1. What are the layers of the stomach wall (mucosa with stratified squamous non-keratinizing, integumentary and glandular epithelium, basement membrane, submucosa, muscular and serous membranes, their fragments).

2. The degree of blood filling of the vessels:

— diffuse pronounced and pronounced venous-capillary plethora, with erythrostases, diapedetic hemorrhages, intravascular leukocytosis, intraluminal thrombosis, parietal thrombi, a picture of acute purulent, productive or polymorphocellular vasculitis;

- uneven blood supply to the vessels (some vessels are in a collapsed state, of weak and moderate blood supply, others are full-blooded);

- weak blood supply (vessels collapsed, with empty gaps or contain a small amount of blood).

3. The condition of the mucous membrane (thickened, thinned, with edema of the stroma, the presence of necrosis, focal or diffuse acute leukocyte infiltration, productive inflammation varying degrees expression, hemorrhage various types and prevalence, cellular reaction in them, Vishnevsky spots - in various stages).

4. Condition of the submucosa (thickened, loosened due to edema, focal or diffuse acute leukocyte infiltration, productive inflammation of varying severity, with hemorrhages of various types and prevalence, cellular reaction in them).

5. Condition of the muscular membrane (in a state of edema, with cell infiltration, necrosis, hemorrhage, replacement of smooth muscle cells with sclerosis or atypical tissue) .

6. The state of the serous membrane (thickened, with the presence of focal or diffuse acute leukocyte infiltration, productive inflammation of varying severity, the presence of hemorrhages of various types and prevalence, cellular reaction in them, the presence of blood deposits, fibrin, purulent-fibrinous exudate, the presence of tuberculous granulomas, giant multinucleated macrophages - cells Pirogov-Langgans or cells of foreign bodies, etc.).

Example number 1.

WALL OF THE STOMACH (2 objects) — pronounced diffuse venous-capillary plethora of all layers of the stomach wall, the lumen of the vessels is dilated, filled with blood, with erythrostasis, intravascular leukocytosis, parietal standing of leukocytes, diapedetic hemorrhages. The walls of a number of vessels with a picture of acute purulent and purulent-necrotic vasculitis. The phenomenon of intraluminal and parietal thrombosis. The sections show a sharply changed mucous membrane: thickened, with its subtotal necrosis, pronounced reactive leukocyte infiltration, the presence of small colonies bacterial microflora, in one of the objects - pronounced focal-diffuse destructive hemorrhages of dark red and brown-brown color, with unevenly expressed hemolysis of erythrocytes against the background of leukocyte infiltration. The submucosal base is sharply thickened, loosened, and defibrated due to edema, with pronounced hemorrhages of a destructive nature, with leukocyte infiltration, merging with each other, partially extending to the muscular membrane. Small and medium size foci of necrosis of the muscular membrane with leukocyte infiltration. The serous membrane is moderately thickened, loosened, with a few segmented neutrophilic leukocytes, focal thin overlays of loose fibrin.

Example #2

WALL OF THE ESOPHAGUS (1 object) - a pronounced diffuse venous-capillary plethora of all layers of the esophageal wall, the lumen of the vessels is dilated, filled with blood, with erythrostasis, intravascular leukocytosis, parietal standing of leukocytes, diapedetic hemorrhages. The mucous membrane is sharply thickened, with focal necrosis and hemorrhagic impregnation, leukocyte infiltration. Epithelial cells of the mucous membrane are sharply swollen . with a pronounced enlightenment of the cytoplasm, in a state of pronounced hydropic dystrophy. The submucosa is in a state of pronounced edema, with the presence of confluent diapedetic-destructive hemorrhages of a dark red color, with uneven hemolysis of erythrocytes, leukocyte infiltration extending to the muscular membrane. The serous membrane is not represented in these sections.

No. 09-8 / XXX 2008

Table № 1

Rice. 1-4. Fungal infection of the esophagus, presumably of a candidal nature. The mucous membrane in a state of necrosis is practically not traced, in its place there is a pronounced growth of the mycelium of the fungus with the presence of yeast-like round-oval bodies. Micellar filaments (hyphae) extend from basement membrane in the form of a dense "palisade". In the submucosa and partly in the muscular membrane against the background of a pronounced edema, between the thickened, loosened, split connective tissue fibers, there are elements of the fungus, macrophages, fibroblasts and round cell elements. Staining: hematoxylin and eosin. Magnification x 100, x 250, x 400. Separate microphotographs were taken with a closed aperture (1, 2, 4), the elements of the fungus gleam in them.

Inflammatory infiltrate. Symptoms and treatment of inflammation of the gastric mucosa

It is known that the degree of activity of the inflammatory process in chronic gastritis is determined by the severity of infiltration of epithelium and lamina propria by polymorphonuclear leukocytes against the background of infiltration by lymphocytes and plasma cells characteristic of chronic gastritis.

Activity - typical feature gastritis caused by H. pylori (Aruin L.I. et al., 1998). Neutrophils and macrophages are topographically associated with Hp colonization and migrate to the site of inflammation with the help of chemotaxis by stimulating the production of epithelial interleukin-8 and chemokines produced by Helicobacteria (Pasechnikov V.D., 2000; Kononov A.V., 1999). The degree of activity of the inflammatory process in chronic hepatitis is determined by the severity of infiltration by neutrophilic granulocytes of the epithelium and lamina propria (Aruin L.I., 1995; Aruin L.I., 1998; Svinitsky A.S. et al., 1999; Stolte M., Meining A , 2001; Khulusi S. et al., 1999). Urease and other mucolytic enzymes produced by HP reduce the viscosity of mucin, which leads to a weakening of intercellular bonds and an increase in the back diffusion of hydrogen ions, as a result, to damage to the gastric mucosa (Rozhavin M.A. et al., 1989; Slomiany B.L. et al. ., 1987).

Neutrophilic granulocytes are the most important morphological marker of an active inflammatory process; this is the first protective barrier against the penetration of bacteria and other pathogenic factors into the internal environment of the body. Neutrophils are highly active regulatory cells, a "single-celled secretory gland", whose products affect the nervous, immune systems, blood coagulation factors and reparative-plastic processes. The active role of iranulocytes and their mediators in the regulation of immunocyte functions was proven, and data were obtained on the production of peptide immunoregulatory factors, neutrophilokins by granulocytes (Dolgushin II et al., 1994). Immune and nervous system take part in the reparative regeneration of damaged tissues. Immunostimulatory neutrophilokines have a pronounced reparative activity. The authors found that the peptide fractions of activated neutrophils have a regulatory effect on lymphocytes, macrophages, neutrophils, on the nervous, endocrine and coagulation systems, and also enhance antimicrobial and antitumor resistance. All regulatory reactions of neutrophils are carried out with the help of various mediators secreted into the pericellular environment, including specific cytokines, which can be called neutrophilokines (Dolgushin II et al., 2000).

The search for antibacterial structures revealed a number of factors in leukocytes nonspecific resistance organism, including non-enzymatic cationic proteins discovered in the 60s of the XX century (Pigarevsky V.E., 1978; Badosi L., Trkeres M., 1985). The antibacterial action of non-enzymatic cationic proteins has been most studied. CB occupy one of the leading places in the implementation and coordination of nonspecific protective reactions of the body. They possess a wide range antimicrobial action, properties of an inflammatory mediator, permeability factors, a stimulator of metabolic processes,
nonspecific opsonins during phagocytosis (Mazing Yu.A., 1990). Deficiency of CB neutrophils, which largely form the antimicrobial potential of these cells, significantly aggravates the inefficiency of the host defense.

