Gastritis. Prevention of stress erosive and ulcerative lesions of the gastroduodenal zone in critically ill patients Dishormonal diseases of the genital organs

The date: 19.07.2019

GASTRITIS (gastritis; Greek, gaster stomach + -itis) - defeat mucous membrane stomach with predominantly inflammatory changes in the acute development of the process and the phenomena of dysregeneration, structural adjustment with its progressive atrophy in hron, during, 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. science. 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 I. P. Pavlov and his school in the field of physiology 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.), depth and severity inflammatory changes in the stomach (leukocytosis, accelerated ESR, elevated body temperature, pain as a result of irritation of nerve endings in the wall of the stomach), on the other hand, involvement in patol, the process of other organs, body systems and some aspects of metabolism (collapse, dehydration of the body, thickening of the blood and 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 leukocytic infiltration of all layers of the stomach wall is observed, 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)- 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 of drugs 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. must begin with cleansing the stomach and intestines and prescribing antibacterial drugs (enteroseptol 0.25-0.5 g 3 times a day, levomycetin up to 2 g per day, etc.) and absorbent substances ( Activated carbon, 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. food. 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: grayish-white spots appear from sulfuric and hydrochloric to-t, yellow and greenish-yellow scabs from nitrogen, brownish-red scabs from chromic, bright white plaque from carbolic. reminiscent of 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 aureus, pneumococcus, Proteus, etc. Sometimes it develops as a complication of an ulcer or decaying gastric cancer, with abdominal trauma 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. General state deteriorates 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 of the chest - mediastinitis (see), purulent pleurisy (see) and abdominal cavity - subphrenic 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 antibiotics a wide range action at high doses. If conservative treatment fails, surgical intervention.

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.-morfol., 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%, mucoprotein concentrations below 23%, a positive reaction to the administration of histamine, a normal content of uropepsinogen.

3. With a pronounced secretory insufficiency: the absence of free hydrochloric acid in all portions of gastric juice, a decrease in the concentration of pepsin (or its complete absence), the absence (or traces) of a mucoprotein, a 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 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 such metabolic products 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.). The mechanism of development of separate 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 pattern of mucus hypersecretion, sometimes with a predominance of the excretion phase over the secretion 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 are revealed own shell rollers (printing, table, Fig. 4). Accessory cells normally located in the isthmus gastric glands, often extending 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, a rarefaction of the cytoplasm in the perinuclear zone and around the intracellular tubules is revealed, 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 an ulcer duodenum(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, etc. (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 rather 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 a wedge, displays of an illness, results of a research of gastric secretion (see. Stomach, research methods), rentgenol, researches, 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 when 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. Only a series of targeted shots of the 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, unlike 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 submucous 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 sighting shots 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 wedge, pictures allows to come to the correct diagnosis.

Gastritis in children

Acute gastritis in children occurs due to infection, eating 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 children of 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 current.

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 diseases of the 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 electrophoregram of gastric juice proteins compared to the electrophoregram 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 effects of 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 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 and 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. 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.

Toxic dystrophy of the liver

Toxic dystrophy of the liver or progressive massive liver necrosis is acute or chronic illness characterized by massive tissue necrosis and the development of liver failure. Toxic dystrophy develops as a result of the action of exogenous (mushrooms, foods 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 which depend on the age 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 the 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 hepatic 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 with the hepatic vein, in the lumen of which a thrombus is visible.

127. Icteric necrotic nephrosis.

The kidney on the cut is yellow-green in color, the border of the cortical and medulla, the stale cortex is 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 pronounced.

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

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:

granular

vacuolar

404. The etiological factors of hepatitis include:

medicines

allergy

dystrophy

405. Morphological form of chronic hepatitis is:

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 vermiform 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.

Appendix thickened serosa 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.

3 ulcerative defects are visible on the mucous membrane of the stomach and duodenum. 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. The 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 cleansed 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. Nonspecific ulcerative colitis of allergic origin is characterized by:

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 the small intestine and the development of shock in the third week of the disease.

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 phenomena, 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 roseola red or Brown color, petechiae, punctate conjunctival hemorrhages 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 preparations for 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 pyknotic 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. Contiguous triads, sinusoid-type vessels, proliferating cholangiols, and lymphohistiocytic infiltrates are visible in the connective tissue fields.

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 .

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 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, the starting moment is Helicobacter bacteria pylori. 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 diseases may include belching, nausea, loose stools, bloating, acid sensation in the mouth. Not pronounced aching pain is 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 are formed 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. This condition requires urgent 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.

