Chronic gastritis. Causes of lymphocytic colitis

Diagnostics

Lymphocytic infiltration is a rare pathology, which resembles other skin and oncological diseases, therefore, diagnosis should be based on mandatory clinical and instrumental methods research.

1. Consultation with an immunologist, oncologist and dermatologist. Specialists conduct an external examination of the patient’s skin, collect complaints and medical history.
2. Histological examination and fluorescent microscopy. Histological examination of skin samples from the affected areas shows the absence of changes in the tissues, and when performing fluorescent microscopy, there is no glow at the border of plaques and papules, which is characteristic of other diseases. To clarify the diagnosis, DNA cytofluorometry is performed to analyze the number of normal cells, the number of which with lymphocytic infiltration is at least 97%.
3. Differential diagnosis. Differential diagnosis is carried out with sarcoidosis, systemic lupus erythematosus, lymphocytoma, and malignant lymphomas of the skin.

Diseases of the gastrointestinal tract are very diverse. Some of them are primary independent diseases and constitute the content of a large section of medicine - gastroenterology, others develop secondary to various diseases of an infectious and non-infectious, acquired and hereditary nature.

Changes in the gastrointestinal tract can be inflammatory, dystrophic, dysregenerative, hyperplastic and tumor in nature. To understand the essence of these changes, the mechanism of their development and diagnosis, morphological study is of great importance biopsy samples esophagus, stomach, intestines obtained by biopsy, since this makes it possible to use subtle research methods, such as histochemical, electron microscopic, and autoradiography.

This section will discuss the most important diseases of the pharynx and pharynx, salivary glands, esophagus, stomach and intestines. Diseases of the dental system and oral cavity organs are described separately (see.

Diseases of the pharynx and pharynx

Among diseases of the pharynx and pharynx, the most important is angina (from lat. angere- to choke), or tonsillitis, - an infectious disease with pronounced inflammatory changes in the lymphadenoid tissue of the pharynx and palatine tonsils. This disease is widespread among the population and is especially common during the cold season.

Sore throats are divided into acute and chronic. Acute sore throat is of greatest importance.

Etiology and pathogenesis. The occurrence of sore throat is associated with exposure to a variety of pathogens, among which the main ones are staphylococcus, streptococcus, adenoviruses, and microbial associations.

The mechanism of development of angina involves both exogenous, so and endogenous factors. Of primary importance is an infection that penetrates transepithelial or hematogenously, but more often it is an autoinfection provoked by general or local hypothermia or trauma. Of the endogenous factors, age-related factors are primarily important -

the stability of the lymphadenoid apparatus of the pharynx and the reactivity of the body, which can explain the frequent occurrence of sore throat in older children and adults under 35-40 years of age, as well as rare cases of its development in young children and the elderly. In development chronic tonsillitis plays a big role allergic factor.

Pathological anatomy. The following clinics are distinguished: morphological forms acute sore throat: catarrhal, fibrinous, purulent, lacunar, follicular, necrotic and gangrenous.

At catarrhal sore throat the mucous membrane of the palatine tonsils and palatine arches is sharply congested or cyanotic, dull, covered with mucus. The exudate is serous or mucous-leukocyte. Sometimes it lifts the epithelium and forms small bubbles with cloudy contents. Fibrinous tonsillitis manifested by the appearance of fibrinous white-yellow films on the surface of the mucous membrane of the tonsils. More often it is diphtheria sore throat, which is usually observed with diphtheria. For purulent sore throat characterized by an increase in the size of the tonsils due to their swelling and infiltration by neutrophils. Purulent inflammation is often diffuse in nature (quinsy), less often it is limited to a small area (tonsil abscess). Transition of the purulent process to adjacent tissues and dissemination of the infection are possible. Lacunar tonsillitis characterized by the accumulation in the depths of lacunae of serous, mucous or purulent exudate with an admixture of desquamated epithelium. As exudate accumulates in the lacunae, it appears on the surface of the enlarged tonsil in the form of whitish-yellow films that are easily removed. At follicular sore throat the tonsils are large, full-blooded, the follicles are significantly increased in size, and areas of purulent melting are visible in their center. In the lymphoid tissue between the follicles, hyperplasia of lymphoid elements and accumulations of neutrophils are observed. At necrotic sore throat There is superficial or deep necrosis of the mucous membrane with the formation of defects with uneven edges (necrotizing ulcerative tonsillitis). In this regard, hemorrhages into the mucous membrane of the pharynx and tonsils are not uncommon. With gangrenous decay of tonsil tissue, they speak of gangrenous sore throat. Necrotizing and gangrenous tonsillitis are observed most often with scarlet fever and acute leukemia.

A special variety is ulcerative membranous sore throat of Simonovsky-Plaut-Vincens, which is caused by the symbiosis of a spindle-shaped bacterium with ordinary spirochetes of the oral cavity. This sore throat is epidemic in nature. The so-called septic sore throat, or sore throat with alimentary-toxic aleukia, occurring after eating products made from grain that has overwintered in the field. Special forms of angina include those that have unusual localization: tonsillitis of the lingual, tubar or nasopharyngeal tonsils, tonsillitis of the lateral ridges, etc.

At chronic sore throat (chronic tonsillitis), which develops as a result of multiple relapses (recurrent tonsillitis), hyperplasia and sclerosis of the lymphoid tissue of the tonsils, sclerosis occur

capsules, expansion of lacunae, ulceration of the epithelium. Sometimes there is a sharp hyperplasia of the entire lymphoid apparatus of the pharynx and pharynx.

Changes in the pharynx and tonsils in both acute and chronic angina are accompanied by hyperplasia of the tissue of the lymph nodes of the neck.

Complications Sore throats can be both local and general in nature. Complications of a local nature are associated with the transition of the inflammatory process to surrounding tissues and the development paratonsillar, or retropharyngeal, abscess, phlegmonous inflammation of the throat tissue, thrombophlebitis. Among the complications of a general sore throat are: sepsis. Angina is also involved in the development rheumatism, glomerulonephritis and other infectious and allergic diseases.

Diseases of the salivary glands

Inflammatory processes are most often found in the salivary glands. Inflammation of the salivary glands is called sialadenitis, and the parotid glands - mumps. Sialadenitis and parotitis can be serous and purulent. They usually occur secondary to infection through the hematogenous, lymphogenous or intraductal route.

A special type of sialadenitis with destruction of glands by cellular lymphomacrophage infiltrate is characteristic of sicca syndrome (sjogren's disease or syndrome).

Sicca syndrome is a syndrome of exocrine gland insufficiency, combined with polyarthritis. Among the etiological factors, the most likely role is viral infection and genetic predisposition. The basis of pathogenesis is autoimmunization, and dry syndrome is combined with many autoimmune (rheumatoid arthritis, Hashimoto's struma) and viral (viral chronic active hepatitis) diseases. Some authors classify dry Sjögren's syndrome as a rheumatic disease.

Independent diseases of the salivary glands are parotitis, caused by myxovirus cytomegaly, the causative agent of which is the cytomegaly virus, as well as tumors(see also Diseases of the dental system and oral cavity organs).

Diseases of the esophagus

Diseases of the esophagus few. The most common causes are diverticula, inflammation (esophagitis) and tumors (cancer).

Esophageal diverticulum- this is a limited blind protrusion of its wall, which can consist of all layers of the esophagus (true diverticulum) or only the mucous and submucosal layer protruding through the cracks of the muscular layer (muscular diverticulum). Depending on the localization And topography distinguish between pharyngoesophageal, bifurcation, epinephric and multiple diverticula, and from characteristics of origin - adhesive diverticula resulting from

inflammatory processes in the mediastinum, and relaxation processes, which are based on local relaxation of the esophageal wall. An esophageal diverticulum can be complicated by inflammation of its mucous membrane - diverticulitis.

The causes of diverticulum formation may be congenital (inferiority of connective and muscular tissues of the wall of the esophagus, pharynx) and acquired (inflammation, sclerosis, cicatricial narrowing, increased pressure inside the esophagus).

Esophagitis- inflammation of the mucous membrane of the esophagus - usually develops secondary to many diseases, rarely - primary. It can be acute or chronic.

Acute esophagitis, observed under the influence of chemical, thermal and mechanical factors, with a number of infectious diseases (diphtheria, scarlet fever, typhus), allergic reactions, maybe catarrhal, fibrinous, phlegmonous, ulcerative, gangrenous. A special form of acute esophagitis is membranous, when the cast of the esophageal mucosa is rejected. After deep membranous esophagitis, which develops from chemical burns, cicatricial stenosis of the esophagus.

At chronic esophagitis, the development of which is associated with chronic irritation of the esophagus (the effects of alcohol, smoking, hot food) or impaired blood circulation in its wall (venous congestion during cardiac decompensation, portal hypertension), the mucous membrane is hyperemic and swollen, with areas of epithelial destruction, leukoplakia and sclerosis. For specific chronic esophagitis, occurring in tuberculosis and syphilis, is characteristic morphological picture corresponding inflammation.

In a special form they allocate reflux esophagitis, in which inflammation, erosions and ulcers are found (erosive, ulcerative esophagitis) in the mucous membrane lower section esophagus due to regurgitation of gastric contents into it (regurgitant, peptic esophagitis).

Esophageal carcinoma most often occurs at the border of the middle and lower thirds, which corresponds to the level of tracheal bifurcation. It is much less common in the initial part of the esophagus and at the entrance to the stomach. Esophageal cancer accounts for 2-5% of all malignant neoplasms.

Etiology. Chronic irritation of the esophageal mucosa (hot rough food, alcohol, smoking), scar changes after a burn, chronic gastrointestinal infections, anatomical disorders (diverticula, ectopia of the columnar epithelium and gastric glands, etc.) predispose to the development of esophageal cancer. Among precancerous changes, leukoplakia and severe dysplasia of the mucosal epithelium are of greatest importance.

Pathological anatomy. The following are distinguished: macroscopic forms of esophageal cancer: ring-shaped dense, papillary and ulcerated. Ring-shaped solid cancer is a tumor formation

tion, which circularly covers the wall of the esophagus in a certain area. The lumen of the esophagus is narrowed. When the tumor disintegrates and ulcerates, the patency of the esophagus is restored. Papillary cancer esophagus is similar to fungal carcinoma of the stomach. It breaks down easily, resulting in the formation of ulcers that penetrate into neighboring organs and tissues. Ulcerated cancer is a cancerous ulcer that is oval in shape and extends along the esophagus.

Among microscopic There are different forms of esophageal cancer carcinoma in situ, squamous cell carcinoma, adenocarcinoma, glandular squamous, glandular cystic, mucoepidermal And undifferentiated cancer.

Metastasis Esophageal cancer occurs predominantly lymphogenously.

Complications are associated with germination into neighboring organs - trachea, stomach, mediastinum, pleura. Esophageal-tracheal fistulas form and develop aspiration pneumonia, abscess and gangrene of the lung, pleural empyema, purulent mediastinitis. With esophageal cancer, cachexia appears early.

Stomach diseases

Among stomach diseases, gastritis, peptic ulcers and cancer are the most important.

Gastritis

Gastritis(from Greek gaster- stomach) - inflammatory disease gastric mucosa. There are acute and chronic gastritis.

Acute gastritis

Etiology and pathogenesis. In the development of acute gastritis, the role of irritation of the mucous membrane from abundant, difficult to digest, spicy, cold or hot food, alcoholic beverages, medications (salicylates, sulfonamides, corticosteroids, biomycin, digitalis, etc.), chemicals (occupational hazards) is great. Microbes (staphylococcus, salmonella) and toxins, products of impaired metabolism, also play a significant role. In some cases, for example, in cases of alcohol poisoning or poor-quality food products, pathogenic factors directly affect the gastric mucosa - exogenous gastritis, in others - this action is indirect and is carried out using vascular, nervous, humoral and immune mechanisms - endogenous gastritis, which include infectious hematogenous gastritis, elimination gastritis with uremia, allergic, congestive gastritis, etc.

Pathological anatomy. Inflammation of the mucous membrane can cover the entire stomach (diffuse gastritis) or certain parts of it (focal gastritis). In this regard, there is a distinction fundal, antral, pyloroantral And pyloroduodenal gastritis.

Depending on the features morphological changes of the gastric mucosa, the following forms of acute gastritis are distinguished: 1) catarrhal (simple); 2) fibrinous; 3) purulent (phlegmous); 4) necrotic (corrosive).