According to research by D.S. Sarkisov and A. A. Paltsyna (1992), during the implementation of the specific function of the neutrophil, its bactericidal and absorbing functions can change non-parallel. Decreased bactericidal activity while maintaining the level of absorption, in addition, the ability to kill bacteria, is depleted in neutrophils before the ability to absorb them, which is another outcome of incomplete phagocytosis. According to researchers, phagocytosis is not the main antibacterial agent microorganism, in particular, with wound infection. Their studies showed that the bulk of microbes in the wound are spatially dissociated from neutrophils and therefore cannot be eliminated directly by phagocytosis. The main point of the mechanism of the antimicrobial action of neutrophils is the melting and removal of dead tissues, and with them the accumulations of microorganisms located in them.

According to research by D.N. Mayansky (1991), neutrophil lysates, including cationic proteins contained in them, cause an influx of monocytes into the infiltration zone. After macrophage monocytes flood the inflammatory focus, the possibility remains for the secondary attraction of neutrophils into it. Macrophages and neutrophils rewarded with leukotrienes and other chemotaxins are subjected to secondary stimulation by living microbes or their products, and they are transformed into fully activated cells with maximally mobilized cytopathogenic potential (Mayansky D.N., 1991). Research by A.N. Mayansky et al. (1983) indicate the functional identity of the circulating and tissue pools of neutrophilic granulocytes.

Cytoplasmic granularity - mirror functional activity blood granulocytes. The functional significance of the cytoplasmic granularity of neutrophilic leukocytes is associated with the concept of lysosomes, which were discovered in 1955 by Christian de Duve. Bone marrow precursors of neutrophilic leukocytes synthesize a large number of lysosomal enzymes, which are isolated in azurophilic granules prior to use in the breakdown of phagocytosed particles. This fact gave grounds to consider azurophilic granules of neutrophils as lysosomes (Baggiolini M. ct al., 1969). Granules are formed sequentially, starting from the promyslocyte stage, to the stab leukocyte (Kozinets G.I., Makarov V.A., 1997; Le Kabec V. et al., 1997).

Azurophilic granularity is subdivided into large defensin-rich granules and smaller defensin-free granules (Borregaard N., Cowland J.B., 1997). After a short period of activity in the focus of inflammation, NGs are destroyed with the release of nuclear histones and lysosomal cationic proteins. This process is preceded by aggregation of granules and their marginal standing under the cell membrane. Damage to NG in the focus of inflammation is determined by staining for cationic proteins according to the modified method of Pigarevsky. A positive reaction to cationic proteins is given by two types of cationic granules: small (specific), creating a uniform staining of the cytoplasm, and larger (azurophilic), available for quantitative determination under a light microscope (Pigarevsky V.E., 1978). In addition, phagocytosed bacteria stain positively after their interaction with cationic proteins. Lysosomes of lymphocytes, monocytes, and macrophages lack cationic proteins, which makes it possible to differentiate granulocytes from other cell types.

Method of cytochemical detection of cationic proteins of granulocytes V.Ye. Pigarevsky (modified) is based on the application
dichromic dyes, somewhat laborious at the preparatory stage, requires precise adherence to the recipe for the preparation of reagents and staining conditions for preparations. It is unacceptable for the dye to dry on the sample during horizontal painting, which gives an indelible deposit. Excessive exposure of toluidine blue leads to restaining of the cellular material, which creates difficulties in the study.

Histones and lysosomal cationic NG proteins have high antibacterial activity and are involved in the formation of nonspecific anti-infective resistance of the organism. Their bactericidal action increases markedly with a decrease in pH. According to Talankin et al. (1989), damage to NG is accompanied by the release of cationic proteins outside the cells, while fatty vacuoles are determined in the cytoplasm, the nuclei of NG are hypersegmented, sometimes they are rounded, imitating a mononuclear cell. During cell decay, nuclei can undergo lysis or rexis (V.L. Belyanin, 1989). In low concentrations, CB contribute to an increase in permeability cell membranes and change the activity of enzymes in cells, in large cells they suppress many biochemical reactions, which indicates a possible regulatory role in the focus of inflammation (Kuzin M.I., Shimkevich, 1990).

G.A. Ivashkevich and D. Ayeggi (1984) as a result of studies of CB of blood neutrophils in purulent diseases observed a clear picture of a decrease in the content of cationic proteins inversely proportional to the severity of the process. The authors suggest that the activation of leukocytes during the inflammatory process is accompanied by the release of not only proteolytic enzymes, but also cationic proteins into the external environment. The same point of view is shared by I.V. Nesterova et al. (2005), whose studies showed a significant decrease in the content of neutrophil CB after stimulation with a bacterial culture, which indicates the potential consumption of CB, i.e. about their reserve capacity. Deficiency of CB neutrophils,
largely forming the antimicrobial potential of these cells, significantly exacerbates the inefficiency of the protection of the host organism (Mazing Yu.A., 1990).

Under light microscopy, the product of the cytochemical reaction to CB is found not only in the granularity of NG, but also extracellularly. Computer analysis of a cellular image, expanding the possibilities of light-optical research and creating mathematical analogues morphological features, allows you to objectify the quantitative assessment of CB (Slavinsky A.A., Nikitina G.V., 2000).

Sequential microspectrophotometry method - scanning. It will make it possible to measure the instantaneous values of the intensity of the light beam, to carry out the logarithm and their summation. Using the reference beam or rescanning the cell-free area of the preparation, the corresponding integral for the background is obtained. The difference between these two sums is the optical density integral, which is directly related to the amount of chromophore in the scan area (Avtandilov G.G., 1984).

When studying colored preparations in the visible part of the spectrum, the amount of dye associated with the test substance is determined. There should be a direct proportional relationship between the optical density, concentration and thickness of the dye layer, as well as the amount of the test substance. A change in the light-absorbing properties of the dye due to a change in its concentration occurs due to a change in the ionization, polymerization of the substance, which transforms the absorption coefficient.

According to research by N.G. A.A. Slavinsky and G.V. Nikitina (2001), CCS healthy people is 2.69 + _0.05 relative units, with peritonitis - 1.64 + _0.12 relative units. A.N. Mayansky et al. (1983) talking about

functional identity of the circulating and tissue pools of neutrophils.

Histopathology chronically infected with Helicobacter pylori (Hp) of the gastric mucosa is characterized by a high number of macrophages, neutrophils, eosinophils, basophils and lymphocytes, as well as tissue damage (Andersen L. et al., 1999). Neutrophils and macrophages are topographically associated with HP colonization and migrate to the site of inflammation via chemotaxis by stimulating the production of epithelial interleukin-8 and HP-produced chemokines. Participating in the phagocytosis of Helicobacteria, leukocytes stimulate the formation of leukotrienes (Pasechnikov VD, 1991). Being a pronounced chemotactic agent, LT-B4 attracts new leukocytes to the inflammation zone, followed by a cascade of vascular reactions, which leads to corresponding morphological changes in the gastric mucosa (Naccache R.N., 1983). Hp phagocytosis depends on bacterial strains and correlates with their ability to induce a "neutrophil respiratory burst" (production of toxic oxygen radicals - TOR), production of vacuolating cytotoxin (VacA). Hp are phagocytosed by both neutrophils and monocytes. The destruction of Hp was observed in vivo only with an excess of phagocytes. Intracellular survival of Hp is species-specific (Kononov A.V., 1999).

Helicobacteria have the ability to produce enzymes that neutralize bactericidal molecules, and use them for intracellular survival (Andersen L. I et al., 1999).

