberculosis

tuberculosis

MICROPRODUCTION No. 18. Septic myocarditis

stained with hematoxylin and eosin

in the myocardium, foci of purulent fusion of tissue, in the center of which bacterial emboli are visible among polymorphonuclear leukocytes

septic myocarditis

causes - sepsis

MICROSLOPE No. 20. Granulation tissue

stained with hematoxylin and eosin

skin section (granulation tissue)

superficial leukocyte-necrotic layer; superficial layer of vascular loops; a layer of vertical vessels; maturing layer (collagen fibers, fewer vessels); a layer of horizontal fibroblasts (black elongated cells); fibrous layer

regeneration through the formation of granulation tissue (outcome - scar formation)

cause is damage

Micropreparation No. 23. Hemosiderin in the focus of hemorrhage (Perls reaction)

Perls reaction (prussian blue)

brain tissue

in the macrophages located in the wall of the cyst, bluish-green granules of the Prussian blue dye are visible, which have settled in the places of accumulation of hemosiderin granules. The formation of Prussian blue is due to the presence of an iron cation in hemosiderin. In the brain tissue, a focus of hemorrhage: in the center under anaerobic conditions, hematoidin (light brown) is formed, on the periphery - hemosiderin (turquoise)

local hemosiderosis

atherosclerosis, cerebral form of hypertension, cerebral aneurysm, stroke, trauma

MICROPRODUCTION No. 25. Squamous cell keratinizing cancer

stained with hematoxylin and eosin

cut of skin

The tumor consists of strands and layers of atypical squamous epithelium that grow into the underlying dermis. At high magnification, signs of polymorphic cells with hyperchromic nuclei of various sizes containing 2 or more nucleoli are visible. Figures of pathological mitoses are found. In the center of the tumor cells, formed bulbous structures from keratinized cells are visible - cancer pearls.

squamous cell keratinizing skin cancer

causes are polyetiological

MICROpreparation No. 27. Adenocarcinoma of the stomach

stained with hematoxylin and eosin

gastric mucosa

in all layers of the wall of the stomach, growths of atypical glands are visible. Gland-forming cells of various sizes and shapes with hyperchromic nuclei, with figures of pathological mitoses

gastric adenocarcinoma

causes are polyetiological

MICRO PREPARATION No. 36. Syphilitic mesaortitis

stained with hematoxylin and eosin

aortic section

In the wall of the aorta, in its middle shell, where the vasa vasorum is located, there is an inflammatory infiltrate consisting of lymphocytes, plasma cells, fibroblasts, and single giant cells of the Pirogov-Langhans type. There are also small foci of necrosis.

syphilitic mesaortitis

causes - syphilis (pale spirochete)

MICROPRODUCTION No. 38. Myocardial hypertrophy

stained with hematoxylin and eosin

muscle cells are thickened, increased in size. The nuclei are large, hyperchromic. There are many blood vessels in the enlarged myocardial stroma

myocardial hypertrophy

MICRO PREPARATION No. 39. Purulent leptomeningitis

stained with hematoxylin and eosin

brain tissue

the pia mater is sharply thickened and diffusely infiltrated with polymorphonuclear leukocytes. Vessels of the shells are dilated, full-blooded. Perivascular and pericellular edema is expressed in the substance of the brain

purulent leptomeningitis

meningococcal infection

stained with picrofuchsin according to Van Gieson

muscle and connective tissue

smooth muscle fibers alternate with bundles of collagen fibers having different thickness. Muscle and collagen fibers are arranged randomly (tissue atypism). Muscle fibers are colored yellow-green, connective tissue is pink. The nuclei are black, randomly arranged

fibromyoma

causes are polyetiological

Micropreparation No. 61. Ischemic infarction of the kidney

stained with hematoxylin and eosin

kidney tissue

against the background of unchanged components of the kidney, a triangular focus is visible, in which only the contours of the glomeruli and tubules are preserved. In the cells of these structures there are no nuclei (karyolysis), in some places the cytoplasm is in a state of lysis, there are areas of pink color, devoid of organization (necrotic detritus). This is the zone of necrosis. It is separated from unaltered tissue by a demarcation zone 9 in which there are full-blooded vessels and an accumulation of leukocytes)

ischemic infarction of the kidney

thrombosis, embolism, prolonged spasm, renal artery atherosclerosis

stained with hematoxylin and eosin

lung tissue

red necrosis. There are no nuclei in the septal cells and epithelium of the alveoli. Some alveolar septa are torn. The area of ​​necrosis is infiltrated with erythrocytes. Around the necrosis - the plethora of blood vessels, the accumulation of leukocytes, and in the lumen of the alveoli - protein liquid. Many branches of the pulmonary artery are thrombosed.

hemorrhagic pulmonary infarction

thrombosis, embolism

MICROSLOPE No. 71. Hemorrhage in the brain

stained with hematoxylin and eosin

brain tissue

brain tissue is edematous. The focus of hemorrhage is represented by an accumulation of erythrocytes in the brain tissue, located in the form of a lake around anatomically intact vessels (diapedetic hemorrhage). In the area of ​​the focus of hemorrhage, arterioles with thickened walls and signs of plasmorrhagia are visible.

hemorrhage in the brain

atherosclerosis, cerebral aneurysm, trauma, GB

MICROSLOPE No. 75. Fatty embolism of the lung (staining Sudan III)

coloring Sudan Sh

lung tissue

interalveolar septa are practically invisible. The lumen of the vessel is obturated with fatty emboli of bright orange color.

pulmonary fat embolism

fractures of tubular bones, crushing of subcutaneous fat, the use of oil preparations in the form of intravenous injections

Stained with hematoxylin and eosin

slice of uterine tissue (endometrial scraping)

the endometrium is thickened, has many elongated glands with a tortuous course. In some places, the lumen of the glands is enlarged and looks like cysts. The epithelium of the glands proliferates, the stroma of the endometrium is rich in cellular elements.

Glandular hyperplasia of the endometrium

causes - ovarian dysfunction, ovarian cyst

MICROPRODUCTION No. 81. Lymphogranulomatosis

stained with hematoxylin and eosin

in the lymph nodes, conglomerates of the remaining cells (lymphatic), some of the tissues are necrotic (a focus without cell infiltrates), areas of fibrosis (bundles of collagen fibers with fibroblasts). In the LU cells that are not characteristic of it: reticular (cells irregular shape large purple with one nucleus), plasmocytes (oval cells with a rounded nucleus, shifted to the periphery), eosinophils (the nucleus is pushed to the periphery, the cytoplasm is orange). Uncharacteristic cells - Berezovsky-Shtenberg-Reed cells (large, reticulocyte-like, but multinucleated - 2 large nuclei next to each other  owlet eye syndrome)

LU in lymphogranulomatosis

causes are polyetiological

stained with hematoxylin and eosin

section of a thyroid tumor

The tumor consists of cavities of various sizes filled with villi - papillary papillae emanating from the walls of the cavities covered with atypical epithelium. In places, tumor papillae grow into the wall of the cavities and the tumor capsule. Virtually no follicles.

papillary thyroid cancer

causes are polyetiological

MICRO PREPARATION No. 88. Actinomycosis

stained with hematoxylin and eosin

section of the ovary

irregularly shaped drusen of fungi are observed in the ovarian tissue. Around the tissue are infiltrated with polymorphonuclear leukocytes. Around the sprawl connective tissue– capsule

actinomycosis

radiant fungus (actinomycetes)

MICROSLOPE No. 89. Cardiosclerosis (staining with picrofuchsin according to Van Gieson)

stained with picrofuchsin according to Van Gieson

among the normal myocardium, extensive fields of scar tissue are visible (colorless with dots - fibroblast cells), surrounded by hypertrophied cardiomyocytes (green with nuclei)

cardiosclerosis

productive inflammation, myocardial infarction, coronary artery disease

MICRO PREPARATION No. 90. Kidney with myeloid leukemia

stained with hematoxylin and eosin

kidney tissue

the tissue is diffusely infiltrated with tumor cells such as myeloblasts. There are areas of hemorrhage, necrosis. In the lumen of blood vessels - leukemic thrombi

kidney in myeloid leukemia

causes are polyetiological

MICROSTREP No. 94. Myocardial infarction

stained with hematoxylin and eosin

3 zones are visible on the preparation: 1) a zone of necrosis with characteristic changes in cardiomyocytes, lysis of nuclei, coagulation and clumpy disintegration of myoplasm, disappearance of transverse striation and cell boundaries; 2) demarcation zone - expansion and plethora of blood vessels, hemorrhages and infiltration by polymorphonuclear leukocytes; 3) a zone of healthy myocardium along the periphery

acute myocardial infarction

spasm of the coronary arteries, thrombosis, embolism, atherosclerosis of the coronary arteries, functional myocardial overstrain with insufficient blood supply

Micropreparation No. 97. Brown induration of the lung (Pearls reaction)

Perls reaction

lung tissue

interalveolar septa are thickened due to the expansion and overflow of blood vessels. Some of the alveoli are filled with edematous fluid, in others - accumulations of siderophages with hemosiderin - bluish-green staining. Part of the interalveolar septa is thickened and sclerosed. Growth of connective tissue around the bronchi

brown induration of the lung

general and chronic venous plethora, heart defects, vascular atherosclerosis, congestion and hypertension in the ICC

MICROSLOPE No. 100. Cirrhosis of the liver (stained with picrofuchsin according to Van Gieson)

stained with picrofuchsin according to Van Gieson

liver tissue

the liver parenchyma is represented by false lobules of various sizes. Fragments of several pre-existing normal hepatic lobules can be seen in each pseudolobule (multiglobular cirrhosis). Hepatic beams are indistinguishable. The central lobular vein is absent or displaced to the periphery of the false lobule. Hepatocytes of false lobules are in a state of protein degeneration and necrosis. There are large hepatocytes with 2 or more nuclei. Areas of the hepatic parenchyma are separated by wide fields of connective tissue stained magenta pink. Contiguous hepatic triads are visible among the connective tissue fields, which are infiltrated by lymphocytes and histiocytes.

multiglobular cirrhosis of the liver

hepatitis, hepatosis of various etiologies

MICROPRODUCTION No. 103. Nutmeg liver

stained with hematoxylin and eosin

slice of liver tissue

in the liver, the veins and sinusoids in the central zone of the lobules are dilated and full-blooded. Also visible are foci of diapedetic hemorrhages in the form of "lakes", discomplexation of the hepatic beams, necrosis and atrophy of hepatocytes. In the peripheral, periportal zone of the lobules, the blood supply to the capillaries and venules is normal, the structure of the hepatic beams is preserved. Hepatocytes are in a state of fatty degeneration (variegation of color)

nutmeg liver

chronic cardiovascular insufficiency, heart defects, hepatic vein thrombosis

MICROpreparation No. 109. Focal influenzal pneumonia

stained with hematoxylin and eosin

lung tissue

airless areas are visible against the background of airy lung tissue. The alveoli are filled with serous-hemorrhagic exudate. In places, accumulations of polymorphonuclear leukocytes forming microabscesses are visible. The epithelium of the bronchi is desquamated and rejected, exudate in the lumen of the bronchi

focal influenza pneumonia

influenza virus, bacterial infection

MICROPRODUCTION No. 110. Mixed thrombus

stained with hematoxylin and eosin

cross section of a vessel

The lumen of the vessel is completely obturated by a thrombus, which consists of platelets, fibrin filaments, hemolyzed erythrocytes and leukocytes. In a mixed thrombus, the quantitative composition of formed elements is proportional to their number in the blood. A significant part of the thrombotic masses has sprouted connective tissue, which grows from the side of the intima of the vessel. Thrombotic masses have gaps lined with endothelium

damage to the vessel wall, disruption of the interaction of blood coagulation and anticoagulation systems, increased blood viscosity, slowing blood flow as a result of cardiovascular insufficiency, decreased muscle tone of the veins

