Changes in the structure of soft tissues. Types of these violations

GASTROINTESTINAL DISEASESTRACT

DISEASES OF THE STOMACH

Among diseases of the stomach, chronic gastritis, peptic ulcer and cancer are of the greatest importance.

Gastritis

Gastritis is an inflammation of the lining of the stomach. Downstream gastritis can be acute and chronic.

Acute gastritis

It develops as a result of irritation of the mucous membrane by alimentary, toxic, microbial factors.

Depending on the characteristics of morphological changes, the following forms of acute gastritis are distinguished:

a. Catarrhal (simple).

b. fibrinous.

in. Purulent (phlegmonous).

d. Necrotic (corrosive).

The most common form is catarrhal gastritis (see "General course", topic 6 "Inflammation").

Chronic gastritis

In the morphogenesis of chronic gastritis, a violation of regeneration and structural restructuring of the mucous membrane play an important role.

Classification of chronic gastritis.

1- According to the etiology and features of pathogenesis allocate gastritis A, B and C. Gastritis B prevails, gastritis A and C are rare.

1) Gastritis A - autoimmune gastritis.

Autoimmune disease associated with the appearance of autoantibodies to parietal cell lipoprotein and intrinsic factor blocking its binding to vitamin B12-

Often combined with other autoimmune diseases (thyroiditis, Addison's disease).

It occurs mainly in children and the elderly.

Localized in the fundus.

Characterized by a sharp decrease in HCL secretion (achlorhydria), G-cell hyperplasia and gastrinemia.

Accompanied by the development of pernicious anemia.

2) Gastritis B - non-immune gastritis.

The most common form of gastritis.

The etiology is associated with Helicobacter pylori, which is found in 100% of patients.

Various endogenous and exogenous factors also play a role in development (intoxication, eating disorders, alcohol abuse).

Localized in the antrum, can spread to the entire stomach.

3) Gastritis FROM- reflux gastritis.

It is associated with the reflux of the contents of the duodenum into the stomach.

It often occurs in people who have had a gastrectomy.

Localized in the antrum.

The secretion of HC1 is not disturbed and the amount of gastrin is not changed.

By process topography distinguish antral, fundic gastritis and pangastritis.

Depending on the morphological picture allocate superficial (non-atrophic) and atrophic gastritis.

Each of these forms is characterized by lymphoplasmacytic infiltration of the mucous membrane.

Depending on the intensity of the cellular infiltrate, there are light, moderate and pronouncedgastritis.

Gastritis can be active or inactive. The active phase is characterized by plethora, edema of the stroma, the appearance of PMN in the infiltrate, and leukopedesis (the penetration of PMN into epithelial cells).

a.Superficial gastritis.

Lymphoplasmacytic infiltrate is located in the superficial sections of the gastric mucosa at the level of the ridges.

The prognosis is usually favorable. In some cases, it can turn into atrophic gastritis.

b.atrophic gastritis.

The mucous membrane is thinned, the number of glands is reduced.

In the lamina propria there is a diffuse lymphoid-plasmacytic infiltrate, severe sclerosis.

Structural reorganization with the appearance of foci of intestinal and pyloric metaplasia is characteristic. In the first case, instead of gastric ridges, intestinal villi appear, lined with intestinal epithelium with numerous goblet cells. In the second case, the glands resemble mucous, or pyloric.

Often there are foci of dysplasia. Against the background of severe dysplasia of the epithelium, gastric cancer may develop.

peptic ulcer

Peptic ulcer is a chronic disease, the morphological substrate of which is a chronic recurrent gastric or duodenal ulcer.

Peptic ulcer must be differentiated from symptomatic ulcers that occur with other diseases and conditions (steroid, aspirin, toxic, hypoxic ulcers, etc.).

* Chronic ulcers in peptic ulcer can be localized in the body of the stomach, pyloroanthral region and duodenum.

Pathogenesis ulcers of the body of the stomach and pyloroduodenal ulcers is different.

1. Pathogenesis of pyloroduodenal ulcers:

° hypertonicity of the vagus nerve with an increase in the activity of the acid-peptic factor,

° dysmotility of the stomach and duodenum,

° increased levels of ACTH and glucocorticoids,

° a significant predominance of the acid-peptic factor of aggression over the factors of protection of the mucous membrane.

2. Pathogenesis of stomach ulcers:

° suppression of the functions of the hypothalamic-pituitary system, a decrease in the tone of the vagus nerve and the activity of gastric secretion,

° weakening of mucosal protective factors.

Morphogenesischroniculcers. During the formation of a chronic ulcer, it passes through the stages of erosion and acute ulcer.

a.Erosion - This is a superficial defect resulting from necrosis of the mucous membrane.

b.acute ulcer - a deeper defect that captures not only the mucous membrane, but also other membranes of the stomach wall. It has an irregular round-oval shape and soft edges.

The bottom of acute erosions and ulcers is colored black due to the accumulation of hematin hydrochloride.

Morphologychroniculcers.

In the stomach, it is more often localized on the lesser curvature, in the duodenum - in the bulb on the back wall.

It has the appearance of a deep defect of an oval or rounded shape, capturing the mucous and muscular membranes.