At catarrhal (simple) gastritis The gastric mucosa is thickened, swollen, hyperemic, its surface is abundantly covered with mucous masses, multiple small hemorrhages and erosions are visible. Microscopic examination reveals dystrophy, necrobiosis and desquamation of the surface epithelium, the cells of which are characterized by increased mucus production. Shedding of cells leads to erosion. In cases where there are multiple erosions, they speak of erosive gastritis. The glands change slightly, but their secretory activity is suppressed. The mucous membrane is permeated with serous, serous-mucosal or serous-leukocyte exudate. Its own layer is plethoric and edematous, infiltrated with neutrophils, and diapedetic hemorrhages occur.

At fibrinous gastritis a fibrinous film of gray or yellow-brown color forms on the surface of the thickened mucous membrane. The depth of necrosis of the mucous membrane can be different, and therefore there are lobar(superficial necrosis) and diphtheritic(deep necrosis) options fibrinous gastritis.

At purulent, or phlegmonous, In gastritis, the wall of the stomach becomes sharply thickened, especially due to the mucous membrane and submucosal layer. The folds of the mucous membrane are rough, with hemorrhages, fibrinous-purulent deposits. A yellow-green purulent fluid drains from the cut surface. A leukocyte infiltrate containing a large number of microbes diffusely covers the mucous membrane, submucosal and muscular layers of the stomach and the peritoneum covering it. Therefore, often with phlegmonous gastritis they develop perigastritis And peritonitis. Cellulitis of the stomach sometimes complicates injury; it also develops with chronic ulcers and ulcerated stomach cancer.

Necrotizing gastritis usually occurs when chemicals (alkali, acid, etc.) enter the stomach, cauterizing and destroying the mucous membrane (corrosive gastritis). Necrosis can involve superficial or deep parts of the mucous membrane, and can be coagulative or colliquative. Necrotic changes usually result in the formation of erosions and acute ulcers, which can lead to the development of phlegmon and gastric perforation.

Exodus acute gastritis depends on the depth of damage to the mucous membrane (wall) of the stomach. Catarrhal gastritis can result in complete restoration of the mucous membrane. At frequent relapses it can lead to the development of chronic gastritis. After significant destructive changes characteristic of phlegmonous and necrotic gastritis, atrophy of the mucous membrane and sclerotic deformation of the stomach wall develop - gastric cirrhosis.

Chronic gastritis

In some cases, it is associated with acute gastritis and its relapses, but more often this connection is absent.

Classification chronic gastritis, adopted by the IX International Congress of Gastroenterologists (1990), takes into account the etiology, pathogenesis, topography of the process, morphological types of gastritis, signs of its activity, and severity.

Etiology. Chronic gastritis develops when it affects the gastric mucosa primarily exogenous factors: violation of diet and eating rhythm, alcohol abuse, the effects of chemical, thermal and mechanical agents, the influence of occupational hazards, etc. Great role and endogenous factors - autoinfections (Campylobacter piloridis), chronic autointoxication, neuroendocrine disorders, chronic cardiovascular failure, allergic reactions, regurgitation of duodenal contents into the stomach (reflux). An important condition for the development of chronic gastritis is long-term exposure pathogenic factors of exogenous or endogenous nature, capable of “breaking” the usual regenerative mechanisms of constant renewal of the epithelium of the gastric mucosa. It is often possible to prove the long-term influence of not one, but several pathogenic factors.

Pathogenesis. Chronic gastritis can be autoimmune (type A gastritis) and non-immune (type B gastritis).

Autoimmune gastritis characterized by the presence of antibodies to parietal cells, and therefore damage to the fundus of the stomach, where there are many parietal cells (fundic gastritis). The mucous membrane of the antrum is intact. There is a high level of gastrinemia. Due to damage to the parietal cells, the secretion of hydrochloric (hydrochloric) acid is reduced.

At non-immune gastritis Antibodies to parietal cells are not detected, so the fundus of the stomach is relatively preserved. The main changes are localized in the antrum (antral gastritis). Gastrinemia is absent, and hydrochloric acid secretion is only moderately reduced. Type B gastritis includes: refluxgastritis(type C gastritis). Type B gastritis is 4 times more common than type A gastritis.

Guided by process topography stomach, secrete chronic gastritis - antral, fundal And Pangastritis.

Morphological types. Chronic gastritis is characterized by long-term dystrophic and necrobiotic changes in the epithelium of the mucous membrane, resulting in disruption of its regeneration and structural restructuring of the mucous membrane, culminating in its atrophy and sclerosis; cellular reactions of the mucous membrane reflect the activity of the process. There are two morphological types of chronic gastritis - superficial and atrophic.

Chronic superficial gastritis characterized by dystrophic changes in the surface (pit) epithelium. In some areas it is flattened, approaching cubic and characterized by reduced secretion, in others it is high prismatic with increased secretion. Translocation of additional cells from the isthmus to the middle third of the glands occurs, the histamine-stimulated secretion of hydrochloric acid by parietal cells and pepsinogen by chief cells decreases. The proper layer (plate) of the mucous membrane is swollen, infiltrated with lymphocytes, plasma cells, and single neutrophils (Fig. 197).

At chronic atrophic gastritis a new and basic quality appears - atrophy of the mucous membrane and its glands, which determines the development of sclerosis. The mucous membrane becomes thinner, the number of glands decreases. In place of the atrophied glands, connective tissue grows. The preserved glands are arranged in groups, the gland ducts are dilated, individual species cells in the glands are poorly differentiated. Due to mucoidization of the glands, the secretion of pepsin and hydrochloric acid is impaired. The mucous membrane is infiltrated with lymphocytes, plasma cells, and single neutrophils. These changes are joined by epithelial restructuring, Moreover, both the surface and glandular epithelium undergo metaplasia (see Fig. 197). The gastric ridges resemble intestinal villi; they are lined with bordered epithelial cells; goblet cells and Paneth cells appear (intestinal metaplasia of the epithelium, “enterolization” of the mucous membrane). The main, accessory (mucosal cells of the glands) and parietal cells of the glands disappear, cubic cells characteristic of the pyloric glands appear; so-called pseudopyloric glands are formed. Metaplasia of the epithelium is accompanied by its dysplasia, the degree of which may vary. Mucosal changes may be mild (moderate atrophic gastritis) or pronounced (severe atrophic gastritis).

A special form is the so-called giant hypertrophic gastritis, or illness Ménétrier, in which an extremely sharp thickening of the mucous membrane occurs, taking on the appearance of a cobblestone street. Cell proliferation is found morphologically glandular epithelium and glandular hyperplasia, as well as infiltration of the mucous membrane with lymphocytes, epithelioid, plasma and giant cells. Depending on the predominance of changes in the glands or interstitium, the severity of proliferative changes are distinguished glandular, interstitial And proliferative variants this disease.

Signs of activity of chronic gastritis allow us to distinguish active (exacerbation) and inactive (remission) chronic gastritis. Exacerbation of chronic gastritis is characterized by stromal edema, vascular congestion, but cellular infiltration with the presence of a large number of neutrophils in the infiltrate is especially pronounced; Sometimes crypt abscesses and erosions appear. During remission, these signs are absent.

Rice. 197. Chronic gastritis (gastrobiopsy):

a - chronic superficial gastritis; b - chronic atrophic gastritis

Severity Chronic gastritis can be mild, moderate or severe.

Thus, chronic gastritis is based on both inflammatory and adaptive-reparative processes of the gastric mucosa with imperfect regeneration of the epithelium And metaplastic restructuring of its “profile”.

The distortion of regeneration of the mucosal epithelium in chronic gastritis is confirmed by electron microscopic examination data on gastrobiopsy material. It has been established that undifferentiated cells, which normally occupy the deep sections of the gastric pits and neck of the glands, in chronic gastritis appear on the gastric ridges, in the area of ​​the body and bottom of the glands. Immature cells show signs of premature involution. This indicates profound disturbances in the coordination of the phases of proliferation and differentiation of the glandular epithelium during the regeneration of the gastric mucosa, which leads to cellular atypia and the development of dysplastic processes.

Due to the fact that in chronic gastritis there are pronounced disturbances in the processes of regeneration and structure formation, leading to cellular atypia (dysplasia), it often becomes the background against which it develops stomach cancer.

Meaning chronic gastritis is extremely high. It ranks second in the structure of gastroenterological diseases. It is also important to note that chronic atrophic gastritis with severe epithelial dysplasia is precancerous disease stomach.

Peptic ulcer

Peptic ulcer- a chronic, cyclical disease, the main clinical and morphological expression of which is a recurrent gastric or duodenal ulcer. Depending on the location of the ulcer and the characteristics of the pathogenesis of the disease, peptic ulcer disease is distinguished with localization of the ulcer in pyloroduodenal zone or body of the stomach although there are also combined forms.

In addition to ulcers as a manifestation peptic ulcer stomach and duodenum, there are so-called symptomatic ulcers, those. ulcerations of the stomach and duodenum, occurring in various diseases. These are the ulcers observed in endocrine diseases (endocrine ulcers with parathyroidism, thyrotoxicosis, Ellison-Zollinger syndrome), with acute and chronic disorders blood circulation (dyscirculatory-hypoxic ulcers), for exo- and endogenous intoxications (toxic ulcers), allergies (allergic ulcers), specific inflammation (tuberculosis, syphilitic ulcers), after operations on the stomach and intestines (postoperative peptic ulcers), as a result of drug treatment (medicinal ulcers, for example, during treatment with corticosteroids, acetylsalicylic acid).

Peptic ulcer disease is a widespread disease, occurring more often in the urban population, especially in men. In the pyloroduodenal zone, ulcers are more common than in the body of the stomach. Peptic ulcer disease is a purely human suffering, in the development of which stressful situations play a major role, which explains the increase in the incidence of peptic ulcer disease in the 20th century in all countries of the world.

Etiology. In the development of peptic ulcer disease, the main importance is stressful situations, psycho-emotional stress, leading to disintegration of those functions of the cerebral cortex that regulate the secretion and motility of the gastroduodenal system (cortico-visceral disorders). The same disintegration processes can develop in the cerebral cortex upon receipt of pathological impulses from organs in which pathological changes appear (viscerocortical disorders). Neurogenic theory peptic ulcer disease can be considered quite substantiated, but it does not explain the occurrence of the disease in all cases. A significant role in the occurrence of peptic ulcers nutritional factors(violation of the regime and nature of nutrition), bad habits(smoking and alcohol abuse), exposure to a number of medicines(acetylsalicylic acid, indomethacin, corticosteroids, etc.). Of absolute importance are hereditary constitutional (genetic) factors, including O (I) blood type, positive Rh factor, “non-secretory status” (the absence of histocompatibility antigens responsible for the production of glycoproteins in gastric mucus), etc. Recently, the occurrence of peptic ulcer has been associated with infectious agent- Campylobacter piloridis, which is detected when duodenal ulcer in 90%, and stomach ulcers - in 70-80% of cases.

Pathogenesis. It is complex and closely related to etiological factors. Not all aspects of it can be considered sufficiently studied. Among pathogenetic factors Peptic ulcer disease is distinguished between general and local. The general ones are represented by disorders of the nervous and hormonal regulation of the activity of the stomach and duodenum, and local - disorders of the acid-peptic factor, mucous barrier, motility and morphological changes in the mucous membrane of the stomach and duodenum.

Meaning neurogenic factors huge. As already mentioned, under the influence of external (stress) or internal (visceral pathology) causes, change in the coordinating function of the cerebral cortex in relation to subcortical formations (diencephalon, hypothalamus). This leads in some cases (ulcer of the pyloroduodenal zone) to excitation of the hypothalamic-pituitary region, the centers of the vagus nerve and increased tone of the nerve itself, increased activity of the acid-peptic factor and increased gastric motility. In other cases (gastric body ulcer), on the contrary, there is a suppression of the function of the hypothalamic-pituitary region by the cortex, a decrease in the tone of the vagus nerve and inhibition of motor skills; in this case, the activity of the acid-peptic factor is normal or reduced.

Among hormonal factors in the pathogenesis of peptic ulcer disease, the main role is played by disorders in the hypothalamic-pituitary-adrenal system in the form of an increase, and subsequent depletion, of the production of ACTH and glucocorticoids, which increase the activity of the vagus nerve and the acid-peptic factor.

These disturbances in hormonal regulation are clearly expressed only in peptic ulcers of the pyloroduodenal zone. With gastric ulcer, the production of ACTH and glucocorticoids is reduced, so the role of local factors increases.