According to Hazell S.T. et al. (1991), Spigelhalder C. et al. (1993), urease, catalase, and superoxide dismutase are enzymes that neutralize bactericidal molecules and help HP avoid destruction in phagocytes. According to research by A.V. Kononova (1999), Hp express polypeptides that disrupt the production of cytokines by macrophages, which is manifested by a lower response of lymphocytes to
mitogen in Hp-associated individuals compared with uninfected individuals. The subminimal antigenic stimulus allows Hp to interact for a long time with the immune system of the mucous membranes, which causes chronic Hp infection. Hp elimination does not occur (Kononov A.V., 1999).

V.N. Galankin et al. (1991) considers the interaction of the NG system with bacterial agents from the standpoint of the concept of emergency response under the predominance of the force of bacterial action. Within the framework of four typical situations: 1st - the conflict between the initially insufficient NG system and the microflora, in which inflammation is an active reaction of the functionally insufficient system of the macroorganism, which, to the best of its ability, counteracts the usual bacterial environment, which, due to the weakness of the system, acquires the character of a pathogenic factor. In the 2nd situation, inflammation acts as a result of an active response of a functionally insufficient system to an opportunistic agent that has turned into a pathogenic one, due to a decrease in the physiological function of the NG system that counteracts it, that is, under conditions that are exclusive to the system. Situation 3 includes cases in which a functionally unchanged NG system interacts with a bacterial agent of an emergency nature. This emergency can be associated not only with the high pathogenicity and virulence of the microorganism, but also with supermassive contamination, in these cases, the system of nonspecific antibacterial protection from the very beginning is in a state of relative functional insufficiency and its response is exclusive. Situation 4 is characterized by a stable function of the NG system, sufficient to suppress the usual environmental bacterial environment. The commensalism of bacteria is determined not only by their internal qualities, but also by the presence of a stable system in the body that counteracts them. Such compromise relationships
resulting in an emergency, the body is able to maintain, subject to the stable constant operation of the antibacterial defense system, incl. NG, maintaining the state of clinical health. Thus, from the standpoint of 4 situations, inflammation can be considered as an exclusive form of response, which carries some inadequacy to the impact due to the emergency, a reflection of the active response of a functionally insufficient NG system to a bacterial impact that exceeds the capabilities of its physiological functioning. The superiority of the impact force over the possibilities of a quick response response - the functional insufficiency of the system, determines the extremeness of the situation. Reactions of an exclusive nature, in contrast to the physiological forms of adaptation, are reactions of a delayed type. They are energetically uneconomical in comparison with physiological ones, and are associated with the use of "reserve forces" of the system that are not included in physiological conditions, and are also characterized by a "cascading" deployment.

Thus, Helicobacter pylori infection, according to the gradation of interactions between macro- and microorganism V.N. Talankin and A.M. Tokmakova (1991), can be considered as an emergency situation, which is associated not only with the high pathogenicity and virulence of the microorganism, but also with supermassive contamination of the gastric mucosa. In this case, the system of nonspecific antibacterial protection from the very beginning is in a state of relative functional insufficiency and its response is really exclusive (Galankin V.N., Tokmakov A.M., 1991).

A.S. Zinoviev and A.B. Kononov (1997) in their studies showed the conjugation of the reactions of inflammation, immunity and regeneration in the mucous membranes, proving that the structure that provides the functions

protection and recognition of "friend or foe", as well as regulating the processes of regeneration, is the lymphoid tissue associated with mucous membranes.

T-lymphocytes of the lamina propria are represented by a population of CO8+-lymphocytes that have cytotoxic properties and make up the bulk of interepithelial lymphocytes, NK-cells that carry out antitumor and antiviral surveillance, and T-xclpsrs with the CD3 phenotype antigen-presenting cells during inflammation. The following types of lymphoproliferative response of the GM in Hp infection are distinguished: lymphoepithelial lesions and minimal infiltration of the lamina propria with lymphocytes, the formation of lymphoid follicles, a combination of lymphoid follicles and diffuse infiltration, as well as an extreme degree of lymphoproliferative response - low-grade lymphoma - MALToma. The immunophenotype of lymphoid cells in reactive processes is B- and T-cell, in lymphoma - B-cell (Kononov A.V., 1999). However, the degree

mononuclear infiltration of the lamina propria does not reflect the intensity of local immunity. It is assumed that HP express polypeptides that disrupt the production of cytokines by macrophages, which is manifested by a lower response of lymphocytes to a mitogen in HP-infected individuals. The subminimal antigenic stimulus allows HP, according to the author, to interact for a long time with the immune system of SO, which leads to the chronicity of HP infection. During the Hp-infectious process, antibodies to the mucosa appear
membrane of the antrum, that is, the autoimmune component is realized in the pathogenesis of Hp-associated diseases.

O.K. Khmelnitsky and B.V. Sarantsev (1999). According to the authors, in the general immune status, the content of T-active lymphocytes in the blood serum averaged 52.9% (normal 28-33%). Celebrated gradual decline of this indicator in cases of presence of dysplastic changes in the epithelium of the gastric mucosa with a tendency to decrease in the presence of early and invasive cancer, but still increased compared to normal indicators. Interepithelial lymphocytes that occurred in chronic hepatitis disappeared in cases of epithelial dysplasia, early and invasive cancer. Plasma cells that produce IgA immunoglobulins, IgM were present in CG and epithelial dysplasia, while they were absent in early and invasive cancer. The fall in the content of MEL and the production of immunoglobulins of the IgA and IgM classes can serve, according to the authors, as indicators that objectify the verification of the pathological process. M.P. Bobrovskikh et al. indicate that the presence of Hp reflects local disturbances in the immunostructural homeostasis of the mucosa and is characterized by phenomena of secondary immunodeficiency, which is confirmed by the high detectability of Hp in the stomach in cancer of extragastric localization. B.Ya. Timofeev et al. (1982) in the study of smears-imprints in precancerous diseases of the stomach, they obtained a dependence of the severity of the stromal reaction on the severity of the proliferation of the epithelium of the gastric mucosa, which, according to
authors, can serve as a method for assessing mononuclear stromal infiltration in the wall of the stomach.

In the early 1990s, a causal relationship was established between Helicobacter pylori infection and the development of primary MALT lymphoma. R. Genta, H. Hamner et al. (1993) showed that Hp is an antigenic stimulus that triggers a complex cascade of B- and T-cell immunological reactions with induction in some cases in B-cell lymphoma of the MALT-type marginal zone. Characteristic features of MALT are predominantly local distribution, association with Hp, they bear the features of a low-grade tumor and the absence of a tendency to early dissemination.

Diffuse changes in the structure of soft tissues can be in the form of atrophy, degeneration [fatty, fibrous (scar-adhesive process) or combined!, inflammatory infiltration. Focal changes in the structure of soft tissues look like cicatricial restructuring, limited inflammatory infiltrate, volumetric formations of traumatic genesis (hematoma, seroma, cyst, neuroma), ectopic (heterotopic) ossificates. According to clinical and radiological research methods, their size, localization, contours, density are determined.

Diffuse changes in the soft tissues of the stump

Atrophy. There are several methods to objectively assess the degree of atrophy of the soft tissues of the stump.

Unlike clinical and functional research methods, based on the results radiodiagnosis it is possible to produce with high certainty:

direct measurements and comparative analysis of the thickness of the soft tissues of the proximal sections of the truncated segment and skin-fascio-muscular flaps above the sawdust;
assessment of the structure and homogeneity of tissues in strictly symmetrical areas of the limbs.

X-ray with atrophy, there is a thinning of the subcutaneous fat, a decrease in its density, a violation of the differentiation of soft tissues. The muscles look heterogeneous, spotting appears in the form of spindle-shaped areas of enlightenment in the projection of individual myofascial groups.

