Pathological anatomy of peptic ulcer disease. Lesson topic

Date: 19.07.2019

GASTRITIS (gastritis; Greek, gaster stomach + -itis) - damage to the gastric mucosa with predominantly inflammatory changes in the acute development of the process and the phenomena of dysregeneration, structural restructuring with progressive atrophy during hron, course, accompanied by dysfunction of the stomach and other body systems.

Representations about G. changed depending on the level of development of honey. Sciences. References to functional and organic disorders of the stomach can be found in the works of Hippocrates, Galen, Razi, Ibn-Sina, and others. The beginning of the study of G. is associated with the name of French. doctor F. Brouss (1803), who considered G. the most common disease and associated with it the development of diseases of the heart, brain, and lungs. Since introduction into a wedge, practice of a method of sounding of a stomach [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. - the beginning of the 20th century. on the basis of new data patol, anatomy, surgery of the abdominal cavity, rentgenol. method, research I.P. Pavlov and his school in the field of physiology digestive tract.

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

Distinguish between acute and hron. G.

Acute gastritis

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

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 caused, on the one hand, by a violation of the secretory and motor function stomach (vomiting, spastic pain, etc.), depth and severity inflammatory changes in the stomach (leukocytosis, accelerated ROE, increased body temperature, pain as a result of irritation of nerve endings in the wall of the stomach), on the other hand, the involvement of other organs, body systems and some aspects of metabolism in the patol process (collapse, dehydration of the body, blood clotting, etc.) etc.).

Pathological anatomy of acute gastritis

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

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

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

At corrosive G. there are necrotic-inflammatory changes in the wall of the stomach (printing. Fig. 9).

At phlegmonous G. (tsvetn. Fig. 10) diffuse leukocytic infiltration of all layers of the stomach wall is observed, but hl. arr. submucosa. Phlegmonous G. is accompanied by perigastritis (see) and can end with peritonitis.

Fibrinous G. is characterized by diphtheria inflammation of the mucous membrane.

Simple gastritis

Simple gastritis (commonplace, catarrhal)- the most common form. Occurs at all ages and regardless of gender. A common cause of simple G. is errors in nutrition, infections, especially foodborne toxicoinfections (see. Food toxicoinfections). The irritating effect of some drugs is known (salicylates, butadion, bromides, iodine, digitalis, antibiotics, sulfonamides, etc.). G.'s development from taking small amounts 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 foodborne diseases) usually develops after 4-8 hours. after exposure to etiol, factor. Patients note 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 bloom. On palpation abdominal wall- soreness in the epigastric region. The pulse is usually fast, the blood pressure is slightly 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 renal damage. There is a lot of mucus in the stomach 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 initiation of 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 of intestinal activity, it is possible to assume gastroenterocolitis (see), it is also necessary to differentiate G. with salmonellosis (see). In this case, bacteriol, and serol, research is of decisive importance.

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, chloramphenicol 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 of 0.1% solution subcutaneously), platifillin (1 ml of 0.2% solution subcutaneously), papaverine (1 ml of 2% solution subcutaneously) are injected. With the development of dehydration, physiol is injected subcutaneously, solution, 5% glucose solution... In acute cardiovascular failure - caffeine, mezaton, norepinephrine. It is necessary to prescribe to lay down. nutrition. The first 1 - 2 days should refrain from eating, drinking is allowed in small portions (strong tea, borzhom). On the 2-3rd day - low-fat broth, slimy soup, semolina and mashed rice porridge, jelly. On the 4th day - meat and fish broth, boiled chicken, fish, steamed cutlets, mashed potatoes, crackers, dried white bread. Then the patient is assigned a table number 1 (see. Therapeutic nutrition), and after 6-8 days - the usual food.

Forecast at simple G. in case of timely started treatment is favorable. If the action of etiol, factors is repeated, then acute G. can go to hron.

Prophylaxis simple G. is reduced to rational nutrition, observance a dignity. - gigabyte. events in everyday life and at catering establishments, dignity. - skylight, work.

Corrosive gastritis

Corrosive gastritis develops as a result of the ingestion of substances such as strong to-you, alkalis, salts of heavy metals, highly concentrated alcohol into the stomach.

Wedge, painting by the 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 the corrosive G, Patients usually complain of pain in the mouth, behind the sternum and in the epigastric region, repeated excruciating 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 changes in the mucous membranes, it is possible to establish the cause of the burn: from sulfuric and hydrochloric acid grayish-white spots appear, from nitrogen - yellow and greenish-yellow scabs, from chrome - brownish-red scabs, from carbolic - a bright white bloom resembling lime, from acetic - superficial whitish-gray burns. In severe cases, a collapse may develop (see). The abdomen is usually swollen, painful on palpation in the epigastric region, sometimes there are signs of irritation of the peritoneum. In some patients, in the first hours after poisoning, acute perforation of the stomach wall occurs, there are signs of toxic damage to the kidneys (in the urine - protein, cylinders) 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, 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, pharynx and larynx).

Treatment should start with gastric lavage large quantity water through a probe, 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 add milk, lime water or burnt magnesia to the water; in case of damage with alkalis - diluted lemon and acetic to - you, antidotes are introduced. For severe pain, morphine, promedol, fentanyl, droperidol are administered; in case of collapse, in addition, caffeine, cordiamine, mezaton, norepinephrine, strophanthin (subcutaneously or intravenously with blood substitute fluids, glucose, physiological solution, etc.). During the first days, fasting, parenteral administration of fiziol, solution and 5% of glucose solution are 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 and destructive changes and therapeutic tactics in the first hours and days of the disease; death can result from shock, bleeding, or peritonitis. The outcome of corrosive G. is usually cicatricial changes stomach, more often in the pyloric and cardiac regions.

Fibrinous gastritis

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

Phlegmonous gastritis

Phlegmonous gastritis occurs, as a rule, primarily as a result of infection directly into the stomach wall. It is caused by streptococcus, often hemolytic, often in combination with Escherichia coli, less often staphylococcus, pneumococcus, Proteus, etc. Sometimes it develops as a complication of an ulcer or disintegrating stomach 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. The general condition deteriorates sharply. Patients refuse to eat and drink; exhaustion quickly sets in. In peripheral blood - neutrophilic leukocytosis, toxigenic granularity in granulocytes, accelerated erythrocyte sedimentation, change 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 operation is placed very rarely.

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

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

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

Chronic gastritis

Chron. G. makes up most of the diseases of the stomach. It is often combined with other diseases of the digestive system.

Chron. G. - the concept of wedge. - morfol., It is shown by a wedge, signs, functional and morfol, changes in various combinations and can proceed with various disorders of secretion, but a decrease in gastric juice 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 different classifications of cron. D. The classification according to Ryss (1966) is given.

I. By etiological basis

1. Exogenous gastritis: long-term violations of the diet - the qualitative and quantitative composition of food; alcohol and nicotine abuse; action of thermal, chemical, fur. and other agents; the influence of professional hazards - systematic tasting of raw meat seasoned with spices (canning industry), ingestion of alkaline vapors 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 action from other affected organs - intestines, gall bladder, pancreas); G., associated with violations in Article. n. With. and endocrine organs; hematogenous G. (hron, infections, metabolic disorders); hypoxemic G. (hron, circulatory failure, pneumosclerosis, pulmonary emphysema, pulmonary heart); allergic G. (allergic diseases).

II. By morphological characteristics

1. Superficial.

2. Gastritis with glandular involvement without atrophy.

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

4. Hypertrophic.

5. Antral.

6. Erosive.

III. Functionally

1.With normal secretory function.

2. With moderately expressed secretory insufficiency: absence of free salt to - you on an empty stomach (or a decrease in its concentration after a test stimulus below 20 titers, units); a decrease in the concentration of pepsin after a test stimulus to 1 g%, a concentration of mucoprotein below 23%, a positive reaction to the introduction 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 mucoprotein, a histamine refractory reaction; decrease in the content of uropepsinogen.

IV. According to the clinical course

1. Compensated (or remission phase): absence of a wedge, symptoms, normal secretory function or moderately expressed 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 (Menetrie's disease).

3. Polyposis.

Vi. Chronic gastritis concomitant with other diseases

1. With Addison-Birmer anemia.

2. With stomach ulcers.

3. With cancer.

Chron, gastritis is a polyetiologic disease, is a consequence 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 consumption of alcoholic beverages, malnutrition, especially with a lack of protein, vitamins and iron. The reason may be long-term intake some medicines (quinine, atophan, digitalis, salicylates, butadion, prednisolone, sulfa drugs, potassium chloride, antibiotics, etc.), the influence of factors such as inhalation of cotton, metal, coal dust, alkali vapors, etc. Violations in endocrine system(diabetes, gout) can cause the development of structural changes in the gastric mucosa. The release through the gastric mucosa of metabolic products such as acetone, indole, skatole, like toxins in infectious diseases and local foci of infection, causes the development of the so-called. elimination G. Chron, diseases of the digestive system (appendicitis, cholecystitis, colitis, etc.) are especially important in development hron. G. Often hron. G. develops in diseases causing tissue hypoxia (hron, circulatory failure, pneumosclerosis, anemia).

From the blood serum of sick hron. G. isolated antibodies, with the help of which the model of autoimmune lesions of the stomach is reproduced. However, the pathogenetic nature of circulating gastric antibodies has not yet been clarified. There is evidence of the role of genetic factors in the emergence of hron. D. 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) G.'s emergence and its rapid transformation into a severe form.

The pathogenesis is complex and not the same at various forms hron. G. At hron. G., which developed from acute, progresses primary inflammatory changes in the stroma and the development of secondary degenerative-regenerative changes in the glandular apparatus (atrophy, hyperplasia, metaplasia, etc.). The mechanism of development of separate forms hron. G., etiologically associated with various nutritional disorders 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 are, in turn, the cause of disruption of the activity of other organs of the digestive apparatus.

According to morfol, superficial G. is distinguished by signs, various stages of atrophy of the mucous membrane. Ts. G. Masevich (1967) allocates G. with defeat of the glands of the bey of atrophy of the mucous membrane and G. is atrophic. Schindler (R. Schindler, 1968) and Elster (K. Elster, 1970) distinguish hypertrophic G.