Local factors significantly realize the transformation acute ulcer into chronic and determine exacerbations and relapses of the disease. For ulcers of the pyloroduodenal zone, increased activity is of great importance acid-peptic factor, which is associated with an increase in the number of gastrin-producing cells, increased secretion of gastrin and histamine. In these cases, aggressive factors (acid-peptic activity) prevail over mucosal protective factors (mucosal barrier), which determines the development or exacerbation of peptic ulcer. In case of an ulcer of the body of the stomach with normal or reduced activity of the acid-peptic factor and depressed motility, the mucous barrier suffers as a result of diffusion of hydrogen ions into the gastric wall (theory of reverse diffusion of hydrogen ions), which determines the release of histamine by mast cells, dyscirculatory disorders (blood shunting) and tissue trophic disorders. Morphological changes in the mucous membrane of the stomach and duodenum are represented by the following picture: chronic gastritis And chronic duodenitis. Damage to the mucous membrane is also likely to involve Campylobacter piloridis.

Thus, the importance of different factors in the pathogenesis of peptic ulcer disease at different localization of the ulcer (pyloroduodenal zone, body of the stomach) is not the same (Table 12). In case of peptic ulcer of the pyloroduodenal zone, the role of vagal-gastrinic influences and increased activity of the acid-peptic factor is great. In case of gastric ulcer, when vagal-gastrinic influences, as well as activation of the acid-peptic factor, are less pronounced, circulatory disorders and trophic disorders in the gastric wall become most important, which creates conditions for the formation of peptic ulcers.

Pathological anatomy. The morphological substrate of peptic ulcer disease is chronic recurrent ulcer. During its formation, it goes through the stages erosion And acute ulcer, which allows us to consider erosion, acute and chronic ulcers as stages morphogenesis peptic ulcer disease. These stages are especially clearly visible in gastric ulcers.

Erosion called defects of the mucous membrane that do not penetrate the muscular plate of the mucous membrane. Erosion is usually spicy, in rare cases - chronic. Acute erosions are usually superficial and are formed as a result of necrosis of an area of ​​the mucous membrane, followed by hemorrhage and rejection of dead tissue. At the bottom of such erosion, hydrochloric acid hematin is found, and at its edges - leukocyte infiltrate.

Table 12. Pathogenetic features of peptic ulcer depending on the location of the ulcer

IN stomach Multiple erosions may occur, which usually epithelialize easily. However, in cases of peptic ulcer development, some erosions do not heal; Not only the mucous membrane, but also the deeper layers of the stomach wall undergo necrosis, and acute peptic ulcers. They have an irregular round or oval shape. As necrotic masses are cleared, the bottom of the acute ulcer is revealed, which is formed by a muscular layer, sometimes by a serous membrane. Often the bottom is colored dirty gray or black due to the admixture of hematin hydrochloride. Deep defects of the mucous membrane often take on a funnel-shaped shape, with the base of the funnel facing the mucous membrane, and the apex facing the serous layer.

Acute stomach ulcers usually appear on the lesser curvature, in the antrum and pyloric sections, which is explained by the structural and functional characteristics of these sections. It is known that the lesser curvature is a “food track” and therefore is easily injured, the glands of its mucous membrane secrete the most active gastric juice, the wall is the richest in receptor devices and the most reactive, but the folds are rigid and, with contraction of the muscle layer, are not able to close the defect. These features are also associated with poor healing of an acute ulcer of this localization and its transition to chronic. That's why chronic ulcer stomach is most often localized in the same place as the acute one, i.e. on the lesser curvature, in the antrum and pylorus; Cardiac and subcardial ulcers are rare.

Chronic stomach ulcer It is usually single, multiple ulcers are rare. The ulcer is oval or round in shape (ulcus rotundum) and sizes from a few millimeters to 5-6 cm. It penetrates the wall of the stomach to varying depths, sometimes reaching the serous layer. The bottom of the ulcer is smooth, sometimes rough, the edges are raised like a roller, dense, calloused (callous ulcer, from lat. callus- callus; rice. 198). The edge of the ulcer facing the esophagus is undermined, and the mucous membrane hangs over the defect. The edge facing the pylorus is gentle (see Fig. 198), sometimes has the appearance of a terrace, the steps of which are formed by layers of the wall - the mucous membrane, submucosal and muscular layers. This type of edges is explained by the displacement of layers during gastric peristalsis. On a cross section, a chronic ulcer has the shape of a truncated pyramid,

Rice. 198. Chronic stomach ulcer:

A - general form chronic ulcer penetrating into the head of the pancreas; b - callous gastric ulcer (histotopographic section); the bottom and edges of the ulcer are represented by fibrous tissue, the cardiac edge of the ulcer is undermined, and the pyloric edge is flat

the narrow end of which faces the esophagus. The serous membrane in the area of ​​the ulcer is thickened, often fused with adjacent organs - the liver, pancreas, omentum, transverse colon.

Microscopic picture chronic gastric ulcers in different periods The course of peptic ulcer disease is different. IN period of remission Scar tissue is found at the edges of the ulcer. The mucous membrane at the edges is thickened and hyperplastic. In the bottom area, the destroyed muscle layer and the scar tissue replacing it are visible, and the bottom of the ulcer may be covered with a thin layer of epithelium. Here, in the scar tissue, there are many vessels (arteries, veins) with thickened walls. In many vessels, the lumens are narrowed or obliterated due to proliferation of intimal cells (endovasculitis) or proliferation of connective tissue. Nerve fibers and ganglion cells undergo dystrophic changes and decay. Sometimes, at the bottom of the ulcer, among the scar tissue, a proliferation of nerve fibers is observed, similar to amputation neuromas.

IN period of exacerbation peptic ulcer, a wide zone appears in the area of ​​the bottom and edges of the ulcer fibrinoid necrosis. On the surface of necrotic masses there is fibrinous-purulent or purulent exudate. The zone of necrosis is delimited granulation tissue With a large number thin-walled vessels and cells, among which there are many eosinophils. Deeper after the granulation tissue is located coarse fibrous scar tissue. Exacerbation of the ulcer is indicated not only by exudative-necrotic changes, but also fibrinoid changes in the walls of blood vessels, often with blood clots in their lumens, as well as mucoid And fibrinoid swelling of scar tissue at the bottom of the ulcer. Due to these changes, the size of the ulcer increases, and there is a possibility of destruction of the entire wall of the stomach, which can lead to serious complications. In cases where exacerbation is replaced by remission (ulcer healing), inflammatory changes subside, the zone of necrosis grows into granulation tissue, which matures into coarse fibrous scar tissue; Epithelization of the ulcer is often observed. As a result of fibrinoid changes in blood vessels and endarteritis, sclerosis of the wall and obliteration of the lumen of blood vessels develop. Thus, exacerbation of peptic ulcer disease, even in cases of a favorable outcome, leads to increased scarring in the stomach And aggravates the violation of the trophism of its tissues, including newly formed scar tissue, which is easily destroyed during the next exacerbation of peptic ulcer disease.

Morphogenesis and pathological anatomy of a chronic ulcer duodenum are not fundamentally different from those for chronic gastric ulcers.

Chronic duodenal ulcer in the vast majority of cases is formed on the anterior or posterior wall of the bulb (bulbar ulcer); only in 10% of cases it is localized below the bulb (postbulbar ulcer). Multiple ulcers are quite common

duodenum, they are located opposite each other along the anterior and posterior walls of the bulb (kissing ulcers).

Complications. Among the complications of a chronic ulcer in peptic ulcer disease there are (Samsonov V.A., 1975): 1) ulcer-destructive (bleeding, perforation, penetration); 2) inflammatory (gastritis, duodenitis, perigastritis, periduodenitis); 3) ulcerative-scar (narrowing of the inlet and outlet sections of the stomach, deformation of the stomach, narrowing of the lumen of the duodenum, deformation of its bulb); 4) malignancy of the ulcer (development of cancer from the ulcer); 5) combined complications.

Bleeding- one of the frequent and dangerous complications of peptic ulcer disease. There is no relationship between the frequency of bleeding and the location of the ulcer in the stomach; when the ulcer is localized in the duodenum, bleeding is more often caused by ulcers located in the posterior wall of the bulb. Bleeding occurs due to corrosion of the walls of blood vessels - arrosive bleeding, therefore, it occurs, as a rule, during an exacerbation of peptic ulcer disease.

Perforation(perforation) is also usually observed during an exacerbation of peptic ulcer disease. More often, pyloric gastric ulcers or ulcers of the anterior wall of the duodenal bulb perforate. Perforation of the ulcer leads to peritonitis. Initially, inflammation in the form of fibrinous deposits on the peritoneum appears only in the area of ​​the perforation, then it spreads and becomes not fibrinous, but fibrinous-purulent. In the presence of adhesions, perforation can lead only to limited peritonitis. Chronic peritonitis is rare. Then the masses of gastric contents are encapsulated, forming on the peritoneum and in the omentum. foreign body granulomas. In rare cases, when the perforation is covered by the liver, omentum, pancreas, or rapidly appearing deposits of fibrin, they speak of covered perforation.

Penetration ulcers are called penetration beyond the walls of the stomach or duodenum into neighboring organs. Ulcers of the posterior wall of the stomach and the posterior wall of the duodenal bulb usually penetrate, and more often into the lesser omentum, head and body of the pancreas (see Fig. 198), into the hepatoduodenal ligament, less often - into the liver, transverse colon, gallbladder. Penetration of a stomach ulcer in some cases leads to digestion of an organ, such as the pancreas.

Complications of an inflammatory nature include periulcerous gastritis and duodenitis, perigastritis and periduodenitis, resulting in the formation of adhesions with neighboring organs. Rarely, a stomach ulcer is complicated phlegmon.

Severe complications of ulcers are caused by Cicatricial stenosis gatekeeper. The stomach expands, food masses are retained in it, and vomiting often occurs. This can lead to dehydration, chloride depletion and development chlorohydropenic uremia(gastric

tania). Sometimes the scar tightens the stomach in the middle part and divides it into two halves, giving the stomach an hourglass shape. In the duodenum, only ulcers of the posterior wall of the bulb lead to cicatricial stenosis and deformation.

Malignancy(malignancy) of chronic gastric ulcer occurs in 3-5% of cases; the transition of a chronic duodenal ulcer to cancer is an extremely rare occurrence. Among combined complications the most common are perforation and bleeding, bleeding and penetration.

Stomach cancer

Stomach cancer in terms of morbidity and mortality since 1981, it ranks second among cancer tumors. Over the past 50 years, many countries around the world have seen a decrease in the incidence of stomach cancer. The same trend existed in the USSR: in 1970-1980. The incidence of stomach cancer decreased by 3.9% in men and by 6.9% in women. Stomach cancer occurs more often in men aged 40 to 70 years. Among cancer deaths, it accounts for about 25%.

Etiology. In an experiment, using various carcinogenic substances (benzopyrene, methylcholanthrene, cholesterol, etc.), it was possible to obtain stomach cancer. It has been shown that as a result of exposure exogenous carcinogens Gastric cancer of the “intestinal” type usually occurs. The development of “diffuse” type cancer is largely associated with the individual genetic characteristics of the body. Plays a significant role in the development of stomach cancer precancerous conditions(diseases in which the risk of developing cancer is increased) and precancerous changes(histological “abnormality” of the gastric mucosa). Precancerous conditions of the stomach include chronic atrophic gastritis, pernicious anemia(with it, atrophic gastritis constantly develops), chronic gastric ulcer, adenomas (adenomatous polyps) of the stomach, gastric stump(consequences of gastrectomy and gastroenterostomy), Ménétrier's disease. The “malignant potential” of each precancerous condition is different, but together they increase the likelihood of developing stomach cancer by 90-100% compared to the general population. Precancerous changes in the gastric mucosa include intestinal metaplasia and severe dysplasia.

Morphogenesis and histogenesis stomach cancer is not well understood. Of undoubted importance for the development of a tumor is the restructuring of the gastric mucosa, observed in precancerous conditions. This restructuring also persists in cancer, which allows us to talk about the so-called background, or profile, cancer stomach.

The morphogenesis of gastric cancer finds a definite explanation in dysplasia and intestinal metaplasia of the epithelium of the gastric mucosa.

Epithelial dysplasia called the replacement of part of the epithelial layer by proliferating undifferentiated cells with varying degrees atypism. There are several degrees of mucosal dysplasia

lining of the stomach, while the severe degree of dysplasia is close to non-invasive cancer (cancer in situ). It is believed that, depending on the predominance of dysplastic processes in the integumentary pitted epithelium or in the epithelium of the necks of the glands, cancer of various histological structures and different differentiation occurs.

Intestinal metaplasia The epithelium of the gastric mucosa is considered as one of the main risk factors for gastric cancer; incomplete intestinal metaplasia with the secretion of sulfomucins by cells, which are capable of absorbing mutant carcinogens, is especially important. In the foci of intestinal metaplasia, dysplastic changes appear, the antigenic properties of cells change (carcinoembryonic antigen appears), which indicates a decrease in the level of cellular differentiation.