With ultrasound, a decrease in the thickness of tissues is determined, a change in their structure: multiple small hyper- and hypoechoic inclusions are visualized, the number of fibrous septa decreases.

The greatest information content in determining the degree of stump atrophy at the studied levels is given by SCT. It allows you to fix signs of minor atrophy, accompanied by thinning of soft tissues by less than 1/4 of their thickness compared to the original (with a healthy limb). If this ratio is 1/2, then the changes are classified as moderate.

Cases where the thickness of the soft tissues in the proximal parts of the stump decreases by more than 1/2 compared with a healthy limb are considered as severe atrophy. Using this research method, moderate atrophic changes in soft tissues are detected in 58.3% of cases and pronounced in 25% of patients with amputated limb stumps.

The skin-fascio-muscular flap over the bone sawdust deserves special attention. Its thickness should average 2.5-3 cm. In some cases, with significant changes, soft tissues in the coronal part of the stump appear only as skin and subcutaneous tissue, their thickness does not exceed 0.5 cm.

Situations that manifest moderate or significant atrophy of the soft tissues of the stump with their sharp thinning over the bone sawdust require a revision of the treatment tactics (surgical correction, changes in the principles of patient rehabilitation) in preparation for prosthetics.

Diffuse degenerative changes in soft tissues can be accompanied by both their thinning and thickening.

In the course of studies of the state of the stump during its formation and preparation for prosthetics, degenerative changes were graded into four types: muscle, fat, fibrous, and combined.

muscle type the stump is characterized by a relative decrease in the volume of tissues, the absence of a violation of the differentiation of muscles and the subcutaneous fat layer of the truncated limb. Structural changes are manifested by cicatricial adhesions, well detected by ultrasound.
fat type differed by the presence of a narrow ring of muscle tissue enveloping the bone, and a pronounced subcutaneous fat layer. In almost 80% of cases, with this type of restructuring, the circumference of the stump decreases compared to a healthy limb at a symmetrical level.
Stumps fibrous type have a cone-shaped or irregular shape, pronounced cicatricial adhesive changes in muscles, subcutaneous fat over a considerable extent. Soft tissues thicken, become thinner, become inactive, soldered to each other and to the bone. The volume of the stump usually decreases, it acquires a cone-shaped or irregular shape, only in 10% of cases these changes are accompanied by an increase in the thickness of tissues in the proximal parts of the stump and above the bone sawdust (up to 5-6 cm).

Diffuse inflammatory infiltration

On radiography, inflammatory infiltration is defined as a zone of increased density with loss of differentiation of all soft tissue structures. The shadow of the subcutaneous fat merges with the shadow of the muscles, their contour becomes fuzzy and uneven.

However, the listed signs cannot be considered as reliable criteria for inflammatory infiltration, they do not allow to accurately determine its severity, to obtain a spatial idea of the localization and prevalence of the process. The most valuable information in these situations is provided by ultrasound and CT.

On echograms, diffuse inflammatory changes look like extensive areas of reduced echogenicity without clear contours, heterogeneous structure, accompanied by lymphoid edema of the subcutaneous fat. The skin thickens up to 0.7-1 cm, while the inner contour of the dermis is not clearly visible. The echogenicity of muscle tissue decreases due to edema. Necrotic changes in individual muscles or muscle groups are also accompanied by a pronounced decrease in echogenicity and “blurring” of the ultrasound pattern. SKT-signs of diffuse inflammatory changes are manifested by thickening of the skin and subcutaneous fat with an increase in their density. In the muscles, zones of liquid or soft tissue density, heterogeneous structure with fuzzy and uneven contours can be traced. Air bubbles can be observed in the tissues, which are the result of revisions of purulent wounds.

Focal change in the structure of soft tissues

Focal cicatricial changes in the stumps of the lower extremities occur in 80-85% of patients after amputations performed for injuries. They are characterized by the presence of areas of deformation and thinning of soft tissues that have arisen as a result of necrobiotic changes due to the mechanism of damage, high intersection of blood vessels and nerves, traumatization of tissues when using a prosthesis, etc. In addition, focal changes in the structure of soft tissues look like limited inflammatory infiltrates, volumetric formations of traumatic origin, the most common of which are hematomas, seromas, false cysts, neuromas.

Abscesses in the area of postoperative wounds of the stumps are diagnosed in 23.3% of patients. The skin over the inflammatory infiltrate is thickened (up to 0.7-1 cm), with an indistinct internal contour, signs of lymphoid edema in the subcutaneous fat.

education fistula inflammatory processes on the stumps are accompanied in 10.8% of cases. On echograms, the fistulous tract is visualized as a tubular structure with smooth and clear contours, reduced echogenicity.

Hematomas limb stumps after amputations performed due to injuries are observed in 20.4% of patients. On the first day after their occurrence, according to ultrasound data, in the soft tissues of the amputated limbs, there are areas of reduced echogenicity, often of an irregular shape, with uneven, fuzzy outline. With prolonged existence of hematomas, heterogeneous echogenic parietal layers are located along their edge - areas of organization and formation of the capsule.

However, according to ultrasound data, it is impossible to accurately determine the amount of blood flowing and the size of hematomas. These characteristics could only be obtained from the results of SCT. Gradually, fibrin settles on the walls of the cavity in which the blood was located, a capsule is formed and the hematoma is transformed into gray and then in false cyst.

Revealing terminal neuromas refers to one of the most difficult tasks in assessing the condition of the stump before prosthetics and requires a particularly thorough standardized approach. There is no direct relationship between complaints and the presence of neuromas in patients with amputated stumps. In half of the cases, they exist as asymptomatic tumor-like growths of nerves associated with their damage and subsequent regeneration.

Only in 50-65% of cases, neuromas are accompanied by local or phantom pain, which occurs if the cut end of the nerve enters a scar, an inflammatory infiltration zone, or is squeezed when using a prosthesis.

As a result of the study of limb stumps after amputations performed for injuries, analysis, standardization and recording of the main semiotic signs of diseases and defects of the stump(an example of a standardized protocol for describing the state of the stump of the lower limb is given).

What is an inflammatory infiltrate

To designate such forms of inflammatory diseases, many authors use the terms "beginning phlegmon", "phlegmon in the stage of infiltration" that are contradictory in meaning, or generally omit the description of these forms of the disease. At the same time, it is noted that forms of odontogenic infection with signs serous inflammation perimaxillary soft tissues are common and in most cases respond well to treatment.

With timely started rational therapy, it is possible to prevent the development of phlegmon and abscesses. And this is justified from a biological standpoint. The vast majority of inflammatory processes should end and undergo involution at the stage of swelling or inflammatory infiltrate. The option with their further development and the formation of abscesses, phlegmon is a disaster, tissue death, i.e. parts of the body, and when spreading purulent process on several areas, sepsis - often death. Therefore, in our opinion, the inflammatory infiltrate is the most frequent, most "expedient" and biologically substantiated form of inflammation. In fact, we often see inflammatory infiltrates in the maxillary tissues, especially in children, with pulpitis, periodontitis, regarding them as reactive manifestations of these processes. A variant of the inflammatory infiltrate are periadenitis, serous periostitis. The most essential for the doctor in the assessment and classification of these processes (diagnosis) is the recognition of the non-purulent stage of inflammation and the appropriate treatment tactics.

What provokes an inflammatory infiltrate

Inflammatory infiltrates make up a group that is diverse in terms of etiological factor. Studies have shown that 37% of patients had a traumatic genesis of the disease, in 23% the cause was an odontogenic infection; in other cases, infiltrates occurred after various infectious processes. This form of inflammation occurs with the same frequency in all age groups.