Micropreparation No. 113. Miliary tuberculosis of the lung

stained with hematoxylin and eosin

lung tissue

numerous tuberculous granulomas are visible in the preparation. In the center of the granulomas there is caseous necrosis, around it are epithelioid, separate multinuclear giant Pirogov-Langhans macrophages, lymphocytes and individual plasmocytes. There are no vessels in the granuloma

miliary pulmonary tuberculosis

Mycobacterium tuberculosis, hematogenous generalization of primary tuberculosis

MICROpreparation No. 117. Colloidal goiter

stained with hematoxylin and eosin

thyroid tissue

thyroid follicles are rounded, dilated. Their wall is thinned, its ruptures and merges of fv among themselves with formation of cysts of various size are visible. The epithelium lining the follicles is flattened. The lumen of the follicles and cysts is filled with a thick mucus-like mass (colloidal). Full-blooded vessels and hemorrhages are visible (brownish contents in the follicles)

mucous (colloid) dystrophy (colloidal goiter)

iodine deficiency, impaired synthesis of thyroid hormone, goitrogenic substances, immunopathology

MICROpreparation No. 126. Skin melanoma

stained with hematoxylin and eosin

section of tumor tissue (skin)

a tumor node is located in the skin - it has an intense brown color due to accumulations of mealnin in tumor cells located along the periphery of the tumor node. Tumor cells vary in size and shape.

skin melanoma

causes are polyetiological (with tumor progression)

MICROpreparation No. 127. Bronchopneumonia

stained with hematoxylin and eosin

lung tissue

the wall of the bronchus is diffusely infiltrated with polymorphonuclear leukocytes (panbronchitis), in the lumen of the bronchi there is serous-leukocytic exudate with an admixture of desquamated epithelial cells. Perifocally, sharply dilated, air-filled alveoli are seen (perifocal emphysema)

bronchopneumonia

causes are polyetiological: inflammation in the respiratory tract, pneumococci, viruses

MICROPRODUCTION No. 133. Emphysema of the lung

stained with hematoxylin and eosin

lung tissue

in dilated acini - complete smoothing of the walls, the walls of the alveoli become thinner, straighten. The capillaries of the interalveolar septa become empty. Alveoli are enlarged. Black inclusion - tobacco

emphysema

chronic bronchitis, age-related changes in the lung tissue, vicarious in the pathology of another lung

MICRO PREPARATION No. 135. Hyalinosis of the pleura

stained with hematoxylin and eosin

lung tissue, pleura

the visceral pleura is thickened, its fibrous structures are hardly distinguished. The mesothelium covering the pleura is atrophic. The thickening of the pleura occurred due to the coarsening of bundles of collagen fibers, which turned into translucent vitreous formations. Around the vessels of the pleura - a pronounced proliferation of connective tissue

hyalinosis of the pleura

causes - metabolic disorders in the connective tissue, the formation of hyaline. The result of the progression of fibrinoid swelling, inflammation, necrosis, sclerosis

Micropreparation No. 136. Healed tuberculous affect in the lung

stained with hematoxylin and eosin

lung tissue

in the lung tissue, purple areas are visible, which are lime deposits. They are surrounded by a connective tissue capsule - this is a healed tuberculous affect. In the field of view, a focus of necrosis surrounded by connective tissue, as well as an island of nascent bone tissue (pseudo-bone). On the periphery in the zone of necrosis - the deposition of calcium salts

healed tuberculosis affect

causes - primary tuberculosis

MICROpreparation No. 141. Skin papilloma

stained with hematoxylin and eosin

skin tissue

numerous outgrowths of stratified squamous keratinized epithelium that make up the tumor parenchyma. The tumor has a well-defined stroma, represented by outgrowths of the dermis, which, like the fingers of a glove, are covered with stratified squamous epithelium. Tissue atypia is characteristic (an increase in the layers of the epithelium, hyperkeratosis). It is a papillary formation covered with stratified squamous epithelium with underlying stroma and vessels.

skin papilloma

causes are polyetiological

MICROPRODUCTION No. 150. Cystic skid

stained with hematoxylin and eosin

uterine tissue

chorionic villi are cystically changed, their stroma is edematous, the central vessel is absent, the trophoblast has a two-row structure, is atrophic in places

hydatidiform mole

causes are polyetiological

MICROSLOPE No. 153. Atherosclerosis of the artery (staining Sudan III)

coloring Sudan Sh

cross section of an artery

yellow spots, stripes (deposits of lipids) and whitish-gray plaques protruding into the lumen are visible on the intima. Some of the plaques are ulcerated. Around the proliferation of connective tissue

artery atherosclerosis

unbalanced diet, hypodynamia, genetic defect of cholesterol receptors (hypercholesterolemia)

MICROPREPARATION No. 159. Tubal pregnancy

stained with hematoxylin and eosin

fallopian tube cut

a decidual reaction is noted in the CO tube. In the lumen of the tube, chorionic villi are visible, penetrating into the thickness of the muscular membrane

tubal pregnancy

causes - violation of the passage of the fetus through the tube (inflammation, swelling, underdevelopment of the tubes, etc.)

MICRO PREPARATION № 163. Fibroadenoma of the mammary gland

stained with hematoxylin and eosin

breast tissue

ducts are visible in the form of cracks of a bizarre shape. Connective tissue grows into them. The coloring is yellow. Visible pink connective tissue

intracanalicular fibroadenoma

causes are polyetiological

Micropreparation No. 178. Cavernous hemangioma of the liver

stained with hematoxylin and eosin

liver tissue

the tumor is well delimited from the surrounding liver tissue by a pronounced fibrous capsule. The tumor consists of large cavernous thin-walled vascular cavities (caverns) lined with endothelium and filled with liquid or clotted blood.

cavernous hemangioma of the liver

causes are polyetiological

MICRO PREPARATION No. 182. Ulcerative enteritis with salmonellosis

stained with hematoxylin and eosin

section of the small intestine

ulcerative defect in the wall of the small intestine. The bottom of the ulcer is filled with necrotic masses. The mucous and submucosal membranes around the ulcer are infiltrated with polymorphonuclear leukocytes.

ulcerative enteritis with salmonellosis

causes - salmonellosis

Micropreparation No. 183. Chorionepithelioma

stained with hematoxylin and eosin

uterine tumor tissue

The tumor is built from tumor cells of two types: monomorphic light epithelial (Langhans) and giant dividing cells with hyperchromic polymorphic nuclei (syncytiotrophoblasts). There is no stroma in the tumor. Instead of vessels, cavities filled with erythrocytes are visible. Cavity walls lined with tumor cells instead of endothelium

chorionepithelioma

causes are polyetiological

stained with hematoxylin and eosin

brain tissue, subarachnoid space

thickened artery wall, erythrocyte diapedesis, signs of plasmorrhagia

subarachnoid hemorrhage

closed craniocerebral injury, cerebral atherosclerosis

stained with hematoxylin and eosin

pancreatic tissue

some lobules are atrophied, others are compensatory hypertrophied. Atrophy of the islets of Langerhans. They are reduced in size. The preparation shows the proliferation of connective tissue (sclerosis), fat deposition (lipomatosis - transparent cells). There is hyalinosis, fibrosis and lymphoid infiltration of microvessels. Sclerosis and lipomatosis, both intralobular and interlobular

pancreatic atrophy in diabetes

causes - SD

Micropreparation No. 196. Croupous tracheitis

stained with hematoxylin and eosin

tracheal tissue

on the surface of the tracheal mucosa there is a fibrinous exudate infiltrated with polymorphonuclear leukocytes. In the underlying tissues, capillaries and venules are sharply expanded and full-blooded.

purulent-nercotic tracheitis with influenza

causes - influenza virus and bacterial infection

Micropreparation No. 198. Phlegmonous-ulcerative appendicitis

stained with hematoxylin and eosin

transverse section of the appendix

the wall of the process is thickened, all its layers are diffusely infiltrated with polymorphonuclear leukocytes. On the serous surface, deposits of fibrinous exudate intensely stained with eosin are noted. Lymph follicles are enlarged.

phlegmonous-ulcerative appendicitis

causes are polyetiological, autoinfection

Micropreparation No. 203. Serous extracapillary glomerulonephritis

stained with hematoxylin and eosin

kidney tissue

there is a sharp plethora of capillaries, the lumen of the Shumlyansky-Bowman capsule is enlarged, filled with serous exudate. As a result of the proliferation of the epithelium of the capsule, podocytes and macrophages, crescent formations (crescents) appear. Capillary loops undergo necrosis, in their lumen there are fibrin thrombi

serous (productive) extracapillary glomerulonephritis

causes - infectious-allergic diseases

MICROpreparation No. 205. Septic verrucous endocarditis

stained with hematoxylin and eosin

massive thrombotic deposits and bacterial colonies appear in the area of ​​necrosis of the valve leaflet. Growing granulation tissue during maturation deforms the valve leaflets. In the interstitial tissue of the myocardium, histiolimphocytic infiltrates and granulomas are found.

septic verrucous endocarditis

causes - rheumatism, sepsis

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Bol w-k.t

Methodological developments

practical classes for students

Diseases of the digestive system and liver

Peptic ulcer of the stomach and duodenum

Examine macroscopic preparations: gastric ulcer, ulcer duodenum, hemorrhagic erosion of the stomach.
Acute stomach ulcers
Describe macroscopic preparation Hemorrhagic erosions of the stomach №88 Hemorrhagic erosion of the stomach	Pay attention to the prevalence of the lesion; determine the shape, color of defects, as well as the type and consistency of the edges of defects. Note the superficial nature of the defect in the stomach wall and find brownish-brown masses of hematin hydrochloride.
Describe macroscopic preparation Chronic stomach ulcer	Pay attention to the prevalence of the lesion, determine the shape, type and consistency of the edges of the defects, the condition and surface of their bottom.
Draw and describe microscopic specimen stomach ulcer Helicobacter pylori (1) in the lumen of the glands (coloring according to Romanovsky Giemsa) Overhanging edge of gastric ulcer Undermined edge of gastric ulcer The bottom of a stomach ulcer during an exacerbation	Find the defect in the stomach wall and determine its depth. To characterize the changes in the bottom of the ulcer and the edges of the defect. Describe the changes in the deeper layers of the stomach wall and determine the nature of the course of the ulcerative process.

Appendicitis. Peritonitis.

To study macroscopic preparations: phlegmonous appendicitis, gangrenous appendicitis, process empyema, chronic appendicitis. Describe one of the macroscopic preparations.
Describe macroscopic preparation Phlegmonous appendicitis Gangrenous appendicitis	Pay attention to the size, wall thickness, condition of the serous membrane of the appendix.
Draw and describe a micropreparation №90 Phlegmonous appendicitis	To characterize the state of the mucous membrane of the process and its lumen. Determine the nature and prevalence of exudate, the degree of blood filling of the vessels.
Draw and describe microscopic specimen Obliteration of the appendix	Determine the topography of connective tissue growth, note the presence of adipose tissue islands, atrophy of the layers of the process wall.
Examine the microscopic preparation Fibrinous-purulent peritonitis	To characterize the state of the peritoneal mesothelium, vessels, exudate. Note changes in underlying fiber and muscle tissue.

Hepatitis. Toxic dystrophy of the liver. Cirrhosis of the liver.