The results of histochemical, and electron microscopic research of biopsy material allow us to consider that the forms hron. G. are phases of violation fiziol, regeneration of the gastric mucosa. According to M. Siurala et al. (1963, 1966), Ts. G. Masevich (1967) and others, superficial G. passes into G. with defeat of the glands, and then into atrophic. Syurala et al. (1968) believe that this process takes approx. 17 years.

Chronic superficial gastritis characterized by a picture of mucus hypersecretion, sometimes with a predominance of the excretion phase over the phase of secretion accumulation: 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 CHIK positive granules over the nuclei indicates increased mucus synthesis (see CHIC response). Sometimes the epithelium lining the gastric fields and dimples looks flattened, with a narrow strip of mucoid, rare supranuclear granules, and a high content of RNA. Revealed granular and vacuolar degeneration of the epithelium, the infiltration of lymphoid and plasma cells of the own shell of the rollers (color, table., Fig. 4). Accessory cells, normally located in the isthmus of the gastric glands, often spread to their middle third.

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

Chronic atrophic gastritis characterized by a decrease (sometimes significant) in the number of main and accessory glandulocytes, deepening of the gastric dimples (color. Fig. 7 and color, table. Fig. 6 and 7), which often have a corkscrew-like appearance (Fig. 3), hyperplasia of accessory glandulocytes. The epithelium covering the gastric fields and dimples is often flattened, contains a lot of RNA and little neutral mucopolysaccharides, in places it is replaced by intestinal epithelium (color table. Fig. 8) with typical enterocytes, goblet cells and Paneth cells (intestinal metaplasia). The stomach glands are often replaced by mucous membranes (pyloric metaplasia). The remaining main glandulocytes are vacuolated; in the ocular 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; there is a reduction in the mitochondrial cristae of the parietal glandulocytes.

Wolf (G. Wolf, 1968) distinguishes three stages of atrophy of the gastric mucosa: incipient atrophy, with a cut the glands are not yet shortened, but look as if squeezed; partial atrophy(glands), with a cut preserved groups of glands containing the main and parietal (lining) glandulocytes; 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 (color. Fig. 6, color. Table Fig. 9 and Fig. 7).

There are three forms of hron, hypertrophic G.: interstitial, proliferative, glandular. The interstitial form is characterized by abundant lymphoplasmacytic infiltration, which occurs at the edges of ulcers; for proliferative - the growth of the superficial epithelium, deepening of the dimples, the glandular apparatus unchanged; with a glandular form, the mucous membrane is thickened 2-7 times due to glandular hyperplasia; this form is hron. G. meets with duodenal ulcer (see. Peptic ulcer), Zollinger-Ellison syndrome (see. Zollinger-Ellison syndrome) and as an independent disease. Some authors refer hron to the glandular form. G. and Menetrie's disease, designating it as gastritis hypertrophica gigantea, although Menetrie 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 Menetrie's disease with G., considering it as an anomaly in the development of the gastric mucosa.

The clinical picture. Depending on the state of the secretory function of the stomach, hron is distinguished. G. with normal and increased secretion and hron. G. with secretory insufficiency.

Chronic gastritis with normal and increased secretion usually occurs 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, the use of alcoholic beverages, including table wines and beer. Patients complain of heartburn, sour belching, a feeling of pressure, burning and distention in the epigastric region, constipation (sometimes diarrhea), rarely vomiting. The pains are usually dull, aching, without a certain irradiation, localized in the epigastric region, their occurrence, as a rule, is associated with food intake. But the pains can be "hungry" and "night", and subside after eating.

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

Massive bleeding from the gastric mucosa is possible, which on average accounts for 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 may be different. Bleeding at G. is most often associated with the development of erosions, but sometimes the mechanism of bleeding remains unclear even after gistol, research of the resected part of the stomach. A certain value in the occurrence of gastric bleeding is attributed to the acidity of gastric juice (the higher the acidity, the more often bleeding). Abundant gastric bleeding usually develops in patients with minor wedge, manifestations, in which, as it is believed, increased permeability of the blood vessels of the stomach. The cause of the development 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 in wedge, manifestations with duodenal ulcer, although not identical to it. IM Fleckel (1958) considered gastroduodenitis to be the pre-stage of peptic ulcer disease or a form of "peptic ulcer disease without an ulcer." The frequency of the disease (during the day and year) is less pronounced than with peptic ulcer disease. Of the wedge, the most characteristic symptoms are pain ("painful gastritis"), which are usually localized under the xiphoid process or to the right of it. Often there is a combination of pain immediately after eating with "hungry" and "night" pains.

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

Chronic gastritis with secretory insufficiency more common in people of mature and old age. In patients, weight usually decreases, weakness appears, symptoms of multivitamin deficiency are revealed - dry skin, loosening and bleeding of the gums, changes in the tongue (thickening, redness, flattened papillae, the presence of dental prints), cracks on the lips, in particular in the corners of the mouth. From stomach symptoms note a violation of appetite and the desire to eat spicy and spicy food outside the period of exacerbation. Some patients cannot take solid food without liquid, which they drink before and during the meal. Patients note an unpleasant taste in the mouth, especially in the morning, nausea, a feeling of fullness and distention in the epigastric region, belching with air. The stool is unstable, with a tendency to diarrhea. Dyspeptic symptoms usually occur soon after eating, especially poorly patients tolerate milk. In some cases, nausea and salivation are persistent and painful for patients, and they seek to alleviate their condition with 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. Some patients show allergic reactions to certain food and medicinal substances.

Sometimes (more often in women) iron deficiency anemia develops (see). Changes in the intestines are often noted, the exocrine function of the pancreas decreases, dysbiosis develops (see), manifested by fermentation or putrefactive dyspepsia.

Special forms hron. G. (rigid, polypous and giant hypertrophic) differ in originality a wedge, manifestations and morfol, features. Some researchers attribute these forms to complications hron. G.

Rigid gastritis first described by A. N. Ryzhikh and Yu. N. Sokolov (1947). It is manifested by persistent dyspepsia (see) and achlorhydria (see). The diagnosis is established with rentgenol. research and based on 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.

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

Giant hypertrophic gastritis, or rather excessive development of the mucous membrane, described by P. Menetrier (1886), is a relatively rare disease, manifested by metabolic disorders (usually 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 table).

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

In the assessment of morfol, the picture of the gastric mucosa, gastrobiopsy data should be preferred. Exfoliative cytodiagnostics, determination of the absorption and excretory functions of the stomach are of secondary importance.

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

With functional disorders of the stomach, there are usually 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 variability of the wedge. manifestations, which is associated with neuropsychic influences, atypical localization of pain on palpation of the abdomen and, finally, a sharp fluctuation in acidity in individual studies.

X-ray diagnostics is based on a thorough rentgenol, examination of the stomach. At the same time, changes in the relief of the gastric mucosa and other X-ray functional and morfol, symptoms are determined. These include: excessive fasting secretion, rapid growth of secretory fluid, changes in tone, persistent deformation of the pyloric part of the stomach, impaired peristalsis, etc. The most constant symptom of increased fasting secretion, sometimes manifested by a horizontal fluid level 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 (the phenomenon of mucus) is small-point enlightenment in the layer of barium suspension - the smallest droplets of mucus suspended in a suspension of barium. The mucus phenomenon is indistinguishable when translucent and can only be ascertained on images with compression. Chron. G. is often accompanied by a decrease in stomach tone. The increase in tone is often local in nature; at antral G. it is manifested by spastic conditions or motor excitation of the output part of the stomach. Violation of the peristaltic function is not always detected. In about half of the cases hron. G. superficial and rare peristalsis is observed. Pronounced disorders of peristalsis up to the appearance of the aperistaltic zone are observed with the so-called. rigid antral G. Evacuation of barium from the stomach usually occurs within normal periods, although occasionally it can be slowed down.

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

Based on the capabilities of rentgenol. the method is distinguished: hron, universal G., hron, antral G. and its wedge, and rentgenol, varieties (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 cron. G. can be taken into account only at the corresponding wedge, picture, anamnesis, etc. Numerous facts are known when expressed rentgenol, G.'s symptomatology was not confirmed by biopsy data and, conversely, morphologically proven G. did not appear radiologically.

At hron, universal G. the area of the rebuilt relief is usually very extensive (the body of the stomach is also captured). As a result of edema, hyperemia and inflammatory cell infiltration, mainly of the submucosal layer and connective tissue stroma, the folds of the mucous membrane swell unevenly (Fig. 4 and 5), sometimes so significantly that their number decreases. In places, the folds form polyp-like thickenings and have a distinct appearance (Fig. 6). Along the greater curvature, the oblique and transversely located bridges between the folds thicken, therefore the contour of the large 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 restructuring of the relief of the mucous membrane at hron. G. is sometimes so disordered and chaotic that it is difficult to distinguish it from the atypical relief in stomach cancer. Series only sighting shots the relief of the mucous membrane helps to establish the still preserved 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.

Chron, antral G. refers to the most often found varieties hron. D. It has a bright, diverse, and most importantly the most convincing roentgenosemiotics. Rentgenol, the picture is characterized by signs of hypersecretion, the phenomenon of mucus, patol, restructuring of the relief of the mucous membrane. In addition, a deformation of the antrum and a violation of its peristalsis are found. The relief pattern varies: more often sharply swollen, widened folds, but retaining the usual longitudinal direction, their number is reduced. With pronounced edema, they form shapeless, pillow-like defects in the relief, the grooves between the folds disappear, the relief is smoothed out. A classic example of a relief at hron. G. of the antrum are rather persistently persistent thickened transverse folds of the mucous membrane (Fig. 7), along the greater curvature of the stomach - an irregularity of the contour in the form of uniform serration. With a long flowing hron. G. with secretory insufficiency, the relief is disordered and consists of shapeless bulges (defects) and spots and strips of barium chaotically located between them. In some cases, atypism of the relief occurs due to the increased mobility of the swollen mucous membrane of a relatively loose, inflammatory altered submucosa. With a wide pyloric canal, partial prolapse of the mucous membrane into the duodenal bulb is possible. With a normal lumen of the pylorus, the gastric mucosa does not fall out. However, periodically "sliding" mucous membrane, accumulating in front of the gatekeeper, here forms a kind of defect, reminiscent of a tumor lesion (Fig. 8). This "phenomenon of crawling" of the mucous membrane was first explained and described by Yu. N. Sokolov and VK Gasmaeva (1969).