The edges of the ulcer are dense, callused. The proximal edge is undermined and the mucous membrane hangs over it, the distal one is gentle, has the form of a terrace, the steps of which are formed by the mucous membrane, submucosal and muscular layers.

Microscopic picture depends on the stage of the peptic ulcer.

a. In remission in the bottom of the ulcer, scar tissue is visible, displacing the muscle layer, with single sclerosed and obliterated vessels. Often there is epithelialization of the ulcer.

b. In the stage of exacerbation 4 layers are clearly distinguishable in the bottom of the ulcer: fibrinous-purulent exudate, fibrinoid necrosis, granulation and fibrous tissue, in which sclerotic vessels are visible. Fibrinoid necrosis is noted in the walls of some vessels.

The presence of a zone of necrosis, delimited by an inflammatory shaft, as well as fibroid changes in the walls of blood vessels indicate an exacerbation of the ulcerative process.

Complications of peptic ulcer illness.

1. Ulcerative-destructive:

o perforation (perforation) of the ulcer,

o penetration (into the pancreas, colon wall, liver, etc.),

about bleeding.

2. Inflammatory:

about gastritis, perigastritis,

° duodenitis, periduodenitis.

3. Ulcerative scars:

° stenosis of the inlet and outlet of the stomach,

o stenosis and deformation of the duodenal bulb.

Malachization of gastric ulcer(no more than 1%).

Combined complications.

Stomach cancer

For many years it was the most common malignant tumor, however, in the last two decades, there has been a trend towards a clear decrease in the incidence and mortality from it throughout the world.

It predominates after the age of 50, more common in men.

* In the occurrence, endogenously formed nitrosamines and exogenously supplied with food nitrites play a role (used in the manufacture of canned food); the possible role of Helicobacter pylori is discussed.

Diseases with an increased risk of stomach cancer include: gastric adenoma (adenomatous polyp), chronic atrophic gastritis, pernicious anemia, chronic ulcer, stomach stump.

Precancerous processes in the stomach currently include only severe epithelial dysplasia.

Classificationcancerstomach.

1 Depending on localization secrete cancer:

a. Pyloric department.

b. Lesser curvature with transition to the posterior and anterior walls of the stomach.

in. Cardiac department.

d. Greater curvature.

D. Fundus of the stomach.

3/4 of all gastric carcinomas are localized in the pyloric region and lesser curvature.

Gastric cancer can be subtotal and total.

2. Clinical and anatomical (macroscopic) forms of gastric cancer.

a. Cancer with predominantly exophytic expansivegrowth:

° plaque-like,

° polyposis,

° mushroom-like (fungose),

° ulcerated cancer:

a) primary ulcer,

b) saucer-shaped (cancer-ulcer),

c) cancer from a chronic ulcer (ulcer-cancer).

b. Cancer with predominantly endophytic infiltrategrowing growth:

° infiltrative-ulcerative,

° diffuse.

in. Cancer with endoexophytic (mixed) growth:

° transitional forms.

From a clinical point of view, it is important to isolate early gastric cancer that grows no deeper than the submucosal layer, i.e. superficial cancer, in which the 5-year postoperative survival is almost 100%.

3. Histological types of stomach cancer (WHO classification).

a. Adenocarcinoma:

° by structure: tubular, papillary, mucinous (mucous cancer),

° according to the degree of differentiation: highly differentiated, moderately differentiated and low-differentiated.

b. undifferentiated cancer.

in. Squamous cell carcinoma.

G. Glandular squamous cell carcinoma.

d. Unclassified cancer.

Adenocarcinoma, as a more differentiated form of cancer, is more common with predominantly exophytic tumor growth.

Undifferentiated forms of cancer (often with a scirrhous type of growth) predominate with predominantly endophytic growth, in particular with diffuse cancer.

Metastasis of stomach cancer.

It is carried out by lymphogenous, hematogenous and implantation methods.

The first metastases occur in regional lymph nodes along the lesser and greater curvature of the stomach.

Among distant lymphogenous metastases, from a diagnostic point of view, retrogrademetastases:

a. In both ovaries - Krukenberg metastases.

b. In pararectal tissue - Schnitzler metastases.

in. In the left supraclavicular lymph node - Virchow's gland.

Implantation metastases lead to carcinomatosis of the peritoneum, pleura, pericardium, diaphragm.

Hematogenous metastases often occur in the liver, lungs, etc.

Appendicitis; -caecum, inflammation of the appendix

There are two clinical and morphological forms of appendicitis: acute and chronic.

Acute appendicitis

Development matters:

a. Obstruction of the appendix (usually by feces) with a decrease in the resistance of the mucous membrane and invasion of microorganisms into the wall of the process.

b. Non-obstructive appendicitis can occur secondary to generalized infectious diseases (usually viral).

Morphological formsacuteuppendicitis.

1. Simple.

Accompanied by circulatory disorders, small hemorrhages, small accumulations of leukocytes - the primary affect.

2. Surface.

A focus of purulent inflammation in the mucous membrane is characteristic.