1. To study macroscopic preparations: toxic liver dystrophy, cirrhosis of the liver, varicose veins of the esophagus. 2. Describe one of the macroscopic preparations.
Describe macroscopic preparation Toxic dystrophy of the liver	Pay attention to the size, consistency; mark the color on the cut surface; determine the stage of the disease.
Examine the microscopic preparation No. 93a Toxic dystrophy of the liver. (Stained with Sudan III)	Note the violation of the structure of the liver, obesity and necrobiosis of liver cells in the center of the lobule.
Draw and describe microscopic specimen №93 Toxic liver dystrophy	Note the violation of the architectonics of the liver, find foci of necrosis. Describe changes in the stroma of the organ. Determine the stage of the process.
Describe macroscopic preparation Postnecrotic cirrhosis of the liver Portal cirrhosis of the liver	Pay attention to the configuration, size, consistency, color of the organ; note the size of the nodes. Pay attention to the size, texture, color of the organ; note the size of the nodes.
Draw and describe microscopic specimen №94 Portal cirrhosis of the liver (stained with picrofuchsin)	To determine the topography of the newly formed connective tissue, the degree of its maturity, to identify the morphological features of the "false lobules". Note changes in liver cells (phenomena of fatty degeneration and perverted regeneration), bile ducts. Note distinctive features various forms of cirrhosis.

Neighbor files in item [UNSORTED]

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Pathological anatomy of peptic ulcer

Pathological anatomy. Initial ulcers do not penetrate deeper than the mucous membrane. A chronic ulcer can spread to the muscular and serous membranes. A callous ulcer is called an ulcer with hard raised edges. An ulcer that involves all layers of the gastric wall can cause it to perforate. An ulcer penetrating into neighboring organs, most often into the pancreas, is called penetrating. After the ulcer heals, scars appear, sometimes deforming the stomach (“hourglass”, stomach in the form of a snail) or causing narrowing (stenosis) of the pylorus. Inflammation of the serous membrane at the location of the ulcer leads to perigastritis or periduodenitis and the formation of adhesions with nearby organs.

Acute ulcers are usually round or oval in shape. The edges of the ulcers are clear, the bottom is usually clean, without overlays. Acute ulcers can cause perforation of the stomach wall and fatal stomach bleeding.

A chronic ulcer, according to most researchers, is the outcome of an acute one and differs from it by a significant development of fibrous tissue in the bottom and edges. A chronic ulcer is usually round or oval in shape, less often it has irregular outlines. The cardial edge of the ulcer is, as it were, undermined, the pyloric edge is gently sloping. The bottom is covered with dirty gray overlays, in the bottom of the penetrating ulcers, the organ into which the penetration has occurred is visible. A stomach ulcer is usually larger than a duodenal ulcer. The size of the niche, determined by x-ray examination, does not always correspond to the size of the ulcer. Due to swelling of the edges, filling of the ulcerative crater with mucus, exudate or food masses, the ulcerative defect may not be completely filled with barium. Most gastric ulcers are located on the lesser curvature and in the pyloric region. Duodenal ulcers are usually localized 1-2 cm from the pylorus, equally often on the anterior and posterior walls of the intestine. Rarely observed postbulbar ulcers. Chronic ulcers are usually solitary, but multiple lesions also occur. During gastroscopy, sometimes several small ones are found near a large ulcer, which are not detected radiologically. In patients with gastric ulcers, duodenal ulcers are sometimes simultaneously detected. Multiple ulcers duodenal ulcers are often located on opposite walls of the intestine ("kissing" ulcers). The most rare localization of ulcers in the stomach are the cardia, fundus and greater curvature.



On microscopic examination, four layers are distinguished in the bottom of the ulcer. On the inside, fibrinous-necrotic overlays, desquamated epithelium, leukocytes, erythrocytes and hydrochloric hematin are visible, staining the bottom of the ulcer in gray or dark brown. Beneath this layer is a layer of fibrinoid necrosis formed by disorganized and necrotic collagen fibers. In rapidly and rapidly progressing ulcers, this layer can reach several millimeters in width. Deeper is the granulation tissue. Often it is not detected, as it is completely involved in the destructive process. Granulation tissue passes into the next, most developed layer - scar tissue, which is formed by loose and dense fibrous connective tissue. There are small lymphoid follicles with pronounced reactive centers. When the ulcer recurs in the scars, you can see a lot of mast cells with signs of increased secretory activity. The scar tissue grows into the muscle layers, the submucosal layer, its volume significantly exceeds the size of the ulcer itself.

With an exacerbation of peptic ulcer, necrosis of the granulation tissue and collagen fibers usually occurs, an inflammatory reaction in the surrounding tissues, rejection of areas of necrosis and, due to this, an increase in the ulcer. Yu. M. Lazovsky believes that the progressive growth of fibrous tissue in the bottom of the ulcer is not associated with the transformation of granulation tissue into a scar, but with the direct formation of collagen fibers from the ground substance.

In the area of ​​the ulcer, changes in blood vessels are usually observed with the development of inflammatory-necrotic processes in them, areas of fibrinoid necrosis of the walls of the arteries, thrombosis of the arteries and veins and their subsequent recalibration. These secondary vascular lesions disrupt tissue trophism and serve as one of the reasons preventing the healing of chronic ulcers. At the bottom of the ulcer, there are nerve trunks immured in scar tissue and growths of nerve fibers such as amputation neuromas. In the ganglion cells of the intramural nerve ganglions, dystrophic changes and irritation phenomena (S. S. Weil, P. V. Sipovsky).



With peptic ulcer, changes occur throughout the mucous membrane of the stomach and duodenum. At the edges of the stomach ulcer, proliferation of the epithelium is observed, which can grow deep into the mucosa and along its surface, taking the form of polyps. The pyloric glands hyperplasia, showing signs of increased mucoid secretion. In a secret, acidic mucopolysaccharides that are not normally present appear. With prolonged existence of an ulcer, atrophic changes in the glands occur, their secretion weakens. In the fundic glands, there are pictures of atrophy, intestinal metaplasia, the so-called pseudopyloric glands of Stern are formed, containing a mucoid secret. In the stroma, one can see diffuse lymphoplasmacytic infiltrates, large lymphoid follicles, growths of smooth muscle fibers. With a duodenal ulcer, the number of parietal cells significantly increases, which are found even in the pyloric region.

Healing of chronic ulcers occurs by scar formation. Before healing begins, edema and inflammatory infiltration of the edges of the ulcer occur. The edges are smoothed out, approaching the bottom, the necrotic masses covering the bottom are rejected. Granulations appear in the bottom and edges, which gradually fill the ulcer crater. The surface epithelium, saturated with RNA, grows on the granulation tissue and lines it. The muscular layer of the mucous membrane, gastric and duodenal glands do not regenerate. In the healing of ulcers, the accumulation of acid mucopolysaccharides is of great importance. An ulcer with mild fibrosis of the bottom and edges takes about 5-7 weeks to heal. Sometimes complete healing occurs after 10 days, sometimes it takes several months. As a result of healing of deep, especially penetrating, ulcers, gastric deformities may occur. Scar healing of pyloric ulcers can lead to pyloric stenosis. Diverticula (ulcus diverticulum) may develop between a healed duodenal ulcer and the pylorus.

Complications. V. M. Samsonov distinguishes five groups of complications of peptic ulcer. 1. Complications of ulcerative-destructive origin: perforation, arrosive bleeding and penetration. Ulcer perforation is one of the most formidable complications. Most often, perforation occurs in the second half of the day. The diameter of the perforation is about 0.5 cm. Histological examination reveals a pattern of exacerbation of peptic ulcer, necrosis and leukocyte infiltration of the edges and bottom of the ulcer, fibrin overlay on the serous cover.

Arrosive bleedings arise from large vessels of a bottom of an ulcer. M. K. Dal et al. found that vessel erosion may be preceded by limited necrosis of the wall with the formation of an aneurysm and its subsequent rupture. Especially dangerous is bleeding from chronic ulcers, the vessels of which are fixed by scar tissue, which prevents the contraction of the arteries. Ulcers of the lesser curvature of the stomach usually penetrate into the lesser omentum, duodenal ulcers into the pancreas.

When ulcers penetrate into hollow organs, gastric fistulas occur (gastrocolic, gastrointestinal, gastro-gall bladder). Ulcers of the cardiac and subcardiac regions may penetrate the diaphragm. In the future, such an ulcer may break through into the pleural cavity, into the pericardial cavity. 2. Complications of an inflammatory nature: gastritis, duodenitis, perigastritis, periduodenitis, stomach phlegmon, hepatocholangitis. 3. Complications of ulcerative cicatricial origin: stenosis of the cardial part of the stomach, pylorus, duodenum, shortening of the lesser curvature, deformity of the stomach in the form of an "hourglass", diverticula of the stomach and duodenum. 4. Malignancy of gastric ulcer, according to AI Abrikosov, occurs in 8-10% of cases. The lack of consensus on the frequency of ulcer malignancy is associated with difficulties differential diagnosis malignant ulcer and primary ulcerative cancer. Malignancy of duodenal ulcers is extremely rare.

Toxic dystrophy of the liver

Toxic dystrophy of the liver or progressive massive liver necrosis is an acute or chronic disease characterized by massive tissue necrosis and the development of liver failure. Toxic dystrophy develops as a result of the action of exogenous (fungi, food products with toxins, etc.) and endogenous (pregnancy toxicosis, thyrotoxicosis) toxins. These substances have a hepatotoxic effect and damage hepatocytes.
Pathological anatomy. Toxic dystrophy of the liver It has various manifestations that depend on the prescription of damage to liver cells. In the first few days, the organ enlarges, it becomes dense, yellow in color. Further, there is a progressive decrease in liver tissue and wrinkling of the capsule. On the cut, the liver is clay-colored or gray. Under a microscope, fatty degeneration of hepatocytes is first found in the center of the lobules, these changes are quickly replaced by necrosis and autolysis of the liver tissue. The progression of necrosis leads to complete necrosis of the lobule by the end of the second week, and only a narrow strip of fatty degeneration remains along the periphery. All this is a stage of yellow dystrophy. On the 3rd week there is a further reduction in the liver and it becomes red. These are manifestations of phagacytosis and resorption of necrotic detritus. In this case, the stroma of the organ with dilated blood vessels is exposed. Changes on the 3rd week are a manifestation of the stage of red liver dystrophy.
With progressive necrosis, patients die from acute hepatic-renal failure. Survivors have liver changes characteristic of postnecrotic cirrhosis.

24. Toxic dystrophy of the liver.

The liver is enlarged, flabby, with a wrinkled capsule. On the section, the structure is erased, variegated color

305. Portal cirrhosis of the liver.

The liver is deformed, compacted, reduced in size, the surface is granular. The section shows large and small nodules of hepatic tissue of various sizes, surrounded by a ring of connective tissue - the so-called "false lobules".

553. Cirrhosis of the liver.

The liver is of a dense consistency, tuberous, on the cut with yellow foci and false lobules.

325. Fatty degeneration of the liver of the "goose" type. Chronic fatty hepatosis.

The liver is enlarged, yellow.

279. Cancer of the liver on the background of cirrhosis.

Against the background of cirrhosis of the liver, a focus of tumor tissue of a variegated appearance is visible.

198. Thrombosis of the hepatic vein.

Part of the liver hepatic vein, in the lumen of which a thrombus is visible.

127. Icteric necrotic nephrosis.

The kidney on the cut is yellow-green, the border of the cortical and medulla stale bark dull, wide.

462. Splenomegaly. Hyalinosis capsule.

The spleen is enlarged, on the capsule there are matte translucent foci

37. Hemorrhoids. Brown varicose veins in the distal colon.

Model 35. Varicose veins of the esophagus in liver cirrhosis.

Sharp plethora and dilatation of the veins of the esophagus with erosion of the vessel wall.

To study micropreparations:

38. Acute viral hepatitis.

Hepatocytes in a state of hydropic (balloon) dystrophy and coagulation necrosis. In the perisinusoidal lumens, hyaline-like bodies of Kaunsilman are found. Cholestasis and lymphohistiocytic infiltration of the portal tracts are expressed.

Indicate in the picture:

1 - balloon dystrophy of hepatocytes.

