Chronic gastritis. Causes of lymphocytic colitis

Diagnostics

Lymphocytic infiltration is a rare disease, which resembles other skin and oncological diseases therefore, the 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 anamnesis.
2. Histological examination and fluorescent microscopy. Histological examination of skin samples from the affected areas shows no changes in the tissues, and during 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 with an analysis of the number of normal cells, the number of which in lymphocytic infiltration is at least 97%.
3. Differential diagnosis. Differential diagnosis is carried out with sarcoidosis, systemic lupus erythematosus, lymphocytoma, malignant lymphomas of the skin.

Diseases of the gastrointestinal tract are of great variety. Some of them are primary independent diseases and make up the content of a large section of medicine - gastroenterology, others develop secondarily in various diseases of an infectious and non-infectious, acquired and hereditary nature.

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

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

Diseases of the throat and throat

Among diseases of the pharynx and pharynx, the most important is angina (from lat. angere- 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 in the cold season.

Angina is divided into acute and chronic. Acute angina is of the greatest importance.

Etiology and pathogenesis. The occurrence of angina is associated with exposure to a variety of pathogens, among which staphylococcus aureus, streptococcus, adenoviruses, microbial associations are of primary importance.

In the mechanism of development of angina are involved as exogenous, so endogenous factors. Of paramount importance is an infection penetrating transepithelially or hematogenously, but more often it is an autoinfection provoked by general or local hypothermia, trauma. Of the endogenous factors, age-related features are of primary importance.

of the lymphadenoid apparatus of the pharynx and the reactivity of the body, which can explain the frequent occurrence of angina in older children and adults up to 35-40 years old, 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. There are the following clinical morphological forms acute angina: catarrhal, fibrinous, purulent, lacunar, follicular, necrotic and gangrenous.

At catarrhal angina the mucous membrane of the palatine tonsils and palatine arches is sharply plethoric or cyanotic, dull, covered with mucus. The exudate is serous or muco-leukocytic. Sometimes it lifts the epithelium and forms small vesicles with cloudy contents. Fibrinous angina manifested by the appearance of fibrinous white-yellow films on the surface of the mucous membrane of the tonsils. More often it diphtheria angina, which is usually observed in diphtheria. For purulent tonsillitis characterized by an increase in the size of the tonsils due to their swelling and infiltration by neutrophils. Purulent inflammation often has a diffuse character (quinsy), less often it is limited to a small area (abscess of the tonsil). Possible transition of the purulent process to adjacent tissues and dissemination of infection. Lacunar angina characterized by 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 angina the tonsils are large, full-blooded, the follicles are significantly enlarged in size, in the center of them areas of purulent fusion are determined. In the lymphoid tissue between the follicles, hyperplasia of the lymphoid elements and accumulations of neutrophils are noted. At necrotizing sore throat there is superficial or deep necrosis of the mucous membrane with the formation of defects with jagged edges (necrotic-ulcerative angina). In this regard, hemorrhages in the mucous membrane of the pharynx and tonsils are not uncommon. With gangrenous decay of the tonsil tissue, they speak of gangrenous angina. Necrotic and gangrenous tonsillitis are observed most often in scarlet fever, acute leukemia.

A special variety is ulcerative membranous angina of Simonovsky-Plaut-Vinsen, which is caused by a symbiosis of a spindle-shaped bacterium with ordinary spirochetes of the oral cavity. This angina is epidemic. The so-called septic angina, or angina with alimentary-toxic aleukia, arising after eating products from overwintered grain in the field. Special forms of angina include those that have unusual location: angina of the lingual, tubal 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

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 angina can be both local and general. Complications of a local nature are associated with the transition of the inflammatory process to the surrounding tissues and the development paratonsillar, or pharyngeal, abscess, phlegmonous inflammation of the tissue of the pharynx, thrombophlebitis. Among the complications of angina of a general nature, one should name sepsis. Angina is also involved in the development rheumatism, glomerulonephritis and other infectious-allergic diseases.

Diseases of the salivary glands

Most often, inflammatory processes are found in the salivary glands. Inflammation of the salivary glands is called sialadenitis, and the parotid glands mumps. Sialoadenitis and parotitis can be serous and purulent. They usually occur secondary to infection by the hematogenous, lymphogenous or intraductal route.

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

Dry syndrome is a syndrome of insufficiency of exocrine glands, combined with polyarthritis. Among the etiological factors, the role of viral infection and genetic predisposition is most likely. The basis of pathogenesis is autoimmunization, and dry syndrome is combined with many autoimmune (rheumatoid arthritis, Struma Hashimoto) and viral (viral chronic active hepatitis) diseases. Some authors classify Sjögren's dry 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 dentoalveolar system and organs of the oral cavity).

Diseases of the esophagus

Diseases of the esophagus few. The most common 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 layers, protruding through the gaps of the muscle layer (muscular diverticulum). Depending on the localization And topography distinguish between pharyngoesophageal, bifurcation, epinephric and multiple diverticula, and from origin features - Adhesive diverticula resulting from

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

Causes of diverticulum formation can 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 is either acute or chronic.

acute esophagitis, observed when exposed to chemical, thermal and mechanical factors, with a number of infectious diseases (diphtheria, scarlet fever, typhoid), allergic reactions, may be catarrhal, fibrinous, phlegmonous, ulcerative, gangrenous. A special form of acute esophagitis is membranous, when there is a rejection of the cast of the mucous membrane of the esophagus. After deep membranous esophagitis, which develops with chemical burns, cicatricial stenosis of the esophagus.

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

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

Esophageal carcinoma most often occurs at the border of the middle and lower thirds of it, which corresponds to the level of tracheal bifurcation. Much less often, it occurs 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. Predispose to the development of cancer of the esophagus chronic irritation of its mucous membrane (hot coarse food, alcohol, smoking), cicatricial changes after burns, chronic gastrointestinal infections, anatomical disorders (diverticula, ectopia of the columnar epithelium and gastric glands, etc.). Among precancerous changes, leukoplakia and severe dysplasia of the mucosal epithelium are of the greatest importance.

Pathological anatomy. There are the following macroscopic forms of cancer of the esophagus: annular dense, papillary and ulcerated. Annular solid cancer is a tumor

ion, which circularly covers the wall of the esophagus in a certain area. The lumen of the esophagus is narrowed. With the collapse and ulceration of the tumor, the patency of the esophagus is restored. papillary cancer the esophagus is similar to mushroom-shaped stomach cancer. It easily breaks down, resulting in 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 types of esophageal cancer carcinoma in situ, squamous cell carcinoma, adenocarcinoma, squamous cell carcinoma, glandular cystic, mucoepidermal And undifferentiated cancer.

Metastasis esophageal cancer is predominantly lymphogenous.

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

Diseases of the stomach

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

Gastritis

Gastritis(from Greek. gaster- stomach) - inflammatory disease mucous membrane of the stomach. 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 with abundant, indigestible, spicy, cold or hot food, alcoholic beverages, drugs (salicylates, sulfonamides, corticosteroids, biomycin, digitalis, etc.), chemicals (occupational hazards) is important. Microbes (staphylococcus, salmonella) and toxins, products of disturbed metabolism also play a significant role. In some cases, for example, in case of alcohol poisoning, poor-quality food products, pathogenic factors directly affect the gastric mucosa - exogenous gastritis, in others, this action is indirect and is carried out with the help of vascular, nervous, humoral and immune mechanisms - endogenous gastritis, which include infectious hematogenous gastritis, eliminative gastritis with uremia, allergic, congestive gastritis, etc.