Symptoms of cancer in the early stages are represented by a decrease in appetite, an 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 can be a sign of 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 signs of 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 secretion 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 establishing the cause of the 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 analysis blood;
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, age, character 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 - pathogen 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: ozokerite 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

Experts do not recommend using folk methods to cure an ulcer because of the risk of aggravating the situation. Such treatment is especially prohibited in complicated acute forms. But in order to prevent exacerbation, doctors allow, for example, a remedy to use some non-traditional recipes:

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 an 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 mashed 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 common. 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 work 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 of the 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:

acute;
chronic.

Diagnosis of the disease

Accurately diagnose the presence of a duodenal ulcer will help FGDS method(fibrogastroduodenoscopy). 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 eliminated with antacids;
antibiotics are prescribed to combat the bacterial cause of the appearance of a lymphofollicular ulcer;
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, ultrasound, the use of microwaves, modulated current therapy to relieve pain. Special physiotherapy exercises will help normalize the motility of the stomach. Gymnastics is good prophylactic from congestion in the intestines and stomach.

In addition to the generally accepted methods of healing intestinal ulcers, traditional medicine has long proven its effectiveness. In the first place for ulcerative lesions is 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 acute period, bed rest is mandatory. 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 recommendations for diet food the following:

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.

In the gastric mucosa, defects of various sizes are visible, the bottom of which is stained with hydrochloric acid hematin in a black-brown color.

Macrodrug CHRONIC GASTRITIS.

Smoothing of the folds of the gastric mucosa is found, the wall is hyperemic, thinned, flattened. Multiple point erosions are noted.

Micropreparation No. 422 Helicobacter pylori in the parietal mucus in the gastric pits (gastrobiopsy, Giemsa stain).

Spiral-shaped bacteria are visible, located near the surface epithelium of the supramucosal barrier. Surface cells are damaged, infiltration of the gastric mucosa with polymorphonuclear leukocytes.

Micropreparation N 423 CHRONIC ACTIVE ANTRUM GASTRITIS WITH GLANDS ATTROPHY AND COMPLETE INTESTINAL METAPLASIA (gastrobiopsy, stained with alcian blue and hematoxylin).

In the lamina propria of the mucous membrane between the glands, a large number of lymphocytes are detected with the formation of lymphoid follicles. There is a destruction of the glands and a decrease in their number, atrophy of the mucous membrane.

Macropreparation CHRONIC GASTRIC ULCER(kaleznaya).

On the lesser curvature of the stomach, a deep defect in the stomach wall is visible, penetrating to the serous membrane, oval in shape, with raised edges. The edge facing the pylorus is flat, has the appearance of a terrace, formed by the mucous, submucosal and muscular membranes. The edge facing the esophagus is undermined. At the bottom of the ulcer, necrotic brown-brown detritus. The folds of the gastric mucosa are smoothed, the rays converge to the ulcerative defect (convergence of the folds).

(E) Micropreparation N 106 CHRONIC GASTRIC ULCER (with exacerbation) (staining with hematoxylin and eosin.

Defect in the wall of the stomach, which captures the mucous, submucosal and muscular membranes. Near the defect, one edge of the mucous membrane is undermined, the other is flat. There are 4 layers at the bottom of the wound defect - from the lumen to the serous membrane: fibrinous-purulent exudate (fibrin, neutrophils, an admixture of necrotic tissue), fibrinoid necrosis, granulation tissue, scar tissue. The muscular membrane at the bottom is not determined, its breakage is visible at the border of the ulcerative defect. In the mucous membrane near the ulcer - a picture of chronic atrophic gastritis.

View a set of macroscopic slides illustrating the complications of a chronic ulcer: PUNCHED GASTRIC ULCER, PENETRATING GASTRIC ULCER, ARROSION OF THE VESSEL IN THE BOTTOM OF THE ULCER, GASTRIC ULCER-CANCER, GASTRIC DEFORMATION

Saucer-shaped stomach cancer on the lesser curvature of the stomach, there is a formation protruding above the surface of the mucous membrane on a wide base with raised dense roller-like edges and a sinking bottom. The bottom is covered with gray-brown decaying masses.

Gross preparations of different forms of GASTRIC CANCER.

Diffuse stomach cancer the wall of the stomach (especially the mucous and submucosal membranes) is diffusely thickened in all departments. The section shows that a gray-pink dense tissue grows through it. The mucous membrane is uneven, its folds are of different thickness, the serous membrane is thickened, dense, bumpy. The lumen of the stomach is narrowed.