2 - Councilmen's bodies.

3 - cholestasis

4 - histiolimphocytic infiltration of the portal tracts

171. Subacute toxic dystrophy of the liver(acute hepatosis, stage of red dystrophy).

The structure of the hepatic lobules is broken. Hepatocytes in a state of cell necrosis are homogeneous, eosinophilic, without nuclei. Many necrotic hepatocytes have undergone phagocytosis and resorption. In these areas, a bare (free) reticular stroma with dilated sinusoids and bile capillaries is visible.

Indicate in the picture:

1 - necrotic hepatocytes.

2 - free stroma.

3 - dilated sinusoids and bile capillaries.

99. Portal cirrhosis.

Growth of the connective tissue along the portal tracts in the form of rings with the formation of the so-called "false lobules", in which the architectonics of the vessels is disturbed. hepatocytes in a state of fatty degeneration (cells in the form of vacuoles) and regeneration (large cells with large or double nuclei)

Indicate in the picture:

1 - connective tissue

2 - false segments

3 - hepatocytes in a state of fatty degeneration

4 - young liver cells

44. Billiary cirrhosis.

Growth of connective tissue along the periphery of the lobules. Cholestasis is pronounced, the bile ducts are dilated, filled with yellow or dark green bile.

76. Postnecrotic cirrhosis (Masson stain).

The structure of the liver is sharply disturbed, extensive areas of blue connective tissue in place of necrotic hepatic tissue. The preserved liver cells in a state of necrosis are homogeneous, pink-violet, without nuclei. Regeneration is not expressed.

397. The basis of toxic dystrophy of the liver is:

inflammation

proteinaceous dystrophy

1. fatty degeneration

398. Outcomes of toxic dystrophy are:

hepatic-renal insufficiency

cirrhosis of the liver

399. The cause of toxic liver dystrophy is:

infection

alcohol poisoning

poisoning with mushrooms and poisons

toxicosis of pregnancy

400. "Goose" liver develops when:

acute hepatosis

chronic hepatosis

401. The mechanism of alteration of hepatocytes in serum hepatitis is:

direct effect of viruses

immune cytolysis

402. AIDS is accompanied by hepatitis:

whey

epidemic

403. Degeneration of hepatocytes in serum hepatitis:

1. granular

   vacuolar

404. The etiological factors of hepatitis include:

1. medicines

allergy

dystrophy

405. Morphological form chronic hepatitis is an:

phlegmonous

persistent

fibrinous

fatty hepatosis

406. Hepatitis is considered chronic:

after 1 month

after 3 months

after 6 months

after 1 year

407. Indications for biopsy in case of clinical diagnosis of hepatitis are:

diagnosis verification

establishing the form and severity of hepatitis

evaluation of treatment outcomes

408. The safest type of biopsy for diffuse liver damage is:

puncture

transvenous

marginal liver resection

pinched at laparoscopy

409. The main histological signs of chronic active hepatitis are:

stepwise necrosis

emperiopolesis

bridging necrosis

410. The main histological sign of persistent hepatitis is:

1- clear boundary of the boundary plate

2- sclerosis of the periportal tracts

3- granulomatous inflammation in the centrilobular zones

4- pericellular fibrosis

411. One of the main histological signs of viral hepatitis is:

1- Councilmen's bodies

2- giant mitochondria

3- granulomatous inflammation

4- pericellular fibrosis

5- sclerosing

412. Histological signs of liver tissue regeneration include:

1- binuclear hepatocytes

2- giant multinucleated hepatocytes, such as simplasts

3- “rosette-like” structures

413. The most common cause of toxic liver dystrophy is:

414. The following stages of toxic liver dystrophy are distinguished:

1- active

2- red dystrophy

3- moderate

4- persistent

415. Signs of the 1st stage of toxic liver dystrophy include:

bright yellow liver

the liver is reduced in size

the liver is dense, sclerotic

diffuse hemorrhages in the liver tissue

416. Histological signs of stage II of toxic liver dystrophy include:

necrosis of hepatocytes in the centrilobular regions

carbohydrate dystrophy

macrofocal sclerosis

mallory bodies

417. Macroscopic sign of the liver in cirrhosis is:

soft-elastic liver

the liver is enlarged

hard liver

nutmeg liver

418. Acute viral hepatitis is characterized by:

extralobular cholestasis

bile lakes

fatty degeneration of hepatocytes

Councilmen's bodies

419. Councilman's bodies are related to hepatitis:

serum

alcoholic

none of the above

420. What changes do hepatocytes undergo during the formation of Kaunsilmen's bodies:

hyalinosis

colliquative necrosis

coagulative necrosis

421. Necrosis spreading between the center of the liver lobules and the branches of the crow's vein are called:

massive

stepped

bridging

422. The inflammatory infiltrates in acute serum hepatitis are dominated by:

neutrophils

macrophages

lymphocytes

423. Inflammatory infiltrates in alcoholic hepatitis necessarily contain:

lymphocytes

neutrophils

macrophages

424. Reddish (light) color of the liver in cirrhosis depends on:

dystrophy

obstruction of blood flow through the inferior vena cava

obstruction of blood flow through the portal vein

425. "Lobular liver" refers to cirrhosis:

1- circulatory

3- infectious

4- exchange.

Theme VI. Diseases of the gastrointestinal tract.

Gastritis is an inflammatory disease of the gastric mucosa. There are acute and chronic gastritis.

Acute gastritis is characterized by:

Macroscopically - thickening of the mucous membrane due to edema, redness, erosion.

FORMS OF ACUTE GASTRITIS:

1. Catarrhal (simple)

2. Fibrinous

3. Purulent

4. Necrotic

Chronic gastritis is a chronic inflammation of the gastric mucosa, accompanied by violations of the clonal renewal of the epithelium.

Morphological forms of chronic gastritis:

surface

atrophic

hypertrophic

combined atrophic-hyperplastic.

Modern international classification of chronic gastritis:

autoimmune (type A)

bacterial (type B)

mixed (type A and B)

chemical-toxic due (type C)

lymphocytic

special forms (Menetrier's disease)

acute ulcer - an ulcer that captures the thickness of the mucous membrane, which does not have sclerotic changes in the bottom and at the edges; is usually secondary.

symptomatic ulcers are observed when:

stressful conditions

endocrine diseases

acute and chronic circulatory disorders

after taking medication

chronic ulcer - an ulcer that penetrates beyond the mucosa into the thickness of the stomach wall, has gross fibrous changes in the bottom and ridge-like raised edges; the proximal edge of the ulcer is undermined.

LAYERS OF CHRONIC GASTRIC ULCER:

1. zone of exudation or necrosis

2. zone of fibrinoid swelling

3. zone of granulation tissue

4. zone of sclerosis.

MAIN COMPLICATIONS OF ULCER:

penetration

perforation

malignancy

pyloric stenosis

bleeding

perigastrid, periduodenitis

diverticulum - protrusion of the wall of the gastrointestinal tract.

Appendicitis is an inflammation of the appendix of the caecum, giving a characteristic clinical syndrome.

Acute appendicitis is:

1. simple

2. superficial

3. destructive (phlegmanous, phlegmanous-ulcerative, apostematous, gangrenous)

chronic appendicitis develops after acute appendicitis and is characterized by sclerotic and atrophic processes, against which inflammatory and destructive changes may appear.

forms of CHOLECYSTITIS:

1. Catarrhal

2. Purulent (phlegmonous)

3. Diphtheritic

4. Chronic

Crohn's disease - a chronic relapsing disease of the gastrointestinal tract, characterized by nonspecific granulomatosis, necrosis, scarring of the intestinal wall.

Explore macros:

79. Phlegmanous appendicitis.

The appendix is ​​thickened, the serous membrane is dull, with fibrinous overlays, the vessels are plethoric. The enlarged lumen is filled with pus (process epiema),

570. Normal gallbladder.

The wall of the gallbladder is thin, the mucous membrane is velvety.

49. Calculous cholecystitis.

The wall of the gallbladder is thickened, sclerosed, there are many stones in the lumen.

50, 180. Cholecystitis.

The wall of the gallbladder is unevenly thickened, the mucous membrane is swollen, dark red

348. Erosion of the gastric mucosa.

On the gastric mucosa, there are multiple superficial mucosal defects with smooth edges, the bottom is black (hematin hydrochloric pigment).

376. Acute stomach ulcers.

On the gastric mucosa, superficial defects with smooth edges of dark red color from 1.5 to 3 cm in diameter are visible

183. Acute duodenal ulcer with perforation.

386. Chronic stomach ulcer.

On the lesser curvature of the stomach, an ulcerative defect of a steep shape up to 1 cm in diameter is visible, the bottom and edges are dense, roll-like.

108. Chronic ulcers of the stomach and duodenum.

On the mucous membrane of the stomach and duodenum, 3 ulcerative defects are visible. In the stomach, an elongated ulcer with undermined dense edges and a dense bottom. In the 12 duodenum there are 2 rounded ulcers located opposite each other (“kissing ulcers”), in one of them there is a perforated hole

128. Melena (bleeding into the lumen of the gastrointestinal tract).

The mucous membrane of the intestine is black (pigment hematin hydrochloride, methemoglobin, iron sulfide)

149, 184. Saucer-shaped stomach cancer. Scirrhus of the stomach.

178. Cancer of the stomach.

Exo- and endophytic growth.

146. Nonspecific ulcerative colitis.

On the mucous membrane of the large intestine, multiple ulcerative defects

various shapes and sizes.

75. Polypoid cancer.

Myoma of the stomach.

To study micropreparations:

62a. Chronic gastric ulcer..

In the bottom of a chronic ulcer, 4 layers are distinguished:

1) on the surface of the ulcerative defect there is a zone of necrosis with leukocytes, 2) under it is a fibrinous exudate, 3) a zone of granulation tissue is visible below, followed by 4) a zone of deep sclerosis with lymphoid infiltrates and sclerosed vessels.

Indicate in the picture:

1 - I zone - necrosis.

2 - II zone - fibrinoid

3 - III zone - granulation tissue.

4 - IV zone - sclerosis.

90. Acute purulent appendicitis (phlegmanous-ulcerative).

(see preparation 151 at the same time. Normal appendix)

All layers of the process are infiltrated with leukocytes, the mucous membrane is ulcerated. In the submucosa, plethoric vessels and hemorrhages

Indicate in the picture:

1 - mucous membrane with ulcerations

2 - submucosa

3 - muscular membrane.

4 - serous membrane

5 - leukocyte infiltration of all layers of the appendix wall.

177. Chronic appendicitis with regeneration of the mucous membrane.

The wall of the process is thickened due to the growth of fibrous connective tissue in all layers. Newly formed low cubic epithelial cells creep onto the ulcerative defect.

140. Cholecystitis.

The wall of the gallbladder is thickened due to the growth of connective tissue. Against the background of sclerosis, there are infiltrates consisting of leukocytes. The mucous membrane is atrophied

74. Solid cancer of the stomach.

The parenchyma and stroma in the tumor are evenly developed. The parenchyma is represented by atypical cells forming cells. The anaplastic epithelium proliferates, in some places it grows beyond the mucosa - infiltrating growth

Tests: choose the correct answers.