Pathological anatomy. Inflammation of the mucous membrane can cover the entire stomach (diffuse gastritis) or certain departments (focal gastritis). In this regard, distinguish fundic, antral, pyloroanthral And pyloroduodenal gastritis.

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

At catarrhal (simple) gastritis the mucous membrane of the stomach is thickened, edematous, 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 formation. Desquamation of cells leads to erosion. In cases where there are multiple erosions, they talk about erosive gastritis. The glands change slightly, but their secretory activity is suppressed. The mucous membrane is permeated with serous, serous-mucous or serous-leukocyte exudate. Its own layer is plethoric and edematous, infiltrated with neutrophils, diapedetic hemorrhages occur.

At fibrinous gastritis a fibrinous film of gray or yellow-brown color is formed on the surface of the thickened mucous membrane. The depth of necrosis of the mucous membrane in this case can be different, and therefore they are isolated croupous(superficial necrosis) and diphtheric(deep necrosis) options fibrinous gastritis.

At purulent, or phlegmonous, 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 overlays. A yellow-green purulent liquid flows from the surface of the incision. 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 develop perigastritis And peritonitis. Phlegmon of the stomach sometimes complicates its injury, it also develops in chronic ulcers and ulcerated stomach cancer.

Necrotizing gastritis usually occurs when chemicals (alkalis, acids, etc.) enter the stomach, cauterizing and destroying the mucous membrane (corrosive gastritis). Necrosis can cover the superficial or deep sections of the mucous membrane, be coagulative or coagulative. Necrotic changes usually end with 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 the lesion of 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 - cirrhosis of the stomach develops.

Chronic gastritis

In some cases, it is associated with acute gastritis, 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, severity.

Etiology. Chronic gastritis develops under the action on the gastric mucosa primarily exogenous factors: violation of the diet and rhythm of nutrition, alcohol abuse, the action of chemical, thermal and mechanical agents, the impact of occupational hazards, etc. great role and endogenous factors - autoinfections (Campylobacter piloridis), chronic autointoxication, neuroendocrine disorders, chronic cardiovascular insufficiency, allergic reactions, regurgitation of duodenal contents into the stomach (reflux). An important condition for the development of chronic gastritis is prolonged 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) or non-immune (type B gastritis).

autoimmune gastritis characterized by the presence of antibodies to parietal cells, and therefore the defeat of 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. In connection with the defeat of 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, secretion of hydrochloric acid is reduced only moderately. Type B gastritis is distinguished reflux gastritis(gastritis type C). Type B gastritis is 4 times more common than type A gastritis.

Guided process topography stomach, secrete chronic gastritis - antral, fundic And pangastritis.

Morphological types. Chronic gastritis is characterized by long-term dystrophic and necrobiotic changes in the epithelium of the mucous membrane, as a result of which there is a violation 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 flattens, approaches the cubic and is characterized by reduced secretion, in others it is high prismatic with increased secretion. There is a translocation of additional cells from the isthmus to the middle third of the glands, the histamine-stimulated secretion of hydrochloric acid by parietal cells and pepsinogen by the main cells decreases. Own layer (lamina) of the mucous membrane is edematous, infiltrated with lymphocytes, plasma cells, single neutrophils (Fig. 197).

At chronic atrophic gastritis a new and basic quality appears - atrophy of the mucous membrane, its glands, which determines the development of sclerosis. The mucous membrane becomes thinner, the number of glands decreases. Connective tissue grows in place of the atrophied glands. The preserved glands are located in groups, the ducts of the glands are dilated, certain types cells in the glands are poorly differentiated. In connection with the mucoidization of the glands, the secretion of pepsin and hydrochloric acid is disturbed. The mucous membrane is infiltrated with lymphocytes, plasma cells, single neutrophils. Added to these changes remodeling of the epithelium moreover, both superficial and glandular epithelium undergoes metaplasia (see Fig. 197). The gastric folds 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, additional (mucous cells of the glands) and parietal cells of the glands disappear, cubic cells appear, characteristic of the pyloric glands; so-called pseudopyloric glands are formed. It joins the metaplasia of the epithelium dysplasia, the degree of which may vary. Mucosal changes may be mild (moderate atrophic gastritis) or pronounced (pronounced atrophic gastritis).

The so-called giant hypertrophic gastritis, or sickness Menetrie, in which there is an extremely sharp thickening of the mucous membrane, which takes on the appearance of a cobblestone pavement. Morphologically find cell proliferation glandular epithelium and glandular hyperplasia, as well as mucosal infiltration with lymphocytes, epithelioid, plasma, and giant cells. Depending on the predominance of changes in the glands or interstitium, the severity of proliferative changes is isolated glandular, interstitial And proliferative variants this disease.

Signs of activity of chronic gastritis allow to allocate active (exacerbation) and inactive (remission) chronic gastritis. Exacerbation of chronic gastritis is characterized by edema of the stroma, plethora of blood vessels, but cell infiltration is especially pronounced with the presence of a large number of neutrophils in the infiltrate; sometimes crypt abscesses and erosions appear. In 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 perversion of the regeneration of the epithelium of the mucous membrane in chronic gastritis is confirmed by the data of an electron microscopic study on the material of gastrobiopsies. It has been established that undifferentiated cells, which normally occupy the deep sections of the gastric pits and the neck of the glands, appear on the gastric ridges, in the area of ​​the body and bottom of the glands in chronic gastritis. Immature cells show signs of premature involution. This indicates a deep violation of the coordination of the phases of proliferation and differentiation of the epithelium of the glands during the regeneration of the gastric mucosa, which leads to cellular atypia, the development of dysplastic processes.

Due to the fact that in chronic gastritis, violations of the processes of regeneration and structure formation are pronounced, 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, cyclically ongoing disease, the main clinical and morphological expression of which is a recurrent gastric or duodenal ulcer. Depending on the localization of the ulcer and the characteristics of the pathogenesis of the disease, peptic ulcer 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 manifestations peptic ulcer stomach and duodenum, there are so-called symptomatic ulcers, those. ulceration 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), with exogenous and endogenous intoxications (toxic ulcers) allergies (allergic ulcers), specific inflammation (tuberculous, syphilitic ulcers), after operations on the stomach and intestines (postoperative peptic ulcers), as a result of medical treatment (drug ulcers, for example, in the treatment of corticosteroids, acetylsalicylic acid).