3. Destructive.

a. Phlegmonous:

° the process is enlarged, the serous membrane is dull, full-blooded, covered with fibrinous plaque; the walls are thickened, purulent contents are released from the lumen,

° microscopically revealed diffuse infiltration of polymorphonuclear leukocytes of the entire thickness of the process.

b. Phlegmonous-ulcerative:

° diffuse purulent inflammation with necrosis and ulceration of the mucous membrane.

in. Apostematous:

° Against the background of diffuse purulent inflammation, abscesses are determined.

G. Gangrenous:

° occurs with thrombosis or thromboembolism of the mesenteric artery of the appendix (primary gangrenous appendicitis) or with its thrombosis due to the development of periappendicitis and purulent mesenteriolite (secondary gangrenous appendicitis),

° the walls of the process acquire a gray-black color, on the serous membrane there are fibrinous-purulent overlays.

Complicationsacuteappendicitis.

0 Occur in destructive forms of appendicitis.

a. Perforation:

° with the development of diffuse purulent peritonitis,

° with the development of a periappendicular abscess, followed by the growth of fibrous tissue and compaction.

b. Process empyema:

° develops with obstruction of the proximal process.

in. Pilephlebitic liver abscesses:

° associated with purulent thrombophlebitis of the vessels of the mesentery and pylephlebitis (inflammation of the vena cava).

Chronic appendicitis

Develops after acute appendicitis

It is characterized by sclerotic and atrophic processes, lymphohistiocytic infiltration.

Inflammatory Bowel Disease

Crohn's disease

Genetic predisposition plays a role in development.

The disease occurs predominantly in young people, although it can occur at any age.

Any parts of the gastrointestinal tract can be affected, but the most characteristic localization is the ileocecal region (the old name for the disease is “terminal ileitis”) -

Often accompanied by extraintestinal manifestations: arthritis, sclerosing cholangitis, various skin manifestations, etc.

Morphological characteristic.

In the wall of the intestine, chronic inflammation develops, capturing all layers of the wall.

In more than half of the cases, nonspecific granulomas are formed without necrosis (reminiscent of sarcoid ones), fibrosis of the submucosal layer is pronounced.

Typically spasmodic lesions of the intestine: the affected areas of the intestine alternate with normal ones.

Thickening of the wall of the affected segment of the intestine with narrowing of the lumen is characteristic.

Deep slit-like transverse and longitudinal ulcers; swelling of the submucosal layer of the remaining sections of the intestine with swelling of the mucous membrane covering them, which gives it the appearance of a cobblestone pavement.

Complications.

Diarrhea, malabsorption syndrome.

Intestinal obstruction (due to cicatricial narrowing).

Fistulas - interintestinal, enterovesical, enterovaginal, external, etc.

Approximately 3% of patients develop colon cancer.

Nonspecific ulcerative colitis

The etiology is unknown.

May be familial.

It occurs at any age, more often young.

Extraintestinal manifestations are frequent: arthritis, iritis and episcleritis, sclerosing cholangitis, skin diseases.

Changes are limited to the colon (in the vast majority of cases); the rectum is involved in the process in all patients; the entire colon may be affected.

Inflammation and ulceration is limited to the mucosa and submucosa; characteristic crypt abscesses (accumulation of polymorphonuclear leukocytes in the crypts of the intestine).

Ulcerations may be extensive, with only small patches of mucosa remaining that form "pseudo-polyps".

Macroscopically, the intestinal mucosa is usually red with a granular surface.

Complications.

Toxic megacolon is a condition in which there is a significant expansion of the intestine.

Bowel perforation.

5-10% of patients develop colon cancer.

Pseudomembranous colitis

It is caused by an enterotoxin produced by Clostridium difficile (a common component of the intestinal microflora).

Occurs (most often) after treatment with broad-spectrum antibiotics.

It is manifested by severe intoxication, diarrhea.

Morphological characteristic.

Limited grayish plaques appear on the surface of the mucous membrane of the colon.

Microscopic picture: in the affected areas are determined muco-necrotic

masses (sometimes with an admixture of fibrin), permeated with leukocytes, attached to areas of damage and ulceration of the mucous membrane. Adjacent mucosal areas usually appear normal.

In the wall of the intestine - pronounced edema.

Ischemic colitis

It develops predominantly in the elderly.

It is associated with sclerosis of the vessels of the intestinal wall, which occurs with atherosclerosis, diabetes mellitus and other diseases accompanied by arteriosclerosis.

Morphological characteristic.

Segmental nature of the lesion, the region of the splenic flexure of the colon is more often involved.

Macroscopic picture: ulceration,

pseudopolyps, wall fibrosis.

Microscopic picture: ulcerations are made by granulation tissue surrounding the bundles of the muscularis lamina and extending into the submucosal layer. A large amount of hemosiderin is determined; in the lumen of small vessels - hyaline thrombi, crypt abscesses may occur. On the surface exudate of fibrin and polymorphonuclear leukocytes, in the acute phase - necrosis of the mucous membrane.

ATrunning out there is a pronounced sclerosis of the lamina propria of the mucous membrane.

Complications:

° bleeding;

° perforation, peritonitis.