Symptoms of the inflammatory infiltrate

Inflammatory infiltrates arise both due to the contact spread of the infection (per continuitatum) and the lymphogenous pathway when the lymph node is affected with further tissue infiltration. The infiltrate usually develops within a few days. The temperature in patients is normal and subfebrile. In the area of the lesion, swelling and thickening of tissues occur with relatively clear contours and spread to one or more anatomical regions. Palpation is painless or slightly painful. Fluctuation is not defined. The skin in the area of the lesion is of normal color or slightly hyperemic, somewhat tense. There is a lesion of all soft tissues of this area - skin, mucous membrane, subcutaneous fat and muscle tissue, often several fascias with the inclusion of lymph nodes in the infiltrate. That is why we prefer the term "inflammatory infiltrate" to the term "cellulite", which also refers to such lesions. The infiltrate can be resolved into purulent forms of inflammation - abscesses and phlegmon, and in these cases it should be considered as a pre-stage of purulent inflammation, which could not be stopped.

Inflammatory infiltrates can have a traumatic origin. They are localized in almost all anatomical regions. maxillofacial region, somewhat more often in the buccal and floor of the mouth. Inflammatory infiltrates of post-infectious etiology are localized in the submandibular, buccal, parotid-masticatory, submental areas. The seasonality of the occurrence of the disease (autumn-winter period) is clearly traced. Children with inflammatory infiltrate often come to the clinic after the 5th day of the disease.

Diagnosis of inflammatory infiltrate

Differential diagnosis of inflammatory infiltrate carried out taking into account the identified etiological factor and the duration of the disease. Diagnosis is confirmed by normal or subfebrile temperature bodies, relatively clear contours of the infiltrate, no signs of purulent fusion of tissues and sharp pain on palpation. Other less pronounced hallmarks serve: the absence of significant intoxication, moderate hyperemia of the skin without revealing tense and shiny skin. Thus, the inflammatory infiltrate can be characterized by the predominance of the proliferative phase of inflammation of the soft tissues of the maxillofacial region. This, on the one hand, indicates a change in the reactivity of the child's body, on the other hand, it is a manifestation of natural and therapeutic pathomorphosis.

The greatest difficulty for differential diagnosis represent purulent foci localized in spaces delimited from the outside by muscle groups, for example, in the infratemporal region, under m. masseter, etc. In these cases, the increase in symptoms acute inflammation determines the forecast of the process. In doubtful cases, the usual diagnostic puncture of the lesion helps.

In the morphological study of the biopsy from the inflammatory infiltrate, cells typical of the proliferative phase of inflammation are found in the absence or a small number of segmented neutrophilic leukocytes, the abundance of which characterizes purulent inflammation.

In infiltrates, accumulations of yeast and filamentous fungi of the genus Candida, Aspergillus, Mucor, Nocardia are almost always found. Around them, epithelioid cell granulomas are formed. Mycelium of mushrooms is characterized dystrophic changes. It can be assumed that the long phase of the productive tissue reaction is supported by fungal associations, reflecting the possible phenomena of dysbacteriosis.

Treatment of inflammatory infiltrate

Treatment of patients with inflammatory infiltrates- conservative. Anti-inflammatory therapy is carried out using physiotherapeutic agents. Give a pronounced effect laser irradiation, dressings with Vishnevsky ointment and alcohol. In cases of suppuration of the inflammatory infiltrate, phlegmon occurs. Then surgical treatment is carried out.

Which doctors should be contacted if you have an inflammatory infiltrate

Infectionist

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Algorithm and examples of description of micropreparations of the wall of the esophagus, stomach, intestines.

Public Health Institution

« SAMARA REGIONAL BUREAU OF FORENSIC MEDICAL EXAMINATION »

To "Expert's Conclusion" No. 09-8 / XXX 2007

Table № 2

Rice. 2. In the sections of one of the objects, a strip-like fragment of adipose tissue with thin layers of fibrous connective tissue, groups of plethoric vessels is shown, along the edge of the sections there is a narrow strip-like fragment of fibrous connective tissue with signs of pronounced polymorphocellular inflammation with a predominance of the productive component (arrow). On the surface of the connective tissue, there are widespread moderately pronounced strip-like overlays of compactly located erythrocyte masses of dark red color, with focal uneven hemolysis of erythrocytes, a small and moderate number of leukocytes, and a thin thread-like inclusion of loose fibrin. Staining: hematoxylin and eosin. Magnification x 100.

Forensic medical expert Filippenkova E.I.

97 STATE CENTER

FORENSIC AND FORENSIC EXAMINATIONS

CENTRAL MILITARY DISTRICT

443099, Samara, st. Venceka, d. 48 tel. 339-97-80, 332-47-60

CONCLUSION OF THE SPECIALIST No.XXX 2011

Table № 3

Specialist E. Filippenkova

Public Health Institution

« SAMARA REGIONAL BUREAU OF FORENSIC MEDICAL EXAMINATION »

To the "Act of Forensic Histological Research" No. 09-8 / XXX 2008

Table № 4




Rice. 1-10. The body of a man, 24 years old. Found on the street unconscious, died in the emergency department of the hospital. In the blood - drug metabolites. During internal examination of the corpse, the stomach, small and large intestines collapsed, with empty gaps. Under microscopy in the thickness of the gastric mucosa of various sizes, hemorrhages are rich and dark red in color, fibrinoid necrosis with hemorrhages (some of them are mushroom-shaped). Thrombosis of a number of vessels of the mucous membrane and submucosa. Stain: hematoxylin-eosin. Magnification x100, x250, x400.

Forensic medical expert E.I.Filippenkova

MINISTRY OF DEFENSE OF THE RUSSIAN FEDERATION

97 STATE CENTER

Digestion is carried out by a single physiological system. Therefore, the defeat of any department of this system causes a disorder of its functioning as a whole. Diseases of the digestive system are detected in more than 5% of the world's population.

The etiology of pathological processes developing in the gastrointestinal tract includes several main factors.

FACTORS DAMAGED TO THE DIGESTIVE ORGANS

Physical nature:

rough, poorly chewed or unchewed food;
foreign bodies - buttons, coins, pieces of metal, etc.;
excessively cold or hot food;
ionizing radiation.

Chemical nature:

alcohol;
tobacco combustion products that enter the gastrointestinal tract with saliva;
drugs, such as aspirin, antibiotics, cytostatics;
toxic substances that penetrate the digestive organs with food - salts heavy metals, mushroom toxins, etc.

biological nature:

microorganisms and their toxins;
helminths;
excess or lack of vitamins, such as vitamin C, group B, PP.

Disorders of the mechanisms of neurohumoral regulation- deficiency or excess of biogenic amines - serotonin, melanin, hormones, prostaglandins, peptides (for example, gastrin), excessive or insufficient effects of the sympathetic or parasympathetic system (with neuroses, prolonged stress reactions, etc.).

Pathogenic factors associated with the defeat of others physiological systems, for example, fibrinous gastroenteritis and colitis with uremia that develops as a result of renal failure.

PATHOLOGY OF INDIVIDUAL DIGESTIVE ORGANS

DIGESTIVE DISORDERS IN THE MOUTH

The main causes of this pathology can be eating disorders as a result:

inflammatory diseases of the oral cavity;
lack of teeth;
jaw injuries;
violations of the innervation of the chewing muscles. Possible consequences:
mechanical damage to the gastric mucosa by poorly chewed food;
violation of gastric secretion and motility.

DISTURBANCES OF EDUCATION AND SALIVATION - SALIVATION

Kinds:

Hyposalivation up to the cessation of formation and secretion of saliva into the oral cavity.