426. The causes of acute gastritis are:

1- alcoholism

2- infection

3- ingestion of traumatic substances

427. The following changes are characteristic of atrophic gastritis:

1 - mucous pink, with well-defined folds

2- pale mucous

3- there is a lot of mucus in the stomach

4- focal regeneration of the epithelium

428. The main severe complication of gastric ulcer is:

1- lymphadenitis of regional nodes

2- perforation

3- perigastritis

4- "inflammatory" polyps around the ulcer

429. The most characteristic changes in blood vessels in the bottom of a chronic ulcer are:

1- inflammation and sclerosis of the wall

2- plethora

3- anemia

4- large thin-walled sinusoidal vessels

430. The local factor that is important in the pathogenesis of gastric and duodenal ulcers includes:

1- infectious

2- violation of trophism

3- toxic

4- decrease in the secretion of gastrin and histamine

5- exogenous

431. Layers of the bottom of a chronic stomach ulcer are:

1- exudate

3- granulation tissue

4- sclerosis

432. An autopsy of the deceased revealed a lot of erosions of the stomach from a burn, covered with hematin hydrochloric acid. Erosion formed:

1- before the burn

2- during a burn

433. Coffee-like liquid on the gastric mucosa. When cleared of it, pinpoint hemorrhages and defects the size of a pinhead are visible. Specify the name of the process:

1- petechiae

3- acute ulcers

434. At autopsy, two round ulcers were found in the stomach, located on the lesser curvature, the edges are even, the bottom is thin. Ulcers are:

1- sharp

2- chronic

435. Signs of a chronic ulcer are:

1 - recurrent bleeding

2- dense sclerosed bottom

3- multiplicity of ulcers

4- one, two ulcers

436. The most common localization of stomach cancer is:

2- big curvature

3- lesser curvature

437. A cancerous tumor spreads diffusely through all layers of the stomach wall, dense, the stomach cavity is reduced. Cancer refers to:

1- differentiated adenocarcinoma

2- mucous cancer

438. A woman has clinically determined solid ovarian tumors on both sides. It is necessary to investigate the presence of metastases first of all:

1- in the lungs

2- in the stomach

439. Acute gastritis usually manifests itself in the form of:

1- atrophic

2- hypertrophic

3- purulent

4- surface

5- with restructuring of the epithelium

440. Chronic atrophic gastritis is characterized by:

1- ulceration

2- hemorrhages

3- fibrinous inflammation

4- enterolization of the mucous membrane

5- plethora and diffuse infiltration by leukocytes of the own layer of the mucous membrane

441. Exacerbation of gastric ulcer is characterized by:

1- hyalinosis

2- enterolization

3- regeneration

4- lymphoplasmacytic infiltrate

5- necrotic changes

442. A characteristic symptom of Menetrier's disease is:

1- enterolization of the gastric mucosa

2- chlorhydrolenic uremia (gastric tetany)

3- Virchow metastases

4- giant hypertrophic folds of the gastric mucosa

5- nonspecific intestinal granulomatosis

443. Ischemic colitis can be detected:

1- with atherosclerosis

2- with scleroderma

3- in diabetes

4- for rheumatoid arthritis

444. Rectal changes are characteristic:

1- for ulcerative colitis

2- for Crohn's disease

3- for Hirschsprung disease

445. When ulcerative colitis is malignant, the intestinal mucosa is:

1- smooth

2- polypoid (granular)

3- atrophic

446. Malignancy of adenomatous polyps is more often detected:

1- in the basal sections

2- in superficial departments

3- in the middle departments

447. Familial multiple colon polyposis is found more often:

1- from birth

4- at the end of the first year of life

5- after 3 years

448. Characteristic histological signs of Whipple's disease are revealed:

1- in the lungs

2- in the myocardium

3- in the liver

4- in the kidneys

449. The most characteristic histological sign of Whipple's disease:

1- hemorrhage

3- macrophage infiltrate

4- leukocytosis

450. Cancer is suspected in an emaciated patient. An enlarged, indurated lymph node is palpated above the left clavicle. It is necessary to examine first of all:

2- stomach

3- esophagus

451. The appendix is ​​thickened in the distal part, the serous cover is dull, hyperemic, there are feces and purulent exudate in the lumen. Microscopically - diffuse infiltration of the process wall with neutrophils, no ulcers. Appendicitis refers to:

1- to simple

2- to destructive

452. The appendix is ​​thickened in the middle segment, the serous cover is covered with fibrinous films. Histologically, against the background of diffuse infiltration of the entire thickness of the ulcer wall.

Appendicitis refers to:

1- to phlegmonous-ulcerative

2- to gangrenous

3- to simple

453. The appendix is ​​thickened, the serous cut is covered with fibrin, the wall is black throughout, dull. Appendicitis refers to:

1- to catarrhal

2- to gangrenous

3- to phlegmonous

454. Abortive appendicitis is characterized by:

1- inflammation is mild

2- primary changes resolved

3- area of ​​inflammation is extremely small

455. Thickening of mucus in the lumen of a sclerosed appendix is ​​called:

1- cystic fibrosis

2- mucocele

3- melanosis

456. Characteristic signs of acute appendicitis are:

2- serous exudate in the mucosa and muscle membrane

3- hyperemia

4- sclerosis of the process wall

5- destruction of muscle fibers

457. Characteristic signs of chronic appendicitis are:

1- sclerosis of the walls of blood vessels

2- sclerosis of the process wall

3- purulent bodies

4- lymphoplasmacytic infiltration

5- granulomas

458. Morphological forms of appendicitis are:

1- acute purulent

2- acute superficial

3- acute destructive

4- chronic

5- croupous

459. Complications of appendicitis are:

1- perforation

2- peritonitis

3- liver abscesses

460. Most often cause subhepatic jaundice:

1- Cancer of Vater's nipple

2- pancreatic head cancer

3- liver cancer

461. Cancer of the head of the pancreas causes jaundice:

1- parenchymal

2- hemolytic

3- mechanical

462. Crohn's disease in the destructive phase is characterized by:

1- mucosa in the form of "cobblestone pavement"

2- deep slit-like longitudinal ulceration of the mucosa

3- superficial ulceration

4- granulomas in the intestinal wall

463. The mucosa of the ileum is divided by deep ulcers in the form of cracks and resembles a cobblestone pavement. Name the disease:

3- typhoid fever

464. For nonspecific ulcerative colitis allergic origin characteristic:

1- fibrinous inflammation

2- multiple ulcers

3 - polypoid protrusions of excessively regenerating epithelium

4- fibrinous necrosis of individual sections of the intestine.

Theme VII. Introduction to infections. Typhus: abdominal, typhus, recurrent.

Infectious diseases are diseases caused by infectious agents: viruses, bacteria, fungi.

Invasive - called diseases when protozoa and helminths are introduced into the body.

Typhoid fever is an acute and long-term infectious disease caused by salmonella (Salmonella typhi), in the first week of the disease it is characterized by symptoms of general intoxication (fever, chills) associated with bacteremia; wide involvement of the reticuloendothelial system, accompanied by a rash, abdominal pain and severe weakness in the second week of the disease; ulceration in Peyer's patches with bleeding from small intestine and the development of shock in the third week of illness.

stages of CHANGES IN GROUP LYMPHATIC FOLLICLES OF THE SMALL INTESTINE IN ABDOMINATE TYPHUS:

1. Cerebral swelling

4. Clean ulcers

5. Regeneration

cellular composition of typhoid granuloma - macrophages, the so-called typhoid and lymphoid cells.

ATYPICAL FORMS OF TYPHUS:

1. Kolotief

2. Laryngotif

3. Pneumotyphoid

4. Cholecystothyphus

THE MOST COMMON AND DANGEROUS COMPLICATIONS OF TYPHUS:

1. Intestinal bleeding

2. Perforation of ulcers with subsequent peritonitis

Epithemic typhus. European typhus (lousy typhus) -

an acute infectious disease caused by rickettsia, characterized by damage to the nervous system and blood vessels. It is manifested by general toxic effects, fever, roseolo-petechial rash and disruption of the activity of internal organs, especially the circulatory system.

Macroscopic characteristics are most often poorly expressed - skin rash in the form of red or brown roseola, petechiae, small-point hemorrhages of the conjunctiva eyeball(chiari symptom). In advanced cases, foci of skin necrosis with areas of gangrene are possible.

Microscopic changes in the capillaries develop - destructive-proliferative-endo-thrombo-vyskulitis.

TYPES OF GRANULOMAS IN TYPHUS:

1. mesenchymal - Davydovsky

microglial - Popova.

Recurrent disease is very rare - this is Brill-Zinser disease. (Repeated sporadic typhus).

Explore macros:

Description of drugs Pathological Anatomy in Lesson No. 28

ACTIVITY #28diseases of the liver and biliary system.

macropreparation "Massive progressive necrosis liver - stage yellow dystrophy" .

The liver is sharply reduced in size, its capsule is wrinkled, the consistency is flabby, on the section, the liver tissue is of a clayey appearance.

micropreparation № "Massive progressive necrosis liver - stage yellow dystrophy.

In the central sections of the lobules, hepatocytes are in a state of necrosis. Among the necrotic masses, individual PMNs are found. In the peripheral sections of the lobules, hepatocytes are in a state of fatty degeneration: when stained with Sudan III, fatty detritus is visible in the hepatocytes of the peripheral sections of the lobules - drops of fat.

macropreparation "Adipose dystrophy liver ( fatty hepatosis ) »

The liver is enlarged in size, the surface is smooth, the edge is rounded, the consistency is flabby, on the cut it is ocher-yellow.

micropreparation № "Spicy viral hepatitis ».

Hepatocytes in a state of hydropic and balloon dystrophy, which is an expression of focal colliquat necrosis. Some hepatocytes are in a state of apoptosis: reduced in size, with eosinophilic cytoplasm and a pycnotic nucleus, or have the appearance of a hyaline-like body that is pushed into the lumen of the sinusoid (Kownsilman's body). Bile capillaries are dilated, filled with bile. Portal tracts are dilated, infiltrated with lymphohistiocytic elements, accumulations of which are visible inside the lobules in the sinusoids, as well as in areas where groups of hepatocytes are in a state of necrosis. In the peripheral parts of the lobules, binuclear and large hepatocytes (regenerative forms) are often found.

electronogram "Balloon dystrophy hepatocyte at sharp viral hepatitis" - demonstration .

micropreparation № "Chronic viral hepatitis AT moderate activity" .

The portal tracts are thickened, sclerosed, abundantly infiltrated with lymphocytes, macrophages (histiocytes), plasma cells with an admixture of PMNs. The infiltrate goes through the border plate into the parenchyma and destroys hepatocytes. Foci of necrotic hepatocytes are surrounded by lymphocytes and macrophages (stepwise necrosis). Foci of infiltration are visible inside the lobules. Outside the areas of necrosis, hepatic cells are in a state of hydropic dystrophy.

electronogram "Hepatocyte destruction by killer lymphocyte in chronic active hepatitis".

At the site of contact of the lymphocyte with the hepatocyte, destruction of its cytoplasmic membrane is visible.

macropreparation "Viral SKD ( postnecrotic ) cirrhosis liver"

The liver is reduced in size, dense, the surface is coarse-nodular: nodes of uneven size, more than 1 cm, separated by wide fields of connective tissue.

micropreparation № "Viral multilobular ( postnecrotic ) cirrhosis liver" - picture . The liver parenchyma is represented by false lobules (regenerate nodes) of various sizes. In each node, fragments of several lobules can be seen (multilobular cirrhosis), hepatic beams are not distinguishable, the central vein is absent or displaced to the periphery. Protein degeneration and necrosis of hepatocytes. There are large hepatocytes, with two or more nuclei. Parenchymal areas are separated by wide fields of connective tissue stained red with picrofuchsin. In the connective tissue fields, contiguous triads, sinusoid-type vessels, proliferating cholangiols, and lymphohistiocytic infiltrates are visible.

macropreparation "Alcoholic small-knot ( portal ) cirrhosis liver"

The liver is enlarged (in the final - reduced) in size, yellow, dense, with a uniform small-hilly (small-nodular) surface; nodes no more than 1 cm in diameter, separated by uniform narrow layers of connective tissue.

micropreparation № "Alcoholic monolobular ( portal ) cirrhosis liver" - picture . The parenchyma is represented by false lobules, uniform in size, built on fragments of one lobule (monolobular cirrhosis). The nodes are separated by narrow strands of connective tissue (septa), hepatocytes with symptoms of fatty degeneration. In the connective tissue septa, lymphohistiocytic infiltration with an admixture of PNL and proliferation of the bile ducts is visible.

macropreparation "Liver at mechanical jaundice" - demonstration .