Thus, in the morphogenesis of gastric cancer plays an important role dysplasia as non-metaplastic(pit, cervical), and metaplastic epithelium(intestinal type). However, we cannot exclude the possibility of development de novo gastric cancer, those. without previous dysplastic and metaplastic changes.

Histogenesis different histological types of gastric cancer are probably common. The tumor arises from single source - cambial elements and precursor cells in and outside the foci of dysplasia.

Classification. Clinical and anatomical classification of gastric cancer takes into account the location of the tumor, the nature of its growth, the macroscopic form of cancer and histological type.

Depending on the localization There are 6 types of cancer in one or another part of the stomach: pyloric(50%), small curvature of the body with transition to the walls(27%), cardiac(15%), great curvature(3%), fundamental(2%) and total(3%). Multicentric gastric cancer is rare. As you can see, in 3/4 of cases the cancer is localized in the pyloric region and on the lesser curvature of the stomach, which is undoubtedly diagnostic value.

Depending on the growth pattern The following clinical and anatomical forms of gastric cancer are distinguished (Serov V.V., 1970).

1. Cancer with predominantly exophytic expansive growth: 1) plaque cancer; 2) polypous cancer (including that developed from an adenomatous polyp of the stomach); 3) fungal (fungal) cancer; 4) ulcerated cancer (malignant ulcers); a) primary ulcerative gastric cancer; b) saucer-shaped cancer (cancer-ulcer); c) cancer from a chronic ulcer (ulcer-cancer).

2. Cancer with predominantly endophytic infiltrating growth: 1) infiltrative ulcerative cancer; 2) diffuse cancer (with limited or total damage to the stomach).

3. Cancer with exoendophytic, mixed growth pattern: transitional forms.

According to this classification, forms of gastric cancer are simultaneously phases of cancer development, which makes it possible to outline certain

variants of the development of stomach cancer with a change in forms - phases over time, depending on the predominance of exophytic or endophytic character.

Based on the characteristics of the microscopic structure, the following histological types of gastric cancer are distinguished: adenocarcinoma(tubular, papillary, mucinous), undifferentiated(solid, scirrhous, signet ring cell), squamous cell, glandular squamous cell(adenocancroid) and unclassified cancer.

Pathological anatomy. Plaque-like cancer (flattened, superficial, creeping) occurs in 1-5% of cases of gastric cancer and is the rarest form. The tumor is often found in the pyloric region, on the lesser or greater curvature in the form of a small, 2-3 cm long, plaque-like thickening of the mucous membrane (Fig. 199). The mobility of the folds of the mucous membrane in this place is somewhat limited, although the tumor rarely grows into the submucosal layer. Histologically, plaque-like cancer usually has the structure of adenocarcinoma, less often - undifferentiated cancer.

Polyposis cancer accounts for 5% of cases of gastric carcinoma. It has the appearance of a node with a villous surface with a diameter of 2-3 cm, which is located on a stalk (see Fig. 199). The tumor tissue is gray-pinkish or

Rice. 199. Forms of stomach cancer:

a - plaque-shaped; b - polypous; c - mushroom-shaped; g - diffuse

grey-red, rich blood vessels. Sometimes polyposis cancer develops from an adenomatous polyp of the stomach, but more often it represents the next phase of exophytic growth of plaque-like cancer. Microscopic examination often reveals adenocarcinoma, sometimes undifferentiated cancer.

Fungal (mushroom) cancer occurs in 10% of cases. Like polypous cancer, it has the appearance of a nodular, lumpy (less often with a smooth surface) formation, sitting on a short wide base (see Fig. 199). On the surface of the tumor node, erosions, hemorrhages or fibrinous-purulent deposits are often found. The tumor is soft, gray-pink or gray-red, well demarcated. Fungal cancer can be considered as a phase of exophytic growth of polyposis cancer, therefore, upon histological examination, it is represented by the same types of carcinoma as polyposis.

Ulcerated cancer occurs very often (in more than 50% of cases of stomach cancer). It combines malignant gastric ulcerations of various genesis, which include primary ulcerative cancer, saucer-shaped cancer (cancer-ulcer) and cancer from a chronic ulcer (ulcer-cancer).

Primary ulcerative cancer stomach (Fig. 200) has been little studied. It is rarely discovered. This form includes exophytic cancer with ulceration in

at the very beginning of its development (plaque cancer), the formation of an acute and then a chronic cancer ulcer, which is difficult to distinguish from a cancer ulcer. Microscopic examination often reveals undifferentiated cancer.

Saucer crayfish(cancer-ulcer) - one of the most common forms stomach cancer (see Fig. 200). It occurs when an exophytically growing tumor ulcerates (polypous or fungosous cancer) and is a round formation, sometimes reaching large sizes, with roller-like whitish edges and ulceration in the center. The bottom of the ulcer may be neighboring organs into which the tumor grows. Histologically, it is more often represented by adenocarcinoma, less often by undifferentiated cancer.

Ulcer-cancer develops from a chronic gastric ulcer (see Fig. 200), so it occurs where a chronic ulcer is usually localized, i.e. at the small curvature. The signs of a chronic ulcer distinguish ulcer-cancer from saucer-shaped cancer: extensive proliferation of scar tissue, sclerosis and thrombosis of blood vessels, destruction of the muscle layer in the scar base of the ulcer and, finally, thickening of the mucous membrane around the ulcer. These signs remain with the malignancy of a chronic ulcer. Particular importance is attached to the fact that in saucer-shaped cancer the muscle layer is preserved, although it is infiltrated by tumor cells, and in ulcer cancer it is destroyed by scar tissue. The tumor grows predominantly exophytically in one of the edges of the ulcer or along its entire circumference. More often it has the histological structure of adenocarcinoma, less often - undifferentiated cancer.

Infiltrative-ulcerative cancer found in the stomach quite often. This form is characterized by pronounced cancrosis infiltration of the wall and ulceration of the tumor, which in time sequence can compete: in some cases it is late ulceration of massive endophytic carcinomas, in others it is endophytic tumor growth from the edges of a malignant ulcer. Therefore, the morphology of infiltrative-ulcerative cancer is unusually diverse - these are small ulcers of varying depths with extensive infiltration of the wall or huge ulcerations with a tuberous bottom and flat edges. Histological examination reveals both adenocarcinoma and undifferentiated cancer.

Diffuse cancer(see Fig. 199) is observed in 20-25% of cases. The tumor grows endophytically in the mucous, submucosal and muscular layers along the connective tissue layers. The wall of the stomach becomes thickened, dense, whitish and motionless. The mucous membrane loses its usual relief: its surface is uneven, folds of uneven thickness, often with small erosions. Stomach damage may be limited (in this case the tumor is most often found in the pyloric region) or total (the tumor covers the entire length of the stomach wall). As the tumor grows, the wall of the stomach sometimes shrinks, its size decreases, and the lumen narrows.

Diffuse cancer is usually represented by variants of undifferentiated carcinoma.

Transitional forms of cancer constitute approximately 10-15% of all gastric cancers. These are either exophytic carcinomas, which at a certain stage of development acquired pronounced infiltrating growth, or endophytic, but limited to a small territory, cancer with a tendency to intragastric growth, or, finally, two (sometimes more) cancer tumors of different clinical and anatomical forms in one and the same same stomach.

In recent years, the so-called early stomach cancer, which has up to 3 cm in diameter and grows no deeper than the submucosal layer. Diagnostics early cancer of the stomach became possible thanks to the introduction of targeted gastrobiopsy into practice. Isolation of this form of cancer has a large practical significance: up to 100% of such patients live after surgery for more than 5 years, only 5% of them have metastases.

Stomach cancer is characterized by spreading beyond the boundaries of the organ itself and germination into neighboring organs and tissues. Cancer, located on the lesser curvature with a transition to the anterior and posterior walls and in the pyloric region, grows into the pancreas, porta hepatis, portal vein, bile ducts and gallbladder, lesser omentum, mesenteric root and inferior vena cava. Cardiac gastric cancer spreads to the esophagus, while fundal cancer grows into the hilum of the spleen and diaphragm. Total cancer, like cancer of the greater curvature of the stomach, grows into the transverse colon, the greater omentum, which shrinks and shortens.

Histological types stomach cancer reflect the structural and functional characteristics of the tumor. Adenocarcinoma, which occurs very often with exophytic tumor growth, may be tubular, papillary And mucinous(Fig. 201), and each of the types of adenocarcinoma - differentiated, moderately differentiated And poorly differentiated. Characteristic of endophytic tumor growth undifferentiated cancer presented in several options - solid, scirrhos(Fig. 202), signet ring cell. Rarely found squamous, glandular-squamous(adenocancroid) and unclassifiable types of stomach cancer.

In addition to the International histological classification, stomach cancer is divided according to the nature of its structure into intestinal And diffuse types (Lauren, 1965). The intestinal type of stomach cancer is represented by glandular epithelium, similar to the columnar epithelium of the intestine with mucous secretion. The diffuse type of cancer is characterized by diffuse infiltration of the stomach wall with small cells containing and not containing mucus and forming glandular structures here and there.

Metastases are very characteristic of stomach cancer, they occur in 3/4-2/3 of cases. Metastasizes stomach cancer in various ways - lymphogenous, hematogenous and implantation (contact).

Lymphogenic pathway metastasis plays a major role in tumor spread and is clinically the most important (Fig. 203). Of particular importance are metastases to regional The lymph nodes located along the lesser and greater curvature of the stomach. They occur in more than half of cases of gastric cancer, appear first and largely determine the volume and nature of surgical intervention. In distant lymph nodes, metastases appear as orthograde (by lymph flow), and retrograde (against the flow of lymph) by. Retrograde lymphogenous metastases, which have important diagnostic value in gastric cancer, include metastases to the supraclavicular lymph nodes, usually the left ones (“Virchow metastases”, or “Virchow gland”), to the lymph nodes of the perirectal tissue (“Schnitzler metastases”). A classic example of lymphogenous retrograde metastases of gastric cancer is the so-called Krukenberg ovarian cancer.

Rice. 203. Spread of cancer through the lymphatic pathways of the peritoneum and mesentery (white stripes). Cancer metastases in mesenteric lymph nodes

As a rule, metastatic lesions affect both ovaries, which sharply enlarge and become dense and whitish. Lymphogenic metastases appear in the lungs, pleura, and peritoneum.

Peritoneal carcinomatosis- a frequent companion to stomach cancer; in this case, the lymphogenous spread of cancer throughout the peritoneum is complemented by by implantation(see Fig. 203). The peritoneum becomes dotted with tumor nodes of various sizes, merging into conglomerates, among which intestinal loops are walled up. Often, a serous or fibrinous hemorrhagic effusion appears in the abdominal cavity (the so-called cancrosis peritonitis).

Hematogenous metastases, spreading through the portal vein system, they primarily affect liver (Fig. 204), where they are found in 1/3-1/2 cases of stomach cancer. These are single or multiple nodes of varying sizes, which in some cases almost completely displace the liver tissue. Such a liver with multiple cancer metastases sometimes reaches enormous sizes and weighs 8-10 kg. Metastatic nodes undergo necrosis and melting, sometimes being a source of bleeding into the abdominal cavity or peritonitis. Hematogenous metastases occur in the lungs, pancreas, bones, kidneys, and adrenal glands. As a result of hematogenous metastasis of gastric cancer, miliary lung carcinomatosis And pleura.

Complications. There are two groups of complications of stomach cancer: the first are associated with secondary necrotic and inflammatory changes

tumors, the second - with the germination of stomach cancer into neighboring organs and tissues and metastases.

As a result secondary necrotic changes carcinoma disintegration occurs wall perforation, bleeding, peritumoral (periulcerous) inflammation, up to development phlegmon of the stomach.

Growth of stomach cancer into the gates of the liver or the head of the pancreas with compression or obliteration of the bile ducts and portal vein leading to the development jaundice, portal hypertension, ascites. Ingrowth of a tumor into the transverse colon or the root of the mesentery of the small intestine leads to its wrinkling, accompanied by intestinal obstruction. When cardiac cancer grows into

The esophagus often narrows

tion of its lumen. With pyloric cancer, as with gastric ulcers, it is also possible pyloric stenosis with a sharp expansion of the stomach and characteristic clinical manifestations, up to “gastric tetany”. Cancer growth into the diaphragm can often be accompanied by contamination of the pleura, development hemorrhagic or fibrinous-hemorrhagic pleurisy. Tumor breakthrough through the left dome of the diaphragm leads to empyema of the pleura.

A common complication of stomach cancer is exhaustion, the genesis of which is complex and determined by intoxication, peptic disorders and nutritional deficiency.