Due to the thickening of the circular and longitudinal muscles, the antrum of the stomach is deformed: it narrows and shortens, in contrast to the deformity in infiltrating cancer, with which 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 elasticity, and the deformation becomes persistent. As a result of inflammatory submucosal sclerosis (so-called sclerosing G.) peristalsis disappears and rigid antral G. arises, which, undoubtedly, is a late stage hron, antral G. with secretory insufficiency. At these patients quite often on the basis of a wedge, data suspect stomach cancer, which is often difficult to refute at rentgenol, research. The deformation of the antrum is very pronounced and persistent. Attention is drawn to the circular narrowing of the pyloric part of the stomach, while its simultaneous shortening often remains 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 covering the entire antrum. The observation of at least short-term peristalsis testifies against cancer, edges can also be caused with the help of morphine.

At polypous (warty) G. patol, changes are often localized in the antrum. They represent multiple, uniform in size, rounded, blurred defects to dia. 3-5 mm, sometimes in the form of elevations on the crests of the folds, but more often forming a disorderly 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, other rentgenol, symptoms are also found. At smaller growths G. is called warty, or verrucous; small defects are usually recognized only on sighting images with compression.

Granular gastritis is recognized by the symptom of "granularity" of the relief (Fig. 11). This symptom was studied by W. Frik using photographs of the relief 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 the data of the study of "fine relief" with the results of gastrobiopsy revealed a parallelism between the picture of the 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 chron. G. gastric fields become more convex - "granular" type, and in far advanced cases - and larger (dia. 3 mm and more), uneven, reminiscent of a warty surface. Along with this symptom, it is necessary to detect other rentgenol described above, G.'s signs.

Erosive G. is rarely recognized roentgenologically, since the possibilities of identifying erosions rentgenol are very limited by the research method.

The so-called. accompanying (accompanying) G. is radiologically constantly found in case of peptic ulcer disease (the exception is the so-called senile stomach ulcers) and less often in case of stomach cancer.

The expressed pictures of accompanying G. are observed with duodenal ulcer, after gastroenterostomy operation. At accompanying G. the outlet part of the stomach is more often amazed. All of the above-described rentgenol are also observed. G.'s symptoms. Often there is a rough drawing of the relief of the mucous membrane, disorder and swelling of the folds. Dynamic wedge. - rentgenol, observations of accompanying G.'s course at peptic ulcer show that if under the influence of conservative treatment the ulcer "niche" disappears, and other rentgenol, G.'s symptoms remain unchanged, then, as a rule, patients do not notice improvement.

At rentgenol, research, the recognition of polyposis G., which should be differentiated with true polyps of the stomach, can present known difficulties. When diagnosing hron. antral G. it is necessary to keep in mind also pernicious anemia, at a cut polymorphic changes in the relief of the mucous membrane of the pyloric part of the stomach can be observed.

In addition to rigid antral gastritis, it is necessary to take into account other types of antral G. 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 "mucosal crawling phenomenon" described above. In case of difficulties, a series of images or X-ray cinematography, fibroscopy and gastrobiopsy are used. With the so-called. systemic diseases only a thorough analysis of the entire wedge, pictures allows you to come to the correct diagnosis.

Gastritis in children

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

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

The 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 a violation of the synthesis of hydrochloric acid, which is confirmed by the presence of persistent achilia (in practically healthy and sick children of G.), to -It can not be explained by any illness or nutritional deficiencies.

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

Morphologically, superficial G. and gastritis with defeat of glands without atrophy prevails in children, atrophic G. is less often 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 course.

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

Malosymptomatic form hron. G. is less common than a form with severe symptoms; often occurs in younger children: pain usually appears after eating, is of low intensity, localized in the epigastrium or diffused. Dyspeptic symptoms are absent in some children. The acid-forming function of the stomach is reduced or histamine reflex achilia is determined.

With hron. G. with severe symptoms, the pain symptom is intense, can occur immediately after a meal, after 1 - 2 hours or at night. Dyspeptic symptoms are persistent. Acid-forming function in most sick children is increased during long-term follow-up. In some children, peptic ulcer disease comes to light in the future, in this case G. is essentially a pre-ulcer state.

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

Differential diagnosis hron. G. at children is carried out with a peptic ulcer (see), liver diseases (see), bile ducts (see Bile ducts) and diseases nervous system... Taking into account the exceptional rarity of malignant neoplasms of the stomach in children and an easier course of hron than in adults. G., sufficient grounds for wide application in pediatric practice, there is no gastrobiopsy method for diagnostic purposes. It is used only for strict indications and necessarily 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 in clinic to peptic ulcer, treatment is carried out as antiulcer, including seasonal preventive courses.

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

Constitutionally weakened children with signs of dysfunction demanded special attention went. - kish. tract (increased acid-forming function, achilia, etc.), with residual effects after 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, to carry out prophylactic anti-relapse courses of treatment and recreational activities.

Gastritis in old and old age

Features of G.'s course are caused by age-related changes in the digestive system and a decrease in general reactivity. Wedge, G.'s manifestations in elderly patients and old age less pronounced than in young people. Dyspeptic symptoms and pain are relatively little expressed, and a decrease in appetite is rarely observed. The digestive ability of gastric juice and the content of gastromucoproteins in it are reduced, as is the acid-forming function of the stomach. The electrophoretogram of gastric juice proteins, in comparison with the electropherogram of young patients, has a more "compressed" appearance, the debit of the protein component is lower in both fractions of gastric mucus, and the carbohydrate component is increased in insoluble mucus. A vitreous basal secret is often found - a jelly-like mass with a large number of desquamated cells of the mucous membrane. Atrophic changes in the gastric mucosa (according to aspiration biopsy) and secretory insufficiency are found in patients hron. G. over the age of 60 is 2-3 times more often than among 30-40-year-olds. After 60 years, atrophic G. is more often observed in women, while at a younger age - more often in men. The great prevalence of atrophic G. in old age is connected, apparently, with the frequent development at this age hron, diseases of the liver, pancreas, intestines, promoting development hron. G.

Treatment and prevention are based on concomitant hron, diseases and characteristics of the reaction of the elderly organism to the introduction medicinal substances... When determining the forecast, one should bear 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 conditions of pathology, as well as to develop issues of therapy, G. on animals reproduce G.

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

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

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 intrasystemic and extrasystemic reactions in the body in response to damage to the stomach. IP Pavlov initiated the classification of types of gastric secretion disorders, which is used in the clinic.

G.'s model caused by the creation of nephysiol. the 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), by adding salt to food or gastric juice 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 the introduction of histamine or pilocarpine. This G.'s model develops gradually against the background of microcirculation disturbances and trophic processes in the mucous membrane, has hron, current.

Clinical and diagnostic characteristics of some clinical forms of chronic gastritis

chronic gastritis	Main clinical signs	Gastric secretion study data	radiological research	Gastroscopy data	Biopsy data
Antral	Pains in the epigastric region are hungry, nocturnal, sometimes subsiding after eating; heartburn, sour belching, often vomiting at the height of pain. Constipation tendency	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 hemorrhage in the submucous layer are found. The tone of the pyloric part is enhanced, sometimes there is a prolonged pyloric spasm. Signs of hypersecretion	Gistol, the picture of the mucous membrane is normal or has signs of hron, gastritis of varying severity. 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 (Menetrie's disease)	Weight loss, signs of hypoproteinemia, iron deficiency anemia. Obstinate gastric dyspepsia. Patients report a feeling of spasm and pressure in the epigastric region. The pains sometimes resemble those of a peptic ulcer; vomiting may be mixed with blood	Decreased, normal or increased	Pronounced changes in the relief of the mucous membrane along the greater curvature (in the sinus and the lower half or third of the body of the stomach) in the form of overly spaced, elastic thickened folds hanging down into the lumen of the stomach, and sometimes into the duodenum	The mucous membrane is swollen, with wide winding 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, overflow. The pains are diffuse, dull, aching, usually moderate, less often intense, last 1 - 11/2 hours. Heartburn, often belching with air, intermittent vomiting	Basal secretion increases to 10 meq / hour, maximum histamine secretion - up to 35 meq / hour. Abundant gastric secretion is often observed at night	Widespread restructuring of the relief of the mucous membrane with thickening of the folds (sometimes their pillow-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, the presence of mucus, single erosion and hemorrhage in the submucosa, signs of hypersecretion. With severe hypertrophy, the mucous membrane has a velvety appearance without the usual shine	Flattening of the mucous membrane due to hyperplasia of the superficial epithelium, less often interstitial tissue. The epithelium is often flattened, with a basal arrangement of nuclei of various sizes; hypersecretion with flour yes, signs of granular and vacuolar degeneration; abundant cellular infiltration of its own layer
Polypoid	Reminds clinic hron, gastritis with secretory insufficiency; can be asymptomatic. The prolapse of polyps into the duodenum and their infringement is clinically manifested by a pronounced pain syndrome. Bleeding may occur	More often reduced	Typical changes are more often localized in the antrum - typical small uniform rounded filling defects, sometimes on the crests of the folds, but usually they form a disorderly or honeycomb pattern. With true polyps, even multiple ones, the relief of the mucous membrane is usually not changed.	Found multiple polyps, the same or different in shape and size, which are often located in the pylorus. The mucous membrane is pale, thinned, its folds are smoothed, blood vessels are visible (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. There is a tendency to diarrhea and the development of anemia	Sharply reduced	Deformation (narrowing, shortening) of the antrum, restructuring of its internal relief; weakening or disappearance of peristalsis	Deformity, rigidity and narrowing of the pyloric stomach, edema of the mucous membrane	In the output section, there is a picture of atrophic and hyperplastic hron, gastritis. In other departments, atrophy of the glandular apparatus of varying severity
Gastritis with secretory insufficiency	Weight loss and decreased appetite, feeling of heaviness and pressure in the epigastric region after eating. Moderate and intermittent pain, 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, tone and peristalsis are often weakened, the evacuation of stomach contents 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, in places covered with mucus, when the stomach is inflated with air, the folds are easily smoothed out. Erosions and punctate hemorrhages are sometimes observed	Various degrees of glandular atrophy (decrease in the main and parietal glandulocytes), flattening of the epithelium of the mucous membrane, deepening of the fossae, intestinal and pyloric metaplasia
Erosive gastritis (hemorrhagic)	Pain in the epigastric region: early, fasting and late; acidic heartburn, sometimes vomiting mixed with blood (from traces to clots). The higher the acidity, the more often bleeding Tendency to constipation	Normal or elevated	The relief of the mucous membrane is changed more often in the pylorus of the stomach. Erosion detection capabilities are very limited	Multiple erosions of a round or stellate shape are determined, mainly in the outlet of the stomach, against the background of the phenomena of superficial gastritis - edema, infiltration, hyperemia of the mucous membrane	Gistol, the picture of the mucous membrane is more often similar to the picture of hron, gastritis with increased secretion. Erosions are more often detected with targeted biopsy

