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

GASTROINTESTINAL DISEASESTRACT

STOMACH DISEASES

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

Gastritis

Gastritis is inflammation of the gastric mucosa. Gastritis can be acute or chronic.

Acute gastritis

Develops as a result of irritation of the mucous membrane by nutritional, toxic, and microbial factors.

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

A. Catarrhal (simple).

b. Fibrinous.

V. 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, impaired regeneration and structural restructuring of the mucous membrane play an important role.

Classification of chronic gastritis.

1- According to etiology and characteristics of pathogenesis gastritis A, B and C are distinguished. Gastritis B predominates, gastritis A and C are rare.

1) Gastritis A - autoimmune gastritis.

An 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 appears 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 (intoxication, eating disorders, alcohol abuse) also play a role in development.

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

3) Gastritis WITH- reflux gastritis.

Associated with the reflux of the contents of the duodenum into the stomach.

Often occurs in people who have undergone gastrectomy.

Localized in the antrum.

HC1 secretion is not impaired and the amount of gastrin is not changed.

According to the topography of the process distinguish antral, fundal gastritis and pangastritis.

Depending on the morphological picture There are 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 expressedgastritis.

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

A.Superficial gastritis.

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

The prognosis is usually favorable. In some cases it can develop 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 and pronounced sclerosis.

Structural restructuring 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.

Foci of dysplasia often occur. Against the background of severe epithelial dysplasia, stomach cancer can develop.

Peptic ulcer

Peptic ulcer is a chronic disease, the morphological substrate of which is a chronic recurrent ulcer of the stomach or duodenum.

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

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

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

1. Pathogenesis of pyloroduodenal ulcers:

° hypertonicity of the vagus nerve with increased activity of the acid-peptic factor,

° impaired motility of the stomach and duodenum,

° increased levels of ACTH and glucocorticoids,

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

2. Pathogenesis of gastric ulcer:

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

° weakening of mucosal protective factors.

Morphogenesischroniculcers During formation, a chronic ulcer goes 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 involves 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 painted black due to the accumulation of hydrochloric acid hematin.

Morphologychroniculcers

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

It looks like a deep defect of oval or round shape, involving the mucous and muscular membranes.

The edges of the ulcer are dense and calloused. The proximal edge is undermined and the mucous membrane hangs over it, the distal edge is flat, looks like 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 at the bottom of the ulcer, scar tissue is visible, displacing the muscle layer, with single sclerotic and obliterated vessels. Epithelization of the ulcer is often observed.

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

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

Complications of ulcer diseases.

1. Ulcerative-destructive:

o perforation (perforation) of the ulcer,

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

about bleeding.

2. Inflammatory:

o gastritis, perigastritis,

° duodenitis, periduodenitis.

3. Ulcerative-scarring:

° stenosis of the gastric inlet and outlet,

o stenosis and deformation of the duodenal bulb.

Malnization of stomach ulcers(no more than 1%).

Combined complications.

Stomach cancer

For many years it was the most common malignant tumor, but in the last two decades there has been a trend towards a clear decrease in morbidity and mortality from it worldwide.

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

* Endogenously formed nitrosamines and exogenously supplied nitrites from food play a role in the occurrence (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, gastric stump.

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

Classificationcancerstomach.

1 Depending on location secrete cancer:

A. Pyloric department.

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

V. Cardiac department.

g. Greater curvature.

d. Fundus of the stomach.

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

Stomach cancer can be subtotal and total.

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

A. Cancer with predominantly exophytic expansileheight:

° plaque-shaped,

° polyposis,

° mushroom-shaped (fungous),

° ulcerated cancer:

a) primary ulcerative,

b) saucer-shaped (cancer-ulcer),

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

b. Cancer with predominantly endophytic infiltrationgrowing growth:

° infiltrative-ulcerative,

° diffuse.

V. Cancer with endoexophytic (mixed) growth:

° transitional forms.

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

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

A. Adenocarcinoma:

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

° by degree of differentiation: highly differentiated, moderately differentiated and poorly differentiated.

b. Undifferentiated cancer.