INFILTRATION(lat. in in + filtratio filtering) - penetration into tissues and accumulation of cellular elements, liquids and various chemicals in them. I. can be active (cellular I. during inflammation, tumor growth) or passive (impregnation of tissues with anesthetic solutions).

The accumulation of cellular elements in tissues and organs is called infiltrate; in its formation during inflammation, along with the formed elements, the blood plasma and lymph leaving the vessels take part. Impregnation of tissues biol, liquids without admixture of cellular elements, for example, blood plasma, bile, is denoted by the terms edema (see), imbibition (see).

And. as a normal fiziol, the process takes place during the differentiation of certain tissues and organs, for example. I. lymphoid cells of the reticular base of the organ during the formation of the thymus gland, limf, nodes.

At patol. I. cells of inflammatory origin - inflammatory I. (see Inflammation) - there are infiltrates from polymorphonuclear leukocytes, lymphoid (round cell), macrophage, eosinophilic, hemorrhagic, etc. Often, tissues are infiltrated with neoplasm cells (cancer, sarcoma) ; in such cases speak about And. fabrics by a tumor, about infiltrative growth of a tumor. Patol. I. is characterized by an increase in the volume of tissues, their increased density, sometimes soreness (inflammatory I.), as well as a change in the color of the tissues themselves: I. polymorphonuclear leukocytes gives the tissues a gray-green tint, lymphocytes - pale gray, erythrocytes - red, etc. d.

The outcome of cellular infiltrates is different and depends on the nature of the process and the cellular composition of the infiltrate. For example, in leukocyte inflammatory infiltrates, proteolytic substances that appear when lysosomal enzymes are released by polymorphonuclear leukocytes often cause the infiltrated tissues to melt and develop abscess(see) or phlegmon (see); cells of infiltrates from polymorphonuclear leukocytes partially migrate from the blood stream, partially decay, partially go to the construction of new tissue elements. I. by tumor cells entails atrophy or destruction of pre-existing tissue. And. with significant destructive changes in tissues in the future most often gives persistent patol. changes in the form of sclerosis (see), decrease or loss of function of tissues or organs. Loose, transient (eg, acute inflammatory) infiltrates usually resolve and do not leave noticeable traces.

Lymphoid (round-cell), lymphocytic and plasmocellular and macrophage infiltrates in most cases are expression hron, inflammatory processes in fabrics. Against the background of such infiltrates, sclerotic changes often occur. They can also be observed in some disorders of tissue metabolism, for example, in the stroma of the thyroid gland with diffuse toxic goiter (see Diffuse toxic goiter), Addison's disease (see), with atrophic changes in the parenchyma of various organs as the initial regenerative act of the elements of the connective tissue of the organ. The same infiltrates can serve as an expression of extramedullary processes of hematopoiesis, for example, lymphocytic infiltrates and lymphomas in various organs with lymphadenosis (see Leukemia), in the initial stages of reticulosis. In some cases round cell infiltrates cannot be considered as patol. process: the infiltrate cells themselves, outwardly resembling lymphocytes, are young forms of the developing sympathetic nervous system. Such, for example, are the groups of sympathogonia in the medullary substance of the adrenal glands. Lymphocytic and plasma cell and macrophage infiltrates can be observed in organs and tissues with various immunol, changes in the body (artificial and natural immunization, allergic immunopatol. processes and allergic diseases). The appearance of lymphocytic-plasmic infiltrates is a reflection of the process of antibody production carried out by plasma cells, the precursors of which are B-lymphocytes, with the participation of macrophages.

From I. chem. substances most common I. glycogen and lipids. I. glycogen of the epithelium of the loops of the nephron (loop of Henle), hepatocytes, epidermis of the skin is observed in diabetes and in the so-called. glycogen disease (see. Glycogenoses), with a cut, there are abundant deposits of glycogen in the liver, striated muscles, myocardium, epithelium of the convoluted tubules of the kidneys, sometimes up to 10% of the weight of the organ. I. lipids can relate to neutral fats, for example, fatty I. liver (with an increase in the amount of fat up to 30% of the weight of the organ). However, the appearance of visible fat in the cells of parenchymal organs does not always indicate infiltration. Decomposition of amino- and protein-lipid complexes of the cytoplasm may take place, but the lipid composition will be different: a mixture of phospholipids, cholesterol and its esters, and neutral fats. And. intima of arteries cholesterol is observed at atherosclerosis (see). I. lipids of the reticuloendothelial system occurs as a manifestation of fermentopathy.

In pulmonary tuberculosis, gelatinous I. (gelatinous, or smooth, pneumonia) is observed, which is one of the manifestations of an exudative reaction in pulmonary tuberculosis, tuberculous pneumonia of a lobular, less often lobar character and is often a prestage of caseous pneumonia; sometimes it occurs as a perifocal process around productive tuberculosis foci (see Tuberculosis of the respiratory system).

Bibliography: Davydovsky I. V. General human pathology, M., 1969; In ii with h n e of F. Allgemeine Pathologie und Atiologie, Miinchen u. a., 1975.

I. V. Davydovsky.

Morphological changes occurring in all types of gastritis are stereotyped reactions of the mucous membrane in response to various pathogenic factors. The main changes that make up the morphological picture of chronic gastritis include inflammation, atrophy, impaired cell renewal, including metaplasia and dysplasia.