Bibliography: Aruin LI Morphological study of biopsies of the gastric mucosa, Arkh. patol., t. 31, No. 3, p. And, 1969; Aruin L. I. and Sh and -r about in V.G. To the question of the morphogenesis of chronic gastritis, in the same place, t. 33, No. 10, p. 21, 1971; Belousov AS Essays on functional diagnostics 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 V. L. Physiology and experimental pathology of the stomach and duodenum, M., 1970; Kanishchev P. A. Methods of diagnosis of diseases of the stomach, L., 1964; Lazovsky Yu. M. Functional morphology of the stomach in norm and pathology, M., 1947; Levin GL Sketches of gastric pathology, M., 1968; L and with about h to and B. G. N., Ultrast ^ structure 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, Pre-tumor diseases of the stomach, L., 1969, bibliogr .; Menshikov FK Diet therapy, M., 1972, bibliogr .; Pavlov I.P. Complete Works, vol. 2, book. 2, M.-L., 1951; Peleschuk A. 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 y with with SM 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 y 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 morphologische Veranderungen des Magens bei Pa-tienten mil umunischer Gastritis im hohe-ren 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 diagnostics G.- Ryzhikh AN 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 NV Diagnostics of gastritis of the distal stomach, Wedge, medical, t. 49, No. 1, p. 69, 1971; With about to about l about in Yu. N. and V l and with about in P. V. Relief of the mucous membrane of the stomach is normal and pathological, M., 1968, bibliogr .; Sokolov Yu. N. and Gasmaev VK About the phenomenon of "crawling" of the gastric mucosa, Vestn, rentgenol, and radiol., No. 2, p. 66, 1969; Sokolov Yu.N. id r. Our experience in the study of the fine relief of the stomach in chronic gastritis, ibid., No. 5, p. 3, 19 73, bibliogr .; Tikhonov KB and Pruchansky VS 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 V. A. N. Radiodiagnosis of diseases of the digestive tract, t. 1, Yerevan, 1961; Sh l and f er 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 r i c h M. Rontgendiagnostik des Magen-Darmka-nals, Stuttgart, 1959, Bibliogr.

G. in children- Balashova TF Enzyme-forming function of the stomach in chronic gastritis in children, Pediatrics, No. 5, p. 14, 1971; And in scarlet about in SM, etc. Endocrine cells of the gastric mucosa in children, in the same place, No. 3, p. 12, 1975, bibliogr .; Queen 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; Cossure M. B. Diseases of the stomach in children, M., 1968, bibliogr .; Lukyanova EM, Korole-z in and RI and Shly to about in IA Endoscopic examinations 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; About s tr about polo-lets S. S. and others. Morphological day-n1st of small gastritis with normal i shdvshtsenoy secretory function of the shlun-ka at d1tey, Ped1at., Obstetrician. i gshek., no. 4, p. 3, 1975; Samarina G. Ya. Clinical features antral gastritis in children, Vopr. okhr. mat. and children., v. 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 (pat.an.), M. B. Cossyura (ped.), H. N. Lebedev (pat. Phys.), A. P. Peleschuk (geront.), Yu. N. Sokolov ( rent.), the compiler of the table F.I.Komarov.

Pathological anatomy... Initial ulcers do not penetrate deeper than the mucous membrane. A chronic ulcer can spread to the muscular and serous membranes. Callous ulcer is called an ulcer with hard raised edges. An ulcer that invades all layers of the gastric wall can cause it. An ulcer that penetrates into neighboring organs, most often the pancreas, is called a penetrating ulcer. After healing, ulcers develop, sometimes deforming the stomach ("hourglass", stomach in the form of a snail) or causing narrowing () of the pylorus. Inflammation serous membrane at the site of the ulcer leads to perigastritis or periduodenitis and formation with nearby organs.

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

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

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

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

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

With a peptic ulcer, changes occur in the entire mucous membrane of the stomach and duodenum. At the edges of the stomach ulcer, there is a proliferation of the epithelium, which can grow deep into the mucous membrane and along its surface, taking the form of polyps. The pyloric glands are gyneplastic, and signs of increased mucoid secretion are visible in them. In a secret, acidic mucopolysaccharides that are absent in the norm appear. With the prolonged existence of an ulcer, atrophic changes in the glands occur, their secretion weakens. In the fundic glands, pictures of atrophy, intestinal metaplasia are noted, the so-called pseudopyloric Stern's glands containing mucoid secretions are formed. In the stroma, you can see diffuse lymphoplasmacytic infiltrates, large lymphoid follicles, proliferation of smooth muscle fibers. With a duodenal ulcer, the number of parietal cells increases significantly, which are found even in the pyloric region.

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

Complications... VM Samsonov identifies five groups of complications of peptic ulcer disease.
1. Complications of ulcerative and destructive origin: perforation, arrosive bleeding and penetration. Ulcer perforation is one of the most formidable complications. Most often, perforation occurs in the afternoon. The diameter of the perforation is about 0.5 cm. Histological examination reveals a picture of exacerbation of peptic ulcer disease, necrosis and leukocyte infiltration of the edges and bottom of the ulcer, fibrin overlay on the serous integument.

Arrosive bleeding arises from the large vessels of the bottom of the ulcer. MK Dahl and others found that arrosion of the vessel can be preceded by a limited necrosis of the wall with the formation of an aneurysm and its subsequent rupture. Bleeding from chronic ulcers is especially dangerous, the vessels of which are fixed with scar tissue, which prevents the arteries from contracting. Ulcers of the lesser curvature of the stomach usually penetrate into the lesser omentum, duodenal ulcers - into the pancreas.

With the penetration of ulcers into the hollow organs, gastric fistulas occur (gastro-colonic, gastrointestinal, gastro-biliary). Ulcers of the cardiac and subcardiac regions can penetrate into the diaphragm. In the future, such an ulcer may break through into the pleural cavity, into the pericardial cavity.

2. Complications of an inflammatory nature: gastritis, duodenitis, perigastritis, periduodenitis, stomach phlegmon, hepatocholangitis.

3. Complications of ulcerative cicatricial origin: stenosis of the cardiac stomach, pylorus, duodenum, shortening of the lesser curvature, deformation of the stomach in the form of an "hourglass", diverticula of the stomach and duodenum.

4. Malignancy of stomach ulcers, according to A. I. Abrikosov, occurs in 8-10% of cases. The lack of consensus on the frequency of ulcer malignancy is associated with the difficulties of differential diagnosis of malignant ulcers and primary ulcerative cancer. Malignancy of duodenal ulcers is extremely rare.

5. Combined complications.

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

Macrodrug CHRONIC gastritis.

Smoothing of the folds of the gastric mucosa is found, the wall is hyperemic, thinned, flattened. There are multiple point erosion.

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

Coiled bacteria are visible, located near the superficial epithelium of the supra-mucous barrier. Superficial cells are damaged, infiltration of the gastric mucosa with polymorphonuclear leukocytes.

Micropreparation N 423 CHRONIC ACTIVE GASTRITIS OF ANTHRUM WITH IRON ATROPHY AND COMPLETE INTESTINAL METAPLASIA (gastrobiopsy specimen, 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.

Macrodrug CHRONIC STOMACH Ulcer(kaleznaya).

On the lesser curvature of the stomach, a deep defect of the stomach wall is visible, penetrating to the serous membrane, oval in shape, with raised edges. The edge facing the gatekeeper is gently sloping, it looks like a terrace, formed by mucous, submucous and muscular membranes. The edge facing the esophagus is undermined. At the bottom of the ulcer there is necrotic brownish detritus. The folds of the gastric mucosa are smoothed, the rays converge to an ulcerative defect (convergence of folds).

(E) Micropreparation N 106 CHRONIC STOMACH Ulcer (with exacerbation) (staining with hematoxylin and eosin.

A defect in the stomach wall that invades the mucous membranes, submucosa and muscular membranes. Near the defect, one edge of the mucous membrane is undermined, the other is shallow. At the bottom of the wound defect there are 4 layers - from the lumen to the serous membrane: fibrinous-purulent exudate (fibrin, neutrophils, an admixture of necrotic tissue), fibrinoid necrosis, granulation tissue, scar tissue. Muscular membrane at the bottom it is not determined, its break is visible at the border of the ulcer defect. In the mucous membrane near the ulcer - a picture of chronic atrophic gastritis.

View a set of macropreparations illustrating complications of chronic ulcers: PASSING STOMACH ULTRA, PENETRATING GASTRIC ULTRA, ARROSION OF THE VASCULAR IN THE BOTTOM OF THE ULTRA, ULTRA-STOMACH CANCER, CURRIC DEFORMATION OF THE STOMACH

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

Macro-preparations of different forms of STOMACH CANCER.

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

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

In the wall of 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 - signet ring (staining with hematoxylin and eosin and alcian blue).

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

INTESTINAL DISEASES

Macrodrug PHLEGMONOUS APPENDICITIS.

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

(E) Micropreparation N 107 PHLEGMONOUS APPENDICITIS (staining 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 by leukocytes.

Macrodrug CHRONIC APPENDICITIS.