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

Etiology. In the development of peptic ulcer are of primary importance stressful situations, psycho-emotional overstrain, leading to the 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 (viscero-cortical disorders). neurogenic theory peptic ulcer can be considered sufficiently substantiated, but it does not allow to explain the occurrence of the disease in all cases. plays an important role in the development of peptic ulcer nutritional factors(violation of the mode and nature of nutrition), bad habits(smoking, and alcohol abuse), exposure to a number of medicines(acetylsalicylic acid, indomethacin, corticosteroids, etc.). Of unconditional importance are hereditary-constitutional (genetic) factors, among which O (I) blood type, positive rh factor, "status of non-secretors" (lack of histocompatibility antigens responsible for the production of gastric mucus glycoproteins), etc. Recently, the occurrence of peptic ulcer has been associated with infectious agent- campylobacter piloridis, which is revealed at duodenal ulcer in 90%, and gastric ulcer - 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 ulcers are divided into 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, mucosal 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 (midbrain, hypothalamus). This leads in some cases (ulcer of the pyloroduodenal zone) to excitation of the hypothalamic-pituitary region, vagus nerve centers and increased tone of the nerve itself, increased activity of the acid-peptic factor and increased gastric motility. In other cases (an ulcer of the body of the stomach), 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 motility; while the activity of the acid-peptic factor is normal or reduced.

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

These violations of hormonal regulation are clearly expressed only in peptic ulcer of the pyloroduodenal zone. With peptic ulcer of the body of the stomach, the production of ACTH and glucocorticoids is reduced, therefore, the role of local factors increases.

Local factors to a large extent implement the transformation acute ulcer into chronic and determine exacerbations, relapses of the disease. With an ulcer of the pyloroduodenal zone, an increase in 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, the factors of aggression (acid-peptic activity) prevail over the factors of protection of the mucous membrane (mucosal barrier), which determines the development or exacerbation peptic ulcer. With a stomach ulcer with normal or reduced activity of the acid-peptic factor and depressed motility, the mucous barrier suffers as a result of diffusion into the gastric wall of hydrogen ions (theory of back diffusion of hydrogen ions), which determines the release of histamine by mast cells, dyscirculatory disorders (blood shunting) and violations of tissue trophism. Morphological changes in the mucous membrane of the stomach and duodenum are presented, respectively, by the picture chronic gastritis And chronic duodenitis. Mucosal damage is also likely to be involved Campylobacter piloridis.

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

Pathological anatomy. The morphological substrate of peptic ulcer is chronic recurrent ulcer. In the course of 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. These stages are especially well observed in gastric ulcer.

erosion called mucosal defects that do not penetrate the muscularis mucosa. Erosion is usually sharp, 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. Hydrochloric acid hematin is found in the bottom of such erosion, and leukocyte infiltrate is found in its edges.

Table 12 Pathogenetic features of peptic ulcer depending on the localization of the ulcer

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

Acute stomach ulcers usually appear on the lesser curvature, in the antrum and pyloric sections, which is explained by the structural and functional features of these sections. It is known that the lesser curvature is a “food path” and therefore is easily injured, the glands of its mucous membrane secrete the most active gastric juice, the wall is richest in receptor devices and the most reactive, but the folds are rigid and, when the muscle layer is reduced, is 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 a chronic one. That's why chronic ulcer stomach is more often localized in the same place as acute, i.e. on the lesser curvature, in the antrum and pyloric regions; cardiac and subcardial ulcers are rare.

Chronic stomach ulcer is usually single, multiple ulcers are rare. The ulcer is oval or round (ulcus rotundum) and sizes from a few millimeters to 5-6 cm. It penetrates the stomach wall to various depths, sometimes reaching the serous layer. The bottom of the ulcer is smooth, sometimes rough; callus- corn; 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 it looks like a terrace, the steps of which are formed by layers of the wall - the mucous membrane, submucosal and muscle layers. This type of edges is explained by the displacement of the layers during the peristalsis of the stomach. On a transverse 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 ulcer of the stomach (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 gently sloping

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

Microscopic picture chronic stomach ulcer in different periods The course of peptic ulcer is different. IN remission period scar tissue is found in the edges of the ulcer. The mucous membrane along the edges is thickened, hyperplastic. In the bottom area, the destroyed muscle layer and the scar tissue replacing it are visible, and the bottom of the ulcer can 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 lumen is 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 in the bottom of the ulcer among the scar tissue there is an overgrowth of nerve fibers by the type of amputation neuromas.

IN period of exacerbation peptic ulcer in the area of ​​the bottom and edges of the ulcer appears a wide area fibrinoid necrosis. On the surface of necrotic masses is located fibrinous-purulent or purulent exudate. The area 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. The exacerbation of the ulcer is evidenced not only by exudative-necrotic changes, but also fibrinoid changes in the walls of blood vessels, often with blood clots in their gaps, as well as mucoid And fibrinoid swelling of scar tissue at the bottom of the ulcer. In connection with these changes, the size of the ulcer increases, it becomes possible to destroy the entire wall of the stomach, which can lead to serious complications. In cases where exacerbation is followed by remission (healing ulcer) inflammatory changes subside, granulation tissue grows into the necrosis zone, which matures into coarse fibrous scar tissue; epithelialization 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 the vessels develop. Thus, exacerbation of peptic ulcer, even in cases of a favorable outcome, leads to increased cicatricial changes in the stomach And exacerbates the violation of the trophism of its tissues, including the newly formed scar tissue, which is easily destroyed during the next exacerbation of peptic ulcer.

Morphogenesis and pathological anatomy of a chronic ulcer duodenum do not fundamentally differ from those in 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 common

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

Complications. Among the complications of chronic ulcers in peptic ulcer disease, there are (Samsonov V.A., 1975): 1) ulcerative-destructive (bleeding, perforation, penetration); 2) inflammatory (gastritis, duodenitis, perigastritis, periduodenitis); 3) ulcerative-cicatricial (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. There is no relationship between the frequency of bleeding and the localization of the ulcer in the stomach; when the ulcer is localized in the duodenum, bleeding is more often caused by ulcers located in the back wall of the bulb. Bleeding occurs due to erosion of the walls of blood vessels - arrosive bleeding, therefore, it occurs, as a rule, during an exacerbation of peptic ulcer.

perforation(perforation) is also usually observed during an exacerbation of peptic ulcer. Pyloric ulcers of the stomach or ulcers of the anterior wall of the duodenal bulb are more often perforated. Perforation of the ulcer leads to peritonitis. Initially, inflammation in the form of fibrinous overlays on the peritoneum appears only in the region of the perforation, then it spreads and becomes not fibrinous, but fibrinous-purulent. In the presence of adhesions, perforation may only lead to limited peritonitis. Chronic peritonitis is rare. Then the masses of gastric contents are encapsulated, on the peritoneum and in the omentum are formed foreign body granulomas. In rare cases, when the perforation is covered by the liver, omentum, pancreas, or rapidly appearing fibrin overlays, they talk about covered perforation.

penetration ulcers are called its penetration beyond the wall 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 the 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, gastric ulcer worsens phlegmon.

Severe ulcer complications are due to cicatricial stenosis gatekeeper. The stomach expands, food masses are retained in it, vomiting often occurs. This can lead to dehydration of the body, depletion of chlorides and the development chlorohydropenic uremia(gastric

tania). Sometimes the scar constricts 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.

Malignization(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 has ranked second among cancerous tumors. Over the past 50 years in many countries of the world there has been a decrease in the incidence of stomach cancer. The same trend was observed in the USSR: for 1970-1980. the incidence of stomach cancer decreased in men by 3.9%, in women - by 6.9%. Stomach cancer is more common in men between the ages of 40 and 70. It accounts for about 25% of cancer deaths.