Consequences:

insufficient wetting and swelling of the food bolus;
difficulty chewing and swallowing food;
development of inflammatory diseases of the oral cavity - gums (gingivitis), tongue (glossitis), teeth.

hypersalivation - advanced education and secretion of saliva.

Consequences:

dilution and alkalization of gastric juice with excess saliva, which reduces its peptic and bactericidal activity;
acceleration of the evacuation of gastric contents into the duodenum.

Angina, or tonsillitis , a disease characterized by inflammation lymphoid tissue pharynx and palatine tonsils.

The reason for the development different types of angina are streptococci, staphylococci, adenoviruses. Importance at the same time, they have sensitization of the body and cooling of the body.

Flow angina can be acute and chronic.

Depending on the characteristics of inflammation, several types of acute tonsillitis are distinguished.

Catarrhal angina characterized by hyperemia of the tonsils and palatine arches, their edema, serous-mucous (catarrhal) exudate.

Lacunar angina , in which the catarrhal exudate is mixed significant amount leukocytes and deflated epithelium. The exudate accumulates in the lacunae and is visible on the surface of the edematous tonsils in the form of yellow spots.

Fibrinous angina characterized by diphtheria. in which a fibrinous film covers the mucous membrane of the tonsils. This sore throat occurs with diphtheria.

Follicular angina characterized by purulent fusion of the tonsil follicles and their sharp swelling.

Quinsy , in which purulent inflammation often passes to the surrounding tissues. The tonsils are swollen, sharply enlarged, plethoric.

Necrotic angina characterized by necrosis of the mucous membrane of the tonsils with the formation of ulcers and hemorrhages.

Gangrenous tonsillitis may be a complication of necrotic and is manifested by the collapse of the tonsils.

Necrotic and gangrenous tonsillitis occur with scarlagina and acute leukemia.

Chronic angina develops as a result of repeated relapses acute tonsillitis. It is characterized by hyperplasia and sclerosis of the lymphoid tissue of the tonsils, their capsules, and sometimes ulceration.

Complications of angina are associated with the transition of inflammation to the surrounding tissues and the development of a peritonsillar or pharyngeal abscess, cellulitis of the pharynx. Recurrent tonsillitis contribute to the development of rheumatism and glomerulonephritis.

PATHOLOGY OF THE ESOPHAGUS

Esophageal disorders are characterized by:

difficulty moving food through the esophagus;
reflux of stomach contents into the esophagus with the development of gastroesophageal reflux, which is characterized by belching, regurgitation, or regurgitation, heartburn, aspiration of food into the respiratory tract.

Belching- uncontrolled release of gases or small amounts of food from the stomach into the esophagus and oral cavity.
regurgitation or regurgitation,- involuntary reflux of part of the gastric contents into the oral cavity, less often - the nose.
Heartburn- burning sensation in the epigastric region. It is the result of the reflux of acidic stomach contents into the esophagus.

DISEASES OF THE ESOPHAGUS

Esophagitis- inflammation of the mucous membrane of the esophagus. The course can be acute and chronic.

Causes of acute esophagitis are the actions of chemical, thermal and mechanical factors, as well as a number of infectious agents (diphtheria, scarlet fever, etc.).

Morphology.

Acute esophagitis is characterized by various types of exudative inflammation, and therefore it can be catarrhal, fibrinous, phlegmonous, gangrenous, and ulcerative. Most often, chemical burns of the esophagus occur, after which the necrotic mucosa is separated in the form of a cast of the esophagus and is not restored, and scars form in the esophagus, sharply narrowing its lumen.

Causes of chronic esophagitis are constant irritations of the esophagus by alcohol, hot food, tobacco smoking products and other irritating substances. It can also develop as a result of circulatory disorders in the esophagus with congestion in it due to chronic heart failure, cirrhosis of the liver and portal hypertension.

Morphology.

In chronic esophagitis, the epithelium of the esophagus is exfoliated, it metaplasia into a keratinized stratified squamous ( leukoplakia), wall sclerosis.

Esophageal cancer accounts for 11-12% of all cancer cases.

Morphogenesis.

The tumor usually develops in middle third esophagus and circularly sprouts its wall, squeezing the lumen, - annular cancer . Often the disease takes the form cancerous ulcer with dense edges, located along the esophagus. Histologically, esophageal cancer has a structure squamous cell carcinoma with or without keratinization. If the cancer develops from the glands of the esophagus, it has the character of adenocarcinoma.

Metastasizes esophageal cancer by lymphogenous route to regional lymph nodes.

Complications associated with germination in the surrounding organs - the mediastinum, trachea, lungs, pleura, while purulent inflammatory processes may occur in these organs, from which the death of patients occurs.

The main function of the stomach is the digestion of food. which includes partial breakdown of the components of the food bolus. This occurs under the influence of gastric juice, the main components of which are proteolytic enzymes - pepsins, as well as hydrochloric acid and mucus. Pepsins loosen food and break down proteins. Hydrochloric acid activates pepsins, causes denaturation and swelling of proteins. Mucus prevents damage to the stomach wall by the food bolus and gastric juice.

Digestive disorders in the stomach. At the heart of these violations are disorders of the functions of the stomach.

Disorders of the secretory function , which cause a discrepancy between the level of secretion of various components of gastric juice and their needs for normal digestion:

violation of the dynamics of secretion of gastric juice in time;
increase, decrease in the volume of gastric juice or its absence;
violation of the formation of hydrochloric acid with an increase, decrease or lack of acidity of gastric juice;
increase, decrease or cessation of formation and secretion of pepsin;
achilia - complete cessation of secretion in the stomach. Occurs with atrophic gastritis, stomach cancer, diseases of the endocrine system. In the absence of hydrochloric acid, the secretory activity of the pancreas decreases, the evacuation of food from the stomach accelerates, and the processes of food decay in the intestine increase.

Motor function disorders

Types of these violations:

violations of the tone of the muscles of the stomach wall in the form of its excessive increase (hypertonicity), excessive decrease (hypotonicity) or absence (atony);
disorders of the tone of the sphincters of the stomach in the form of its decrease, which causes the gaping of the cardiac or pyloric sphincter, or in the form of an increase in the tone and spasm of the muscles of the sphincters, leading to cardiospasm or pylorospasm:
violations of the peristalsis of the stomach wall: its acceleration - hyperkinesis, slowing down - hypokinesis;
acceleration or delay in the evacuation of food from the stomach, which leads to:
- - fast satiety syndrome with a decrease in tone and motility of the antrum of the stomach;
- - heartburn - burning sensation in the lower part of the esophagus as a result of a decrease in the tone of the cardiac sphincter of the stomach, lower
- it is the sphincter of the esophagus and the reflux of acidic gastric contents into it;
- - vomiting - an involuntary reflex act, characterized by the release of the contents of the stomach out through food and water, pharynx and oral cavity.

DISEASES OF THE STOMACH

The main diseases of the stomach are gastritis, peptic ulcer and cancer.

Gastritis- inflammation of the gastric mucosa. Allocate spicy And chronic gastritis, however, these concepts mean not so much the time of the process as morphological changes in the stomach.

Acute gastritis

Causes acute gastritis can be:

nutritional factors - Poor quality, coarse or spicy food;
chemical irritants - alcohol, acids, alkalis, some medicinal substances;
infectious agents - Helicobacter pylori, streptococci, staphylococci, salmonella, etc.;
acute circulatory disorders in shock, stress, heart failure, etc.

Classification of acute gastritis

By localization:

diffuse;
focal (fundal, antral, pyloroduodenal).