Micropreparation N 424 HIGHLY DIFFERENTIATED GASTRIC ADENOCARCINOMA (intestinal type) (staining with hematoxylin and eosin).

In the wall of the growth of atypical glandular structures of various sizes and shapes, built from atypical polymorphic cells. The nuclei are large, hyperchromic.

Micropreparation N 225 UNDIFFERENTIATED CANCER - cricoid (stained with hematoxylin and eosin and alcian blue).

In the cytoplasm of tumor cells, mucin (mucus), stained blue. Tumor cells are cricoid in shape, the nucleus is pushed to the periphery, the cytoplasm is filled with mucus.

DISEASES OF THE INTESTINE

Macropreparation PHEGMONOUS APPENDICITIS.

The appendix is enlarged, thickened. The serous membrane is hyperemic, dull, with fibrin overlays. When the process is cut, greenish-gray thick contents are released from its lumen.

(E) Micropreparation N 107 PHEGMONOUS APPENDICITIS (stained with hematoxylin and eosin). The mucous membrane of the appendix is focally destroyed, in the lumen of the appendix there is a mass of pus, the layers of the wall are diffusely infiltrated with leukocytes.

Macropreparation CHRONIC APPENDICITIS.

The lumen is filled with mucus. Cavity obliteration. Mucus turns into globules. Muscular atrophy and sclerosis.

Micropreparation N 133 CHRONIC APPENDICITIS (staining with hematoxylin and eosin).

Fibrous obliteration is formed. The lamina propria undergoes lipomatosis, muscle layer atrophy, and sclerosis. There is an inflammatory infiltration characteristic of chronic inflammation.

Macropreparation of LIVER ABSCESSES(pylephlebitic), as a complication of appendicitis

In the region of the gate of the liver there are cavities with thick grayish-white walls filled with greenish-gray dense contents. On section, the liver tissue is yellowish.

View a set of gross specimens of intestinal tumors.

Circular stenosing cancer of the sigmoid colon - in sigmoid colon- a ring-shaped formation with raised edges and an ulcerated bottom. On section, grayish-white tissue with hemorrhages growing into the layers of the intestinal wall.

LIVER DISEASES

Macropreparation TOXIC LIVER DYSTROPHY (fatty hepatosis). The liver is enlarged in size, flabby, yellow-white in color (clay type), on the cut has a greasy sheen ("goose liver")

Micropreparation N 4 MASSIVE LIVER NECROSIS - subacute form (staining with hematoxylin and eosin). In the central sections of the lobules, necrotic detritus in the peripheral sections in the cytoplasm of hepatocytes, large vacuoles.

Micropreparation N 5 CHRONIC HEPATITIS OF WEAK ACTIVITY, STAGE I (staining with hematoxylin and eosin). Note the signs of hepatitis activity: intralobular lobular lymphoid infiltrates, "spreading" of lymphocytes along the sinusoids, degenerative changes in hepatocytes, lymphohistiocytic infiltration of the portal tracts. Note the signs of chronic inflammation (hepatitis stage): fibrosis of the portal portal tracts, fibrous septa growing into the lobules. Pay attention to cholestasis: expansion of bile capillaries, imbibition of hepatocytes by bile pigments.

The lobular structure of the liver is broken. In the portal tracts - sclerosis, a pronounced lymphoid infiltrate with the formation of lymphoid follicles. In some places, the infiltrate penetrates into the lobules through the border plate and surrounds groups of hepatocytes. Proliferation in the portal tracts of the bile ducts and periportal sclerosis are visible. Hepatocytes along the course of infiltration are in a state of necrosis, in other areas there are signs of hydropic and fatty degeneration.

Electronogram HYDROPIC DYSTROPHY OF HEPATOCYTE IN VIRAL HEPATITIS(atlas, fig. 14.5). Pay attention to the expansion of the endoplasmic reticulum of the hepatocyte and the sharp swelling of mitochondria.

An electron microscopic examination of the EPS cistern was sharply expanded, the mitochondria were swollen.

Gross preparations of liver cirrhosis. Mark the size, color, consistency, appearance of the liver from the surface and in section. Assess the size of regenerated nodes and determine the macroscopic form of cirrhosis by this feature.

Alcoholic small nodular portal cirrhosis- the liver is deformed, yellow in color, the surface is small-hilly.