Etiology. In the experiment, with the help of various carcinogenic substances (benzpyrene, methylcholanthrene, cholesterol, etc.), it was possible to obtain stomach cancer. It is shown that as a result of exposure exogenous carcinogens there is usually cancer of the stomach "intestinal" type. The development of cancer of the "diffuse" type is largely associated with the individual genetic characteristics of the organism. important 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 constantly developing atrophic gastritis), chronic stomach ulcer, adenomas (adenomatous polyps) of the stomach, stomach stump(consequences of resection of the stomach and gastroenterostomy), Menetrier's disease. The "malignant potential" of each of the precancerous conditions is different, but in sum, they increase the likelihood of gastric cancer by 90-100% compared with the general population. Precancerous changes in the gastric mucosa include intestinal metaplasia and severe dysplasia.

Morphogenesis and histogenesis gastric cancer are not well understood. The restructuring of the gastric mucosa, observed in precancerous conditions, is of unconditional importance for the development of a tumor. This restructuring is also preserved in cancer, which allows us to speak of the so-called background, or profile, cancerous stomach.

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

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

membranes of the stomach, with a severe degree of dysplasia close to non-invasive cancer (cancer in situ). It is believed that depending on the predominance of dysplastic processes in the integumentary pit epithelium or in the epithelium of the gland necks, cancer of a different histological structure and different differentiation occurs.

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

Thus, in the morphogenesis of gastric cancer, an important role is played by dysplasia as non-metaplastic(pit, cervical), and metaplastic epithelium(intestinal type). However, the possibility of developing gastric cancer de novo, those. without previous dysplastic and metaplastic changes.

Histogenesis different histological types of gastric cancer, probably common. The tumor originates from single source - cambial elements and progenitor cells in the foci of dysplasia and outside them.

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

Depending on the localization Cancer in a particular part of the stomach is divided into 6 types: pyloric(50%), less curvature of the body with the transition to the walls(27%), cardiac(15%), greater curvature(3%), fundamental(2%) and total(3%). Multicentric gastric cancer is rare. As can be seen, in 3/4 cases, cancer is localized in the pyloric region and on the lesser curvature of the stomach, which has an undoubted diagnostic value.

Depending on the growth pattern allocate the following clinical and anatomical forms of stomach cancer (Serov VV, 1970).

1. Cancer with predominantly exophytic expansive growth: 1) plaque-like cancer; 2) polyposis cancer (including those developed from an adenomatous polyp of the stomach); 3) fungous (mushroom) 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 patterns: transitional forms.

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

options for the development of gastric cancer with a change in forms - phases in time, depending on the predominance of exophytic or endophytic character.

Guided by the features of the microscopic structure, the following histological types of gastric cancer are distinguished: adenocarcinoma(tubular, papillary, mucinous), undifferentiated(solid, scirrhous, cricoid), squamous, glandular squamous(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 found more often 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 2-3 cm in diameter, which is located on the leg (see Fig. 199). Tumor tissue is grey-pinkish or

Rice. 199. Forms of stomach cancer:

a - plaque-like; b - polyposis; 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.

Fungous (mushroom) cancer occurs in 10% of cases. Like polyposis cancer, it looks like a nodular, tuberous (less often with a smooth surface) formation, sitting on a short, wide base (see Fig. 199). Erosions, hemorrhages, or fibrinous-purulent overlays are often found on the surface of the tumor node. 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, in histological examination, it is represented by the same types of carcinoma as polyposis.

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

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

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

Saucer-shaped cancer(cancer-ulcer) - one of the most frequent forms stomach cancer (see Fig. 200). Occurs with ulceration of an exophytically growing tumor (polypous or fungal cancer) and is a rounded formation, sometimes reaching large sizes, with roller-like whitish edges and ulceration in the center. The bottom of the ulcer may be adjacent organs into which the tumor grows. Histologically, it is more often represented by adenocarcinoma, less often by undifferentiated cancer.

Cancer ulcer develops from a chronic stomach ulcer (see Fig. 200), so it occurs where a chronic ulcer is usually localized, i.e. on a small curvature. Signs of a chronic ulcer distinguish cancer ulcer from saucer-shaped cancer: extensive growth of scar tissue, sclerosis and thrombosis of blood vessels, destruction of the muscle layer in the cicatricial bottom 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 case of saucer-shaped cancer, the muscle layer is preserved, although it is infiltrated by tumor cells, and in case of 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 cancrotic infiltration of the wall and ulceration of the tumor, which can compete in time sequence: in some cases, this is late ulceration of massive endophytic carcinomas, in others, endophytic growth of the tumor from the edges of the malignant ulcer. Therefore, the morphology of infiltrative-ulcerative cancer is unusually diverse - these are small ulcers of various depths with extensive infiltration of the wall or huge ulcerations with a bumpy 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 immobile. The mucous membrane loses its usual relief: its surface is uneven, folds of uneven thickness, often with small erosions. Gastric injury may be limited (in this case, the tumor is most often found in the pyloric region) or total (the tumor covers the wall of the stomach throughout). 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 make up approximately 10-15% of all gastric cancers. These are either exophytic carcinomas, which acquired a pronounced infiltrating growth at a certain stage of development, or endophytic, but limited to a small area, cancer with a tendency to intragastric growth, or, finally, two (sometimes more) cancerous tumors of different clinical and anatomical forms in one and the same volume. 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 due to the introduction of targeted gastrobiopsy into practice. Isolation of this form of cancer has a large practical value: up to 100% of such patients live after surgery for more than 5 years, only 5% of them have metastases.

Gastric cancer is characteristic spreading outside the organ itself germination to neighboring organs and tissues. Cancer, located on the lesser curvature with the transition to the anterior and posterior walls and in the pyloric region, grows into the pancreas, the portal of the liver, the portal vein, the bile ducts and the gallbladder, the lesser omentum, the root of the mesentery and the inferior vena cava. Cardiac cancer of the stomach passes to the esophagus, fundic - grows into the hilum of the spleen, the diaphragm. Total cancer, like cancer of the greater curvature of the stomach, grows into the transverse colon, the greater omentum, which shrinks, shortens.

Histological types gastric cancer reflect the structural and functional features of the tumor. adenocarcinoma, which occurs very often with exophytic tumor growth, may be tubular, papillary And mucinous(Fig. 201), and each of the varieties of adenocarcinoma - differentiated, moderately differentiated And undifferentiated. characteristic of endophytic tumor growth undifferentiated cancer represented by several options - solid, scirrhous(Fig. 202), cricoid cell. Rarely found squamous, glandular-squamous(adenocancroid) and unclassifiable types of stomach cancer.

In addition to the International histological classification, gastric cancer is divided according to the nature of the structure into intestinal And diffuse types (Lauren, 1965). The intestinal type of gastric 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 in some places.

Metastases are very characteristic of gastric cancer, they occur in 3/4-2/3 cases. Metastasizes gastric 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 the surgical intervention. In distant lymph nodes, metastases appear as orthograde (according to the lymph flow), and retrograde (against the flow of lymph) by. Retrograde lymphogenous metastases, which are of great diagnostic importance in gastric cancer, include metastases to the supraclavicular lymph nodes, usually the left ("Virchow's metastases", or "Virchow's gland"), to the lymph nodes of pararectal tissue ("Schnitzler's 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 the mesenteric lymph nodes

As a rule, a metastatic lesion affects both ovaries, which increase sharply, become dense, whitish. Lymphogenic metastases appear in the lungs, pleura, peritoneum.