CHAPTER 11

II. PRIVATE PATHOLOGICAL ANATOMY. CHAPTER 12

CHAPTER 19. INFECTIONS, GENERAL CHARACTERISTICS. PARTICULARLY DANGEROUS INFECTIONS. VIRAL INFECTIONS

III. OROFACIAL PATHOLOGY. CHAPTER 23

CHAPTER 26. EPITHELIAL TUMORS, PRECANCER DISEASES AND LESIONS OF THE SKIN OF THE FACE, HAIRY PART OF THE HEAD, NECK AND MUCOSA OF THE MOUTH. TUMORS AND TUMOR-LIKE FORMATIONS OF SOFT TISSUES OF THE OROFFACIAL REGION AND NECK FROM DERIVATIVES OF MESENCHYME, NEUROECTODERM AND MELANIN-PRODUCING TISSUE

CHAPTER 28

CHAPTER 17. DISEASES OF THE GASTROINTESTINAL TRACT

CHAPTER 17. DISEASES OF THE GASTROINTESTINAL TRACT

DISEASES OF THE pharynx and throat. DISEASES OF THE STOMACH. IDIOPATHIC DISEASES OF THE INTESTINE (CROHRON'S DISEASE AND ULCERATIVE COLITIS)

PROCESS OF THE CECAQUS

Angina (tonsillitis)- an infectious disease characterized by inflammatory changes in the lymphoid tissue of the pharynx and palatine tonsils (Pirogov rings). Forms of tonsillitis: acute, chronic (recurrent).Forms of acute tonsillitis:exudative - catarrhal, fibrinous, purulent; necrotic - necrotic, gangrenous, ulcerative-membranous (a special form is Simanovsky-Plaut-Vincent's angina); by localization - lacunar, follicular.Complications of tonsillitis:local - paratonsillar abscess, cellular phlegmon, thrombophlebitis; common - sepsis, rheumatism, glomerulonephritis.

Gastritis- inflammation of the gastric mucosa.Types of gastritis:acute and chronic;by topography- diffuse and focal (antral, fundal, pyloroanthral, ​​pyloroduodenal).

Forms of acute gastritis:catarrhal, fibrinous, purulent (phlegmonous), necrotic. In any form - erosion and acute ulcers.Erosion- a superficial defect of the mucous membrane is not deeper than its muscular plate.Ulcer- a deep defect, the bottom of which is the muscular or even serous layer of the organ wall.

Chronic gastritisis a group of diseases of the stomach of different etiologies, characterized by a combination of chronic inflammation and violations of regeneration with structural restructuring of the gastric mucosa.Chro-classification

nic gastritis:by etiology and pathogenesis- Helicobacter pylori (type B), autoimmune (type A), reflux gastritis (type C);by topography; by morphological type- superficial and atrophic;by activity.Take into account the presence, nature and severityintestinal metaplasia and dysplasia (intraepithelial neoplasia).Chronic atrophic pangastritis is an optional precancer.

peptic ulcer- a chronic, cyclically current disease, the main clinical and morphological manifestation of which is a chronic recurrent gastric or duodenal ulcer.Complications of peptic ulcer:destructive- bleeding, perforation (perforation with the development of peritonitis), penetration (into the liver, gallbladder, omentum, pancreas);cicatricial- deformation and stenosis of the inlet and outlet sections of the stomach and duodenal bulb;malignancy- malignancy (very rare).

Tumors of the stomach:epithelial(adenoma and cancer) and non-epithelial(mesenchymal, lymphomas). Macroscopically, exophytic formations of the stomach (hyperplastic growths, adenomas) are calledpolyps.Classification of stomach cancer:macroscopic form of growth- exophytic (polypous, mushroom-shaped, saucer-shaped), endophytic (plaque-like), ulcerative-infiltrative, plastic linitis;on

histological type- intestinal type (intestinal - types of adenocarcinomas, etc.) and diffuse (skirr, solid, cricoid, etc.);according to the depth of invasion and the stage of generalization of the tumor process(TNM system). Diagnostically significant lymphogenous metastases:to the left supraclavicular lymph node(Virchow's metastasis),retrograde - to the ovaries(cancer of Krukenberg)into the pararectal tissue(Schnitzler metastases).

Idiopathic bowel disease: Crohn's disease(granulomatous inflammation of any part of the digestive tract) andulcerative colitis.Ulcerative colitis is a facultative precancerous disease.

Appendicitis- inflammation of the appendix of the caecum. In surgical practice, it belongs to the group of diseases referred to as acute abdomen (peptic ulcer with perforation, peptic ulcer with bleeding, acute intestinal obstruction, strangulated hernia, acute cholecystitis, acute appendicitis).Forms of appendicitis:acute - simple, superficial, phlegmonous (options - apostematous, phlegmonous-ulcerative), gangrenous (primary and secondary); chronic.Complications of acute appendicitis:peritonitis, mezenteriolit, pylephlebitis, pylephlebitic liver abscesses.

Rice. 17-1. Micropreparation. Chronic tonsillitis in the acute stage: the surface epithelium is damaged (dystrophic and necrotic changes, areas of ulceration), infiltrated by neutrophilic leukocytes (1). Lymphoid follicles are atrophied, there is sclerosis in the stroma (2). In dilated lacunae, neutrophilic leukocytes and bacterial colonies are determined (3).

Staining with hematoxylin and eosin: x160

Rice. 17-2. Macropreparations (a, b). Chronic multifocal atrophic gastritis: gastric mucosa with smoothed folds, thinned, pale, grayish in color, with small punctate hemorrhages, erosions (b - preparation by I.N. Shestakova)

Rice. 17-3. Micropreparations (а-d). Chronic atrophic gastritis: the mucous membrane of the fundus of the stomach is sharply thinned, the glands are reduced in size, the distance between them is increased, the epithelium of the glands acquires more primitive features, loses the ability to produce gastric juice and hydrochloric acid, and secretes mucus. There are foci of intestinal metaplasia with goblet cells (1). In the lamina propria of the mucous membrane diffuse lymphoplasmacytic infiltrate, lymphoid follicles (2), severe sclerosis; c, g - Helicobacter pylori in the lumen of the glands.

a, b - hematoxylin and eosin staining, c - Vartin-Stari staining, d - immunohistochemical method: a - x 100, b - x200, c, d - x400

Rice. 17-4. Macropreparations (a-e). Acute erosions and ulcers of the stomach: in the gastric mucosa, there are multiple small superficial (erosions) and deeper, capturing submucosal and muscular layers of the stomach wall (acute ulcers), rounded defects with soft, even edges and a brownish-black or gray-black bottom ( due to hematin hydrochloride, which is formed from erythrocyte hemoglobin under the action of hydrochloric acid and gastric juice enzymes); (see also Fig. 3-4, 4-10) (a, c - preparations by I.N. Shestakova, d, e - preparations by N.O. Kryukov)

Rice. 17-4. Continuation

Rice. 17-4. The ending

Rice. 17-5. Micropreparations (a, b). Erosion of the gastric mucosa: in the gastric mucosa, a superficial (within the mucous membrane) focus of necrosis is determined with the formation of a shallow defect - erosion with perifocal leukocyte inflammatory infiltration. At the bottom of the erosion there are deposits of hematin hydrochloric acid (1). Staining with hematoxylin and eosin: x 100 (b - preparation by N.O. Kryukov)

Rice. 17-6. Macropreparations (a-n). Chronic ulcer of the stomach (a, c-d, g-n) and duodenal ulcer (b, f): chronic ulcers with bleeding - arrosed and thrombosed vessels in the bottom of the ulcers (c, f, l, n), perforation (e, k - view from the outside, from the side of the abdominal cavity - j) and penetration (b, d, g-i, n). Round-shaped defects of the mucous membrane and the wall of the stomach (or duodenum) with roller-shaped compacted edges. The cardial edge of the ulcer is undermined, overhangs, and the edge facing the pyloric section of the stomach is flat, has the form of a terrace, the steps of which are formed by the mucous membrane, submucosal and muscle layers. This configuration is due to the constant displacement of the edges of the ulcer during peristalsis. The mucous membrane around the ulcer is changed, its folds can be located radially in relation to the ulcer defect (fold convergence -

a, g, i, m); (а-c, f - preparations of I.N. Shestakova,

b, d, i-n, - preparations of N.O. Kryukov)

R is. 17-6. Continuation

Rice. 17-6. Continuation

Rice. 17-6. Continuation

Rice. 17-6. Continuation

Rice. 17-6. The ending

Rice. 17-7. Micropreparations (a, b). Chronic gastric ulcer (a) and duodenal ulcer (b): a defect in the wall of the stomach or duodenum, involving the mucosa, submucosa and muscle membrane. There are 4 layers in the bottom of the defect: 1 - fibrinous-purulent exudate; 2 - fibrinoid necrosis; 3 - granulation tissue; 4 - scar tissue with sclerosed and hyalinized vessels. At the edges of a chronic gastric ulcer, the processes of restructuring of the epithelium (hyperplasia of the cervical epithelium, atrophy of the glands, intestinal metaplasia, mild or moderate dysplasia). Staining with hematoxylin and eosin: a - x 120, b - x60 (b - preparation by N.O. Kryukov)

Rice. 17-8. Macropreparations (a, b). Polyp of the stomach: a small exophytic formation protruding into the lumen of the stomach on a wide base, covered with a mucous membrane (histologically: a - adenoma, b - leiomyoma); (a - preparation by N.O. Kryukov, b - preparation by I.N. Shestakova)

Rice. 17-9. Macropreparations (а-d). Gastric cancer (nodular or diffuse forms): a - fungous, b - saucer-shaped, c, d - endophytic diffuse cancer (d - view from the outside of the stomach, from the side of the serous membrane); nodular form - on the lesser curvature of the stomach, a large mushroom-shaped or saucer-shaped node with raised jagged edges and a lowered ulcerated bottom is determined. The tissue of the node is whitish in color, dense in consistency, grows through all layers of the stomach wall, has no clear boundaries. Diffuse form: the wall of the stomach is sharply thickened over a considerable extent due to the growth of a dense whitish tissue that does not have clear boundaries. The mucous membrane with smoothed folds, rigid (see also Fig. 9-5, 10-7); (a - preparation by N.O. Kryukov, b - preparation by I.N. Shestakova)

Rice. 17-9. The ending

Rice. 17-10. Micropreparations (a, b). Adenocarcinoma of the stomach: in the thickness of the mucous membrane and muscular layer of the stomach there are atypical glandular complexes of different sizes and shapes (tissue atypia). Tumor cells and their nuclei are polymorphic, of different sizes and shapes, the nuclei are hyperchromic (cellular atypia). Mitoses (typical and atypical) are not numerous, the level of tumor proliferative activity is moderate. Tumor complexes invade the lamina propria and muscle layer- invasive growth (see also Fig. 9-6). Staining with hematoxylin and eosin: x 160

Rice. 17-11. macropreparation. Phlegmonous appendicitis: appendix increased in size, the walls are thickened, diffusely saturated with pus (when pressed, pus is also released from the lumen of the process), the surface is dull, reddish-bluish, with full-blooded vessels; the mesentery of the process is also full-blooded, with foci of suppuration, hemorrhages (see also Fig. 6-6); (preparation by I.N. Shestakova)

Rice. 17-12. Micropreparations (a, b). Phlegmonous-ulcerative appendicitis: pronounced leukocyte infiltration of all layers of the appendix wall, edema, inflammatory hyperemia, necrosis and ulceration of the mucous membrane, atrophy of the lymphoid tissue.