Chronic inflammation in gastritis

The presence of inflammation is evidenced by infiltration of the lamina propria and epithelium with mononuclear elements. The infiltrate of the gastric mucosa includes plasma cells, lymphocytes, macrophages, and leukocytes. All these cells are associated with immune responses, which indicates the involvement of immune mechanisms in the development of chronic gastritis.

Currently, it is believed that normally the gastric mucosa contains no more than 2-5 lymphocytes, plasma cells and macrophages in the field of view (objective 40) or 2-3 mononuclear cells in one roller. The presence of even 1-2 plasma cells in the field of view already indicates chronic inflammation.

Lymph nodules (follicles) with gastritis

Small lymphoid aggregates without germinal centers in the basal part of the gastric mucosa can also occur in normal conditions. The presence of germinal centers is always evidence of pathology and, above all, Hp-associated gastritis.

Neutrophil infiltration in gastritis

Neutrophil infiltration is the main indicator of chronic gastritis activity. Neutrophils can infiltrate their own plate, epithelium, fill the gaps of the glands, forming the so-called pit abscesses. Typically, leukocyte infiltration correlates with the severity of mucosal injury.

Mucosal atrophy

Mucosal atrophy is characterized by a decrease in the number of normal glands. The biological basis of atrophic gastritis is proliferation and apoptosis disorders induced by various pathogenic factors. It is proposed to consider that normally 3-4 transversely cut glands are visible in the high magnification field of view. If there are fewer of them, then atrophy can be diagnosed. With atrophy, along with the irreversible loss of the gastric glands, they are replaced by metaplastic epithelium or fibrous tissue.

A.Kalinin and others.

"Morphological changes in gastritis" and other articles from the section

5.14. Lymphocytic ("Varioloform";, "Chronic erosive";) gastritis

Lymphocytic gastritis is characterized by a number of features that make it possible to distinguish it as a special form of gastritis (178). Its main symptom is pronounced lymphocytic infiltration of the epithelium. It is known that an increase in the content of MEL is observed in all gastritis, but the infiltration of the epithelium is combined with the infiltration of the lamina propria of the mucous membrane. With lymphocytic gastritis, there is, as it were, selective or predominant infiltration of the epithelium; there are relatively few lymphocytes and plasma cells in the lamina propria, including in areas of erosion.

Lymphocytes with a characteristic light rim are located in groups only on the ridges (Fig. 5.88) and the superficial part of the fossae, they are not present in the deeper sections. We can talk about lymphocytic gastritis when the number of lymphocytes exceeds 30/100 epitheliocytes.

Endoscopic examination of such patients reveals nodules, thickened folds and erosion. The constant presence of nodules with an ulcerated surface determined the designation of this type of gastritis as varioloform. In the latest edition of the manual R. Whitehead (1990) it is included in the group of "chronic erosive gastritis"; (fourteen).

In the classification of the German Society of Pathologists "lymphocytic gastritis"; listed as a special pathogenetic form of gastritis, "on an equal footing"; with autoimmune, bacterial and reflux gastritis. As for the term "erosive gastritis", it is removed from the German and Sydney classifications. The presence and features of erosions in these classifications are indicated in the diagnosis, but as a "suffix"; (16.18). Nevertheless, we consider it possible in this section to discuss the relationship between gastritis and erosions.

The nodular mucosa with lymphocytic gastritis is found in 68% of patients, with "nonspecific gastritis"; in 16%, thickened folds in 38 and 2%, respectively (178).

The localization of lymphocytic gastritis also differs from "non-specific" gastritis; In 76% it is pangastritis, in 18% it is fundic and only in 6% it is antral. "Non-specific"; gastritis is antral in 91%, fundic in 3%, and total in 6% (178).

Lymphocytic gastritis accounts for about 4.5% of all gastritis (179).

The etiology and pathogenesis of this "new"; (178) forms of gastritis are unknown.

It can be assumed that we are talking about an immune reaction to the local effect of some kind of antigens. Such antigens could be HP or food ingredients. Indeed, HP was found in 41% of patients, but much less frequently than in patients with chronic active gastritis in the control group, where HP was detected in 91% (179). At the same time, serological signs of infection with HP were so common that it gave grounds to consider HP as the antigen responsible for the occurrence of lymphocytic gastritis (179). True, not all researchers agree with this (180). It should be noted that immunomorphological changes differ from those observed in type B gastritis: in the nodular mucosa, the content of IgM plasmacytes is reduced, but the number of IgG and IgE cells is increased (178).

Infiltration of the epithelium in lymphocytic gastritis is remarkably similar to the patterns that are constantly observed in the small intestine of patients with celiac disease (Fig. 5.89). In this regard, it has even been suggested that lymphocytic gastritis is a manifestation of celiac disease (181). Indeed, lymphocytic gastritis was found in 45% of patients with celiac disease, which is 10 times more common than among patients with all forms of chronic gastritis. The content of MEL in the small intestine was almost the same as in the stomach (47.2 and 46.5/100 epitheliocytes) (180,181). At the same time, there are no macroscopic signs of lymphocytic gastritis (“varioloformity” of the mucous membrane) in celiac disease (180).