V. 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 routes.

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

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

A. There are Krukenberg metastases in both ovaries.

b. There are Schnitzler metastases in the perirectal tissue.

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

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

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

Appendicitis; -cecum, inflammation of the appendix

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

Acute appendicitis

What matters in development are:

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 appendix.

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

Morphological formsacuteuppendicitis.

1. Simple.

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

2. Superficial.

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, diffuse infiltration of polymorphonuclear leukocytes throughout the thickness of the process is revealed.

b. Phlegmonous-ulcerative:

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

V. Apostematous:

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

G. Gangrenous:

° occurs with thrombosis or thromboembolism of the artery of the mesentery of the appendix (primary gangrenous appendicitis) or with its thrombosis in connection with the development of periappendicitis and purulent mesenteriolitis (secondary gangrenous appendicitis),

° the walls of the process become gray-black, and there are fibrinous-purulent deposits on the serous membrane.

Complicationsacuteappendicitis.

0 Occur in destructive forms of appendicitis.

A. Perforation:

° with the development of diffuse purulent peritonitis,

° with the development of a periappendiceal abscess with subsequent proliferation of fibrous tissue and compaction.

b. Empyema of the appendix:

° develops with obstruction of the proximal parts of the process.

V. Pylephlebitic liver abscesses:

° are associated with purulent thrombophlebitis of the mesenteric vessels 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 diseases

Crohn's disease

Hereditary 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 typical 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 characteristics.

Chronic inflammation develops in the intestinal wall, affecting all layers of the wall.

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

Typically, spasmodic damage to the intestine: the affected areas of the intestine alternate with normal ones.

Characteristic is thickening of the wall of the affected segment of the intestine with narrowing of the lumen.

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

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

Etiology unknown.

May be familial in nature.

Occurs at any age, most often young.

Extraintestinal manifestations are common: 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 are limited to the mucous membrane and submucosal layer; characterized by crypt abscesses (accumulation of polymorphonuclear leukocytes in the crypts of the intestine).

Ulcerations can be extensive, with only small areas of mucous membrane remaining, which form “pseudopolyps.”

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

Complications.

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

Bowel perforation.

5 - 10% of patients develop colon cancer.

Pseudomembranous colitis

Caused by an enterotoxin produced by Clostridium difficile (a common component of intestinal microflora).

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

Manifests itself as severe intoxication and diarrhea.

Morphological characteristics.

Limited grayish plaques appear on the surface of the colon mucosa.

Microscopic picture: in the affected areas mucous-necrotic

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

There is pronounced swelling in the intestinal wall.

Ischemic colitis

Develops mainly in older people.

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

Morphological characteristics.

The lesion is segmental in nature, often involving the area of the splenic flexure of the colon.

Macroscopic picture: ulcerations,

pseudopolyps, wall fibrosis.

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

INoutcome severe sclerosis of the lamina propria of the mucous membrane occurs.

Complications:

° bleeding;

° perforation, peritonitis.

INFILTRATION(lat. 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 in nature (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 formed elements, blood plasma and lymph leaving the vessels take part. Impregnation of tissues with biol, liquids without admixture of cellular elements, for example, blood plasma, bile, is designated by the terms edema (see), imbibition (see).

And. as a normal physiol, 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, lymph nodes.

With pathol. 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, they speak of tissue inflammation as a tumor, or infiltrative tumor growth. Patol. I. is characterized by an increase in the volume of tissues, their increased density, sometimes pain (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 during the release of lysosomal enzymes of polymorphonuclear leukocytes often cause melting of the infiltrated tissues and the development abscess(see) or phlegmon (see); infiltrated cells from polymorphonuclear leukocytes partially migrate from the bloodstream, partially disintegrate, and partially go to build new tissue elements. I. tumor cells entails atrophy or destruction of pre-existing tissue. I. 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 marks.