The lumen is filled with mucus. Obliteration of the cavity. The mucus turns into globules. Atrophy of the muscle layer and sclerosis.

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

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

Macro-preparation of the Liver abscess(pylephlebitic), as a complication of appendicitis

In the area of the gate of the liver - cavities with thick grayish-white walls, filled with greenish-gray dense contents. On the cut, the liver tissue is yellowish.

View a set of intestinal tumors macro-preparations.

Circular stenosing cancer of the sigmoid colon - v sigmoid colon- an annular formation with raised edges and an ulcerated bottom. The section shows a grayish-white tissue with hemorrhages, growing into the layers of the intestinal wall.

LIVER DISEASES

Macrodrug TOXIC LIVER DYSTROPHY (fatty hepatosis). The liver is enlarged, flabby consistency, yellow-white (clay-like), has a greasy sheen in the cut ("goose liver")

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

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

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

Electronogram HYDROPIC HEPATOCYTE DYSTROPHY 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.

During electron microscopic examination, the EPS cisterns are sharply expanded, the mitochondria are swollen.

Macro-preparations of LIVER CIRROSIS... Mark the size, color, consistency, surface and section view of the liver. Estimate the size of the regenerated nodes and determine the macroscopic form of cirrhosis based on this feature.

Alcoholic small-node portal cirrhosis of the liver- the liver is deformed, yellow color, the surface is shallow.

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

Macro-preparations: PRIMARY LIVER CANCER, LIVER METASTASES OF TUMORS OF ANOTHER PRIMARY LOCALIZATION.

MORPHOLOGICAL EQUIVALENTS OF GLOMERULONEPHRITIS

Micropreparation N 112 INTRACAPILLARY PROLIFERATIVE GLOMERULONEPHRITIS (stained 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 IMUNE COMPLEXES IN THE RENAL BLOOD IN ACUTE GLOMERULONEFRITIS(atlas, fig. 15.2).

Along the course of the basement membrane, a granular glow is visible (deposits in the form of lumps glow)

Macro-preparation SUBCUTE GLOMERULONEPHRITIS("large variegated kidney").

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

Micropreparation N 113 SUBCUTE, MOSTLY EXTRACAPILLARY GLOMERULONEPHRITIS (stained with hematoxylin and eosin).

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

MORPHOLOGICAL OPTIONS OF CHRONIC GLOMERULONEPHRITIS

Electron diffraction pattern MEMBRANOSE NEPHROPATHY(atlas, fig. 15.6).

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

Electron diffraction pattern MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS(atlas, fig. 15.9).

Electron microscopic examination reveals subepithelial electron-dense deposits.

Electronogram MESANGIOPROLIFERATIVE GLOMERULONEPHRITIS(atlas, fig. 15.10).

Electron microscopic examination shows deposits in the mesangium.

Macrodrug SECONDARY SHRINKED KIDNEY (CHRONIC GLOMERULONEPHRITIS WITH OUTCOME TO NEPHROSCLEROSIS).

The buds 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, in the preserved hypertrophied glomeruli proliferation of mesangial cells, sclero-vascular loops. There are sclerosis and hyalinosis of arterioles. Hyaline cells in the lumen of the tubules.

SECONDARY KIDNEY DAMAGE

Macrodrug AMYLOID NEPHROSIS("large white", "large sebaceous kidney").
Note the increase in the size of the kidney, dense consistency, greasy appearance of the surface.

The kidneys are enlarged in size, dense texture, smooth surface. On the cut with a greasy sheen. The border between cortical and medulla is erased

(E) Micropreparation N 16 AMYLOID NEPHROSIS (coloration of Congo-mouth). Designate deposits of amyloid in the capillary loops of the glomerulus, along the tubular membrane of its own, in the walls of blood vessels, as well as in the stroma of the kidney along the reticular fibers.
Mark 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 deposits of amyloid.

ACUTE RENAL FAILURE (ARF)

(E) Micropreparation N 6 NECROTIC NEPHROSIS (staining with hematoxylin and eosin). The glomeruli and epithelium of the rectus tubules are preserved. Their cells contain nuclei. The epithelium of the convoluted tubules does not contain nuclei (karyolysis).

ORGANOPATHOLOGY OF CHRONIC RENAL FAILURE

View a set of macro-preparations reflecting the morphological manifestations of uremia: fibrinous pericarditis ("hairy heart"), gross tracheitis, diphtheritic colitis.

DISHORMONAL DISEASES OF THE GENITAL ORGANS

Macro-preparation POLYP UTERUS. Mark the localization of the polyp, its shape, size, surface nature, connection with the underlying tissue.

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

(E) Micropreparation N 142 IRON HYPERPLASIA ENDOMETRY (staining with hematoxylin and eosin).

The endometrial glands are built from the epithelium of the proliferating type, have a different size and shape, have a convoluted course and cystic expansion, are very closely located, branching and budding of the glands is noted.

Micropreparation N 57 PSEUDOEROSIS OF THE CERVIC (staining with hematoxylin and eosin).

In the area of cervical erosion, there are two types of epithelium: the epithelium is stratified squamous non-keratinizing and prismatic. Ectopia of the columnar epithelium in the exocervix is noted.

PATHOLOGY OF PREGNANCY

Macro-preparation POSITIVE ENDOMETRITIS.

The lining 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 slightly open.

Macrodrug LIVER IN ECLAMPSION.

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

Description of drugs in Pathological Anatomy in Lesson No. 26

(This is an indicative description, not a cathedral, some drugs may be missing, since the description of past years)

LESSON number 26stomach diseases: gastritis, peptic ulcer, stomach tumors

Micropreparation № 37 "Acute catarrhal gastritis" - description .

The mucous membrane of the stomach is covered with purulent exudate, which penetrates into all layers of the stomach wall. The openings of the glands are widened. The cytoplasm of the epithelium is vacuumed. Own layer of the mucous membrane with congested vessels, in places with diapedesic hemorrhages, polymorphonuclear leukocytes (PMN).

Micropreparation № 112 "Chronic superficial gastritis" - demo .

Micropreparation № 229 "Chronic atrophic gastritis" - description .

The mucous membrane of the stomach is sharply thinned, the number of glands is reduced, in place of the glands, fields of growing connective tissue are visible. The fossa epithelium with symptoms of hyperplasia. Epithelium of the glands with signs of intestinal metaplasia. The entire wall of the stomach is diffusely infiltrated by histolymphocytic elements with an admixture of polymorphonuclear leukocytes.

Macrodrug "Acute erosions and stomach ulcers" - description .

The mucous membrane of the stomach with smooth folds and numerous defects of the mucous membrane of a round and oval shape, the bottom of which is painted black.

Macrodrug "Chronic stomach ulcer" - description .

On the lesser curvature of the stomach, a deep defect of the mucous membrane is determined, affecting the muscular layer, of a rounded shape with dense, raised, amosolized edges. The edge of the defect facing the esophagus is undermined, to the gatekeeper it is shallow.

Micropreparation № 121 "Chronic stomach ulcer in the acute stage" - description .

A defect in the wall of the stomach is determined, capturing the mucous and muscular layer, with an undermined edge facing the esophagus, and shallow, facing the gatekeeper. At the bottom of the defect, 4 layers are determined. The first is external - fibrinous-purulent exudate. The second is fibrinoid necrosis. The third is granulation tissue. The fourth is scar tissue. At the edges of the defect, strips of muscle fibers, amputation neuroma are visible. Vessels of the cicatricial zone with sclerosed thickened walls. The mucous membrane at the edges of the defect with symptoms of hyperplasia.

Macrodrug "Polyp of the stomach" - description .

On the gastric mucosa, a tumor formation on a broad base (pedicle) is determined.

Macrodrug "Saucer-shaped stomach cancer" - description .

The tumor looks like a rounded flat formation on a wide base. The central part of the tumor sinks, the edges are somewhat raised.

Macrodrug "Diffuse stomach cancer" - description .

The wall of the stomach (mucous and submucous layers) is sharply thickened, represented by a uniform grayish-white dense tissue. The mucous membrane over the tumor with symptoms of atrophy with smoothed folding.

Micropreparation № 77 "Adenocarcinoma of the stomach" - description .

Micropreparation № 79 Cricoid cell carcinoma - demo .

The tumor is built of atypical glandular complexes formed by cells with pronounced cellular polymorphism. The stroma is not developed.

Micropreparation № 70 "Metastasis of adenocarcinoma in the lymph node" - description .

The pattern of the lymph node is erased, the growth of tumor tissue is represented by atypical glandular cosplexes.

9. What is, on average, the total duration of the first three stages of development of lobar pneumonia?

10. Specify the ways of spreading inflammation in lobar pneumonia.

11. List pulmonary complications lobar pneumonia caused by Streptococcus pneumoniae.

12. Describe the composition of the exudate in case of lobar pneumonia in the tidal stage.

13. Describe the composition of the exudate in case of lobar pneumonia in the stage of red hepatization.

14. Describe the composition of the exudate in lobar pneumonia in the stage of gray hepatization.

15. Specify the extrapulmonary complications of lobar pneumonia caused by Streptococcus pneumoniae.

16. Give the macroscopic characteristics of changes in the lungs with bronchopneumonia.

17. Give a microscopic characterization of changes in the lungs with focal pneumonia.

18. Name the features of the causative agents of nosocomial pneumonia.

19. Name the complication of lobar pneumonia that develops with excessive activity of neutrophils with massive destruction lung tissue.

20. Specify the complication of lobar pneumonia that develops with insufficient activity of neutrophils and the development of the organization of fibrinous exudate.

21. Name the reasons for the formation of a lung abscess.

22. List the reasons for the formation of a lung abscess.

23. Give a definition of the term atelectasis.

24. What develops when the airway is completely closed?

25. What develops when the pleural cavity is partially filled with liquid exudate?

26. What develops when respiratory distress syndrome, due to the destruction of the surfactant?

27. What is the cause of hemodynamic pulmonary edema?

28. A 25-year-old patient fell ill suddenly after hypothermia while intoxicated. Complains of a rise in body temperature to 390C, chills, dagger pain in the right side and severe weakness for 7 days. Objectively: a dull sound is heard above the lower lobe of the right lung during percussion, during auscultation, breathing is not performed, a pleural friction noise is heard. Radiographically - darkening of the lower lobe of the right lung, in the region of the 8th segment there is a cavity, thickening of the pleura. Your conclusion.