The surface localization of lymphocytes is associated with the action of gluten. It is possible that gluten may be passively absorbed by the gastric mucosa of gluten-sensitive patients, causing an immune response, the expression of which is lymphocytic gastritis (181). This assumption is not contradicted by the fact that the gastric mucosa, unlike the mucous membrane of the small intestine, is intended not for absorption, but for the secretion of mucus. As is known, the rectum also secretes mucus, but the introduction of gluten into it leads to a significant increase in the number of MELs (182 ).

Lymphocytic gastritis, as a rule, is accompanied by erosions of the gastric mucosa and, on this basis, is included in the group of chronic erosive gastritis.

R. Whitehead (1990) believes that there are at least 2 forms of chronic erosive gastritis (14).

One is related to Helicobacter pylori gastritis B and is combined with peptic ulcer, perhaps even precedes it. Such gastritis is localized mainly in the antrum.

It can be assumed that inflammation of the mucous membrane, reducing its resistance

resistance to various damaging factors, predisposes to the development of erosion. Such erosions look like superficial necrosis infected with leukocytes (Fig. 5.90). In their circle is a picture of chronic active gastritis. Such erosions are sharp.

The second form of chronic erosive gastritis is characterized by the presence of chronic erosions, the bottom of which is formed by necrotic masses, fibrinoid, and a thin, unstable layer of granulation tissue (Fig. 5.91). In their circumference are hyperplastic, elongated, twisted and branching pits, often lined with immature epitheliocytes. There are many MELs in the surrounding mucosa. The muscular plate is either intact or hyperplastic.

Moreover, 99% of patients with chronic erosions find HP. The intensity of HP seeding and gastritis activity were significantly higher than in patients with chronic H. pylori gastritis, but without erosion. On this basis, an assumption was made about the leading role of Helicobacter pylori gastritis in the pathogenesis of chronic erosions. This is due to the high cytotoxicity of microorganisms, which initially cause surface microerosion. HCL penetrates through the mucous barrier destroyed due to this, it damages the underlying tissue, which, moreover, is relatively poorly supplied with blood in these areas. These topographic features against the background of pronounced gastritis impede reparative regeneration and erosion becomes chronic (183).

The concept of the role of HP in the pathogenesis of chronic erosions makes it possible to understand the origin of the so-called distant leukocytosis (38). We are talking about the constant detection at some distance from erosion of areas of leukocyte infiltration of the lamina propria and epithelium. There is every reason to attribute them to the foci of active Helicobacter pylori gastritis, their subsequent manifestation and ensures the recurrent nature of erosion.

Judgments about the pathogenesis and morphogenesis of erosions are complicated by the fact that the erosions that the endoscopist sees are not always found in histological preparations. A multicentric European study (184) showed that surface epithelial defects were found in biopsy specimens in only 42% of patients with endoscopically diagnosed erosions. In most biopsies, only areas of acute inflammation, intestinal metaplasia, and subepithelial hyperemia were visible.

5.15. Pseudolymphoma.

Pseudolymphomas are characterized by pronounced hyperplasia of the lymphoid tissue, with infiltration not only of the mucous membrane, as in all types of chronic gastritis, but also of the submucosa. Nevertheless, they are classified as chronic gastritis.

there (1.158), using as a synonym the term lymphatic (lymphoblastoid) gastritis, proposed back in the 30s by R. Schindler (1937) and G.H. Konjetzny (1938).

Usually, pseudolymphomas are combined with peptic ulcer, less often they are independent.

Most pseudolymphomas are localized in a place typical for chronic gastritis - in the pyloroantrapal region, mainly on its lesser curvature.

During gastroscopy, diffuse polypoid hyperplasia of the folds is revealed, sometimes the mucous membrane looks like a cobblestone pavement. Similar changes are usually seen in the circumference of gastric ulcers.

The mucous membrane is abundantly infiltrated with mature small lymphocytes, always with an admixture of plasma cells and macrophages (Fig. 5.92). Eosinophils are also common. The infiltrate pushes the glands apart and can penetrate through the muscular plate into the submucosa (Fig. 5.93). Less commonly, infiltrates occur in their own muscle layer (Fig. 5.94).

Pseudolymphomas are characterized by the presence of lymphatic nodules (follicles) with large light (embryonic) centers (Fig. 5.95a). They are located, like all follicles, mainly in the basal part of the mucous membrane, but due to their size, their groups can occupy almost its entire thickness. Follicles are also frequent in the submucosa (Fig. 5.956). The infiltrate, as it were, pushes the pre-existing network of argyrophilic fibers, their neoplasms are not observed (Fig. 5.96).

Three subtypes of gastric pseudolymphomas have been identified (186).

1. Ulcerations surrounded by abundant lymphocytic infiltrate. Apparently, these pictures should be regarded as a reactive process.

2. Nodular lymphoid hyperplasia. Ulceration and post-ulcerative fibrosis are absent in these cases. There are large superficially located lymphatic aggregates deforming gastric fields. In such patients, hypogammaglobulinemia and giardiasis are noted.