Lymphoid (round cell), lymphocytic-plasma cell and macrophage infiltrates in most cases are an expression of hron, inflammatory processes in tissues. 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 hematopoietic processes, 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, which outwardly resemble lymphocytes, are young forms of the developing sympathetic nervous system. These are, for example, groups of sympathogonia in the medullary substance of the adrenal glands. Lymphocytic plasma cell and macrophage infiltrates can be observed in organs and tissues with various immunol, changes in the body (artificial and natural immunization, allergic immunopathol. processes and allergic diseases). The appearance of lymphocytic plasma 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. the most common substances are glycogen and lipids. I. glycogen of the epithelium of nephron loops (loops of Henle), hepatocytes, and skin epidermis is observed in diabetes and the so-called. glycogen disease (see Glycogenosis), in which there are abundant deposits of glycogen in the liver, striated muscles, myocardium, and the epithelium of the convoluted tubules of the kidneys, sometimes amounting to up to 10% of the weight of the organ. I. lipids can concern 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 composition of lipids will be different: a mixture of phospholipids, cholesterol and its esters, neutral fats. I. intima of arteries with cholesterol is observed in atherosclerosis (see). I. lipids of the reticuloendothelial system arises as a manifestation of fermentopathy.

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

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

I. V. Davydovsky.

Morphological changes that occur in all types of gastritis represent stereotypical 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 cellular renewal, including metaplasia and dysplasia.

Chronic inflammation with gastritis

The presence of inflammation is indicated 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 reactions, which indicates the participation of immune mechanisms in the development of chronic gastritis.

It is currently believed that normally the gastric mucosa contains no more than 2-5 lymphocytes, plasma cells and macrophages in the field of view (lens 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 normally. 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 the activity of chronic gastritis. Neutrophils can infiltrate the lamina propria, epithelium, and fill the lumens of the glands, forming so-called pit abscesses. Typically, leukocyte infiltration correlates with the severity of mucosal damage.

Mucosal atrophy

Atrophy of the mucous membrane is characterized by a decrease in the number of normal glands. The biological basis of atrophic gastritis is disorders of proliferation and apoptosis induced by various pathogenic factors. It has been suggested that 3-4 transversely cut glands are normally visible in a 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, etc.

"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 into 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 infiltration of the epithelium is combined with infiltration of the lamina propria of the mucous membrane. With lymphocytic gastritis, there is a 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 pits; they are not present in the deeper sections. We can speak of lymphocytic gastritis when the number of lymphocytes exceeds 30/100 epithelial cells.

Endoscopic examination of such patients reveals nodules, thickened folds and erosions. 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 by R. Whitehead (1990), it is included in the group of “chronic erosive gastritis”; (14).

In the classification of the German Society of Pathologists “lymphocytic gastritis”; listed as a special pathogenetic form of gastritis, “on equal terms”; with autoimmune, bacterial and reflux gastritis. As for the term “erosive gastritis”, it has been removed from the German and Sydney classifications. The presence and characteristics 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 connection between gastritis and erosions.

Nodular mucous membrane 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 “nonspecific” 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).

Etiology and pathogenesis of this “new”; (178) The forms of gastritis are unknown.

It can be assumed that we are talking about an immune reaction to the local influence of some 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 HP infection were so common that this gave reason to consider HP to be the antigen that is responsible for the occurrence of lymphocytic gastritis (179). However, not all researchers agree with this (180). It should be noted that immuno-morphological changes differ from those observed in type B gastritis: in the nodularly changed mucous membrane the content of IgM plasma cells is reduced, but the number of IgG and IgE cells is increased (178).

Infiltration of the epithelium in lymphocytic gastritis is surprisingly reminiscent of 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 MEL content in the small intestine was almost the same as in the stomach (47.2 and 46.5/100 epithelial cells) (180,181). At the same time, there are no macroscopic signs of lymphocytic gastritis (“varioloformity” of the mucous membrane) in celiac disease (180).