Bowel diseases

Intestinal pathologies of greatest clinical importance include malformations (megacolon, megasigma, diverticula, stenosis and atresia), inflammatory diseases (enteritis, appendicitis, colitis, enterocolitis) and dystrophic (enteropathy) nature, tumors (polyps, carcinoid, colon cancer intestines).

Developmental defects. A peculiar developmental defect is congenital expansion entire colon (megacolon- megacolon congenitum) or just the sigmoid colon (megasigma- megasigmoideum) with a sharp hypertrophy of the muscle layer of its wall. Congenital diseases include intestinal diverticula- limited protrusions of the entire wall (true diverticula) or only the mucous membrane and submucosal layer through defects in the muscular layer (false diverticula). Diverticula are observed in all parts of the intestine. Diverticula of the small intestine are more common at the site of the umbilical-intestinal tract - Meckel's diverticulum and diverticula of the sigmoid colon. In cases where multiple diverticula develop in the intestine, they speak of diverticulosis. In diverticula, especially the colon, intestinal contents stagnate, fecal stones form, and inflammation occurs (diverticulitis), which can lead to perforation of the intestinal wall and peritonitis. Congenital stenosis and atresia intestines are also found in different departments intestines, but more often at the junction of the duodenum into the jejunum and the end of the ileum into the cecum. Stenosis and atresia of the intestine lead to intestinal obstruction (see. Diseases of childhood).

Intestinal inflammation may occur predominantly in thin (enteritis) or colon (colitis) or spread more or less evenly throughout the intestine (enterocolitis).

Enteritis

With enteritis, inflammation does not always cover the entire length of the small intestine. In this regard, inflammation of the duodenum is distinguished - duodenitis, jejunum - jeunitis and ileum - ileitis. Enteritis can be acute and chronic.

Acute enteritis

Acute enteritis- acute inflammation of the small intestine.

Etiology. Often occurs with many infectious diseases (cholera, typhoid fever, colibacillary, staphylococcal and viral infection, sepsis, giardiasis, opisthorchiasis, etc.), especially in case of food toxic infections (salmonellosis, botulism), poisoning (chemical poisons, poisonous mushrooms, etc.). Famous acute enteritis nutritional (overeating, consumption of rough food, spices, strong alcoholic drinks, etc.) and allergic (idiosyncrasy to foods, drugs) origin.

Pathological anatomy. Acute enteritis can be catarrhal, fibrinous, purulent, necrotic-ulcerative.

At catarrhal enteritis, which occurs most often, the congested and edematous intestinal mucosa is abundantly covered with serous, serous-mucosal or serous-purulent exudate. Edema and inflammatory infiltration cover not only the mucous membrane, but also the submucosal layer. Dystrophy and desquamation of the epithelium are noted, especially at the tips of the villi. (catarrhal desquamative enteritis), goblet cell hyperplasia (“goblet transformation”), small erosions and hemorrhages.

At fibrinous enteritis, more often ileite, the intestinal mucosa is necrotic and permeated with fibrinous exudate, as a result of which gray or gray-brown filmy deposits appear on its surface. Depending on the depth of necrosis, inflammation may be lobar or diphtheritic, in which deep ulcers form after the fibrinous films are rejected.

Purulent enteritis characterized by diffuse saturation of the intestinal wall with pus (phlegmonous enteritis) or the formation of pustules, especially at the site of lymphoid follicles (apostematous enteritis).

At necrotic ulcerative enteritis destructive processes can concern mainly group and solitary lymphatic follicles of the intestine, as is observed with typhoid fever, or cover the mucous membrane without connection with the intestinal lymphatic system. In this case, necrosis and ulceration are widespread (influenza, sepsis) or focal character(allergic vasculitis, periarteritis nodosa).

Regardless of the nature of the inflammatory changes in the mucous membrane, hyperplasia and reticulomacrophagic transformation of the intestinal lymphatic system develop in acute enteritis. Sometimes it is expressed extremely sharply (for example, the so-called brain-like swelling of group and solitary follicles in typhoid fever) and causes subsequent destructive changes in the intestinal wall.

In the mesenteric lymph nodes Reactive processes are observed in the form of hyperplasia of lymphoid elements, plasmacytic and reticulomacrophagal transformation, and often inflammation.

Complications acute enteritis include bleeding, perforation of the intestinal wall with the development of peritonitis (for example, with typhoid fever), and

also dehydration and demineralization (for example, with cholera). In some cases, acute enteritis can become chronic.

Chronic enteritis

Chronic enteritis- chronic inflammation of the small intestine. It can be an independent disease or a manifestation of other chronic diseases (hepatitis, cirrhosis of the liver, rheumatic diseases, etc.).

Etiology. Chronic enteritis can be caused by numerous exogenous and endogenous factors that, with prolonged exposure and damage to enterocytes, can disrupt the physiological regeneration of the mucous membrane of the small intestine. Exogenous factors are infections (staphylococcus, salmonella, viruses), intoxication, exposure to certain medications (salicylates, antibiotics, cytostatic agents), long-term nutritional errors (abuse of spicy, hot, poorly cooked foods), excessive consumption of coarse plant fiber, carbohydrates, fats, insufficient intake of proteins and vitamins. Endogenous factors may be autointoxication (for example, with uremia), metabolic disorders (with chronic pancreatitis, cirrhosis of the liver), hereditary deficiency of small intestinal enzymes.

Morphogenesis. The basis of chronic enteritis is not only inflammation, but also a violation physiological regeneration mucous membrane of the small intestine: proliferation of the crypt epithelium, differentiation of cells, their “advancement” along the villi and rejection into the intestinal lumen. At first, these disorders consist of increased proliferation of the crypt epithelium, which seeks to replenish the quickly rejected damaged enterocytes of the villi, but the differentiation of this epithelium into functionally complete enterocytes is delayed. As a result, most of the villi turn out to be lined with undifferentiated, functionally incompetent enterocytes, which quickly die. The shape of the villi adapts to the reduced number of epithelial cells: they become shorter and atrophy. Over time, the crypts (cambial zone) are unable to provide a pool of enterocytes and undergo cystic transformation and sclerosis. These changes are the final stage of impaired physiological regeneration mucous membrane, it develops atrophy And structural restructuring.

Pathological anatomy. Changes in chronic enteritis have recently been well studied using enterobiopsy material.

There are two forms of chronic enteritis - without atrophy of the mucous membrane and atrophic enteritis.

For chronic enteritis without mucosal atrophy The uneven thickness of the villi and the appearance of club-shaped thickenings in their distal sections are very characteristic, where destruction of the basal membranes of the epithelial lining is noted. The cytoplasm of the enterocytes lining the villi is vacuolated (Fig. 205). Activity of redox and hydrolytic (alkaline phosphatase) enzymes

the cytoplasm of such enterocytes is reduced, which indicates a violation of their absorption capacity. Between the enterocytes of the apical sections of nearby villi, adhesions and “arcades” appear, which is apparently associated with the formation of surface erosions; the villous stroma is infiltrated with plasma cells, lymphocytes, and eosinophils. The cellular infiltrate descends into the crypts, which may be cystically dilated. The infiltrate expands the crypts and reaches the muscular layer of the mucous membrane. If the changes described above affect only the villi, they speak of superficial version this form of chronic enteritis, but if they involve the entire thickness of the mucous membrane - o diffuse version.

Chronic atrophic enteritis characterized primarily by shortening of the villi, their deformation, and the appearance of a large number of fused villi (see Fig. 205). In shortened villi, collapse of argyrophilic fibers occurs. Enterocytes are vacuolated, and alkaline phosphatase activity in their brush border is reduced. A large number of goblet cells appear.

The crypts are atrophied or cystically enlarged, they are infiltrated by lymphohistiocytic elements and replaced by proliferations of collagen and muscle fibers. If atrophy concerns only the villi of the mucous membrane, and the crypts are little changed, they speak of hyperregenerative version this form of chronic enteritis, if

Rice. 205. Chronic enteritis (enterobiopsy) (according to L.I. Aruin):

a - chronic enteritis without atrophy; uneven thickness of the villi, club-shaped thickening of their distal sections, dystrophy of enterocytes, polymorphic cell infiltration of the stroma; b - chronic atrophic enteritis; shortening of the villi, their deformation and fusion; pronounced lymphohistiocytic infiltration of the stroma

the villi and crypts are atrophic, the number of which is sharply reduced - about the hyporegenerative option.

With long-term, severe chronic enteritis, anemia, cachexia, hypoproteinemic edema, osteoporosis, endocrine disorders, vitamin deficiency, and malabsorption syndrome may develop.

Enteropathies

Enteropathies are called chronic diseases of the small intestine, which are based on hereditary or acquired enzyme disorders of enterocytes (intestinal fermentopathy). A decrease in activity or loss of certain enzymes leads to insufficient absorption of those substances that these enzymes normally break down. As a result, the syndrome develops impaired absorption certain nutrients (malabsorption syndrome).

Among enteropathies there are: 1) disaccharidase deficiency (for example, alactasia); 2) hypercatabolic hypoproteinemic enteropathy (intestinal lymphangiectasia); 3) celiac enteropathy (non-tropical sprue, celiac sprue).

Pathological anatomy. Changes in various enteropathies are more or less the same type and come down to varying degrees of severity of dystrophic and atrophic changes in the mucous membrane of the small intestine. Particularly characteristic are shortening and thickening of the villi, vacuolization and a decrease in the number of enterocytes with their loss of microvilli (brush border), deepening of the crypts and thickening of the basement membrane, infiltration of the mucous membrane with plasma cells, lymphocytes, and macrophages. In the later stages, an almost complete absence of villi and severe sclerosis of the mucous membrane are noted.

At hypercatabolic hypoproteinemic enteropathy the described changes are combined with a sharp expansion of the lymphatic capillaries and vessels of the intestinal wall (intestinal lymphangiectasia). Histoenzyme-chemical study of biopsy samples of the intestinal mucosa makes it possible to determine enzyme disorders characteristic of a certain type of enteropathy, for example, deficiency of enzymes that break down lactose and sucrose, with disaccharidase enteropathy. At celiac enteropathy the diagnosis is made based on the study of material from two enterobiopsies performed before and after a gluten-free diet.

Enteropathy is characterized by the same consequences as severe chronic enteritis. They lead, in addition to the malabsorption syndrome, to hypoproteinemia, anemia, endocrine disorders, vitamin deficiencies, and edema syndrome.

Whipple's disease

Whipple's disease(intestinal lipodystrophy) is a rare chronic disease of the small intestine, which is characterized by malabsorption syndrome, hypoprotein and hypolipidemia, progressive weakness and weight loss.

Etiology. Many researchers, in connection with the discovery of bacilli-shaped bodies in macrophages of the mucous membrane, attach importance to the infectious factor. The infectious nature of the disease is also supported by the fact that these bodies, when treated with antibiotics, disappear from the mucous membrane and reappear when the disease worsens.

Pathological anatomy. As a rule, compaction of the wall of the small intestine and its mesentery is noted, as well as an increase in mesenteric lymph nodes, which is associated with the deposition of lipids and fatty acids and severe lymphostasis. Characteristic changes are detected by microscopic examination. They are manifested by pronounced infiltration of the lamina propria of the intestinal mucosa by macrophages, the cytoplasm of which is stained with Schiff's reagent (CHIK-positive macrophages). In addition to the mucous membrane, the same type of macrophages appear in mesenteric lymph nodes (Fig. 206), liver, synovial fluid. In macrophages and epithelial cells of the mucous membrane, electron microscopic examination reveals bacilli-like bodies (see Fig. 206). Lipogranulomas are found in the intestine, lymph nodes and mesentery, in areas of fat accumulation.

Colitis

For colitis inflammatory process covers predominantly the blind (typhlitis), transverse colon (transversit), sigmoid (sigmoiditis) or direct (proctitis) intestine, and in some cases extends to the entire intestine (pancolitis). Inflammation can be either acute or chronic.

Acute colitis

Acute colitis- acute inflammation of the colon.

Etiology. There are infectious, toxic and toxicoallergic colitis. TO infectious include dysentery, typhoid, colibacillary, staphylococcal, fungal, protozoal, septic, tuberculous, syphilitic colitis, toxic - uremic, sublimate, medicinal, and to toxicoallergic - nutritional and coprostatic colitis.

Pathological anatomy. The following forms of acute colitis are distinguished: catarrhal, fibrinous, purulent, hemorrhagic, necrotic, gangrenous, ulcerative.

At catarrhal colitis the intestinal mucosa is hyperemic, swollen, and accumulations of exudate are visible on its surface, which can be serous, mucous or purulent in nature (serous, mucous or purulent catarrh). The inflammatory infiltrate penetrates not only the thickness of the mucous membrane, but also the submucosal layer, in which hemorrhages are visible. Dystrophy and necrobiosis of the epithelium are combined with desquamation of the surface epithelium and hypersecretion of glands.