(E) Micropreparation N 48 CHRONIC MODERATE HEPATITIS WITH TRANSITION TO LIVER CIRRHOSIS (staining with hematoxylin and eosin and picrofuchsin). The presence of moderately pronounced signs of inflammation activity (lymphoid infiltration of the stroma, extending to the parenchyma, fatty degeneration of hepatocytes), fibrosis dominance (porto-portal, porto-central septa with the formation of false lobules) and regeneration of hepatocytes (loss of the beam structure, the presence of cells with large nuclei .

Gross preparations: PRIMARY LIVER CANCER, LIVER METASTASES OF TUMORS OF ANOTHER PRIMARY LOCATION.

MORPHOLOGICAL EQUIVALENTS OF GLOMERULONEFRITIS

Micropreparation N 112 INTRACAPILLARY PROLIFERATIVE GLOMERULONEFRITIS (staining with hematoxylin and eosin).

An enlarged multicellular glomerulus is noted. Hypercellularity is associated with proliferation and swelling of endothelial and mesangial cells. There is a narrowing of the lumen of the capillary loops that fill the cavity of the capsule, as well as their massive neutrophilic infiltration.

Micropreparation FIXATION OF DEPOSITS OF IMMUNE COMPLEXES IN THE RENAL GLUMER IN ACUTE GLOMERULONEPHRITIS(atlas, fig. 15.2).

A granular glow is visible along the basement membrane (deposits in the form of lumps glow)

Macropreparation SUBACCUTE GLOMERULONEPHRITIS("large motley kidney").

The kidney is enlarged, flabby, pale with petechial hemorrhages on the surface.

Micropreparation N 113 SUBACUTE PREFERREDLY EXTRACAPILLARY GLOMERULONEPHRITIS (staining with hematoxylin and eosin).

The crescents are visible, formed due to the proliferation of the epithelium of the outer leaf of the Shumlyansky-Bowman capsule and the migration of monocytes and macrophages into the space between the capsule and the capillary glomerulus. Between the layers of cells in the crescents is an accumulation of fibrin. The glomeruli are compressed - they show focal necrosis, diffuse and focal proliferation of the endothelium, and mesangial proliferation. Part of the tubules is atrophic, in the epithelium of some convoluted tubules - hydropic or hyaline-drop dystrophy. In the stroma of the kidney - sclerosis, lymphomacrophage infiltration.

MORPHOLOGICAL VARIANTS OF CHRONIC GLOMERULONEPHRITIS

Electronogram MEMBRANOUS NEPHROPATHY(atlas, fig. 15.6).

Electron microscopic examination shows subepithelial deposits in the glomerular basement membrane, accumulation of the basement membrane substance between the peduncles of podocytes, loss of processes by podocytes and their spreading on the thickened and deformed basement membrane.

Electronogram MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS(atlas, fig. 15.9).

Electron microscopic examination reveals subepithelial electron-dense deposits.

Electron diffraction pattern(atlas, fig. 15.10).

Electron microscopic examination shows deposits in the mesangium.

Macropreparation SECONDARY SHRINKLED KIDNEY (CHRONIC GLOMERULONEPHRITIS WITH OUTCOME IN NEPHROSCLEROSIS).

The kidneys are symmetrically wrinkled and have a fine-grained surface.

(E) Micropreparation N 114 FIBROPLASTIC GLOMERULONEPHRITIS (terminal) (staining with hematoxylin and eosin).

Sclerosis and hyalinosis of most glomeruli, proliferation of mesangial cells, sclerovascular loops in the remaining hypertrophied glomeruli. Sclerosis and hyalinosis of arterioles are noted. Hyaline cylinders in the lumen of the tubules.

SECONDARY KIDNEY DAMAGE

Macropreparation AMYLOID NEPHROSIS("big white", "big greasy kidney").
Note an increase in the size of the kidney, a dense texture, a greasy appearance of the surface.

The kidneys are enlarged in size, dense texture, smooth surface. On the cut with a greasy sheen. The boundary between the cortex and medulla is blurred

(E) Micropreparation N 16 AMYLOID NEPHROSIS (congo-mouth stain). Designate amyloid deposits in the capillary loops of the glomerulus, along the proper membrane of the tubules, in the walls of blood vessels, and also in the stroma of the kidney along the reticular fibers.
Note the color of the amyloid.

Under the basement membrane of the tubules, in the glomeruli, along the reticular fibers of the stroma in the intima of the vessels, there are red-colored amyloid deposits.