According to the nature of inflammation:

catarrhal gastritis, which is characterized by hyperemia and thickening of the mucous membrane, hypersecretion of mucus, sometimes erosion. In this case, one speaks of erosive gastritis. Microscopically observed degeneration and desquamation of the surface epithelium, serous-mucous exudate, blood vessels, edema, diapedetic hemorrhages;
fibrinous gastritis is characterized by the fact that a fibrinous film of gray-yellow color is formed on the surface of the thickened mucous membrane. Depending on the depth of mucosal necrosis, fibrinous gastritis may be croupous or diphtheritic;
purulent (phlegmonous) gastritis is a rare form of acute gastritis that complicates injuries, ulcers, or ulcerated stomach cancer. It is characterized by a sharp thickening of the wall, smoothing and coarsening of the folds, purulent overlays on the mucous membrane. Microscopically, diffuse leukocyte infiltration of all layers of the stomach wall, necrosis and hemorrhages in the mucous membrane are determined;
necrotic (corrosive) gastritis is a rare form that occurs with chemical burns of the gastric mucosa and is characterized by its necrosis. With the rejection of necrotic masses, ulcers form.

Complications of erosive and necrotic gastritis there may be bleeding, perforation of the stomach wall. With phlegmonous gastritis, mediastinitis, subphrenic abscess, liver abscess, purulent pleurisy occur.

Outcomes.

Catarrhal gastritis usually ends in recovery; with inflammation caused by infection, a transition to a chronic form is possible.

Chronic gastritis- a disease characterized by chronic inflammation gastric mucosa, impaired regeneration and morphofunctional restructuring of the epithelium with the development of glandular atrophy and secretory insufficiency, underlying digestive disorders.

The leading symptom of chronic gastritis is dysregeneration- violation of the renewal of epithelial cells. Chronic gastritis accounts for 80-85% of all stomach diseases.

Etiology chronic gastritis is associated with prolonged action of exogenous and endogenous factors:

infections, primarily Helicobacter pylori, which accounts for 70-90% of all cases of chronic gastritis;
chemical (alcohol, autointoxication, etc.);
neuroendocrine, etc.

Classification chronic gastritis:

chronic superficial gaschrit;
chronic atrophic gastritis;
chronic helicobacter gastritis;
chronic autoimmune gastritis;
special forms of chronic gastritis - chemical, radiation, lymphocytic, etc.

Pathogenesis diseases at various types chronic gastritis is not the same.

Morphogenesis.

With chronic superficial gastritis there is no atrophy of the mucous membrane, the gastric pits are poorly expressed, the glands are not changed, diffuse lympheosinophilic infiltration is characteristic, and slight fibrosis of the stroma.

Chronic atrophic gastritis is characterized by low pit epithelium, reduction of gastric pits, a decrease in the number and size of glands, dystrophic and often metaplastic changes in the glandular epithelium, diffuse lympheosinophilic and histiocytic infiltration, and stromal fibrosis.

In chronic Helicobacter pylori gastritis, Helicobacter pylori plays a leading role, which mainly affects the antrum of the stomach. The pathogen enters the stomach through the mouth and is located under a layer of mucus that protects it from the action of gastric juice. The main property of a bacterium is the synthesis ureases- an enzyme that breaks down urea with the formation of ammonia. Ammonia shifts pH to the alkaline side and disrupts the regulation of hydrochloric acid secretion. Despite the emerging hypergastrinemia, HC1 secretion is stimulated, which leads to hyperacid syndrome. The morphological picture is characterized by atrophy and impaired maturation of the integumentary pit and glandular epithelium, pronounced lymphoplasmacytic and eosinophilic infiltration of the mucous membrane and lamina propria with the formation of lymphoid follicles.

Chronic autoimmune gastritis.

Its pathogenesis is due to the formation of antibodies to parietal cells of the glands of the fundus of the stomach, endocrine cells of the mucous membrane, as well as to gastromucoprotein ( internal factor), which become self-antigens. In the fundus of the stomach, there is a pronounced infiltration with B-lymphocytes and T-helpers, the number of IgG-plasmocytes increases sharply. Atrophic changes in the mucous membrane progress rapidly, especially in patients older than 50 years.

Among special forms of chronic gastritis highest value It has hypertrophic gastritis, which is characterized by the formation of giant folds of the mucous membrane, similar to the convolutions of the brain. The thickness of the mucous membrane reaches 5-6 cm. The pits are long, filled with mucus. The epithelium of the glands is flattened, as a rule, its intestinal metaplasia develops. The glands often lack chief and parietal cells, which leads to a decrease in the secretion of hydrochloric acid.

Complications.

Atrophic and hypertrophic gastritis can be complicated by the formation of polyps, sometimes ulcers. In addition, atrophic and Helicobacter pylori gastritis are precancerous processes.

Exodus superficial and Helicobacter pylori gastritis with appropriate treatment is favorable. Therapy of other forms of chronic gastritis only slows down their development.

peptic ulcer - chronic illness, the clinical and morphological expression of which is a recurrent gastric or duodenal ulcer.

Therefore, they distinguish peptic ulcer stomach and duodenal ulcer, which differ somewhat from each other mainly in pathogenesis and outcomes. Peptic ulcer suffers from predominantly men aged 50 years and older. Duodenal ulcers occur 3 times more often than gastric ulcers.

Etiology peptic ulcer disease is associated mainly with Helicobacter pylori and with general changes that occur in the body and contribute to the damaging effect of this microorganism. Certain strains of Helicobacter pylori are highly adherent to surface epithelial cells and cause marked neutrophilic infiltration of the mucosa, leading to mucosal damage. In addition, urease formed by bacteria synthesizes ammonia, which is highly toxic to the mucosal epithelium and also causes its destruction. At the same time, microcirculation and trophism of tissues in the area are disturbed. necrotic changes epitheliocytes. In addition, these bacteria contribute to a sharp increase in the formation of gastrin in the blood and hydrochloric acid in the stomach.

General changes that occur in the body and contribute to the damaging effect of Helicobacter pylori:

psycho-emotional overstrain to which a modern person is exposed ( stressful conditions violate the coordinating influence of the cerebral cortex on the subcortical centers);
violations of endocrine influences as a result of a disorder in the activity of the hypothalamic-pituitary and pituitary-adrenal systems;
increased influence of the vagus nerves, which, together with an excess of corticosteroids, increases the activity of the acid-peptic factor of gastric juice and the motor function of the stomach and duodenum;
decrease in the effectiveness of the formation of the mucous barrier;
microcirculation disorders and an increase in hypoxia.

Among other factors contributing to the formation of ulcers,

drugs such as aspirin, alcohol, smoking are important, which not only damage the mucous membrane themselves, but also affect the secretion of hydrochloric acid and gastrin, microcirculation and trophism of the stomach.

Morphogenesis.

The main expression of peptic ulcer is a chronic recurrent ulcer, which in its development goes through the stages of erosion and acute ulcer. Most frequent localization stomach ulcers - lesser curvature in the antrum or pyloric region, as well as in the body of the stomach, in the area of transition to the antrum. This is explained by the fact that the lesser curvature, like the “food path”, is easily injured, its mucous membrane secretes the most active juice, erosions and acute ulcers in this area are poorly epithelialized. Under the influence of gastric juice, necrosis captures not only the mucous membrane, but also spreads to the underlying layers of the stomach wall and erosion turns into acute peptic ulcer. Gradually acute ulcer becomes chronic and can reach 5-6 cm in diameter, penetrating to various depths (Fig. 62). The edges chronic ulcer raised in the form of rollers, dense. The edge of the ulcer facing the entrance to the stomach is undermined, the edge facing the pylorus is flat. The bottom of the ulcer is scar connective tissue and scraps of muscle tissue. The walls of the vessels are thick, sclerotic, their lumens are narrowed.