The superficial localization of lymphocytes is associated with the action of gluten. It is possible that gluten can be passively absorbed by the gastric mucosa of gluten-sensitive patients and cause an immune reaction, the expression of which is lymphocytic gastritis (181). This assumption is not contradicted by the fact that the mucous membrane of the stomach, 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 MEL (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 gastritis B and is combined with peptic ulcer disease, perhaps even preceding it. This 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 erosions. Such erosions have the appearance of superficial necrosis infected with leukocytes (Fig. 5.90). Surrounding them is a picture of chronic active gastritis. Such erosions are acute.

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). They are surrounded by hyperplastic, elongated, convoluted and branching pits, often lined with immature epithelial cells. There are many MEL in the surrounding mucosa. The muscular plate is either intact or hyperplastic.

Moreover, HP is found in 99% of patients with chronic erosions. The intensity of HP contamination and the activity of gastritis were significantly higher than in patients with chronic Helicobacter pylori gastritis, but without erosions. On this basis, it has been suggested that Helicobacter pylori gastritis plays a leading role in the pathogenesis of chronic erosions. This is due to the high cytotoxicity of microorganisms, which initially cause superficial microerosions. HCL penetrates through the mucous barrier destroyed due to this, it damages the underlying tissue, which, moreover, in these areas is relatively poorly supplied with blood. These topographical features against the background of severe gastritis complicate reparative regeneration and erosion becomes chronic (183).

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

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 in biopsies were found 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 lymphoid tissue, with infiltration of not only the mucous membrane, as in all types of chronic gastritis, but also the submucosa. Nevertheless, they are classified as chronic gastri

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 disease, and less often they are independent.

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

Gastroscopy reveals diffuse polypoid hyperplasia of the folds, sometimes the mucous membrane has the appearance of a cobblestone pavement. Similar changes are usually visible 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 often found. The infiltrate expands the glands and can penetrate through the muscular plate into the submucosa (Fig. 5.93). Less commonly, infiltrates are found in the muscle layer proper (Fig. 5.94).

Pseudolymphomas are characterized by the presence of lymph nodes (follicles) with large light (germinal) 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 common in the submucosa (Fig. 5.956). The infiltrate seems to push apart the pre-existing network of argyrophilic fibers; their new formation is 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. Ulcerations and post-ulcerative fibrosis are absent in these cases. There are large superficially located lymphatic aggregates that deform the 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. Based on the histological structure, they are distinguished into monomorphic cell, polymorphic cell and mixed variants (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 it is “monomorphic”; here, in contrast to the “true”; lymphoma is not complete. Therefore, it is better to talk about “predominantly monomorphic pseudolymphoma”;.

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

Table 5.5. Differential diagnosis between malignant lymphomas and pseudolymphomas of the stomach (1 each).

Criteria	Malignant lymphoma	Peevdol mphoma
	usually short(< 1 года)	usually long-term (1-5 years)
Generalization	often (lymph nodes, spleen, liver)	absent
Localization	all departments	usually pyloroantral
Depth of invasion	to the serous membrane	usually within the mucous membrane, but can penetrate deeper layers
Sprouting of blood vessels		absent
Condition of blood vessels	not changed	the walls are often thickened
Polymorphonuclear infiltration		always available
Sizes of lymphocyte nuclei	usually large
Shape of kernels	oval
Lymphatic follicles	rarely (with the exception of pseudofollicles in follicular lymphoma), without light centers	reactive hyperplasia
Mantle zone	lymphoplasmacytoid cells,	small lympholiths, plasma
follicles	immunoblasts	magic cells
Immunomorphology	monoclonal cell proliferation	polyclonal cell proliferation
Mitotic index
		none

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

Pseudolymphoma can be diagnosed using gastrobiopsy, but the pathologist's conclusion can only be speculative due to the small size of the biopsy.

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

Foma in a superficially excised biopsy does not exclude the presence of lymphoma in deeper areas. In addition, lymphoid cell infiltration may be a reaction to malignant lymphoma. It also cannot be ruled out that if 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 “pretumor” (186). It has even been suggested that the so-called pseudolymphoma is a lymphoma, but of a low grade (188). It has been found 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 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 and form large clusters that protrude into the lumen.