Fibrinous colitis depending on the depth of necrosis of the mucous membrane and penetration of fibrinous exudate, they are divided into lobar And diphtheritic (cm. Dysentery). Purulent colitis usually characterized by phlegmonous inflammation - phlegmonous colitis, phlegmon of the colon. In cases where multiple hemorrhages occur in the intestinal wall due to colitis, areas of hemorrhagic impregnation appear, they speak of hemorrhagic colitis. At necrotizing colitis necrosis often affects not only the mucous membrane, but also the submucosal layer. Gangrenous colitis- necrotic variant. Spicy ulcerative colitis usually completes diphtheritic or necrotic changes in the intestinal wall. In some cases, for example with amoebiasis, ulcers in the colon appear at the very beginning of the disease.

Complications acute colitis: bleeding, perforation and peritonitis, paraproctitis with pararectal fistulas. In some cases, acute colitis takes a chronic course.

Chronic colitis

Chronic colitis- chronic inflammation of the colon - occurs primarily or secondary. In some cases, it is genetically associated with acute colitis, in other cases this connection is not traced.

Etiology. The factors causing chronic colitis are essentially the same as those in acute colitis, i.e. infectious, toxic And toxicoallergic. The duration of action of these factors in conditions of increased local (intestinal) reactivity becomes important.

Pathological anatomy. Changes in chronic colitis, studied on biopsy material, differ little from those in chronic enteritis, although in colitis they are more clearly expressed inflammatory phenomena, which are combined with disregenerative and lead to atrophy And sclerosis mucous membrane. Guided by this, a distinction is made between chronic colitis without atrophy of the mucous membrane and chronic atrophic colitis.

At chronic colitis without mucosal atrophy the latter is swollen, dull, granular, gray-red or red, often with multiple hemorrhages and erosions. Flattening and desquamation of the prismatic epithelium and an increase in the number of goblet cells in the crypts are noted. The crypts themselves are shortened, their lumen is widened, sometimes they resemble cysts (cystic colitis). The lamina propria of the mucous membrane, in which hemorrhages occur, is infiltrated with lymphocytes, plasma cells, eosinophils, and the cellular infiltrate often penetrates into its muscular layer. The degree of cellular infiltration can be different - from very moderate focal to pronounced diffuse with the formation of individual abscesses in the crypts (crypt abscesses) and areas of ulceration.

For chronic atrophic colitis characterized by flattening of the prismatic epithelium, a decrease in the number of crypts, and hyperplasia of smooth muscle elements. In the mucous membrane histiolim-

focytic infiltration and proliferation of connective tissue; in some cases, epithelializing and cicatricial ulcers occur.

Among the forms of chronic colitis, the so-called collagen colitis, which is characterized by the accumulation of collagen, amorphous protein and immunoglobulins around the crypts of the mucous membrane (“pericryptal fibroblast disease”). The development of this form of colitis is associated with a distortion of collagen synthesis or with autoimmunization.

Complications. Parasigmoiditis and paraproctitis, in some cases hypovitaminosis.

Nonspecific ulcerative colitis(synonyms: idiopathic ulcerative colitis, ulcerative proctocolitis) is a chronic relapsing disease based on inflammation of the colon with suppuration, ulceration, hemorrhage and outcome in sclerotic deformation of the wall. This is a fairly common disease that occurs more often in young women.

Etiology and pathogenesis. Local allergies, which are apparently caused by intestinal microflora, are certainly important in the occurrence of this disease. The allergic nature of colitis is supported by its combination with urticaria, eczema, bronchial asthma, rheumatic diseases, and Hashimoto's goiter. Autoimmunization is of great importance in the pathogenesis of the disease. This is confirmed by the discovery of autoantibodies in ulcerative colitis that are fixed in the epithelium of the intestinal mucosa, the nature of the cellular infiltrate of the mucous membrane, which reflects a delayed-type hypersensitivity reaction. The chronic course of the disease and the imperfection of reparative processes are apparently associated not only with autoaggression, but also with trophic disorders due to the pronounced destruction of the intramural nervous apparatus of the intestine.

Pathological anatomy. The process usually begins in the rectum and gradually spreads to the cecum. Therefore, there are both relatively isolated lesions of the rectum and sigmoid or rectum, sigmoid and transverse colon, as well as total lesions of the entire colon (Fig. 207).

Morphological changes depend on the nature of the disease - acute or chronic (Kogoy T.F., 1963).

Acute form corresponds to an acute progressive course and exacerbation of chronic forms. In these cases, the wall of the colon is swollen, hyperemic, with multiple erosions and superficial ulcers of irregular shape, which merge and form large areas of ulceration. The islands of mucous membrane preserved in these areas resemble polyps (fringed pseudopolyps). Ulcers can penetrate into the submucosal and muscular layers, where fibrin-

Rice. 207. Nonspecific ulcerative colitis (preparation by Zh.M. Yukhvidova)

obvious necrosis of collagen fibers, foci of myomalacia and karyorrhexis, extensive intramural hemorrhages. At the bottom of the ulcer, both in the zone of necrosis and along their periphery, vessels with fibrinoid necrosis and arrosion of the walls are visible. Perforation of the intestinal wall in the area of ​​the ulcer and intestinal bleeding often occur. Such deep ulcers form pockets with necrotic masses, which are rejected, the intestinal wall becomes thinner, and the lumen becomes very wide (toxic dilatation). Individual ulcers undergo granulation, and granulation tissue grows in excess in the area of ​​the ulcer and forms polypoid outgrowths - granulomatous pseudopolyps. The intestinal wall, especially the mucous membrane, is abundantly infiltrated with lymphocytes, plasma cells, and eosinophils. During the period of exacerbation, the infiltrate is dominated by neutrophils, which accumulate in the crypts, where they form crypt abscesses(Fig. 208).

For chronic form characterized by a sharp deformation of the intestine, which becomes much shorter; There is a sharp thickening and compaction of the intestinal wall, as well as diffuse or segmental narrowing of its lumen. Reparative-sclerotic processes prevail over inflammatory-necrotic ones. Granulation and scarring of ulcers occur, but their epithelization is usually incomplete, which is associated with the formation of extensive scar fields and chronic inflammation.

Rice. 208. Nonspecific ulcerative colitis (preparation by Zh.M. Yukhvidova):

a - accumulation of leukocytes in the crypt (crypt abscess); b - pseudopolyp

The manifestation of perverse reparation is multiple pseudopolyps(see Fig. 208) and not only as a result of excessive growth of granulation tissue (granulomatous pseudopolyps), but also reparative regeneration of the epithelium around areas of sclerosis (adenomatous pseudopolyps). Productive endovasculitis, wall sclerosis, and obliteration of the lumen are noted in the vessels; fibrinoid vascular necrosis is rare. Inflammation is predominantly productive in nature and is expressed in infiltration of the intestinal wall with lymphocytes, histiocytes, and plasma cells. Productive inflammation is combined with crypt abscesses.

ComplicationsNonspecific ulcerative colitis can be local and general. TO local relate intestinal bleeding, perforation of the wall and peritonitis, stenosis of the lumen and polyposis of the intestine, development of cancer, to general - anemia, amyloidosis, exhaustion, sepsis.

Crohn's disease

Crohn's disease- a chronic recurrent disease of the gastrointestinal tract, characterized by nonspecific granulomatosis and necrosis.

Crohn's disease previously meant a nonspecific granulomatous lesion of only the final part of the small intestine and therefore was called terminal (regional) ileitis. It was later shown that changes characteristic of this disease can occur in any part of the gastrointestinal tract. Descriptions of Crohn's disease of the stomach, colon, appendix, etc. appeared.

Etiology and pathogenesis.The cause of Crohn's disease is not known. Suggestions have been made about the role of infection, genetic factors, and hereditary predisposition of the intestine to respond to various

exposure to a stereotypical granulomatous reaction, autoimmunization. Among the pathogenetic theories, in addition to the autoimmune one, the so-called lymphatic one is widespread, according to which primary changes develop in the lymph nodes of the mesentery and lymphoid follicles of the intestinal wall and lead to “lymphatic edema” of the submucosal layer, resulting in destruction and granulomatosis of the intestinal wall.

Pathological anatomy. Most often, changes are found in the terminal segment of the ileum, in the rectum (especially in the anus) and appendix; other localizations are rare. Affected the entire thickness of the intestinal wall, which becomes sharply thickened and swollen. The mucous membrane is lumpy, reminiscent of a “cobblestone street” (Fig. 209), which is associated with the alternation of long, narrow and deep ulcers, which are located in parallel rows along the length of the intestine, with areas of normal mucous membrane. There are also deep slit-like ulcers, located not along the length, but along the diameter of the intestine. The serous membrane is often covered with adhesions and multiple whitish nodules, which are similar to tuberculosis. The intestinal lumen is narrowed, and fistula tracts form in the thickness of the wall. The mesentery is thickened and sclerotic. Regional lymph nodes are hyperplastic and white-pink in section.

The most characteristic microscopic feature is nonspecific granulomatosis, which covers all layers of the intestinal wall. Granulomas have a sarcoid-like structure and consist of epithelioid and giant cells of the Pirogov-Langhans type (see Fig. 209). Edema and diffuse infiltration of lymphocytes, histiocytes, and plasma cells are also considered characteristic submucosal layer, hyperplasia of its lymphoid elements, formation of slit-like ulcers (see Fig. 209). These changes are often accompanied by abscesses in the thickness of the wall, sclerosis and hyalinosis as a result of the evolution of diffuse infiltrate cells and granulomas. With a long course, a sharp cicatricial deformation of the wall occurs.

Complication in Crohn's disease there is perforation of the intestinal wall with the formation of fistulous tracts, and therefore purulent or fecal peritonitis develops. There are frequent stenoses of various parts of the intestine, but more often the ileum, with symptoms of intestinal obstruction. Crohn's disease is considered a precancer of the intestine.

Appendicitis

Appendicitis- inflammation of the vermiform appendix of the cecum, giving a characteristic clinical syndrome. It follows from this that in clinical and anatomical terms, not every inflammation of the appendix (for example, with tuberculosis, dysentery) is appendicitis. Appendicitis is a common disease that often requires surgical intervention.

Rice. 209. Crohn's disease affecting the colon:

a - macropreparation (according to Zh.M. Yukhvidova); b - epithelioid cell granuloma with giant cells of the Pirogov-Langhans type (according to L.L. Kapuller); c - slit-like ulcer (according to L.L. Kapuller)

Etiology and pathogenesis. Appendicitis is an enterogenous autoinfection. The flora vegetating in the intestines becomes pathogenic; E. coli and enterococcus are of greatest importance. The study of possible conditions contributing to the invasion of microbes into the wall of the appendix and the manifestation of the virulent properties of the intestinal flora showed the importance of various factors, which served as the basis for the creation of pathogenetic theories of appendicitis.

Angioneurotic theory The pathogenesis of appendicitis has become widespread. Built on a physiological basis (disturbances in the kinetics of the process as a trigger point for the disease), it easily explains initial manifestations diseases (simple, superficial appendicitis) and those clinical cases where there are no morphological changes in the removed appendix. At the same time, from the standpoint of the neurovascular theory, it is difficult to explain the dynamics of the development of destructive forms of appendicitis, which is easily explained by the concept of progression of primary affect by L. Aschoff.

Pathological anatomy. There are two clinical and anatomical forms of appendicitis: acute and chronic. Each of them has a certain morphological characteristic.

Acute appendicitis. The following morphological forms of acute appendicitis are distinguished: 1) simple, 2) superficial, 3) destructive (phlegmonous, apostematous, phlegmonous-ulcerative, gangrenous). These forms are a morphological reflection of the phases of acute inflammation of the appendix, ending with destruction and necrosis. Usually it lasts 2-4 days.

Changes characteristic of acute simple appendicitis, develop during the first hours from the onset of the attack. They consist of a disorder of blood and lymph circulation in the form of stasis in capillaries and venules, edema, hemorrhages, accumulation of siderophages, as well as marginal standing of leukocytes and leukodiapedesis. These changes are expressed mainly in the distal appendix. Disorders of blood and lymph circulation are combined with dystrophic changes in the intramural nervous system of the appendix.

In the following hours, against the background of dyscirculatory changes in the distal appendix, foci of exudative purulent inflammation of the mucous membrane appear, called primary affect. At the top of such a cone-shaped focus, facing the lumen of the process, surface defects of the epithelium are noted. These microscopic changes characterize acute superficial appendicitis, in which the process becomes swollen, and its serous membrane becomes full-blooded and dull. Changes characteristic of simple or superficial appendicitis are reversible, but if they progress, it develops acute destructive appendicitis.