Peritoneal carcinomatosis- a frequent companion of stomach cancer; at the same time, the lymphogenous spread of cancer along the peritoneum is supplemented by implantation(see fig. 203). The peritoneum becomes dotted with tumor nodes of various sizes, merging into conglomerates, among which intestinal loops are immured. Often, in this case, a serous or fibrinous-hemorrhagic effusion appears in the abdominal cavity (the so-called cancrotic peritonitis).

hematogenous metastases, spreading through the portal vein system, affecting primarily liver (Fig. 204), where they are found in 1/3-1/2 cases of gastric cancer. These are single or multiple nodes of various sizes, which in some cases almost completely replace the liver tissue. Such a liver with multiple cancer metastases sometimes reaches a huge size and weighs 8-10 kg. Metastatic nodes undergo necrosis and fusion, 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 gastric cancer: the first are associated with secondary necrotic and inflammatory changes.

tumors, the second - with the germination of gastric cancer in neighboring organs and tissues and metastases.

As a result secondary necrotic changes breakdown of carcinoma occur wall perforation, bleeding, peritumorous (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 leads to the development jaundice, portal hypertension, ascites. Tumor ingrowth 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

its lumen. In pyloric cancer, as in gastric ulcer, it is also possible pyloric stenosis with a sharp expansion of the stomach and characteristic clinical manifestations, up to "gastric tetany". Germination of cancer in the diaphragm can often be accompanied by seeding of the pleura, development hemorrhagic or fibrinous-hemorrhagic pleurisy. The breakthrough of the tumor through the left dome of the diaphragm leads to pleural empyema.

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

Bowel disease

The pathology of the intestine, which has the greatest clinical significance, includes 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 kind of malformation is congenital extension the entire colon (megacolon- megacolon congenitum) or just the sigmoid colon (megasigma- megasigmoideum) with a sharp hypertrophy of the muscular layer of its wall. Congenital diseases are 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 of the large intestine, the intestinal contents stagnate, fecal stones form, inflammation joins (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 blind. Stenosis and atresia of the intestine lead to its obstruction (see. diseases of childhood).

Inflammation of the intestine can take place predominantly in the thin (enteritis) or large intestine (colitis) or spread more or less evenly throughout the intestines (enterocolitis).

Enteritis

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

Acute enteritis

Acute enteritis- acute inflammation of the small intestine.

Etiology. Often occurs in many infectious diseases (cholera, typhoid fever, colibacillary, staphylococcal and viral infection, sepsis, giardiasis, opisthorchiasis, etc.), especially with food toxic infections (salmonellosis, botulism), poisoning (chemical poisons, poisonous mushrooms, etc.). Famous acute enteritis alimentary (overeating, eating roughage, spices, spirits, etc.) and allergic (idiosyncrasy to food, drugs) origin.

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

At catarrhal enteritis, which occurs most often, the full-blooded and edematous intestinal mucosa is abundantly covered with serous, serous-mucous or serous-purulent exudate. Edema and inflammatory infiltration cover not only the mucous membrane, but also the submucosal layer. Degeneration and desquamation of the epithelium are noted, especially at the tops of the villi (catarrhal desquamative enteritis), hyperplasia of goblet cells ("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 membranous overlays appear on its surface. Depending on the depth of necrosis, inflammation may be croupy or diphtheria, in which, after rejection of fibrinous films, deep ulcers form.

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

At necrotizing ulcerative enteritis destructive processes can mainly concern the group and solitary lymphatic follicles of the intestine, as is observed in typhoid fever, or cover the mucous membrane out of touch with the lymphatic apparatus of the intestine. At the same time, necrosis and ulceration are widespread (flu, sepsis) or focal character(allergic vasculitis, periarteritis nodosa).

Regardless of the nature of inflammatory changes in the mucous membrane, acute enteritis develops hyperplasia and reticulomacrophage transformation of the lymphatic apparatus of the intestine. 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, their plasmacytic and reticulomacrophage 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, in 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, liver cirrhosis, 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 small intestine mucosa. exogenous factors are infections (staphylococcus, salmonella, viruses), intoxication, exposure to certain drugs (salicylates, antibiotics, cytostatic agents), long-term alimentary errors (abuse of spicy, hot, poorly cooked food), excessive consumption of coarse vegetable 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 intestine 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 epithelium of the crypts, differentiation of cells, their “advancement” along the villus and rejection into the lumen of the intestine. At first, these disorders consist in increased proliferation of the crypt epithelium, which seeks to replenish the rapidly shedding damaged villi enterocytes, but the differentiation of this epithelium into functionally complete enterocytes is delayed. As a result, most of the villi are 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, undergo cystic transformation and sclerosis. These changes are the final stage of disturbed physiological regeneration mucous membrane, develop it atrophy And structural adjustment.

Pathological anatomy. Changes in chronic enteritis have recently been well studied on the material of enterobiopsies.

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

For chronic enteritis without mucosal atrophy very characteristic is the uneven thickness of the villi and the appearance of club-shaped thickenings of their distal sections, 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. Adhesions, "arcades" appear between the enterocytes of the apical parts of the nearby villi, which is apparently associated with the formation of surface erosions; the stroma of the villi is infiltrated with plasma cells, lymphocytes, and eosinophils. The cellular infiltrate descends into crypts, which may be cystically dilated. The infiltrate pushes the crypts apart and reaches the muscular layer of the mucous membrane. If the changes described above concern only the villi, they speak of surface version this form of chronic enteritis, if they capture the entire thickness of the mucous membrane - about diffuse version.

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

Crypts are atrophied or cystically enlarged, their infiltration with lymphohistiocytic elements and replacement with growths of collagen and muscle fibers are noted. If atrophy concerns only the villi of the mucous membrane, and the crypts are little changed, they speak of hyper-regenerative variant 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, enterocyte dystrophy, polymorphic cell infiltration of the stroma; b - chronic atrophic enteritis; shortening of the villi, their deformation and fusion; pronounced lymphohistiocytic infiltration of the stroma

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

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

enteropathy

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

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

Pathological anatomy. Changes in various enteropathies are more or less the same and are reduced 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 the loss of microvilli (brush border), deepening of the crypts and thickening of the basement membrane, infiltration of the mucous membrane by plasma cells, lymphocytes, and macrophages. In the later stages, there is an almost complete absence of villi and a sharp sclerosis of the mucous membrane.

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). Histoenzymatic study of biopsies of the intestinal mucosa allows you to determine the enzyme disorders characteristic of a certain type of enteropathy, for example, a lack of enzymes that break down lactose and sucrose, with disaccharidase enteropathy. At celiac disease the diagnosis is made on the basis of the study of two enterobiopsies taken before and after the gluten-free diet.

Enteropathy is characterized by the same consequences as for severe chronic enteritis. They lead, in addition to the syndrome of impaired absorption, to hypoproteinemia, anemia, endocrine disorders, beriberi, edematous syndrome.