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

Pseudolymphoma can be combined with gastric cancer (Fig. 5.98). Two possibilities are accepted: first, pseudolymphoma represents a reaction to cancer, and second, pseudolymphoma stimulates the development of adenocarcinoma (190). It cannot be ruled out that the long-term existence of a defect in the mucous membrane leads to constant stimulation of the proliferative activity of the epithelium, which creates certain preconditions for malignancy due to impaired reparative regeneration caused by altered tissue trophism (191).

Chronic gastritis, L.I. Aruin, 1993

In the tissue space, compactions consisting of various biological structural elements can occur. This circumstance is of a polyetiological nature. For this reason, it is important to know what diseases provoke the development of this kind of pathological formations.

What is infiltration

Medical practice describes many cases of this condition developing in patients. Infiltration (infiltratus) is usually understood as the formation in 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 research, tissue infiltration is mainly of a post-traumatic nature. A more dangerous option for the development of pathology is the reactive proliferation of atypical cells during 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.

Appendiceal infiltrate

Inflammation of the appendix of the cecum is the main factor contributing to the accumulation of affected tissue elements in this area. The appendicular infiltrate is characterized by clear boundaries with the inclusion of the dome of the colon and loops of the small intestine, peritoneum and greater omentum in the process. It is worth noting that the formation of a pathological formation occurs already in the early stages of the development of the disease. In later stages, as a rule, resorption of the resulting conglomerate of cells or its transition into a periappendiceal abscess is observed.

Inflammatory infiltrate

Traumatic genesis is of decisive importance in this form of pathological changes. An infectious cause for the accumulation of exudate is often identified. Some authors prefer to synonymize phlegmon and inflammatory infiltrate - what these conditions are can be found out more reliably from the medical encyclopedia. According to the information presented there, identification of these diagnoses is impossible due to differences in their clinical manifestations. Thus, the inflammatory infiltrate is accompanied by:

damage to the skin, mucous membrane, subcutaneous fat and muscles;
inclusion of lymphoid tissue in inflammation;
low-grade fever;
thickening and hyperemia of the skin.

Infiltrate in the lungs

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

Abdominal infiltrate

This kind of negative state can have completely different etiological directions. Thus, infiltration of the abdominal cavity is often formed as a result of staphylococcal or streptococcal infection, candidiasis. It is extremely important to promptly eliminate the resulting pathological compaction. The accumulation of exudate in the abdominal cavity 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 of the drug in the tissues. Infiltration after an injection develops when 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 some patients occurs extremely rarely, while in others it occurs after each insertion of a 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 surgery develops at the site of scar formation. The resulting compaction is preferably opened surgically. Experts do not rule out 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 different origins into the body’s tissues: sarcoma, carcinoma, etc. In this case, the affected tissue areas are characterized by high density and sometimes pain. This type of formation is characterized by proliferative tumor growth.

Cause of infiltrates

The 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. An equally important role in the formation of exudative formations is given to various infectious diseases. Other causes of the infiltrative process include:

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

Infiltration - treatment

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

Appendiceal infiltration is treated exclusively in a hospital setting. Treatment for this condition includes following a diet, taking antibiotics, and limiting physical activity. Abscess formation requires surgical intervention to open and sanitize the abscess. Most tumor malignancies are also eliminated through surgery.

Treatment of post-injection infiltrate involves applying an iodine grid and topical application of Vishnevsky ointment. If exudate accumulates in the lungs, additional diagnostic tests should be performed. Thus, Diaskintest allows you to detect incipient tuberculosis. If the body reacts positively, you should not give up. Modern medicines are very successful in combating the causative agents of this disease.

Treatment of infiltration with folk remedies

The accumulation of exudate in the internal organs must be eliminated only on a permanent basis. Treatment of infiltration with folk remedies is possible only with post-injection complications in the form of bruises and minor inflammations. For odontogenic infections in a child without the addition of a purulent process, parents are recommended to use salt compresses and rinses. You should not try to treat other types of exudative processes at home: this can lead to the development of abscesses and phlegmons.