Staining with hematoxylin and eosin: a - x 60, b - x 200

Rice. 17-13. macropreparation. Chronic appendicitis: appendix of normal size (but can be enlarged or reduced), the serous membrane is smooth, shiny, whitish, with scraps of adhesions. The wall of the process is thickened, compacted (sclerosis). The mucous membrane is pale pink (atrophy). The lumen of the process is obliterated in places

Rice. 17-14. Micropreparations (a, b). Crohn's disease: deep slit-like ulcerative defect of the mucous membrane, lymphomacrophage, with an admixture of plasmocytes, infiltration and sclerosis of all layers of the intestinal wall (a), granuloma with giant multinucleated cells in the submucosal layer (b). Staining with hematoxylin and eosin: a - x 100, b - x 200

Rice. 17-15. Micropreparations (a, b). Ulcerative colitis: pronounced diffuse lymphomacrophage with an admixture of leukocytes, inflammatory infiltrate, edema, microcirculatory disorders of the colon mucosa, crypt abscess (1).

Staining with hematoxylin and eosin: a - x 100, b - x 200

Rice. 17-16. Macropreparations (a, b). Gangrene of the intestine: ischemic necrosis of a part of the small or large intestine with obstruction of the mesenteric arteries by blood clots, thromboembolism, atherosclerotic plaques (acute ischemic bowel disease); (a - preparation by A.N. Kuzin and B.A. Kolontarev)

Rice. 17-17. Macropreparations (a, b). Diverticulosis of the colon: multiple finger-like protrusions in the wall of the colon, from the side of the mucous membrane, the entrances to the diverticula look like dark spots (arrows); (preparations by I.N. Shestakova)

Rice. 17-18. macropreparation. Meckel's diverticulum (preparation by I.N. Shestakova)

• 1 Causes of pain
• 2Gastritis
• 3 Peptic ulcer
• 5Food poisoning
• 6Duodenitis and pancreatitis
• 7Diagnosis and treatment

1 Causes of pain

If you feel severe discomfort, you should consult a specialist. An important aspect of diagnosis is to clarify the nature of the pathology. Pain in the stomach is most often concentrated in the projection of the organ on the abdominal wall. This region is called the epigastric region. Pain in the stomach area can be localized, diffuse, radiating, acute, dull, paroxysmal, burning and cutting.

To establish the cause of its occurrence, it is necessary to identify the intensity of the syndrome. In this case, the main characteristics of pain are determined:

• character;
• appearance time;
• duration;
• localization;
• connection with food intake;
• weakening or strengthening during movement, after defecation or when changing posture;
• combination with other symptoms (nausea, loss of appetite, vomiting, bloating).

The sensation of pain in the stomach in most cases is associated with damage to the organ. The most common reasons are:

• acute and chronic gastritis;
• stomach ulcer;
• the presence of polyps;
• damage to the mucous membrane of an organ during food poisoning (intoxication or toxic infection);
• damage due to abdominal trauma;
• severe stress;
• intolerance to certain products;
• injury to the mucosa by accidentally swallowed objects.

Pain in the stomach area can be due to other reasons. These include pancreatitis, peptic ulcer of the 12th intestine, colitis, enterocolitis, cholecystitis, dyskinesia biliary tract, irritable bowel syndrome, appendicitis, heart disease.

2Gastritis

The most common causes of stomach pain are acute or chronic gastritis. These forms of the disease are characterized by inflammation of the mucous layer of the organ against the background of exposure to irritating factors. Quite often, gastritis has an infectious nature. In this case, Helicobacter pylori bacteria act as a starting point. The disease occurs in children, young and old people. When it hurts in the stomach, in this case there is an acute gastritis, which is divided into simple, catarrhal, erosive, fibrinous and phlegmonous. If the disease becomes chronic, organ atrophy often develops. The main provoking factors for the occurrence of gastritis are:

• abuse of spicy, fried, hot or cold foods;
• alcohol consumption;
• smoking;
• infection with Helicobacter bacteria;
• accidental or intentional use of acids or alkalis;
• uncontrolled intake of medications (drugs of the NSAID group).

The symptoms of gastritis are varied. In children and adults, discomfort in the stomach is the main symptom of the disease. Most often worried Blunt pain. Sharp manifestations are typical for acute inflammation of the mucosa. With gastritis, the pain syndrome can be paroxysmal or constant. There is a clear connection with food intake (spasm appears after eating and when a person is hungry). Additional symptoms of the disease may include belching, nausea, loose stools, bloating, and a feeling of acid in the mouth. not pronounced It's a dull pain characteristic of chronic gastritis with normal acidity.

3 Peptic ulcer

Acute pain in the stomach associated with eating may indicate the presence of a peptic ulcer. It proceeds in a chronic form. The pain syndrome is most pronounced during the period of exacerbation. Ulcers form on the background of stress, gastritis, the use of certain drugs, endocrine diseases. The pathogenesis of the formation of this defect is associated with the suppression of protective mechanisms (impaired synthesis of mucus covering the stomach), as well as with an increase in the acidity of gastric juice. The symptoms of stomach ulcers are similar to those of gastritis. The main signs of the disease include:

• severe pain in the epigastric region;
• nausea and vomiting after eating;
• weight loss;
• loss of appetite.

With ulcerative lesions, the stomach hurts after eating. This is the main difference from the pathology of the 12th intestine. Pain syndrome occurs almost immediately after eating (within one and a half hours). There is a certain connection of exacerbation with the time of year. Most often, a person suffers from attacks of pain in the fall and spring. In the case of complications (perforation, bleeding), symptoms can increase dramatically. Such a state requires emergency care. The processes occurring in the stomach, the causes of which may be different, are often reversible.

4Cancer

If the stomach hurts, the cause may lie in oncology. This is one of the most common malignant pathologies. Nearly a million people worldwide die from stomach cancer every year. For a long time, the disease may not manifest itself. Quite often, cancer is detected already at stage 3 or 4, when treatment is ineffective. Men suffer from this disease more often than women. Cancer is dangerous because the tumor in the later stages is capable of metastasizing to other organs, which is why patients die. The exact cause of the disease is still unknown. Possible etiological factors are: the presence of atrophic gastritis, infection of the organ with Helicobacter bacteria, exposure to toxic and carcinogenic substances, poor nutrition, medication, alcoholism, aggravated heredity, Menetrier's disease.

Cancer symptoms on early stages presented by decreased appetite, aversion to meat, nausea, bloating, weight loss, malaise, weakness, and swallowing disorders. In the later stages, patients may be disturbed by aching pain. In most cases, it is due to the germination of the tumor in neighboring organs. Persistent shingles pains appear when the neoplasm is introduced into the pancreas. Operative treatment should be started as soon as possible. Acute pain, resembling an angina attack, is characteristic of a tumor that has grown into the diaphragm. If the pain syndrome is combined with a transfusion in the abdomen, a violation of the stool by the type of constipation, this may indicate the involvement of the transverse colon in the process.

5Food poisoning

Sharp pain in the stomach may be a sign food poisoning. This is a disease that develops when eating poor-quality food containing pathogenic microorganisms, their decay products, or various toxic compounds. All food poisonings are divided into the following forms:

• microbial;
• non-microbial etiology;
• mixed.

The first group includes food toxic infections and intoxications. In this situation, the causative agents are bacteria (clostridia, coli, proteus, streptococci), fungi, toxins. Poisoning is also possible with poisonous plants, mushrooms, berries, fish caviar, seafood, salts of heavy metals, pesticides, pesticides. Symptoms in this pathology are caused by inflammation of the stomach against the background of exposure to toxins.

In most cases, there are signs of gastroenteritis. These include constant pain in the muscles, head, nausea, vomiting, fever, weakness, frequent stools. Often there are symptoms of dehydration. Diagnostic features food poisoning are:

• acute, sudden onset;
• connection of pain with food intake;
• simultaneous onset of symptoms in a group of individuals;
• the speed of the disease.

6Duodenitis and pancreatitis

Pain in the epigastric region may be a symptom of duodenitis (inflammation of the mucous membrane of the 12th intestine). It can occur in acute and chronic form. This is the most common pathology of this organ. Quite often, this disease is combined with enteritis and gastritis. The main causes of inflammation of the 12th intestine are:

• nutritional errors;
• the use of alcoholic beverages;
• bacterial infection;
• the presence of an ulcer or gastritis;
• violation of blood supply;
• chronic pathology of the liver and pancreas.

The main symptoms of the disease depend on its form. Duodenitis, which arose against the background of an ulcer or infectious gastritis, is characterized by pain on an empty stomach, at night and a few hours after eating. Strong manifestations are characteristic of the acute type of pathology. When combined with inflammation of other parts of the small intestine, symptoms may include malabsorption syndrome, dyspeptic disorders. In case of stagnation of the secret of the 12th intestine, there are paroxysmal pains, belching, nausea, vomiting, bloating, rumbling. With duodenitis, the outflow of bile can be disturbed. In this situation, pain appears in the epigastric region. The clinical picture resembles biliary dyskinesia.

If something hurts in the stomach, the cause may be pancreatitis, the symptoms of which, as a rule, are quite pronounced. The pain syndrome is most pronounced in acute inflammation of the pancreas. The latter is located next to the stomach. This pathology is characterized by the appearance of pain in the upper abdomen. It can last from several minutes to several days. The pain is intense, constant and disturbs the patient. It can give to the left or right half of the body, depending on which part of the organ is affected (head, body or tail). The pain syndrome intensifies during meals and requires treatment. Often it takes on a shingling character. Additional signs of the disease include nausea, vomiting, bloating, tenderness on palpation, and an increase in general body temperature.

7Diagnosis and treatment

If the stomach is sick, then you should not put off a visit to the doctor on the back burner, because the consequences can be dangerous. Treatment is carried out only after the cause is established. pain syndrome. Diagnostics includes:

• a detailed survey of the patient;
• physical examination (palpation of the abdomen, auscultation of the lungs and heart);
• general and biochemical blood test;
• conducting FGDS;
• determination of the acidity of gastric juice;
• a blood test for the presence of Helicobacter pylori;
• Ultrasound of the abdominal organs;
• laparoscopy;
• study of feces;
• contrast radiography;
• CT or MRI;
• duodenal sounding;
• Analysis of urine.

Colonoscopy may be done if colitis is suspected. A biopsy is done to rule out stomach cancer. How to get rid of stomach pain? Therapy should be aimed at eliminating the underlying cause. If the stomach is inflamed, what to do in this situation? Treatment of gastritis involves adherence to a strict diet, the use of drugs (antacids, proton pump blockers, gastroprotectors). The use of Almagel, Phosphalugel and Omez is indicated for the form of the disease with high acidity. If Helicobacter bacterium is detected, antibiotics and Metronidazole are used.

Therapy for acute pancreatitis includes temporary fasting, application of cold to the abdomen, the use of antispasmodics, omeprazole, diuretics, infusion therapy.

With purulent pancreatitis, treatment necessarily includes antibiotics. If vomiting is present, antiemetics (metoclopramide) are used. With the development of peritonitis and necrosis of the organ, an operation is indicated. The chronic form of pancreatitis involves dieting, taking enzyme preparations (Panzinorma, Pancreatin, Mezima). In case of gastric cancer, surgical treatment (resection of the organ or its removal). Thus, the causes of abdominal pain can be very different. If any, you should consult your doctor.

What to do in case of exacerbation of peptic ulcer of the stomach?

If the patient has an acute critical condition associated with perforation of a stomach ulcer, then emergency treatment is necessary, since peritonitis in this case is rapidly progressing. The symptoms of perforation are:

• the appearance of a sharp pain, rapidly spreading throughout the abdomen;
• muscle tension of the walls of the peritoneum;
• phenomena preceding fainting (dizziness, ringing in the ears, weakness);
• chills;
• nausea;
• dry mouth.