Whipple disease

Whipple 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 detection 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 disappear from the mucous membrane during antibiotic treatment and reappear when the disease is exacerbated.

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

Colitis

With colitis inflammatory process covers mostly the blind (typhlitis), transverse colon (transverse), 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 toxic-allergic colitis. TO infectious include dysentery, typhoid, colibacillary, staphylococcal, fungal, protozoal, septic, tuberculous, syphilitic colitis, to toxic - uremic, sublimate, medicinal, and to toxic-allergic - alimentary and coprostatic colitis.

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

At catarrhal colitis the mucous membrane of the intestine is hyperemic, edematous, accumulations of exudate are visible on its surface, which may have a serous, mucous or purulent character (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. Degeneration and necrobiosis of the epithelium are combined with desquamation of the surface epithelium and hypersecretion of the glands.

fibrinous colitis depending on the depth of necrosis of the mucous membrane and the penetration of fibrinous exudate, they are divided into croupous And diphtheritic (cm. Dysentery). Purulent colitis usually characterized by phlegmonous inflammation - phlegmonous colitis, phlegmon of the large intestine. In cases where multiple hemorrhages occur in the intestinal wall during colitis, areas of hemorrhagic impregnation appear, they speak of hemorrhagic colitis. At necrotizing colitis necrosis is often subjected not only to the mucous membrane, but also to the submucosal layer. gangrenous colitis- a variant of necrotic. Spicy ulcerative colitis usually completes diphtheritic or necrotic changes in the intestinal wall. In some cases, for example, with amebiasis, 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 secondarily. In some cases, it is genetically associated with acute colitis, in other cases this relationship is not traced.

Etiology. The factors causing chronic colitis are essentially the same as for acute colitis, ie. infectious, toxic And toxic-allergic. Of great importance is the duration of these factors in conditions of increased local (intestinal) reactivity.

Pathological anatomy. Changes in chronic colitis, studied on biopsy material, differ little from those in chronic enteritis, although they are more pronounced in colitis. inflammatory events, which are combined with dysregenerative and lead to atrophy And sclerosis mucous membrane. Guided by this, chronic colitis without mucosal atrophy and chronic atrophic colitis are distinguished.

At chronic colitis without mucosal atrophy the latter is edematous, dull, granular, gray-red or red, often with multiple hemorrhages and erosions. Flattening and desquamation of the prismatic epithelium, 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, in which hemorrhages occur, is infiltrated by 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 foci of ulceration.

For chronic atrophic colitis flattening of the prismatic epithelium, a decrease in the number of crypts, and hyperplasia of smooth muscle elements are characteristic. The mucosa is dominated by histioli-

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

Among the forms of chronic colitis, the so-called collagen colitis, which is characterized by the accumulation around the crypts of the mucous membrane of collagen, amorphous protein and immunoglobulins ("pericryptal fibroblast disease"). The development of this form of colitis is associated with a perversion 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, which is based on inflammation of the colon with suppuration, ulceration, hemorrhages and outcome in sclerotic deformation of the wall. This is a fairly common disease that occurs more often in young women.

Etiology and pathogenesis. In the occurrence of this disease, of course, the importance of local allergies, which is apparently caused by the intestinal microflora. In favor of the allergic nature of colitis, its combination with urticaria, eczema, bronchial asthma, rheumatic diseases, Hashimoto's goiter testifies. In the pathogenesis of the disease, autoimmunization is of great importance. This is confirmed by the detection in ulcerative colitis of autoantibodies fixed in the epithelium of the intestinal mucosa, the nature of the mucosal cellular infiltrate, 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 severe destruction of the intramural nervous apparatus of the intestine.

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

Morphological changes depend on the nature of the course 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 edematous, hyperemic, with multiple erosions and irregularly shaped superficial ulcers that coalesce and form large areas of ulceration. The islands of the mucous membrane preserved in these areas resemble polyps. (fringed pseudopolyps). Ulcers can penetrate into the submucosal and muscle layers, where fibrino-

Rice. 207. Nonspecific ulcerative colitis (drug Zh.M. Yukhvidova)

id 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 erosion of the walls are visible. Often there is perforation of the intestinal wall in the area of ​​the ulcer and intestinal bleeding. Such deep ulcers form pockets with necrotic masses that are rejected, the intestinal wall becomes thinner, and the lumen becomes very wide. (toxic dilatation). Individual ulcers undergo granulation, and the 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, neutrophils predominate in the infiltrate, which accumulate in crypts, where 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 epithelialization is usually incomplete, which is associated with the formation of extensive scar fields and chronic inflammation.

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

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

A manifestation of perverted reparation are 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). In the vessels, productive endovasculitis, sclerosis of the walls, obliteration of the lumen are noted; fibrinoid necrosis of the vessels is rare. Inflammation is predominantly productive and is expressed in the 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 intestinal polyposis, development of cancer, to general - anemia, amyloidosis, exhaustion, sepsis.

Crohn's disease

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

Crohn's disease previously meant a nonspecific granulomatous lesion of only the final section of the small intestine and therefore called it terminal (regional) ileitis. Later it was shown that the 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. have appeared.

Etiology and pathogenesis.The cause of Crohn's disease is not known. There are suggestions about the role of infection, genetic factors, hereditary predisposition of the intestine to the response to various

exposure to a stereotypical granulomatous reaction, autoimmunization. Among the pathogenetic theories, in addition to autoimmune, 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, culminating in destruction and granulomatosis of the intestinal wall.

Pathological anatomy. Most often, changes are found in the terminal ileum, in the rectum (especially in the anal part) and appendix; other localizations are rare. Amazed the entire thickness of the intestinal wall, which becomes sharply thickened and edematous. The mucous membrane is tuberous, reminiscent of a "cobblestone pavement" (Fig. 209), which is associated with the alternation of long, narrow and deep ulcers, which are arranged in parallel rows along the length of the intestine, with areas of normal mucous membrane. There are also deep slit 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 that look like tuberculosis. The lumen of the intestine is narrowed, fistulous passages are formed in the thickness of the wall. The mesentery is thickened, sclerosed. Regional lymph nodes are hyperplastic, white-pink in section.

The most characteristic microscopic sign 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 by lymphocytes, histiocytes, and plasma cells are also considered characteristic. submucosal layer, hyperplasia of its lymphoid elements, formation of slit-like ulcers (see fig. 209). Abscesses in the thickness of the wall, sclerosis and hyalinosis as a result of the evolution of diffuse infiltrate cells and granulomas often join these changes. With a long course, a sharp cicatricial deformation of the wall occurs.

Complication in Crohn's disease, there is a perforation of the intestinal wall with the formation of fistulous passages, in connection with which purulent or fecal peritonitis develops. Stenosis of various parts of the intestine is not uncommon, but more often the ileum, with symptoms of intestinal obstruction. Crohn's disease is considered a pre-cancer of the intestine.

Appendicitis

Appendicitis- inflammation of the appendix of the caecum, giving a characteristic clinical syndrome. From this it follows that in clinical and anatomical terms, not every inflammation of the appendix (for example, with tuberculosis, dysentery) is appendicitis. Appendicitis is a widespread disease that often requires surgery.