29. In a patient with a stroke and left-sided hemiparesis on the 14th day, the body temperature increased to 380C, which was accompanied by the appearance of cough and small bubbling rales in the lower parts of the left lung. Your conclusion.

30. A 67-year-old man who is inpatient treatment for phlegmon of the scalp developed shortness of breath, coughing, and his body temperature rose to 38.50C. 4 weeks after the massive antibiotic therapy, the body temperature dropped, dyspnea decreased, and moderate leukocytosis persisted. During an X-ray examination, an annular shadow with a fluid level appeared in the second segment of the right lung. Your diagnosis.

II lesson

CHRONIC NON-SPECIFIC LUNG DISEASES. INTERSTITIAL LUNG DISEASES. PNEUMOCONIOSIS. LUNG CANCER.

1. Diffuse chronic lung lesions: definition of the concept and classification. Chronic obstructive pulmonary disease. General characteristics.

2. Chronic obstructive pulmonary emphysema- definition, classification, epidemiology, etiology, pathogenesis, morphological characteristics, clinical manifestations, complications, outcomes, causes of death. Other types of emphysema (compensatory, senile, vicarious, interstitial): clinical and morphological characteristics.

3. Chronic obstructive bronchitis: definition, classification, etiology, epidemiology, pathogenesis, morphological characteristics, clinical manifestations, complications, outcomes.

4. Bronchiectasis and bronchiectasis. Concept, classification, etiology, pathogenesis, morphological characteristics, clinical manifestations, complications, outcomes, causes of death. Kartagener's syndrome. Clinical and morphological characteristics.

5. Diffuse interstitial lung disease. Classification, clinical and morphological characteristics, pathogenesis. Alveolitis. Morphological characteristics, pathogenesis. Pneumoconiosis (anthracosis, silicosis, asbestosis, beryllium). Pathogenesis and morphogenesis, clinical manifestations, complications, causes of death. Sarcoidosis Clinical and morphological characteristics, morphology of extrapulmonary lesions.

6. Idiopathic pulmonary fibrosis. Classification, etiology, pathogenesis and morphogenesis, stages and variants, clinical and morphological characteristics, prognosis.

7. Pneumonitis(desquamative interstitial pneumonitis, hypersensitivity pneumonitis): patho - and morphogenesis, clinical and morphological characteristics, causes of death. Eosinophilic lung infiltrate. Classification, causes, clinical and morphological characteristics.

8. Tumors of the bronchi and lungs. Epidemiology, principles of classification. Benign tumors. Malignant tumors. Lung cancer. Bronchogenic cancer. Epidemiology, etiology. Biomolecular markers of lung cancer. Precancerous changes in the bronchi and lung. The concept of "cancer in the rumen". Clinical manifestations. Diagnostic methods, morphological characteristics, macroscopic variants, histological types (squamous cell, adenocarcinoma, small cell, large cell). Bronchioloalveolar cancer: clinical and morphological characteristics.

1. Lecture material.

vol. 2, part I: p. 415-433, 446-480.

vol. 2, part I: pp. 293-307, 317-344.

4. Guide to practical exercises on pathological anatomy(, 2002) p. 547-567.

5. Atlas on pathological anatomy (2003) p. 213-217.

LEARNING CARD

PURPOSE INSTALLATION OF THE LESSON: to study the morphology of the main forms of chronic lung diseases using macrospecimens, microspecimens and electron diffraction patterns and conduct clinical and anatomical comparisons.

CHRONIC NON-SPECIFIC

LUNG DISEASES

View macropreparations, the main clinical and anatomical forms of chronic nonspecific lung diseases. Describe CHRONIC LUNG ABSCESS, CHRONIC BRONCHITIS WITH BRONCHEECTASES, LUNG EMFYZEMA.

Micropreparation No. 12 CHRONIC DEFORMAL BRONCHITIS (staining with hematoxylin and eosin). To note the components of chronic inflammation of the bronchi: peribronchial sclerosis, vascular pericalibration, inflammatory infiltration in the wall of the bronchi and peribronchial tissue, metaplasia of the bronchial epithelium.

Electronogram Intracapillary sclerosis in pulmonary emphysema (atlas, fig. 11.13). Note the formation of a capillary with a sclerosed wall and the destruction of the air-blood barrier.

PNEUMOCONIOSIS

Macrodrug ANTHRAKO-LUNG SILICOSIS. Pay attention to the change in volume and decrease in the airiness of the lung tissue. To characterize the sclerotic areas in the lung: their shape, size, color, prevalence.

Micropreparation No. 000 LUNG ANTHRAKO-SILICOSIS (staining with hematoxylin and eosin). Outline the structure of the silicotic nodule, concentrically located collagen fibers around the sclerosed vessels. Pay attention to the significant amount of coal dust contained both in the cytoplasm of macrophages (coniophages) and freely lying in the interalveolar septa.

LUNG CANCER

By a set of macro-preparations to determine the forms of growth and localization of cancerous tumors in the lungs.

Micropreparation No. 33 SQUAT CELL LUNG CANCER (staining with hematoxylin and eosin). Pay attention to the degree of atypia of tumor cells, signs of infiltrating growth.

Micropreparation No. 34 UNDIFFERENTIATED (anaplastic) LUNG CANCER (stained with hematoxylin and eosin). Assess the degree of anaplasia of cancer cells (shape, size, layout). Pay attention to the invasive nature of tumor growth.

BASIC Vocabulary for Lesson

Bronchiectasis- chronic pathological expansion of the bronchi.

Obstructive pulmonary disease- a group of diseases characterized by obstruction of the airways.

Restrictive lung diseases- a group of diseases characterized by the predominance of restrictive (restrictive) changes, usually in the intermediate tissue.

Pneumoconiosis- the general name for occupational lung diseases caused by exposure to industrial dust.

Epidermoid cancer- squamous cell carcinoma.

Hammen-Rich syndrome- idiopathic pulmonary fibrosis, diffuse fibrosing alveolitis, chronic interstitial pneumonitis.

Emphysema- excessive and stable expansion of the airways and respiratory structures located distal to the terminal bronchioles.

Bullous emphysema- emphysema, characterized by the formation of large subpleural bubbles (bullae).

Emphysema vicar (compensatory)- emphysema, which develops with the loss of a significant part of the lung (for example, with pulmonectomy, lobectomy).

Interstitial emphysema (interstitial)- emphysema, localized in the interstitium (stroma) of the lung.

Irregular emphysema- emphysema affecting the acini unevenly, which is almost always associated with scarring changes in the lung tissue.

Obstructive emphysema- emphysema caused by incomplete blockage (obstruction) of the airways with the formation of a valve mechanism.

Panacinar emphysema (panlobular)- emphysema, capturing acini from respiratory bronchioles to terminal alveoli.

Emphysema paraseptal- emphysema, characterized by changes in the distal part of the acin, while the proximal part remains normal.

Emphysema centriacinar (centrilobular)- emphysema, affecting the central or proximal part of the acinus, leaving the distal alveoli intact.

The list of questions for the lesson,

1. Specify the change in the myocardium underlying the development of cor pulmonale in COPD.

2. Select obstructive pulmonary disease.

3. What is the name of the excessive and persistent expansion of air and respiratory structures (or spaces) located distal to the respiratory bronchioles, with destruction of the walls of these structures without subsequent fibrosis?

4. Name the types of pulmonary emphysema.

5. What causes the predisposition to chronic obstructive pulmonary emphysema?

6. Select the most important factors in the development of chronic bronchitis.

7. Name the pathogenetic variants of chronic bronchitis.

8. Name the possible complications of chronic obstructive bronchitis.

9. In what disease does the increased reactivity of the mucous membrane of the airways occur?

10. Specify the pathogenetic variant of bronchial asthma.

11. Specify a molecule that fixes on mast cells in atopic bronchial asthma.

12. Name the changes in the bronchial wall during bronchiectasis.

13. Name the macroscopic types of bronchiectasis.

14. Name the complications of bronchiectasis.

15. What is the name Occupational Illness associated with exposure to industrial dust and characterized by the gradual development of sclerotic changes in the lung parenchyma?

16. Name the etiological factors in the development of silicosis.

17. Name the etiological factors in the development of asbestosis.

18. Name the etiological factors in the development of anthracosis.

19. Select the components of the sarcoid granuloma.

20. In what disease are asteroid inclusions found in the cytoplasm of multinucleated cells?

21. Name the types of lung cancer classified by location.

22. Name the most common histological type of central lung cancer.

23. Name the most common histological type of peripheral lung cancer.

24. What is called lung cancer developing from the epithelial lining of the distal third of the segmental bronchi, bronchioles, or alveolar epithelium?

25. What is the name of lung cancer that develops from the epithelial lining of the main, lobar and proximal third of the segmental bronchi?

26. Indicate precancerous conditions in the lungs.

27. What are the complications of bronchial cancer?

28. A 53-year-old patient has been smoking 2 packs of cigarettes a day for 30 years. I went to the clinic with complaints of persistent productive cough, worsening in the morning after waking up, and progressive shortness of breath. On X-ray images, an increase in the airiness of the lung tissue and an increase in the pulmonary pattern are determined. Your conclusion.

29. A 30-year-old patient was admitted to the clinic with complaints of shortness of breath, general cyanosis, weakness. It is known from the anamnesis that the woman long time works on a poultry farm. In the study: the level of immunoglobulins in the blood is increased, immune complexes are determined. X-ray examination shows a picture of a "cellular lung". Indicate the most likely diagnosis.

30. A 67-year-old patient, suffering from chronic diffuse bronchitis for a long time, died with increasing symptoms of pulmonary heart disease. At postmortem examination of the lungs of increased airiness, in the peripheral regions there are many different-sized bubbles. Indicate the changes in the internal organs found at the autopsy.

DISEASES OF THE DIGESTIVE ORGANS

(the section is studied in two laboratory sessions)

Learning objectives

The student must know :

1. The cause and the main nosological forms of diseases of the digestive system.

2. Classification, morphological manifestations of diseases of the digestive system, their complications and causes of death.