Traditional Therapies

Therapeutic care in the phase of exacerbation of gastric ulcer is determined based on the patient's condition, his age, the nature of clinical symptoms. However, the treatment of uncomplicated forms is almost always based on the use of bactericidal agents, for example, Amoxicillin, Metranidazole, Clarithromycin. Due to these drugs and some others, also belonging to the group of antibiotics, it becomes possible to cure the pathology of the gastric mucosa, since they eliminate the main cause - the pathogenic microorganism Helicobacter pylori.

In addition to antibacterial drugs in the treatment of acute ulcers, the following can be used:

1. means that normalize the level of acidity of the digestive juice (Omeprazole, Ranitidine);

2. drugs with a gastroprotective (protective) property (De-nol and other bismuth-containing medicines);

3. dopamine central receptor blockers (Primperan, Reglan, Cerucal);

4. drugs with a psychotropic effect, if the patient suffers from irritability, insomnia, a feeling of constant anxiety (Tazepam, Elenium);

5. adrenergic agents that have antisecretory and suppressive gastrin release action (Obzidan, Inderal).

In the treatment of exacerbation of gastric ulcer, certain physiotherapeutic methods have also proven themselves: ozocerite and paraffin applications, magnetic and hydrotherapy, sessions of modulated sinusoidal currents.

Carrying out all activities in combination with a diet in 80-90% of cases allows you to achieve a stable remission of the pathology. However, conservative treatment does not always help, and then the patient is shown surgical intervention in various ways depending on the circumstances (selective proximal vagotomy, resection, endoscopy).

Indications for gastric surgery:

• perforation ulceration;
• an ulcer complicated by bleeding of a profuse nature (bleeding leading to hypovolemia);
• pyloric stenosis;
• defect penetration.

Folk recipes for treatment

Apply folk ways to cure an ulcer, experts do not recommend due to the risk of aggravating the situation. Such treatment is especially prohibited in complicated acute forms. But in order to prevent exacerbation, use some unconventional recipes doctors allow, for example, a remedy:

1. from birch leaves (1 teaspoon of crushed fresh leaves of this tree is poured with a glass of boiling water, infused for 1-2 hours);

2. from coltsfoot (the infusion is prepared similarly to the previous method with one difference that not only the leaves of the plant, but also the flowers themselves can be used); besides, this folk recipe helps to treat both the stomach and the bronchi;

3. from medicinal marshmallow (1 large spoonful of its ground rhizome is poured with 250 ml of boiling water, everything languishes over low heat for 30 seconds, and then infused for about half an hour).

All of the listed traditional medicine should be drunk before meals 3 times a day.

Diet for ulcers

Compliance with dietary nutrition is equally important during exacerbation of the inflammatory process, and in the stage of its remission, and in case of complications with stenosis, bleeding and other life-threatening factors. Therefore, the doctor prescribes a personal diet to the patient, based on:

• sparing of the gastroduodenal mucosa with the elimination of all chemical, thermal and mechanical stimuli;
• fractional nutrition (the patient is recommended to eat and drink in small portions, but every 3-4 hours);
• correction of fats in the direction of increase;
• increasing the protein quota;
• reducing the proportion of carbohydrates in the daily diet.

Diet in the treatment of stomach ulcers should be observed for at least 6-9 months. When the disease recedes, going into a remission phase, and food does not cause discomfort to the stomach, you can gradually return to the usual type of dishes (not pureed and not very boiled), but you still have to completely abandon coarse and harmful industrial products.

In addition to diet, an important role in the prevention and treatment of acute ulcers is played by the exclusion of alcohol and energy drinks because they cause bleeding and the growth of erosive inflammation.

Ulcer of the duodenal bulb

One of the most common types of erosive formations of the gastrointestinal tract is the ulcer of the duodenal bulb. The disease is widespread. According to official data, up to 10% of the world's population is ill. Deformation develops due to a failure in the chemical processing of food. The anatomy of erosive formations is different, but more often they form on a bulb that has the shape of a ball. The bulb of the duodenum is located at the very beginning of the intestine, at the exit from the stomach. Treatment is long and difficult.

It can be deformed on the front and back wall(kissing sores). The duodenal ulcer also has a special location - at the end or at the beginning (mirror). Mirror erosions are treated like other forms. Negative factors affecting the functioning of the stomach and intestines provoke the appearance of ulcers of various shapes. The risk group includes middle-aged people and those who are forced to work the night shift.

If there is a failure in the processing of food by the stomach, an ulcer of the duodenal bulb may occur.

Causes of duodenal ulcer

Most often, inflammation of the duodenum occurs due to the aggressive action of acid. In the absence of therapy, the development of perforated ulcers and bleeding is possible. There can be a number of reasons:

• disturbed diet (a lot of fatty, spicy, diet abuse, carbonated drinks);
• bacterium Helicobacter - the cause of ulcerative formations in most cases;
• smoking, alcohol;
• severe stress or systematic stay in a state of emotional stress;
• hereditary predisposition;
• long-term use of certain anti-inflammatory drugs;
• incorrectly prescribed treatment at the initial stage of the disease.

Kissing ulcers in the intestines may appear due to concomitant causes: HIV infection, liver cancer, hypercalcemia, renal failure, Crohn's disease, etc.

Symptoms

Symptoms of a duodenal ulcer are also characteristic of other types of gastrointestinal ulcers, and they appear depending on the stage of the disease:

• heartburn;
• nausea in the morning or after eating;
• pain in the epigastric region;
• pain in the stomach at night;
• flatulence;
• the appearance of a feeling of hunger after a short period of time after eating;
• if the disease is in advanced form, bleeding may open;
• vomit;
• pain localized in the lumbar region, or retrosternal part.

The inflammatory lymphofollicular form of the duodenum has a different nature of pain: stabbing pain, sharp or aching. Sometimes it goes away after the person has eaten. Hunger pains usually occur at night, and to eliminate discomfort, it is recommended to drink a glass of milk or eat a little. Night pain is caused by a sharp increase in acidity.

stages

The intestinal healing process is divided into 4 main stages:

• Stage 1 - initial healing, the creeping of layers of the epithelium is characteristic;
• stage 2 - proliferative healing, in which protrusions in the form of papillomas appear on the surface; these formations are covered with regenerating epithelium;
• Stage 3 - the appearance of a polysade scar - an ulcer on the mucous membrane is no longer visible; a more detailed study shows many new capillaries;
• Stage 4 - scar formation - the bottom of the ulcer is completely covered with new epithelium.

Erosive kissing formations on the duodenum 12 heal after therapy. Many ulcers in a small area of ​​the intestine leads to the formation of several scars. The result of such healing is cicatricial and ulcerative deformity of the duodenal bulb. The appearance of fresh scars leads to a narrowing of the lumen of the bulbous sector. Inflammatory cicatricial deformity duodenal bulb has negative consequences, for example, stagnation of food and malfunctions of the entire gastrointestinal tract.

There is also a distribution by stage: exacerbation, scarring, remission.

One of the forms of intestinal ulcers is lymphoid hyperplasia of the duodenal bulb, which is characterized by inflammation due to a violation in the outflow of lymph. The causes of occurrence are exactly the same as those of a duodenal ulcer. Also have similar symptoms. Lymphofollicular dysplasia is a pathology in the mucous membrane of the intestine or stomach. It is characterized by the appearance of rounded formations on a wide base. Lymphofollicular dysplasia is deformed and has a dense texture and punctate dimensions. The lymphofollicular mucosa is infiltrated. Development stages:

1. acute;
2. chronic.

Diagnosis of the disease

The FGDS method (fibrogastroduodenoscopy) will help to accurately diagnose the presence of a duodenal ulcer. Using a special probe with a camera, the surface of the intestine is examined. It is this diagnostic method that will determine the location of the ulcer, its size and stage of the disease. Usually inflammation is observed, or the surface is hyperemic, covered with dotted erosions of a dark red color. The area of ​​the intestine is inflamed in the region of the mouth, and the mucosa is hyperemic.

Be sure to appoint tests to determine the bacterium Helicobacter. As a material for testing, not only blood and feces are used, but also vomit, material after a biopsy. Auxiliary diagnostic methods include x-ray, palpation in the stomach, complete blood count.

Treatment

After the diagnosis of "inflammation of the duodenal bulb" is made, treatment should be started immediately, since serious complications may develop. Kissing ulcers are treated mainly with medication. During an exacerbation, hospitalization is necessary.

The doctor selects drugs and physiotherapy individually for each patient, taking into account the characteristics of the body and stage. For example, the chronic or lymphofollicular stage is treated differently than during an exacerbation. This scheme usually includes such medicines:

• bismuth-based drugs, in case of detection of Helicobacter bacteria; such drugs have a depressing effect on pathogenic microflora;
• drugs that reduce the amount of gastric juice produced: blockers, inhibitors, anticholinergics;
• prokinetics - improve intestinal motility;
• unpleasant pain is eliminated with the help of antacids;
• to fight bacterial cause the appearance of a lymphofollicular ulcer, antibiotics are prescribed;
• gastroprotectors will help prevent the negative effects of hydrochloric acid on the affected area;
• inflammation is relieved by analgesics and antispasmodics.

The combination of medication and physiotherapy contributes to a faster recovery of the body. These techniques include: electrophoresis, ultrasonic exposure, the use of microwaves, modulated current therapy for pain relief. Special physiotherapy exercises will help normalize the motility of the stomach. Gymnastics is a good prophylactic against stagnation in the intestines and stomach.

In addition to the generally accepted methods of healing intestinal ulcers, traditional medicine has long proven its effectiveness. In first place at ulcerative lesions worth freshly squeezed potato juice. It must be drunk three times a day, and only freshly squeezed. Pre-peel the potatoes, rub on a grater, and squeeze through gauze. The first few days, the dosage is one tablespoon. Gradually, it can be increased to half a glass. It is necessary to drink before eating.

Other equally effective remedies include honey, herbs (calendula, St. John's wort, plantain), olive and sea buckthorn oils.

During the period acute form obligatory observance of a bed rest. After the aggravation has passed, you can take short walks. Heavy physical activity and exercise are prohibited. The army is contraindicated for those who have an ulcer. In order not to provoke new attacks, it is important to avoid stress and protect the nervous system.

Compliance with the diet is one of the important factors on the way to recovery and reduction of inflammatory processes. General dietary guidelines are as follows:

• small portions;
• chew each piece thoroughly;
• temporarily exclude foods that provoke the active production of gastric juice (vegetable soups, fish and meat broths);
• in order not to additionally irritate the mucous membrane, the food should be frayed;
• fruit juices should be diluted with water;
• consume milk more often;
• do not use spices in dishes;
• cook grated cereals;
• eat food at the optimum temperature, not too hot and not too cold;
• fractional meals, up to 5 times a day.

Cooking food should be steamed or in the oven. The diet must include non-acidic fruits, kefir, milk, cottage cheese, boiled or steamed vegetables. It is necessary to stop drinking alcohol and smoking, as this can lead to the development of serious complications.

Forecast

A favorable prognosis for recovery can be if the treatment was carried out on time and the correct diet was observed. In case of untimely access to a doctor or incorrectly prescribed drugs, serious complications may develop: lymphofollicular ulcer, bleeding (vomiting blood), perforation of the ulcer ( sharp pain under the sternum) and penetration (due to adhesions, intestinal contents enter neighboring organs). In each of these cases, the only option is surgery.

Duodenal stenosis is a complication. After healing, there are cicatricial changes, which later can cause swelling and spasm. Stenosis usually manifests itself during the acute form or after therapy. There is stenosis in those patients in whom the ulcer does not heal for a long time. Stenosis is accompanied by impaired motility of the intestines and stomach.