3. Angiofollicular lymphoid hyperplasia. This subtype is rare and differs markedly from the previous two. According to the histological structure, monomorphic cell, polymorphic cell and mixed variants are distinguished (187).

The infiltrate in the monomorphic-cellular variant of pseudolymphoma is formed mainly by mature lymphocytes, but there is always an admixture of plasma cells and eosinophils, so that “monomorphism”; here, in contrast to the "true"; lymphoma is incomplete. Therefore, it is better to speak of "predominantly monomorphic pseudolymphoma";.

In the polymorphic cellular variant, along with lymphocytes, there are many plasma cells, eosinophils, and lymphoblasts are found. In this variant, a deeper infiltration of the stomach wall was noted.

Table 5.5. Differential diagnosis between malignant lymphomas and gastric pseudolymphomas (1 each).

Criteria	Malignant lymphoma	Peevdol imfoma
	usually short< 1 года)	usually long (1-5 years)
Generalization	often (lymph nodes, spleen, liver)	missing
Localization	all departments	usually pyloroanthral
Depth of invasion	to the serosa	usually within the mucosa, but may penetrate deeper layers
Sprouting of blood-nasal vessels		missing
condition of the blood vessels	not changed	walls are often thickened
Polymorphonuclear infiltration		always available
The size of the nuclei of lymphocytes	usually large
Shape of nuclei	oval
Lymph follicles	rare (exception - pseudofollicles in follicular lymphoma), without light centers	reactive hyperplasia
mantle zone	lymphoplasmacytoid cells,	small lympholiths, plasma
follicles	immunoblasts	magical cells
Immunomorphology	monoclonal cell proliferation	polyclonal cell proliferation
Mytotic index
		missing

The mixed variant is characterized by the fact that monomorphic-cellular areas alternate with polymorphic-cellular ones.

It is possible to diagnose pseudolymphoma with the help of a gastrobiopsy, but the conclusion of a pathologist can only be conjectural in this case due to the small size of the biopsy.

The main thing with a biopsy is the differential diagnosis between pseudolymphoma and malignant lymphoma. In this case, it should be taken into account that the picture of the pseudolim-

Foma in a superficially cut biopsy does not exclude the presence of lymphoma in deeper areas. In addition, lymphoid cell infiltration may be a reaction to malignant lymphoma. It cannot also be ruled out that since lymphoma originates from pre-existing reactive elements, then those changes that are regarded as pseudolymphoma may turn out to be an early stage of the tumor (14), or “pre-tumor” (186). It has even been suggested that the so-called pseudolymphoma is a lymphoma, but of a low degree of malignancy (188). It has been established that primary B-cell lymphoma of the stomach can remain a local process for a long time, the lymph nodes may not be involved, and the long-term results of surgical treatment are very favorable (189).

Some criteria for the differential diagnosis between pseudolymphomas and malignant lymphomas are given in Table 5.5.

When studying biopsy material, lymphoma should be suspected in the presence of dense infiltration of the mucous membrane that has retained its structure without signs of ulceration (14). Lymphoma is characterized by the phenomenon of epithelial tropism of tumor cells with the formation of so-called lymphoepithelial lesions with progressive destruction of the epithelium (189). These pictures are easy to distinguish from active gastritis, in which the epithelium is destroyed by leukocytes, and non-lymphocytes. Unlike interepithelial lymphocytes, they do not have a characteristic light rim, they form large clusters that protrude into the lumen.

With pseudolymphomas, there are often damage to the surface epithelium in the form of severe dystrophy (Fig. 5.97), necrobiosis and necrosis with the formation of merosions. These processes, apparently, are caused by impaired microcirculation due to abundant infiltration of the mucous membrane. This can explain the presence of long-term non-healing erosions in many patients.

Pseudolymphoma can be combined with stomach cancer (Fig. 5.98). Two possibilities are admitted: the first is that pseudolymphoma is a reaction to cancer, and the second is that pseudolymphoma stimulates the development of adenocarcinoma (190). It cannot be ruled out that the prolonged existence of a mucosal defect leads to constant stimulation of the proliferative activity of the epithelium, which creates certain prerequisites for malignancy due to disturbances in reparative regeneration due to altered tissue trophism (191).

Chronic gastritis, L.I. Aruin, 1993

Seals may occur in the tissue space, consisting of different biological structural elements. This circumstance is polyetiological in nature. For this reason, it is important to know what diseases provoke the development of this kind of pathological formations.

What is an infiltrate

Medical practice describes many cases of the development of this condition in patients. Under the infiltrate (infiltratus) it is customary to understand the formation in the soft tissues of a limited or widespread formation containing exudate of different composition. The latter is a kind of effusion from blood vessels, consisting of biological fluids (blood, lymph), chemicals, foreign microorganisms, and cellular elements.

According to studies, tissue infiltration is mainly post-traumatic in nature. A more dangerous option for the development of pathology is the reactive reproduction of atypical cells in a malignant proliferative process. It is important to note that the internal exudate of cancerous tumors is extremely specific: they consist of their own tissues, pathogenic agents, calcifications and other elements.