Rice. 209. Crohn's disease with damage to 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 enterogenic autoinfection. The flora vegetating in the intestine becomes pathogenic, the most important are Escherichia coli, Enterococcus. The study of possible conditions that promote the invasion of microbes into the wall of the process 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.

Angioedema theory pathogenesis of appendicitis is widespread. Built on a physiological basis (violations of the process kinetics as the starting point of the disease), it easily explains initial manifestations diseases (simple, superficial appendicitis) and those clinical cases when there are no morphological changes in the removed process. 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 L. Ashoff's concept of the progression of the primary affect.

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

Acute appendicitis. There are the following morphological forms of acute appendicitis: 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 in destruction and necrosis. It usually lasts 2-4 days.

Changes specific to acute simple appendicitis, develop within the first hours from the onset of an attack. They consist in 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 degenerative changes in the intramural nervous system of the process.

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, superficial 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 process wall - it develops phlegmonous appendicitis(Fig. 210). The dimensions of the process increase, its serous membrane becomes dull and full-blooded, a fibrinous coating appears on its surface (Fig. 211, see on color incl.); the wall on the incision is thickened, pus is released from the lumen. The mesentery is edematous, hyperemic. If multiple small pustules (abscesses) appear against the background of diffuse purulent inflammation of the process, they speak of apostematous appendicitis, if ulceration of the mucous membrane joins phlegmonous appendicitis - o phlegmonous-ulcerative appendicitis. Completes purulent-destructive changes in the process gangrenous appendicitis, which is called secondary, since it occurs as a result of the transition of the purulent process to the surrounding tissues (periappendicitis, see fig. 211), including on the mesentery of the process (mesenteriolite), which leads to thrombosis of the appendicular artery.

Secondary gangrenous appendicitis must be distinguished from gangrene of the appendix developing with primary thrombosis or thromboembolism of his artery. Obviously, therefore, gangrene of the appendix is ​​not quite aptly called primary gangrenous appendicitis.

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

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

Complications. In acute appendicitis, complications are associated with the destruction of the process and the spread of pus. Often occurs 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 process is closed, then the lumen of the distal part is stretched and develops. process empyema. The spread of the purulent process to the tissues surrounding the process and the caecum (periapendicitis, perityphlitis) accompanied by the formation of encysted abscesses, the transition of inflammation to the retroperitoneal tissue. Very dangerous development purulent thrombophlebitis of the vessels of the mesentery with its spread to the branches of the portal vein and the occurrence pylephlebitis(from Greek. pile- gates, flebos- vein). In such cases, thrombobacterial embolism of the portal vein branches 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 which inflammatory and destructive changes may appear. Usually, inflammation and destruction are replaced by the growth of granulation tissue in the wall and lumen of the process. Granulation tissue matures, turns into scar tissue. There is a sharp sclerosis and atrophy of all layers of the wall, obliteration of the lumen process, adhesions appear between the appendix and surrounding tissues. These changes can be combined with granulating and acute ulcers, histiolimphocytic and leukocyte infiltration of the appendix wall.

Sometimes, with cicatricial obliteration of the proximal process, serous fluid accumulates in its lumen and the process turns into a cyst - it develops edema of the process. If the contents of the cyst becomes the secret of the glands - mucus, then they talk about mucocele. Rarely, mucus due to the peristalsis of the process is collected in spherical formations (myxoglobules), which leads to myxoglobulosis process. When the cyst breaks and the mucus and cells that form it enter the abdominal cavity, these cells can be implanted on the peritoneum, which leads to its changes resembling a tumor - myxoma. In such cases, one speaks of pseudomyxome peritoneum.

About false appendicitis they say in cases where the clinical signs of an attack of appendicitis are not due to an 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 process is thinned, the mucous membrane is atrophic.

Intestinal tumors

Among intestinal tumors, epithelial - benign and malignant - are of the greatest importance.

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, blind and thin. Among intestinal adenomas, there are tubular, tubulo-villous And villous. Villous adenoma, which is a soft pink-red tissue with a villous surface (villous tumor) has a glandular-papillary structure. She can become malignant. With multiple adenomatous polyps, they talk about intestinal polyposis, which is familial.

Cancer occurs in both the small and large intestines. small intestine cancer rare, usually duodenum, in the area of ​​​​her large (vater's) nipple. The tumor does not reach a large size, very rarely causes difficulty in the outflow of bile, which is the cause of subhepatic jaundice, and is complicated by inflammation of the biliary tract.

colon cancer tends to increase, mortality from it increases. Of the various parts of the colon, cancer is more common in rectum, less often in the sigmoid, blind, hepatic and splenic angles of the transverse colon.

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

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

TO exophytic crayfish include plaque-like, polypous and large-tuberous, to 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, cricoid, squamous, glandular squamous, undifferentiated, unclassifiable cancer. Exophytic forms of cancer usually have the structure of adenocarcinoma, endophytic forms - the structure of cricoid or undifferentiated cancer.

Separately allocate anal cancers: squamous, 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 complicating diseases of the digestive system: perforation of a stomach or duodenal ulcer, intestinal ulcers in typhoid fever, ulcerative colitis, dysentery; it occurs as a complication of appendicitis, liver disease, cholecystitis, acute pancreatitis, etc.

Peritonitis can be limited to one or another part of the abdominal cavity - limited peritonitis or be common - diffuse peritonitis. More often it acute exudative peritonitis(serous, fibrinous, purulent), sometimes it can be feces, bile. At the same time, the visceral and parietal peritoneum is sharply hyperemic, with areas of hemorrhage, accumulations of exudate are visible between the intestinal loops, which, as it were, glues the loops. The 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, easily torn, 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. In the outcome of fibrinous peritonitis, adhesions are formed in the abdominal cavity, in some cases it develops chronic adhesive peritonitis(adhesive disease), which leads to intestinal obstruction.

Sometimes chronic peritonitis emerges "originally". It is usually limited perigastritis with gastric ulcer, perimetritis And perisalpingitis after childbirth or with a long-term infection (gonorrhea), pericholecystitis with calculosis of the gallbladder, periappendicitis without clinical manifestations of appendicitis in history. In such cases, sclerosis usually appears in a limited area of ​​the peritoneum, adhesions are formed, often disrupting the function of the abdominal organs.

Gastritis is a disease in which there is inflammation of the stomach lining. With gastritis, food in the stomach will be digested with some difficulty, which means that much more time will be spent on digesting food. To date, there are several types of 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 presented disease is diagnosed with the help of 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;
• Violation 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, then you should immediately contact a gastroenterologist. Otherwise, the disease will go into a more severe form, and then its treatment will require much more effort. Treatment must necessarily take place after consultation with a gastroenterologist, since the recovery process requires different therapeutic approaches.

Treatment for this form of gastritis usually consists of taking antibiotics and drugs that reduce the level of acid in the stomach. In addition, in the treatment of a superficial form of active gastritis, not only regular medication is required, but also a strict diet. The diet requires the following foods to be excluded from the diet:

• roast;
• salty;
• acute;
• fatty;
• 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 main functions of the stomach will not be affected, but the long-term course of the disease may be poorly reflected in the state 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 the study of biotite. Results may be affected by:

• low secretory activity of the glands of the gastric mucosa;
• wide gastric pits;
• thinned walls of the stomach;
• 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 12 duodenal ulcer, 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, it is imperative to take into account the course of the disease. Patients who suffer from this disease should be under the constant supervision of a gastroenterologist.