ACUTE RENAL FAILURE (ARF)

(E) Slide No. 6 NECROTIC NEPHROSIS (staining with hematoxylin and eosin). The glomeruli and epithelium of the direct tubules are preserved. Their cells contain nuclei. The epithelium of the convoluted tubules does not contain nuclei (karyolysis).

ORGANOPATOLOGY OF CHRONIC RENAL INSUFFICIENCY

View a set of macropreparations reflecting the morphological manifestations of uremia: FIBRINOSIS PERICARDITIS ("hairy heart"), croupous tracheitis, diphtheritic colitis.

DISHORMONAL DISEASES OF THE GENITAL ORGANS

Macropreparation UTERINE POLYP. Note the localization of the polyp, its shape, size, nature of the surface, connection with the underlying tissue.

The outgrowth of the endometrium is gray-red in color, with an uneven surface.

(E) Micropreparation N 142 Glandular endometrial hyperplasia (staining with hematoxylin and eosin).

The endometrial glands are built from proliferating type epithelium, have different sizes and shapes, have a tortuous course and cystic expansion, are very closely located, branching and budding of the glands are noted.

Micropreparation N 57 PSEUDOEROSION OF THE CERVICE (staining with hematoxylin and eosin).

In the area of erosion of the cervix, there are two types of epithelium: stratified squamous non-keratinized and prismatic epithelium. There is an ectopic columnar epithelium in the exocervix.

PATHOLOGY OF PREGNANCY

Macropreparation POSTPARTUM ENDOMETRITIS.

The membrane of the vagina and cervix is hyperemic, edematous, sometimes with hemorrhages. In the lumen of the vagina, especially in the cervix, there is exudate released from the uterus. The cervical canal is ajar.

Macropreparation LIVER IN ECLAMPSIA.

Single or confluent white-yellow foci of necrosis and multiple hemorrhages of different sizes appear in the liver - a landcart-shaped liver.

Stained with hematoxylin and eosin. There is a fibrinous-purulent exudate in the area of the defect in the stomach wall (a), with an underlying extensive area of fibrinoid necrosis (b), the presence of granulation tissue (c) and the growth of coarse fibrous connective tissue penetrating to different depths muscle layer (d). The serous membrane of the stomach wall is preserved (e).

2. Chronic atrophic gastritis. Heme coloring

toxin and eosin. In the gastric mucosa, atrophy of the integumentary epithelium (a) and epithelium of the glands with restructuring

which glands intestinal type- "intestinal metaplasia" (b), in the lamina propria of the mucous membrane of the field of sclerosis

3. Adenocarcinoma. Stained with hematoxylin and eosin. All layers of the stomach wall are infiltrated with tumor tissue with signs of cellular atypism (a). Multiple pathological mitoses are seen in hyperchromic (b) and polymorphic tumor cells (c).

4. Mucous cancer of the stomach. Stained with hematoxylin and

eosin. The tumor tissue is represented by an abundance of large atypical "cricoid" cells (a) with the formation of a large amount of mucus (b). The infiltrative character of tumor growth is visible (c). Demonstration.

5. Scirrhus of the stomach. Stained with hematoxylin and eosin. In the wall of the stomach, a group of atypical cells with large hyperchromic nuclei (a), in the stroma of the tumor, the growth of fibrous connective tissue (b). Demonstration.

MACRO PREPARATIONS.

1. Acute catarrhal gastritis: in the preparation of the stomach, the mucous membrane is thickened, with high hyperemic folds covered with thick viscous mucus, with petechial hemorrhages. The reasons: poor-quality food, the use of alcohol surrogates, antitumor chemotherapy drugs, burns with acids and alkalis, uremia, salmonellosis, shock, severe stress.

Complications: acute ulcers, transition to chronic gastritis. Exodus: mucosal restoration.

2. Erosions and acute stomach ulcers: in the preparation of the stomach,

the mucous membrane is edematous, on the surface there are multiple petechial hemorrhages and conical defects of various sizes, their bottom and edges are black. Erosions are localized within the mucosa, and ulcers penetrate

cabins at different depths of the mucous membrane, some reach the muscular membrane.

The reasons: endocrine diseases (Zolinger-Ellison syndrome, hyperparathyroidism), acute and chronic circulatory disorders, intoxication, allergies, chronic infections (tuberculosis, syphilis), postoperative, steroid and stress ulcers.

Complications: perforation, peritonitis.

Exodus: erosions are epithelialized, the ulcerative defect is replaced by scar tissue.