By the end of the first day, the leukocyte infiltrate spreads to the entire thickness of the wall of the appendix - it develops phlegmonous appendicitis(Fig. 210). The size of the appendix increases, its serous membrane becomes dull and full-blooded, and a fibrinous coating appears on its surface (Fig. 211, see color on); the wall of the incision is thickened, pus is released from the lumen. The mesentery is swollen and hyperemic. If, against the background of diffuse purulent inflammation of the appendix, multiple small pustules (abscesses) appear, they speak of apostematous appendicitis, if phlegmonous appendicitis is accompanied by ulceration of the mucous membrane - o phlegmonous-ulcerative appendicitis. Completes purulent-destructive changes in the appendix gangrenous appendicitis, which is called secondary, since it occurs as a result of the transition of a purulent process to surrounding tissues (periappendicitis, see fig. 211), including on the mesentery of the process (mesenteriolitis), which leads to thrombosis of the appendicular artery.

Secondary gangrenous appendicitis should be distinguished from gangrene of the appendix, developing as a result of primary thrombosis or thromboembolism of its artery. Obviously, this is why gangrene of the appendix is ​​not quite aptly called primary gangrenous appendicitis.

Rice. 210. Phlegmonous appendicitis. Swelling of the wall and its separation with purulent exudate

Type of appendix gangrenous appendicitis very characteristic. The process is thickened, its serous membrane is covered with dirty green fibrinous-purulent deposits. The wall is also thickened, gray-dirty in color, and pus is released from the lumen. Microscopic examination reveals extensive foci of necrosis with bacterial colonies, hemorrhages, and blood clots in the vessels. The mucous membrane is ulcerated almost throughout.

Complications. In acute appendicitis, complications are associated with destruction of the appendix and the spread of pus. Often occurring with phlegmonous-ulcerative appendicitis perforation walls leads to the development of limited and diffuse peritonitis, which also appears during self-amputation of a gangrenous appendix. If, with phlegmonous appendicitis, the proximal part of the appendix closes, then the lumen of the distal part stretches and develops empyema of the appendix. Spread of the purulent process to the tissues surrounding the process and the cecum (periappendicitis, peritiphlitis) accompanied by the formation of encysted abscesses, the transition of inflammation to the retroperitoneal tissue. Very dangerous development purulent thrombophlebitis of mesenteric vessels with its spread to the branches of the portal vein and the appearance pylephlebitis(from Greek pile- gates, flebos- vein). In such cases, thrombobacterial embolism of the branches of the portal vein in the liver and the formation of pylephlebitic abscesses.

Chronic appendicitis. It develops after acute appendicitis and is characterized by sclerotic and atrophic processes, against the background of which inflammatory and destructive changes may appear. Typically, inflammation and destruction are replaced by the proliferation of granulation tissue in the wall and lumen of the process. Granulation tissue matures and turns into scar tissue. Severe sclerosis and atrophy of all layers of the wall occur, lumen obliteration appendix, adhesions appear between the appendix and surrounding tissues. These changes can be combined with granulating and acute ulcers, histiolymphocytic and leukocyte infiltration of the appendix wall.

Sometimes, with cicatricial obliteration of the proximal part of the process, serous fluid accumulates in its lumen and the process turns into a cyst - it develops dropsy of the appendix. If the contents of the cyst become the secretion of the glands - mucus, then they talk about mucocele. Rarely, due to peristalsis of the appendix, mucus collects into spherical formations (mixoglobules), which leads to myxoglobulosis process. When a cyst breaks through and the mucus and the cells that form it enter the abdominal cavity, these cells can implant on the peritoneum, which leads to its changes resembling a tumor - a myxoma. In such cases we talk about pseudomyxoma peritoneum.

About false appendicitis they say in cases where the clinical signs of an attack of appendicitis are caused not by the inflammatory process, but dyskinetic disorders. In cases of hyperkinesis, the process

As its muscle layer is reduced, the follicles are enlarged, the lumen is sharply narrowed. With atony, the lumen is sharply expanded, filled with feces (coprostasis), the wall of the appendix is ​​thinned, the mucous membrane is atrophic.

Intestinal tumors

Among intestinal tumors, the most important are epithelial ones - benign and malignant.

From benign epithelial tumors are the most common adenomas(as adenomatous polyps). They are usually localized in the rectum, then in frequency - in the sigmoid, transverse colon, cecum and small colon. Among intestinal adenomas there are tubular, tubulovillous And villous. Villous adenoma, which is represented by soft pink-red tissue with a villous surface (villous tumor), has a glandular-papillary structure. It may become malignant. With multiple adenomatous polyps they talk about intestinal polyposis, which has a family character.

Cancer occurs in both the small and large intestines. Small bowel cancer rare, usually in duodenum, in the area of ​​her large (Vater) nipple. The tumor does not reach large sizes, very rarely causes difficulty in the outflow of bile, which is the cause of subhepatic jaundice, and is complicated by inflammation of the bile ducts.

Colon cancer tends to become more frequent, and the mortality rate from it increases. Of the different parts of the colon, cancer is most common in rectum, less often in the sigmoid, cecum, hepatic and splenic corners of the transverse colon.

Rectal cancer usually preceded by chronic ulcerative colitis, polyposis, villous tumor or chronic rectal fistulas (precancerous diseases).

Depending on the growth pattern There are exophytic, endophytic and transitional forms of cancer.

TO exophytic crayfish include plaque-like, polypous and large-tuberous, endophytic- ulcerative and diffuse-infiltrative, usually narrowing the intestinal lumen (Fig. 212), to transitional- saucer-shaped cancer.

Among histological types bowel cancer isolated adenocarcinoma, mucinous adenocarcinoma, signet ring cell, squamous cell, glandular squamous cell, undifferentiated, unclassified cancer. Exophytic forms of cancer usually have the structure of adenocarcinoma, endophytic forms - the structure of signet ring cell or undifferentiated cancer.

Separately allocate cancers of the anal canal: squamous cell, cloacogenic, mucoepidermal, adenocarcinoma.

Metastasizes rectal cancer to regional lymph nodes and liver.

Rice. 212. Diffuse infiltrative rectal cancer

Peritonitis

Peritonitis, or inflammation of the peritoneum, often complicates diseases of the digestive system: perforation of a stomach or duodenal ulcer, intestinal ulcers due to typhoid fever, nonspecific ulcerative colitis, dysentery; it occurs as a complication of appendicitis, liver diseases, cholecystitis, acute pancreatitis, etc.

Peritonitis may be limited to one or another part of the abdominal cavity - limited peritonitis or be widespread - diffuse peritonitis. More often it is acute exudative peritonitis(serous, fibrinous, purulent), sometimes it can be feces, bile. The visceral and parietal peritoneum is sharply hyperemic, with areas of hemorrhage; between the intestinal loops, accumulations of exudate are visible, which seems to glue the loops together. Exudate is located not only on the surface of the organs and walls of the abdominal cavity, but also accumulates in the underlying sections (lateral canals, pelvic cavity). The intestinal wall is flabby, ruptures easily, and there is a lot of liquid content and gases in the lumen.

With diffuse peritonitis, the organization of purulent exudate is accompanied by the formation of encysted interintestinal accumulations of pus - “abscesses”; with limited peritonitis, a subdiaphragmatic “abscess” appears in the area of ​​the diaphragm. As a result of fibrinous peritonitis, adhesions are formed in the abdominal cavity, and in some cases it develops chronic adhesive peritonitis(adhesive disease), which leads to intestinal obstruction.

Sometimes chronic peritonitis arises “primarily”. Usually it is limited: perigastritis for gastric ulcers, perimeteritis And perisalpingitis after childbirth or with a long-term infection (gonorrhea), pericholecystitis with calculosis of the gallbladder, periappendicitis without clinical manifestations of appendicitis in the anamnesis. In such cases, sclerosis usually appears in a limited area of ​​the peritoneum, and adhesions form, often disrupting the function of the abdominal organs.

Gastritis is a disease in which there is inflammation of the gastric mucosa. With gastritis, food in the stomach will be digested with some difficulty, which means much more time will be spent on digesting food. Currently, there are several types of the disease and here are the main ones:

• Surface;
• Atrophic.

Superficial active gastritis

Active superficial gastritis is a harbinger of atrophic inflammation of the stomach and early stage chronic. It is characterized by minimal damage to the gastric mucosa and few clinical symptoms. The disease is diagnosed using endoscopy.

Surface active gastritis characterized by the following symptoms:

• Metabolic disorders;
• Discomfort in the upper abdomen that occurs on an empty stomach and after eating;
• Disturbance of the digestive process.

As a rule, superficial active gastritis does not have pronounced symptoms, but if you find any of the above symptoms in yourself, you should immediately contact a gastroenterologist. Otherwise, the disease will develop into a more severe form and then its treatment will require much more effort. Treatment must take place after consultation with a gastroenterologist, since the recovery process requires various therapeutic approaches.

Treatment for this form of gastritis usually involves taking antibiotics and medications that reduce the level of acidity in the stomach. In addition, when treating the superficial form of active gastritis, not only regular medication is required, but also adherence to a strict diet. The diet requires excluding the following foods from the diet:

• roast;
• salty;
• spicy;
• fat;
• smoked;
• soda;
• products with various dyes;
• coffee and alcoholic drinks.

Active chronic gastritis is accompanied by various inflammatory processes, which in turn lead to damage to the lower region of the stomach. In this case, the basic functions of the stomach will not be affected, but a prolonged course of the disease may have a bad effect on the condition of the gastric cells, which can lead to a pathological decrease in its functionality.

Symptoms of active chronic gastritis may begin to develop due to a decrease in the level of acid in the gastric juice. The disease is diagnosed on the basis of a physical examination, and differentiation is carried out on the basis of laboratory, instrumental and functional abilities. Of particular importance in this case is endoscopy, as well as biotite examination. Results may be affected by:

• low secretory activity of the glands of the gastric mucosa;
• wide gastric pits;
• thinned stomach walls;
• vacuolization of stomach cells;
• moderate infiltration of leukocytes outside the vessels.

Chronic active atrophic gastritis may be accompanied by bleeding in the stomach, peptic ulcer disease duodenum, as well as stomach cancer. A patient with a chronic form of the disease must undergo not only drug treatment, but also follow a strict diet, which must be selected individually. When creating a diet, you must take into account the course of the disease. Patients who suffer from this disease should be under constant supervision of a gastroenterologist.

Chronic atrophic gastritis must be treated for a week. In addition, in most cases, atrophic active gastritis is aggravated due to frequent stressful situations. It is because of this that quite often gastroenterologists, in addition to prescribing certain drugs and diets, write out a referral to a psychologist to provide psychological assistance.

Chronic gastritis is a disease based on chronic inflammation of the gastric mucosa, prone to progression and leading to digestive disorders and metabolic disorders.

One of the key elements of treatment remains diet for chronic gastritis. Without the right diet, the effectiveness of therapy decreases sharply and full recovery becomes impossible. About who and what menu is prescribed, what and how you can eat, what dishes you need to exclude from your diet, and also a little about recipes ─ later in this article.

Principles of therapeutic nutrition

Nutrition for chronic gastritis is based on several principles:

• You need to eat mechanically, temperature and chemically neutral food.
• You need to eat often, but in small portions.
• The menu should contain enough vitamins and microelements and have the necessary energy value.
• You should exclude or significantly limit foods high in fiber, meat dishes, alcohol, fried and mushroom dishes, bakery products, coffee and strong teas, chocolate, chewing gum and carbonated drinks. These restrictions are especially strict for those who have concomitant diseases (cholecystitis, pancreatitis).

What determines the choice of diet?

What does a doctor focus on when giving advice on his patient’s menu? Depending on the form of the disease, the presence of concomitant diseases (cholecystitis, pancreatitis) will be different and therapeutic nutrition for chronic gastritis. Next, a little about anatomy, which will help to better understand the differences in prescribed diets.

Depending on the morphological changes in the stomach wall, gastritis occurs:

• nutrition for chronic gastritis with high acidity
• what to eat for acute gastritis
• what to take for chronic gastritis

• Surface. It is characterized by disruption of the processes of nutrition and restoration of the gastric epithelium, the gastric mucosa is inflamed. Although the gland cells are changed, their function is not significantly impaired. This form of the disease occurs most often with normal and high acidity.
• Atrophic. Chronic atrophic gastritis is manifested by the same structural changes that occur with superficial gastritis, but here the inflammatory infiltration of the gastric mucosa is already continuous, and the number is also reduced - in fact, atrophy of the glands. As a result of the above processes, there are signs of gastritis with low acidity. What else can this type of gastritis be associated with and who gets it? Often occurs in patients with cholecystitis, pancreatitis. Low acidity in this case, it may be caused by the reflux of the contents of the duodenum into the stomach (since it has an alkaline reaction).