Appendicular infiltrate

Inflammation of the appendix of the caecum is the main factor contributing to the accumulation of affected tissue elements in this area. Appendicular infiltrate is characterized by clear boundaries with the inclusion in the process of the dome of the large and loops of the small intestine, peritoneum and greater omentum. It should be noted that the formation of a pathological formation occurs already in the early stages of the development of the disease. In the later stages, as a rule, there is a resorption of the formed conglomerate of cells or its transition to a periappendicular abscess.

Inflammatory infiltrate

Traumatic genesis is of decisive importance in this form of pathological changes. Often, an infectious cause of exudate accumulation is also detected. Some authors prefer to synonymize phlegmon and inflammatory infiltrate - what kind of condition these are, you can learn more reliably from the medical encyclopedia. According to the information presented there, the identification of these diagnoses is impossible due to differences in their clinical manifestations. So, the inflammatory infiltrate is accompanied by:

• damage to the skin, mucous membrane, subcutaneous fat and muscles;
• inclusion in the inflammation of the lymphoid tissue;
• subfebrile temperature;
• thickening and hyperemia of the skin.

Infiltrate in the lungs

The human respiratory system is constantly attacked by pathogens. Infiltration in the lungs, as a rule, develops against the background of inflammation and requires immediate treatment. The accession of a purulent process is dangerous by the occurrence of organ dysfunction with all the negative consequences arising from this state. Unlike edema, pulmonary infiltration occurs against the background of the accumulation of not only fluid, but also cellular inclusions. A moderate increase in the volume of the organ is evidence of the development of inflammation with the further formation of exudative formation.

Abdominal infiltrate

This kind of negative state can have a completely different etiological orientation. So, an infiltrate of the abdominal cavity is often formed as a result of a staphylococcal or streptococcal infection, candidiasis. It is extremely important to eliminate the resulting pathological compaction in a timely manner. The accumulation of exudate in the abdomen can cause an abscess and bleeding. Separately, it is worth mentioning peritonitis with subsequent focal perivesical tissue infiltration. This condition requires immediate surgical intervention.

Post-injection infiltrate

This type of pathological changes occurs against the background of penetration and temporary accumulation in the tissues of the drug. An infiltrate after an injection develops if the rules of antiseptic treatment are not followed or the drug is administered too quickly. The development of such a post-injection complication depends on the characteristics of each individual organism. The accumulation of exudate in this case in some patients is extremely rare, while in others it is observed after each injection of the syringe needle.

Postoperative infiltrate

The formation of such a formation often occurs due to poor-quality suture material used during surgery. In this case, the infiltrate after the operation develops at the site of scar formation. The resulting seal is mainly opened surgically. Experts do not exclude that the body can independently eliminate the infiltrate of the postoperative scar. However, in order to avoid serious complications, doctors recommend not to hesitate and contact surgeons at the first sign of suture failure.

Tumor infiltrate

The likelihood of developing such pathological changes is present to the same extent in each person. The term "tumor infiltrate" is used to refer to the penetration of atypical cells of various genesis into the tissues of the body: sarcomas, carcinomas, etc. In this case, the affected tissue areas are characterized by high density, sometimes painful. Such a plan of education is characterized by proliferative tumor growth.

Cause of infiltrates

Accumulation of exudate in body tissues can occur under the influence of endogenous and exogenous factors. Experts say that the main cause of infiltrates is a traumatic source. No less important role in the formation of exudative formations is assigned to various infectious diseases. Other causes of the infiltrative process include:

• odontogenic infection;
• accumulation of cholesterol (atherosclerosis) or glycogen (diabetes);
• postoperative complications;
• growth of the tumor mass;
• accumulation of triglycerides in liver cells;
• acute appendicitis and other pelvic inflammations;
• accumulation in the lungs of blood cells, fibrin;
• compaction of the skin area due to its impregnation with chemicals (drugs);

Infiltrate - treatment

Therapy of the inflammatory exudative process is based on the use of conservative methods to resolve the problem. In this case, the treatment of the infiltrate is carried out by means of drug electrophoresis. It should be said that high-intensity physiotherapy with a thermal effect is allowed only in the absence of a purulent inflammatory focus.

Appendicular infiltrate is treated exclusively in a hospital setting. Therapy for this condition includes diet, antibiotics, restriction of motor activity. Abscess formation process requires surgical intervention to open and sanitize the abscess. Most of the malignant tumors are also eliminated through surgery.

Treatment of post-injection infiltrate involves the application of an iodine mesh and topical application of Vishnevsky ointment. With the accumulation of exudate in the lungs, additional diagnostic studies should be carried out. So, diaskintest allows you to identify incipient tuberculosis. In case of a positive reaction of the body, do not give up. Modern medicines are very successful in fighting the causative agents of this disease.

Treatment of infiltration with folk remedies

The accumulation of exudate in the internal organs must be eliminated only permanently. Treatment of infiltrate with folk remedies is possible only with post-injection complications in the form of bruises and minor inflammation. With odontogenic infections in a child without the addition of a purulent process, parents are advised to use saline compresses and rinses. Do not try to treat other types of exudative processes at home: this can lead to the development of abscesses and phlegmon.

Video: post-injection infiltrate - treatment