3. Chronic stomach ulcer in remission: in the preparation of the stomach, on the lesser curvature, there is a pathological focus in the form of a deepening of the mucous membrane, rounded, 3 cm in diameter. The mucosal folds radially converge to the defect, the edges of which are dense, raised in a roller-like manner, callused (calculous ulcer). On the cut, the inlet is a crater, smaller than the inner part of the ulcer. The edge facing the cardia is undermined, the mucous membrane hangs over it. The edge facing the gatekeeper is flat - terraced. The thickness of the ulcer is represented by connective tissue, gray-white, 2.5 cm. At the bottom of the ulcer, the vessels are sclerotic, their lumen is gaping.

The reasons: genetic predisposition, Helicobacter pylori, inflammatory and dysregenerative changes in the mucous membrane, leading to exposure to peptic aggression factors (hydrochloric acid and pepsinogen).

Complications: perigastritis, bleeding, perforation, penetration, cicatricial deformity of the stomach with the development of stenosis behind the inlet or outlet. Against the background of a chronic ulcer, a second disease can develop - stomach cancer.

4. Polyps of the stomach (adenomas): in the antrum

The stomach has two tumor-like formations the size of pigeon eggs, on thin legs, irregular oval shape with a villous surface, soft consistency.

On the section, pathological neoplasms are abundantly vascularized and localized exclusively on the surface of the mucous membrane, without sprouting the underlying tissues.

Complications: bleeding, torsion of the leg, obturation of the exit or inlet.

Exodus: malignancy.

5. Various forms stomach cancer.a) Fungal cancer:

on the surface of the mucous membrane there is a tumor-like formation growing into the lumen of the stomach, of an irregular round shape, 5 cm in diameter, on a wide base in the form of a mushroom cap, with a retraction in the center. The cut shows that the tumor sprouts the entire wall of the stomach.

b) Diffuse gastric cancer: the organ is reduced in size, the wall is thickened up to 1 cm along its entire length, of a dense "woody" consistency, on the section it is represented by a gray-pinkish tissue. The mucous membrane is uneven, its folds of various thicknesses, the serous membrane is thickened, dense, tuberous. The lumen of the stomach is narrowed.

c) Saucer-shaped stomach cancer: on the lesser curvature there is a pathological focus in the form of a formation rising above the surface of the mucous membrane with dense roller-like edges and a sinking bottom, measuring 3.5 cm by 2.0 cm. The bottom is covered with gray-brown decaying masses. On section, the tumor tissue infiltrates the entire thickness of the organ wall.

The reasons: nutrition (smoked meats, canned food, pickled vegetables, peppers), biliary reflux (after stomach operations, especially according to Billroth II), Helicobacter pylori (contributes to the development of mucosal atrophy, intestinal metaplasia, epithelial dysplasia). Metastasis: 1. Orthograde lymphogenous metastases to regional nodes on the lesser and greater curvature, retrograde lymphogenic metastases in the left supraclavicular lymph node - Virchow's metastasis, in the ovaries - Krukenbergovsky

cancer, pararectal tissue - Schnitzler metastases, 3. Hematogenous metastases to the liver, lungs, brain, bones, kidneys, less often to the adrenal glands and pancreas. 4. Implantation- carcinomatosis of the pleura, pericardium, diaphragm, peritoneum, omentum.

TEST CONTROL

Choose one or more correct answers

1. SIGNS OF ACUTE CATHARAL GASTRITIS

1) thickening of the mucosa

2) glandular atrophy

3) multiple erosions

4) mucosal sclerosis

5) neutrophilic infiltration of the mucosa

6) lymphoid infiltration of the mucosa

2. MORPHOLOGICAL FORMS OF ACUTE GASTRITIS

1) fibrinous

2) atrophic

3) hypertrophic

4) catarrhal

5) corrosive (necrotic)