The student must be able to :

1. Describe the morphological changes of the studied macro-preparations and micro-preparations.

2. Based on the descriptions, compare the structural manifestations of diseases of the heart and blood vessels at various levels of the structure of organs, tissues and cells.

The student must understand :

Mechanisms of the formation of structural changes that occur in organs in diseases of the digestive system.

Iclass

DISEASES OF THE STOMACH AND INTESTINAL

1. Gastritis. Definition. Acute gastritis: etiology, pathogenesis, clinical and morphological characteristics. Chronic gastritis, concept, etiology, pathogenesis, classification principles. Forms identified on the basis of the study of gastrobiopsies, and their morphological characteristics. Complications, outcomes, prognosis. Chronic gastritis as a precancerous condition.

2. Peptic ulcer disease. Definition. General characteristics of peptic (chronic) ulcers of different localizations. Epidemiology, etiology, patho - and morphogenesis, its features in pyloric-duodenal and medio-gastric ulcers. Morphological characteristics of chronic ulcers during exacerbation and remission. Complications, outcomes. Acute stomach ulcers: etiology, pathogenesis, morphological characteristics, outcomes.

3. Tumors of the stomach. Classification. Hyperplastic polyps. Adenoma of the stomach. Morphological characteristics. Malignant tumors of the stomach. Stomach cancer. Epidemiology, etiology, classification principles. Features of metastasis. Macroscopic and histological forms.

4. Idiopathic inflammatory bowel disease. Nonspecific ulcerative colitis. Crohn's disease. Epidemiology, etiology, pathogenesis and morphogenesis, clinical manifestations, complications, outcomes, prognosis. Criteria for the differential diagnosis of chronic colitis.

5. Intestinal epithelial tumors. Benign tumors. Adenomas: epidemiology, classification, clinical and morphological characteristics, prognosis. Familial adenomatous polyposis. Adenoma and cancer: a concept of multistage colon carcinogenesis. Colon cancer. Epidemiology, etiology, classification, macro- and microscopic morphological characteristics, clinical manifestations, prognosis.

6. Diseases appendix cecum. Appendicitis. Classification, epidemiology, etiology, pathogenesis. Morphological characteristics and clinical manifestations of acute and chronic appendicitis. Complications.

1. Lecture material.

2. Textbook on pathological anatomy (, Anichkov N. M, 2000) vol. 2, part I: pp. 537-562, 586-593, 597-618.

3. Textbook on pathological anatomy (, Anichkov N. M, 2005) vol. 2, part I: p. 384-405, 416-422, 425-441.

4. Guide to practical training in pathological anatomy (, 2002) p.580-585, 601-612.

5. Atlas on pathological anatomy (2003) p. 256-265.

LEARNING CARD

PURPOSE INSTALLATION OF THE LESSON: to study the morphology of certain nosological forms of organ diseases using macropreparations and micropreparations gastrointestinal tract and conduct clinical and anatomical comparisons.

DISEASES OF THE STOMACH

Macrodrug MULTIPLE STOMACH EROSION. Pay attention to the gastric mucosa with multiple superficial defects, note the color of the bottom of the erosion.

Macrodrug CHRONIC GASTRITIS. Pay attention to the relief of the mucous membrane in various parts (body, pyloric canal), the presence of erosion.

Micropreparation No. 000 Helicobacter pylori in parietal mucus in the gastric fossa (gastrobiopsy, Giemsa stain). View, note the ability of bacteria to adhere to the epithelial cell.

Micropreparation No. 000 CHRONIC ACTIVE GASTRITIS OF ANTHRUM WITH IRON ATROPHIA AND COMPLETE INTESTINAL METAPLASIA (gastrobiopsy, staining with alcian blue and hematoxylin). Describe and evaluate semi-quantitatively morphological signs chronic gastritis: activity (presence of neutrophilic leukocytes) and the severity of inflammation (density of mononuclear infiltrate), the degree of atrophy of the lamina propria glands, the prevalence of intestinal metaplasia of the integumentary fossa epithelium.

Macrodrug CHRONIC STOMACH Ulcer (kalezny). Pay attention to the localization of the ulcer, its shape, edges, depth, the nature of the bottom. Determine which edge is facing the esophagus and which is the gatekeeper.

Micropreparation No. 000 CHRONIC STOMACH Ulcer (with exacerbation) (staining with hematoxylin and eosin). Designate the layers in the bottom of the ulcer that characterize the chronic course of the disease. Note fibrinoid necrosis and leukocyte infiltration, indicating an exacerbation of the process.

View a set of macro-preparations, illustrating the complications of chronic ulcers: PASSING STOMACH ULTRA, PENETRATING STOMACH ULTRA, ARROSION OF THE VASCULAR IN THE BOTTOM OF THE ULTRA, ULTRA-CANCER OF THE STOMACH, CURRIC DEFORMATION OF THE STOMACH. Pay attention to the localization of ulcers, the shape, nature of the edges, changes in the bottom and edges of the ulcer.

Macro preparations different forms of STOMACH CANCER. Determine the macroscopic forms of the tumor. Describe one of the forms.

Micropreparation No. 000 HIGHLY DIFFERENTIATED GASTRIC ADENOCARCINOMA (intestinal type) (stained with hematoxylin and eosin). Identify the signs of tissue and cellular atypism, the invasive nature of tumor growth.

Micropreparation No. 000 UNDIFFERENTIATED CANCER - signet ring (staining with hematoxylin and eosin and alcian blue). Pay attention to tumor cells with alcyanophilic cytoplasm, located in the "pools" of mucus. Mark the shape of the cell - cricoid, the nucleus is pushed back to the periphery, the cytoplasm is filled with mucus.

INTESTINAL DISEASES

Macrodrug PHLEGMONOUS APPENDICITIS. Pay attention to the size of the appendix, the state of the serous membrane (appearance, degree of blood filling), wall thickness, the nature of the contents in the lumen.

Micropreparation No. 000 PHLEGMONOUS APPENDI-CITY (staining with hematoxylin and eosin). Describe. To note the degree of preservation of the mucous membrane, the nature of the exudate, its distribution in the layers of the wall and the mesentery (mesenteriolitis).

Macrodrug CHRONIC APPENDICITIS. Pay attention to the size of the appendix, the state of the serous membrane, the thickness and the appearance of its wall in section.

Micropreparation No. 000 CHRONIC APPENDICITIS (staining with hematoxylin and eosin). Describe. Mark sclerotic changes in the wall and obliteration of the lumen of the appendix. Pay attention to lipomatosis and diffuse chronic inflammatory infiltration.

Macrodrug Liver abscesses (pylephlebitic), as a complication of appendicitis. View.

View set of macro-preparations intestinal tumors.

BASIC Vocabulary for Lesson

Acute gastritis- diseases manifested by inflammation of the gastric mucosa.

Chronic gastritis- Dative inflammation-dysregenerative diseases of the gastric mucosa.

Hematomesis- bloody vomiting.

Colitis- a group of inflammatory diseases of the colon.

Crohn's disease- terminal ileitis, regional ileitis.

Mallory-Weiss syndrome- longitudinal ruptures of the mucous membrane in the region of the esophageal-gastric junction.

Penetration- penetration of the defect into adjacent organs ("covered" perforation).

Perforation- perforation.

Pylorospasm- a steady contraction of the pyloric sphincter of the stomach, leading to a violation of the evacuation function.

Polyp- any exophytic node that rises above the surface of the mucous membrane.

Enteritis- a group of inflammatory diseases of the small intestine.

Erosion- a defect that does not go beyond the mucous membrane.

Ulcer- a defect extending beyond the mucous membrane.

Stricture- stenosis, narrowing.

The list of questions for the lesson,

which are the basis of the control test

1. Give the definition of Barrett's esophagus.

2. Specify the features of Zenker's diverticulum.

3. Indicate the positions characteristic of Mallory-Weiss syndrome.

4. Indicate the factors providing the cytoprotective function of the gastric mucosa.

5. Indicate the most common reason(etiological factor) chronic gastritis.

6. Specify the methods for detecting H. pylori in biopsy.

7. Indicate the positions typical for chronic stomach ulcers.

8. List the factors that significantly reduce the synthesis of prostaglandins and have an ulcerogenic effect.

9. Specify the microscopic features of an acute stomach ulcer.

10. Describe the perforation of the gastric ulcer.

11. Note statements specific to Zollinger-Ellisson syndrome.

12. Specify the preferred localization of stomach ulcers.

13. Select the positions characteristic of the cambial cells of the intestinal epithelium.

15. The predisposing factors for the development of hemorrhoids are.

16. Select the extraintestinal manifestations of Crohn's disease.

17. Specify the complications of Crohn's disease.

18. Specify a disease characterized by a combination of the following microscopic characteristics - crypt-abscesses, granulomas with the presence of giant cells of Pirogov-Langhans.

19. Specify microscopic signs of exacerbation of Crohn's disease.

20. Select statements specific to volvulus.

21. Specify the pathogenetic factors of colon diverticulosis.

22. Describe the pseudopolyps in ulcerative colitis.

23. What disease is characterized by a macroscopic appearance of the mucous membrane of the large intestine of the "cobblestone" type?

24. What disease can be suspected in the presence of following signs: skin hyperpigmentation, lymphadenopathy and the presence of a large number of macrophages with swollen cytoplasm and PAS-positive granules in the intestinal biopsy?

25. Indicate the characteristic features of celiac disease.

26. In what conditions does malabsorption syndrome occur?

27. A 64-year-old patient has diabetes mellitus there were sharp pains in the epigastric region, which after a few hours moved to the right iliac region, fever up to 39 ° C, single vomiting. The patient was hospitalized 12 hours after the onset of the disease. On examination by the doctor of the emergency room, confusion, fever of 39.6 ° C, symptoms of peritoneal irritation are positive. Indicate the presumptive diagnosis.

28. A 28-year-old patient has been losing weight, pain in the epigastric region for several years, in the last month, pallor of the skin, black feces, girdle pain at the epigastric level, yellowness of the skin and visible mucous membranes have appeared. With FGDS, a callous ulcer of the posterior wall of the stomach with undermined edges was found, the bottom is deep, filled with dirty gray contents. What complication of the ulcer are we talking about in this case?