The diet for chronic gastritis depends mainly on the above classification: on whether the disease occurs with low, normal or high acidity, as well as on what phase it is in - exacerbation or remission.

The most strict diet is prescribed in the acute phase. For those patients whose condition improves, its menu is gradually expanded.

Diet during an exacerbation

There is only one diet during an exacerbation, regardless of acidity. Food should be as gentle as possible on the gastric mucosa, which will reduce inflammation and stimulate its recovery. In the hospital, patients with exacerbations are prescribed diet number 1, namely its subtype number 1a. All dishes are prepared in water or steamed, taken in grated form, and the use of table salt is limited. You need to eat 6 times a day. The diet is observed especially strictly if there is also pancreatitis or cholecystitis.

• On the first day of an exacerbation, it is recommended to abstain from food, drinking is allowed, for example, sweet tea with lemon.
• From the second day you can eat liquid food, add jelly, jelly, meat soufflé.
• On the third day, you can eat crackers, steamed cutlets, lean meat broth, and compotes.

Diet without exacerbation

When the acute period subsides, switch from diet number 1a (the first 5–7 days) to diet number 1b (up to 10–15 days).

The principle of sparing the gastric mucosa remains, but it is not as radical as in the acute period. Foods and dishes that stimulate the secretion of gastric juice are limited. The amount of salt is still limited. Meals six times a day.

Features depend on acidity:

• Patients with increased acidity of gastric juice are not recommended to eat fatty broths, fruits, or drink juices. Dairy products and cereals are shown.
• In the diet of patients who have low acidity of gastric juice, they use meat soups and broths, vegetable salads, juices, fermented milk products.

For gastritis with reduced secretion, diet number 2 can also be prescribed. According to this diet, you should not eat spicy foods, snacks and spices, and fatty meats. Avoid foods containing large amounts of fiber, whole milk, and flour products.

Outside of an exacerbation, you need to stick to basic diet number 1 or number 5.

Concomitant pathology

Gastritis rarely occurs on its own. If it is combined with diseases of the liver, gall bladder, biliary tract, for example, cholecystitis, it is advisable, especially during an exacerbation, to adhere to diet number 5.

About drinking

Adequate amount of water is necessary for successful treatment chronic gastritis is no less than all other food. There are several rules according to which:

• What matters is what kind of water you drink ─ it’s better to boil tap water or buy bottled water.
• You can drink water during the day as the need arises, the total volume can reach 2 liters per day.
• It is important to drink a small amount of water 30 minutes before meals ─ this will prepare the stomach for eating.
• During an exacerbation, it is prohibited; outside of it, it is extremely undesirable to drink cold or hot water. This once again irritates the gastric mucosa and worsens the condition.
• It is necessary to reduce the intake of coffee and strong tea to a minimum; during an exacerbation, they should not be taken at all.
• Give up carbonated drinks!

The main treatment for gastritis can be supplemented with mineral water. But it should be remembered that to be effective, the course of treatment must be at least 1–1.5 months.

With high acidity, the choice usually stops at Essentuki-1 or Borjomi.

There are features of taking mineral water in this case:

• Drink 250 ml of warm mineral water 3 times a day 1 hour - 1 hour 30 minutes before meals.
• The specified volume is drunk at once, quickly evacuated from the stomach and reflexively reduces increased secretion.

At decreased secretion prefer Essentuki-4 and 17. Features of reception:

• Water can be taken warm, with a volume of about 250 ml, 3 times a day, 15-20 minutes before meals.
• Drink in small sips ─ this will lengthen the time of contact of mineral water with the gastric mucosa and normalize reduced secretion.

Fruits and berries

If acidity is high, sour fruits and berries are prohibited; if acidity is low, you can eat them little by little; melons and grapes are not recommended. You should also not take risks by trying exotic things: avocado, papaya.

But you can afford such a tasty berry as watermelon even with gastritis.

After all, especially in the summer, many patients are interested in whether it is possible to include watermelons in their menu. It is allowed to eat watermelons, but you should not abuse them either, this will provoke another exacerbation. If you eat a few small slices of watermelon, you can do this every day.

Although in fresh Fruits are strictly limited, you can bake them! Recipe books are filled with a huge number of delicious and healthy recipes.

Recipe for apples baked with cottage cheese and raisins.

• The apples are washed and cored.
• The pureed cottage cheese is mixed with sugar and raw egg and vanilla.
• The apples are filled with the resulting mass and placed in the oven, preheated to 180°C for 10 minutes.

A recipe for apples filled with a mixture of cottage cheese and raisins will allow you to diversify your menu.

Illness and pleasure from eating

It may seem that the therapeutic diet for gastritis contains too many restrictions. Many foods must be completely excluded from the diet, many dishes the patient cannot eat at all, and what remains is completely impossible to eat. But this is not true.

If you search, you will find many recipes for dishes that you can and should please yourself with, even if you have chronic gastritis and need to eat according to a diet and cannot eat a lot of things.

Gastric biopsy - procedure, risks

A biopsy is the removal of a small fragment of material from the gastric mucosa for subsequent analysis in a laboratory.

The procedure is usually performed with classical fibrogastroscopy.

The technique reliably confirms the existence of atrophic changes and makes it possible to judge with relative confidence the benign or malignant nature of neoplasms in the stomach. When identifying Helicobacter pylori its sensitivity and specificity are at least 90% (1).

Procedure technology: how and why is a biopsy performed during FGDS?

The study of gastrobiopsy specimens became a routine diagnostic technique only in the mid-twentieth century.

It was then that the first special probes began to be widely used. Initially, the collection of a tiny piece of tissue was not done precisely, without visual control.

Modern endoscopes are equipped with fairly advanced optical equipment.

They are good because they allow you to combine sample collection and visual examination of the stomach.

Nowadays, not only devices are in use that mechanically cut off material, but also electromagnetic retracting devices of a fairly advanced level. The patient does not have to worry that a medical specialist will blindly damage his mucous membrane.

A targeted biopsy is prescribed when it comes to:

• confirmation of Helicobacter pylori infection;
• various focal gastritis;
• suspected polyposis;
• identification of individual ulcerative formations;
• suspected cancer.

The standard process of fibrogastroscopy is not too lengthened by taking a sample - in total, the process requires 7-10 minutes.

The number of samples and the site from which they are obtained are determined taking into account the acceptable diagnosis. In cases where infection with Helicobacter bacteria is suspected, material is studied at least from the antrum, and ideally from the antrum and body of the stomach.

Having discovered a picture characteristic of polyposis, a piece of the polyp is examined directly.

Suspecting a ulcer, they take 5-6 fragments from the edges and bottom of the ulcer: it is important to capture the possible focus of degeneration. Laboratory research gastrobiopsy data allows you to exclude (and sometimes, alas, detect) cancer.

If there are already signs indicating oncological changes, 6-8 samples are taken, sometimes in two steps. As noted in the “Clinical Guidelines for the Diagnosis and Treatment of Patients with Gastric Cancer” (2),

With submucosal infiltrative tumor growth, a false negative result is possible, which requires a repeat deep biopsy.

X-rays help to draw final conclusions about the presence or absence of a diffuse-infiltrative malignant process in the stomach, but early stages for the development of such cancer, it is not carried out due to low information content.

Preparing for the biopsy procedure follows the standard procedure for FGDS.

Isn't this harmful to the organ?

The question is logical. It’s unpleasant to imagine that something will be cut off from the stomach lining.

Professionals say that the risk is almost zero. The instruments are miniature.

The muscle wall is not affected; the tissue is taken strictly from the mucous membrane. There should be no subsequent pain, much less full-blown bleeding. Standing up almost immediately after taking a tissue sample is usually not dangerous. The examined person will be able to go home calmly.

Then, naturally, you will have to consult a doctor again - he will explain what the answer he received means. A “bad” biopsy is a serious cause for concern.

If alarming laboratory data is received, the patient may well be referred for surgery.

Contraindications for biopsy

1. suspected erosive or phlegmonous gastritis;
2. physiologically determined probability of a sharp narrowing of the esophagus;
3. lack of preparedness at the top respiratory tract(roughly speaking, a stuffy nose that forces you to breathe through your mouth);
4. the presence of an additional disease that is infectious in nature;
5. a number of cardiovascular pathologies (from high blood pressure to heart attack).

In addition, a gastroscope tube should not be inserted into neurasthenics or patients with severe mental disorders. They may react inadequately to the sore sensation in the throat that accompanies the introduction of a foreign body.

Literature:

1. L.D.Firsova, A.A.Masharova, D.S.Bordin, O.B.Yanova, “Diseases of the stomach and duodenum”, Moscow, “Planida”, 2011
2. “Clinical guidelines for the diagnosis and treatment of patients with stomach cancer”, project of the All-Russian Union of Public Associations “Association of Oncologists of Russia”, Moscow, 2014

gastritis diagnosis cancer diagnosis ulcer diagnosis

Infiltration - what is it and how dangerous is this phenomenon? This term refers to the accumulation in tissues of cells (including blood and lymph) that are not characteristic of them. Infiltrates can form in various organs human - liver, lungs, subcutaneous fatty tissue, muscles. There are several forms of formation that appear due to various reasons.

There are two forms of infiltrates - inflammatory and tumor. The first variety is detected during the rapid proliferation of cells. In the problem area, an accumulation of leukocytes, lymphocytes, blood and lymph is observed, which leak through the walls of blood vessels.

Tumor infiltrate refers to the development of various tumors - fibroids, sarcomas, malignant tumors. It is the process of infiltration that stimulates their active growth. In this case, a change in the volume of affected tissues is observed. They acquire a characteristic color, become dense to the touch and painful.

A separate group includes surgical infiltrates. They form on the surface of the skin or tissues of internal organs due to their artificial saturation various substances- anesthetics, alcohol, antibiotics.

Types of inflammatory formations

IN medical practice the most common is an inflammatory infiltrate. Depending on the cells that fill the formation, they are divided into the following types:

• Purulent. The tumor contains polymorphonuclear leukocytes.
• Hemorrhagic. Contains a large number of red blood cells inside.
• Lymphoid. The component of the infiltrate is lymphoid blood cells.
• Histiocytic-plasma cell. Inside the seal there are elements of blood plasma, histiocytes.

Regardless of the nature of its origin, the inflammatory infiltrate may disappear on its own within 1-2 months or develop into an abscess.

Causes of pathology

There are many reasons for the appearance of infiltrates. The most common are the following:

The cause of the pathology may also be the development of an allergic reaction, weak immunity, presence of chronic diseases, individual feature body.

Symptoms

Inflammatory infiltrates develop over several days. At this time, the following symptoms are observed:

• Body temperature remains normal or rises to low-grade levels. In the latter case, its decline does not occur for a long time.
• The affected area becomes slightly swollen. Upon palpation, a compaction is determined, which has clearly defined boundaries.
• When pressing on the formation, pain is felt and discomfort appears.
• The area of ​​skin in the affected area is slightly tense and has hyperemia.
• In the presence of infiltration, all layers of tissue are drawn into the pathological process - the skin, mucous membrane, subcutaneous fat, muscles, and nearby lymph nodes.

Traditional treatment

If symptoms of infiltration are detected, a number of therapeutic measures must be taken. All of them are aimed at eliminating the inflammatory process and preventing the development of an abscess. Used for treatment special means and methods to eliminate tissue swelling, restore blood flow in the affected area and get rid of pain. In most cases, therapy comes down to the following:

• Taking antibiotics is important if the inflammatory process is caused by an infection.
• Symptomatic therapy. Involves taking painkillers.
• Local hypothermia is a decrease in body temperature artificially.
• Physiotherapy. They use special therapeutic mud, laser exposure, and UV irradiation. These methods are prohibited if pus accumulates in the infiltrate.

If conservative treatment does not bring a positive result, minimally invasive intervention is resorted to. Most often, under the control of ultrasonic devices, the affected area is drained and the accumulated fluid is removed. At severe course Diseases of the formation are opened surgically using laparoscopy or laparotomy.

Traditional treatment

If the infiltration is not accompanied by severe symptoms, it can be treated folk remedies at home. They are very effective, helping to make the skin soft and eliminate all seals in just a few days. The most popular traditional medicine recipes are:

It is not difficult to cure infiltration with folk remedies. The main thing is to follow the recommendations and consult a doctor even if your condition worsens slightly.