3. CHANGES IN THE EPITHELIUM IN CHRONIC GASTRITIS

1) atrophy

2) intestinal metaplasia

3) hyperplasia

4) dysplasia

5) the appearance of Mallory bodies in the cytoplasm

4. CHARACTERISTIC FEATURES OF CHRONIC GASTRITIS A

2) autoantibodies in the blood

to parietal cells

3) Helicobacter pylori -

5. PATHOGENESIS OF PERNICIOUS ANEMIA IN AUTOIMMUNE GASTRITIS

1) cessation of HCl production

2) production of antibodies to Helicobacter pylori

3) production of antibodies to parental cells

4) production of antibodies to intrinsic factor

5) destruction of the glands and atrophy of the mucous membrane

6. CHARACTERISTIC FEATURES OF CHRONIC GASTRITIS IN

1) predominant localization - antrum

2) autoantibodies in the blood

to parietal cells

3) Helicobacter pylori -

main etiological factor

4) accompanied by G-cell hyperplasia, gastrinemia

5) often associated with pernicious anemia

6) is localized in the fundus

7) reflux of duodenal contents into the stomach - the basis of pathogenesis

ACUTE EROSION OF THE STOMACH IS

mucosal inflammation

mucosal necrosis,

nonmuscular

3) atrophy of the mucous membrane

4) mucosal sclerosis

5) necrosis involving the muscle layer

8. CLINICAL AND MORPHOLOGICAL SIGNS OF CHRONIC ATROPHIC GASTRITIS

IN THE STAGE OF EXAMINATION

1) often occurs in patients with alcoholism

2) the mucous membrane is not changed

3) diffuse lymphoid-plasmacytic infiltration with a significant admixture of PMN

4) foci of pyloric and intestinal metaplasia

5) increased acidity of gastric juice

9. MORPHOLOGICAL SUBSTRATE OF ULCER

1) inflammation of the gastric mucosa

2) erosion of the gastric mucosa

and 12 duodenal ulcer

3) acute stomach ulcer

and duodenum

4) chronic recurrent gastric and duodenal ulcer

5) inflammation of the mucous membrane of the duodenum

10. Sclerotic deformity of the stomach IS THE OUTCOME

1) catarrhal gastritis

2) diphtheritic gastritis

3) corrosive gastritis

4) phlegmonous gastritis

11. SIGNS of chronic atrophic gastritis as a precancerous disease

1) lymphoplasmacytic infiltration

2) sclerotic processes

3) structural restructuring of the epithelium

(intestinal metaplasia)

4) all answers are correct

5) all answers are wrong

12. ULCEROGENIC PROMOTORS

1) corticosteroids

3) aspirin

4) smoking

5) increased tone of the vagus nerve

13. Stomach ulcers include

1) endocrine ulcers of the stomach

2) allergic ulcers

3) peptic ulcers

4) postoperative ulcers

5) tuberculous ulcers

14. LOCAL FACTORS IN THE DEVELOPMENT OF Peptic Ulcer

1) increased aggressiveness of gastric juice

2) campillobacteria

3) the presence of chronic gastritis

4) circulatory disorders

5) all answers are correct

6) all answers are wrong

15. REASONS FOR THE DEVELOPMENT OF ACUTE GASTRIC ULCER

1) corticosteroids

3) aspirin

4) smoking

5) increase in tone

vagus nerve

16. MORPHOLOGICAL SIGNS OF ACUTE gastric ulcer

1) funnel shape

2) the shape of a truncated pyramid

in cross section

3) soft jagged edges

4) dense callused edges

7) multiple ulcers

17. MORPHOLOGICAL SIGNS of chronic gastric ulcer

1) funnel shape

2) the shape of a truncated pyramid

in cross section

3) soft jagged edges

4) dense callused edges

5) the bottom of the ulcer, as it is cleansed, is stained black with hematin hydrochloride

6) the edge of the ulcer, facing the pylorus, looks like a terrace, the cardial edge is undermined

18. SIGNS OF CHRONIC GASTRIC ULCER

DURING REMISSION

1) the presence of exudate on the surface

2) scar tissue interrupts muscular layer to different depths

3) endovasculitis

4) fibrinoid changes in the bottom and vessels

5) surface epithelialization

19. SIGNS OF CHRONIC GASTRIC ULCER

IN THE PERIOD OF EXAGENCE

1) the presence of fibrinous-purulent exudate

on the surface 2) scar tissue interrupts muscle

shell at different depths

3) endovasculitis

4) fibrinoid changes in the walls of blood vessels and in the bottom of the ulcer