29. In the gastrobiopsy of a 43-year-old patient, the presence of a lymphoplasmacytic infiltrate in the lamina propria of the mucous membrane is determined, there are accumulations of lymphocytes with light centers. Histobacterioscopically, when staining according to Giemsa, S-shaped sticks are determined in the layer of superficial mucus. What is the presumptive diagnosis?

IIclass

DISEASES OF THE LIVER, GALL BLADDER

AND PANCREAS

1. Hepatitis: definition, classification. Acute viral hepatitis. Epidemiology, etiology, transmission routes, patho - and morphogenesis, clinical and morphological forms, viral markers, outcomes. Chronic hepatitis: concept, etiology, clinical and morphological characteristics and classification, signs of activity, outcomes, prognosis.

2. Alcoholic liver damage. Alcoholic obesity of the liver. Alcoholic hepatitis. Alcoholic cirrhosis of the liver. Epidemiology, pathogenesis and morphogenesis, clinical manifestations, complications and causes of death, outcomes, prognosis.

3. Cirrhosis of the liver. Concept. Pathomorphological signs and classification of cirrhosis by etiology, pathogenesis, macro-, microscopic changes, etc. Clinical and morphological characteristics of the most important types of cirrhosis. Alcoholic cirrhosis. Cirrhosis after viral hepatitis. Biliary cirrhosis (primary, secondary). Liver changes in hemochromatosis, Wilson-Konovalov disease, alpha-1-antitrypsin deficiency. Pathogenesis, clinical and morphological characteristics.

4. Liver tumors. Classification, epidemiology. Benign neoplasms. Hepatocellular adenoma. Intrahepatic bile duct adenoma. Malignant neoplasms. Classification. Hepatocellular adenocarcinoma. Epidemiology, etiology. Classification according to macro - and microscopic features. Complications. Regularities of metastasis. Levels of spread of hepatocellular adenocarcinoma according to the TNM system. Cholangiocellular carcinoma.

5. Diseases of the gallbladder and bile ducts. Cholelithiasis (cholelithiasis). Etiology, pathogenesis, types of stones. Cholecystitis, definition. Acute and chronic cholecystitis: etiology, pathogenesis, clinical and morphological characteristics, complications, causes of death.

6. Diseases of the exocrine pancreas. Acute pancreatitis (pancreatic necrosis) and chronic. Epidemiology, etiology, pathogenesis, morphological characteristics, clinical manifestations, complications and causes of death. Tumors of the exocrine pancreas. Cystadenoma. Pancreas cancer. Epidemiology, classification, morphological characteristics, prognosis.

1. Lecture material.

2. Textbook on pathological anatomy (, Anichkov N. M, 2000) vol. 2, part I: pp. 637-669, 672-682, 687-709.

3. Textbook on pathological anatomy (, Anichkov N. M, 2005) vol. 2, part I: pp. 452-477, 479-487, 489-501.

4. Guide to practical training in pathological anatomy (, 2002) p.634-654, 585-589.

5. Atlas on pathological anatomy (2003) p. 282-288.

LEARNING CARD

PURPOSE INSTALLATION OF THE LESSON: to study the morphology of individual nosological forms of liver diseases using macropreparations, microspecimens and electron diffraction patterns and conduct clinical and anatomical comparisons.

LIVER DISEASES

Macrodrug TOXIC LIVER DYSTROPHY (fatty hepatosis). Pay attention to the size of the liver, its color, consistency, the state of the capsule.

Micropreparation No. 4 MASSIVE LIVER NECROSIS - subacute form (staining with hematoxylin and eosin). To note the discomplexation of the beams, signs of fatty degeneration and necrosis of hepatic cells. Compare the state of hepatocytes in the center and periphery of the lobules. Pay attention to the incipient stromal fibrosis and infiltration of the portal tracts with lymphoid-macrophage elements.

Micropreparation No. 5 CHRONIC HEPATITIS OF WEAK ACTIVITY, STAGE I (staining with hematoxylin and eosin). To note signs of hepatitis activity: intralobular lobular lymphoid infiltrates, "spreading" of lymphocytes along sinusoids, dystrophic changes in hepatocytes, lymphohistiocytic infiltration of portal tracts. Note the signs of chronic inflammation (stage of hepatitis): fibrosis of the portal portal tracts, fibrous septa growing into the lobules. Pay attention to cholestasis: expansion of bile capillaries, imbibition of hepatocytes with bile pigments.

Electronogram HYDROPIC HEPATOCYTE DYSTROPHY 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.

Macro preparations LIVER CIRROSIS. Mark the size, color, consistency, surface and section view of the liver. Estimate the size of the regenerated nodes and determine the macroscopic form of cirrhosis based on this feature.

Micropreparation No. 48 CHRONIC HEPATITIS OF MODERATE ACTIVITY WITH TRANSITION TO LIVER CIRROSIS (staining with hematoxylin and eosin and picrofuchsin). Pay attention to the presence of moderately pronounced signs of inflammatory activity (lymphoid infiltration of the stroma, extending to the parenchyma, fatty degeneration of hepatocytes), dominance of fibrosis (port-portal, port-central septa, formation of false lobules) and regeneration of hepatocytes (loss of the beam structure, presence of cells with large nuclei).

Macro preparations: PRIMARY LIVER CANCER, LIVER METASTASES, TUMORS OF ANOTHER PRIMARY LOCALIZATION.

BASIC Vocabulary for Lesson

Budd-Chiari syndrome- obstruction of the main hepatic veins as a result of thrombosis.

Hepatitis- any diffuse inflammatory liver disease.

Hepatosis- a group of liver diseases characterized by the dominance dystrophic changes and necrosis of hepatocytes.

Jellyfish head- expansion of the veins of the anterior abdominal wall with portal hypertension.

Portal hypertension- increased hydrodynamic pressure in the portal vein system.

Kaiser-Fleischer rings- greenish-brown or yellowish-green pigment rings in the cornea of the eyes in Wilson's disease.

Kaunsilmana Taurus- eosinophilic rounded formations in the perisinusoidal space.

Mallory Taurus- alcoholic hyaline, homogeneous eosinophilic inclusions in the cytoplasm of hepatocytes.

Massive liver necrosis (confluent)- extensive widespread necrosis of most of the hepatic parenchyma.

Liver necrosis bridged (bridge necrosis)- confluent necrosis of a large number of hepatocytes with the formation of "bridges" between adjacent lobules.

Graded liver necrosis (periportal)- destruction of hepatocytes along the border of the parenchyma and stroma, i.e. in the peripheral parts of the lobule.

Focal liver necrosis (macular)- death of individual small groups of hepatocytes in different parts of the acinus.

Pancreatitis- an inflammatory disease of the pancreas, often accompanied by its necrosis.

Goose liver- a macroscopic view of an organ with fatty degeneration.

Hepatolienal syndrome- enlargement of the spleen in liver diseases, accompanied by hypersplenism.

Wilson's disease (Wilson-Konovalov's disease)- hepatolenticular degeneration, hepatocerebral dystrophy.

Cholangitis- inflammatory disease of the bile ducts.

Cholelithiasis- cholelithiasis.

Cholestasis- insufficiency of bile flow.

Cholecystitis- inflammatory disease of the gallbladder.

Cirrhosis- Excessive proliferation of connective tissue in the organ against the background of degenerative and regenerative processes, accompanied by a change in the shape of the organ.

The list of questions for the lesson,

which are the basis of the control test

1. Specify the options for the structure of the liver.

2. List the variants of liver parenchyma necrosis.

3. What results in the formation of Kaunsilman's little bodies?

4. List the forms of acute hepatitis.

5. Specify the route of transmission of the virus in acute hepatitis A.

6. Specify the routes of transmission of the virus in acute hepatitis B.

7. Name the indirect markers viral lesion hepatocytes.

8. Specify the predominant localization of HBcAg in hepatocytes.

9. What kind does the accumulation of HBsAg in the hepatocyte impart to the cytoplasm?

10. List the etiological variants of chronic hepatitis.

11. Specify the microscopic signs of chronic hepatitis.

12. List the morphological forms of chronic hepatitis.

13. Specify characteristic signs alcoholic liver damage.

14. List the options for alcoholic liver damage.

15. Name the cells responsible for collagen formation in alcoholic liver damage.

16. Describe the macroscopic changes in the liver in alcoholic steatosis.

17. List the microscopic signs of a false lobule in liver cirrhosis.

18. Name the morphological forms of liver cirrhosis.

19. List the acquired forms of liver cirrhosis.

20. List the hereditary forms of liver cirrhosis.

21. Indicate the signs of portal hypertension.

22. List the causes of death of patients with liver cirrhosis.

23. Give the characteristics of primary sclerosing cholangitis.

24. Give a characteristic of primary biliary cirrhosis of the liver.

25. Give a characteristic of Wilson-Konovalov's disease.

26. Changes in the wall of the gallbladder in acute cholecystitis.

27. Changes in the wall of the gallbladder in chronic cholecystitis.

28. A 60-year-old patient has suffered from chronic alcoholism for 30 years. On examination, the liver is dense, the surface is bumpy. On the anterior abdominal wall, the veins are dilated, the spleen is palpable. Indicate the possible histological manifestations in the biopsy material.

29. A 50-year-old woman has suffered from fatigue and itching for 8 months. At laboratory research a minimum increase in the level of transaminases, a significant increase in the level of alkaline phosphatase, and high titers of antimitochondrial antibodies were found. A biopsy study revealed a granulomatous nature of inflammation in the cholangioli and a decrease in the number of bile ducts with pronounced lymphoma-macrophage infiltration along the portal tracts with symptoms of sclerosis. Your conclusion.

30. A 63-year-old sick man who has suffered from chronic viral hepatitis B, was admitted to the clinic with complaints of heaviness in the right hypochondrium, yellowness skin... On examination, the liver is dense, its edge is bumpy, there is an increase in the spleen and expansion of the veins of the anterior abdominal wall. Note possible histological manifestations in the biopsy material.