It is necessary to treat chronic atrophic gastritis for a week. In addition, in most cases, atrophic active gastritis is exacerbated due to the transfer of 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 indigestion and metabolic disorders.

One of the key elements of treatment is still a diet for chronic gastritis. Without the right diet, the effectiveness of therapy is sharply reduced and full recovery becomes impossible. About who and what menu is assigned, what and how you can eat, what dishes you need to exclude from your diet, as well as 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, have the necessary energy value.
• You should exclude or significantly limit foods with a lot of 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 is the doctor guided by when giving advice on the menu of his patient? Depending on the form of the disease, the presence of concomitant diseases (cholecystitis, pancreatitis) will be different and medical nutrition with 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 can be:

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

• Surface. It is characterized by a violation of the processes of nutrition and restoration of the epithelium of the stomach, the gastric mucosa is inflamed. Although the cells of the glands are altered, 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 are with superficial gastritis, but here the inflammatory infiltration of the gastric mucosa is already continuous, and the amount is also reduced - in fact, atrophy of the glands. As a result of these processes, there are signs of gastritis with low acidity. What else can be associated with and who has this type of gastritis? Often occurs in patients with cholecystitis, pancreatitis. Decreased acidity in this case, it can 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 proceeds with low, normal or high acidity, and also on what phase it is in - exacerbation or remission.

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

Diet during an exacerbation

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

• On the first day of exacerbation, it is recommended to refrain from eating, 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, steam cutlets, lean meat broth, compotes.

Diet without exacerbation

With the attenuation of the acute period, they 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 is preserved, 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. Six meals a day.

Features depend on acidity:

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

With gastritis with reduced secretion, diet number 2 can also be prescribed. According to this diet, you can not eat spicy dishes, snacks and spices, fatty meat. Exclude foods containing a large amount of fiber, whole milk, flour products.

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

Concomitant pathology

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

About drinking

An adequate amount of water is essential for successful treatment chronic gastritis is no less than all other nutrition. There are several rules according to which:

• The important thing is what kind of water to drink ─ it is better to boil tap water or buy bottled water.
• Water during the day can be drunk 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 the meal.
• During an exacerbation it is impossible, outside of it ─ it is highly undesirable to use 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 cannot be done at all.
• Avoid carbonated drinks!

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

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

There are features of taking mineral water in this case:

• 250 ml of warm mineral water is drunk 3 times a day for 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. Reception features:

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

Fruits and berries

With increased acidity, sour fruits and berries are prohibited, with low acidity, you can eat them little by little, melons and grapes are not recommended. You should also not take risks by trying the exotic: avocado, papaya.

But such a tasty berry as a watermelon can be afforded with gastritis.

Indeed, 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 aggravation. If you eat a few small slices of watermelon, then this can be done 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.

• Wash the apples and cut out the core.
• The mashed cottage cheese is mixed with sugar and raw egg and vanilla.
• The apples are filled with the resulting mass and sent to the oven, heated to 180 ° C for 10 minutes.

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

Illness and the pleasure of eating

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

If you search, there are many recipes for dishes that you can and should please yourself, even if you have chronic gastritis, and there is a need to eat according to a diet and you can’t eat a lot of things.

Biopsy of the stomach - conduct, risks

A biopsy is the taking of a small piece 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, allows you to relatively confidently judge the benign or malignant nature of neoplasms in the stomach. When identifying Helicobacter pylori its sensitivity and specificity is at least 90% (1).

Procedure technology: how and why is a biopsy done with EGD?

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

It was then that the first special probes began to be widely used. Initially, the sampling of a tiny piece of tissue was carried out without aiming, without visual control.

Modern endoscopes are equipped with sufficiently advanced optical equipment.

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

Now in use are not only devices that mechanically cut the material, but also electromagnetic retractors of a fairly perfect level. The patient does not have to worry that a medical specialist will blindly damage his mucosa.

A targeted biopsy is indicated when it comes to:

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

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

The number of specimens and the site from which they are obtained is determined taking into account the admitted diagnosis. In the case when infection with Helicobacter bacteria is assumed, material is studied at least from the antrum, and ideally from the antrum and body of the stomach.

Having found a picture characteristic of a polyposis, they examine directly a piece of the polyp.

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

If there are already signs indicating oncological changes, 6-8 samples are taken, and 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 repeated deep biopsy.

Radiography helps to make final conclusions about the presence or absence of a diffuse-infiltrative malignant process in the stomach, but early stages the development of such cancer is not carried out - due to low information content.

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

Is it harmful to the body?

The question is legitimate. It is unpleasant to imagine that something will be cut off from the gastric mucosa.

Professionals say that the risk is almost zero. The tools are tiny.

The muscle wall is not affected, the tissue is taken strictly from the mucous membrane. Subsequent pain, and even more so full-fledged bleeding, should not occur. Standing up almost immediately after taking a tissue sample is usually not dangerous. The patient will be able to safely go home.

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

In case of receiving alarming laboratory data, the patient may well be referred for surgery.

Contraindications for biopsy

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

In addition, it is impossible to insert a gastroscope tube into neurasthenics, patients with severe mental disorders. They may respond inappropriately to the sore 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", a project of the All-Russian Union of Public Associations "Association of Oncologists of Russia", Moscow, 2014

diagnosis of gastritis diagnosis of cancer diagnosis of ulcers

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

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

Tumor infiltrate refers to the development of various tumors - fibroids, sarcomas, malignant formations. 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 are formed on the surface of the skin or tissues of internal organs due to their artificial saturation. various substances- anesthetics, alcohol, antibiotics.

Varieties of inflammatory formations

IN medical practice the most common inflammatory infiltrate. Depending on the cells that fill the formation, the division into the following types is carried out:

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

Regardless of the nature of the origin, the inflammatory infiltrate can 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 appearance of pathology can also be the development of an allergic reaction, weak immunity, the presence of chronic diseases, idiosyncrasy organism.

Symptoms

Infiltrates of an inflammatory nature develop over several days. At this time, the following symptoms are observed:

• Body temperature remains normal or rises to subfebrile levels. In the latter case, its decrease does not occur for a long time.
• The affected area becomes slightly swollen. On palpation, a compaction is determined, which has clearly defined boundaries.
• When pressing on the formation, pain is felt, discomfort appears.
• The skin area in the affected area is slightly tense, has hyperemia.
• In the presence of an infiltrate, all layers of tissues are drawn into the pathological process - the skin, mucous membrane, subcutaneous fat, muscles, and the nearest 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 is reduced to the following:

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

If conservative treatment does not bring a positive result, resort to minimally invasive intervention. Most often, under the control of ultrasound devices, the affected area is drained with the removal of accumulated fluid. At severe course disease formation is opened surgically using laparoscopy or laparotomy.

Alternative treatment

If the infiltrate is not accompanied by severe symptoms, it is allowed to be treated folk remedies at home. They are very effective, help 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 infiltrate with folk remedies. The main thing is to follow the recommendations and consult a doctor even with a slight deterioration in the condition.