12. Bleeding mechanism in peptic ulcer

arrosive

diapedetic

due to rupture of a blood vessel

as a result of purulent fusion

21. Chlorhydropenic uremia - the result

1) bleeding from an ulcer

2) chronic nephritis

3) ulcer penetration

4) cicatricial pyloric stenosis

5) all answers are correct

6) all answers are wrong

22. Peritonitis complicating a chronic ulcer is the result of

1) penetration

2) perforations

3) gastritis

4) duodenitis

5) cicatricial stenosis of the pylorus

23. COMPLICATIONS OF CHRONIC ULCER

1) penetration

2) perforations

3) empyema

4) hypercalcemia

5) cicatricial stenosis

and wall deformation

6) bleeding

24. TYPES OF GASTROPATHIES

1) Meniere's disease

2) Menetrier's disease

3) Wernicke's syndrome

4) Zollinger-Ellison syndrome

5) hypertrophic hypersecretory gastropathy

25. HISTOLOGICAL SIGNS OF GASTROPATHIES

1) hypertrophy of the gastric mucosa

2) atrophy of the gastric mucosa

3) hyperplasia of the integumentary pit epithelium

4) hyperplasia of the glandular epithelium

5) severe sclerosis

26. MORPHOLOGICAL SIGNS OF THE INFLAMMATORY POLYP

1) inflammatory infiltrate in the stroma

2) atypical cells

3) without a clear differentiation into the leg and body

4) dysplasia of the glandular epithelium

5) surface erosion

27. BENIGN TUMORS OF THE STOMACH

1) angiosarcoma

2) adenoma

3) leiomyoma

4) adenocarcinoma

5) hyperplasiogenic polyp

28. BACKGROUND FOR THE DEVELOPMENT OF GASTRIC ADENOMA

1) chronic superficial gastritis

2) acute erosive-hemorrhagic gastritis

3) acute fibrinous gastritis

4) chronic gastritis with enterolization

29. ADENOMA IS THIS

1) benign tumor

from glandular epithelium

2) malignant tumor from glandular epithelium

3) epidermal cancer

4) malignant tumor from transitional cell epithelium 5) benign tumor from squamous epithelium

30. DISEASES WITH A RISK OF CANCER

1) superficial gastritis

2) chronic stomach ulcer

3) sharp erosive gastritis

4) chronic atrophic gastritis

5) adenomatous polyps

31. HISTOLOGICAL VARIANTS OF GASTRIC CANCER

1) adenocarcinoma

2) sarcoma

3) cricoid

4) undifferentiated

32. CLINICAL AND MORPHOLOGICAL CHARACTERISTICS OF INTESTINAL TYPE GASTRIC CANCER

1) occurs more often before the age of 30 years

2) has a high degree of differentiation

3) develops against the background of chronic gastritis

4) 2 times more likely to affect men

5) develops from metaplastic epitheliocytes

33. CLINICAL AND MORPHOLOGICAL CHARACTERISTICS OF DIFFUSE TYPE GASTRIC CANCER

1) develops from epitheliocytes

2) occurs at a relatively young age

3) histologically cricoid-cell

4) occurs against the background of chronic gastritis

5) has a low degree of differentiation

34. PROGNOSTIC SIGN IN GASTRIC CANCER

1) histological variant

2) macroscopic form

3) depth of invasion

4) mucus formation

5) secondary changes

35. HISTOLOGICAL SIGNS OF POLYPOID STOMACH CANCER

1) atypical glandular structures of a bizarre shape

2) cricoid cells

3) an abundance of mucus in the lumen of the glands

4) atypical polymorphic cells with large hyperchromic nuclei

5) atypical cells characterized by monomorphism

36. HISTOLOGICAL SIGNS OF CRIC CELL GASTRIC CANCER

1) extensive hemorrhages are characteristic

2) the nuclei of atypical cells are displaced

to the cell membrane

3) poorly differentiated cells with very large irregularly shaped hyperchromic nuclei

4) atypical glandular structures

5) massive sclerosis and hyalinosis in the wall

37. MICROSCOPIC CHARACTERISTICS OF SCIRRHOUS GASTRIC CANCER

1) atypical cells with large

nuclei are arranged in groups

2) atypical cells form glands

3) massive growths of connective tissue

4) an abundance of mucus in the lumen of the glands

5) atypical cells do not form glands

38. KRUKENBERG AND SCHNITZLER METASTASES OF GASTRIC CANCER

1) hematogenous

2) implantation

3) lymphogenous orthograde

4) lymphogenous retrograde

39. COMPLICATIONS OF GASTRIC CANCER

1) hemoptysis

2) dilatation of the pylorus

3) perforation

4) exhaustion

5) stomach bleeding

40. SIGNS OF VIRCHOV METASTASIS

1) hematogenous metastasis

2) retrograde lymphogenous metastasis

3) peritoneal carcinomatosis

4) damage to the left supraclavicular lymph node

5) ovarian damage

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