Rice. 62. Chronic stomach ulcer.

With an exacerbation of peptic ulcer, purulent-necrotic exudate appears in the bottom of the ulcer, and fibrinoid necrosis appears in the surrounding scar tissue and in the sclerotic walls of blood vessels. Due to the growing necrosis, the ulcer deepens and expands, and as a result of corroding the walls of the vessels, their rupture and bleeding may occur. Gradually, in place of necrotic tissues, granulation tissue develops, which matures into coarse connective tissue. The edges of the ulcer become very dense, callused, in the walls and in the bottom of the ulcer there is an overgrowth of connective tissue, vascular sclerosis, which disrupts the blood supply to the stomach wall, as well as the formation of a mucous barrier. This ulcer is called callous .

With duodenal ulcer the ulcer is usually located in a bulb and only sometimes is localized below it. Multiple duodenal ulcers are not very common and are located on the anterior and back walls bulbs against each other - "kissing ulcers".

When the ulcer heals, the tissue defect is compensated for by the formation of a scar, and an altered epithelium grows on the surface, and there are no glands in the area of the former ulcer.

Complications of peptic ulcer.

These include bleeding, perforation, penetration, gastric phlegmon, rough scar, chlorhydropenic uremia.

Bleeding from a necrotic vessel is accompanied by "coffee grounds" vomiting due to the formation of hematin hydrochloride in the stomach (see Chapter 1). The stool becomes tarry due to great content they have blood in them. Bloody stool is called melena«.

Perforation, or perforation, of the wall of the stomach or duodenum leads to acute diffuse peritonitis - purulent-fibrinous inflammation of the peritoneum.

penetration- a complication in which the perforated hole opens in the place where, as a result of inflammation, the stomach was soldered to nearby organs - the pancreas, transverse colon, liver, gallbladder.

Penetration is accompanied by digestion of the tissues of the adjacent organ by the gastric juice and its inflammation.

A rough scar can form at the site of the ulcer as it heals.

Chlorhydropenic uremia accompanied by convulsions, develops if the scar sharply deforms the stomach, pylorus, duodenum, almost completely closing the exit from the stomach. In this case, the stomach is stretched by food masses, patients experience uncontrollable vomiting, in which the body loses chlorides. Callous ulcer of the stomach can become a source of cancer.

Stomach cancer seen in more than 60% of all neoplastic diseases. Mortality in this case is 5% of the total mortality of the population. This disease often occurs in people aged 40-70 years; men get sick about 2 times more often than women. The development of gastric cancer is usually preceded by precancerous diseases such as gastric polyposis, chronic gastritis, chronic gastric ulcer.

Rice. 63. Forms of stomach cancer. a - plaque-shaped, b - polypous, c - mushroom-shaped, d - diffuse.

Forms of cancer stomach, depending on the appearance and nature of growth:

plaque-like has the form of a small dense, whitish plaque, located in the mucous and submucosal layers (Fig. 63, a). Asymptomatic, usually preceded by carcinoma in situ. Grows predominantly exophytic and precedes polyposis cancer;
polycomplete has the form of a small knot on a stem (Fig. 63, b), grows mainly exophytically. Sometimes develops from a polyp (malignant polyp);
mushroom, or fungic, represents a tuberous knot on a wide base (Fig. 63, c). Fungal cancer is further development polypous, since they have the same histological structure:
ulcerated forms of cancer found in half of all stomach cancers:
- -primary ulcerative cancer (Fig. 64, a) develops with ulceration of plaque-like cancer, histologically usually poorly differentiated; proceeds very malignantly, gives extensive metastases. Clinically, it is very similar to gastric ulcer, which is the insidiousness of this cancer;
- -saucer-shaped cancer , or cancer-ulcer , occurs with necrosis and ulceration of polypous or fungal cancer and at the same time resembles a saucer (Fig. 64, b);
- - ulcer-cancer develops from a chronic ulcer (Fig. 64, c);
- - diffuse, or total , cancer grows predominantly endophytic (Fig. 64, d), affecting all parts of the stomach and all layers of its wall, which become inactive, the folds are thick, uneven, the stomach cavity decreases, resembling a tube.

According to the histological structure, there are:

adenocarcinoma , or glandular cancer , which has several structural variants and is a relatively differentiated tumor (see Chapter 10). Usually makes up the structure of plaque-like, polyposis and fundic cancer;

Undifferentiated forms of cancer:

Rare forms of cancer described in specific manuals. These include squamous And glandular squamous cell carcinoma.

Metastasis gastric cancer is carried out mainly by the lymphogenous route, primarily to the regional lymph nodes, and as they are destroyed, distant metastases to various organs. Can occur in stomach cancer retrograde lymphogenous metastasis when an embolus from cancer cells moves against the lymph flow and, getting into certain bodies, gives metastases bearing the name of the authors who described them:

krukenberg cancer - retrograde lymphogenous metastases in the ovaries;
Schnitzler's metastasis - retrograde metastasis to pararectal tissue;
Virchow's metastasis - retrograde metastasis to the left supraclavicular lymph nodes.

The presence of retrograde metastases indicates the neglect of the tumor process. In addition, Krukenberg's cancer and Schnitzler's metastasis can be mistaken for independent tumors, respectively, of the ovaries or rectum.

Hematogenous metastases usually develop after lymphogenous and affect the liver, less often - the lungs, kidneys, adrenal glands, pancreas, bones.

Complications of stomach cancer:

bleeding with necrosis and ulceration of the tumor;
inflammation of the stomach wall with the development of its phlegmon:
tumor growth in nearby organs- pancreas, transverse colon, greater and lesser omentums, peritoneum with the development of the corresponding symptoms.

Exodus gastric cancer with early and radical surgical treatment may be beneficial in most patients. In other cases, it is only possible to prolong their life.

INTESTINAL PATHOLOGY

Digestive disorders in the intestines associated with a violation of its basic functions - digesting, absorption, motor, barrier.

Disorders of the digestive function of the intestine cause:

violation of abdominal digestion, i.e., digestion in the intestinal cavity;
disorders of parietal digestion, which occurs on the surface of the membranes of microvilli with the participation of hydrolytic enzymes.

Disorders of the absorption function of the intestine, The main reasons for which can be:

defects in cavity and membrane digestion;
acceleration of the evacuation of intestinal contents, for example, with diarrhea;
atrophy of the villi of the intestinal mucosa after chronic enteritis and colitis;
resection of a large fragment of the intestine, for example, with intestinal obstruction;
disorders of blood and lymph circulation in the intestinal wall with atherosclerosis of the mesenteric and intestinal arteries, etc.

Violation of the curtain function of the intestine.

Normally, the intestine provides mixing and movement of food from the duodenum to the rectum. The motor function of the intestine can be upset in varying degrees and forms.

Diarrhea, or diarrhea, - rapid (more than 3 times a day) stools of a liquid consistency, combined with increased intestinal motility.

Constipation- prolonged stool retention or difficulty in emptying the bowels. It is observed in 25-30% of people, especially after the age of 70 years.

Violation of the barrier-protective function of the intestine.

Normally, the intestinal wall is a mechanical and physico-chemical protective barrier for the intestinal flora and toxic substances formed during the digestion of food, secreted by microbes. entering the intestines through the mouth. etc. Microvilli and glycocalyx form a microporous structure that is impermeable to microbes, which ensures the sterilization of digested food products during their absorption in the small intestine.

In pathological conditions, a violation of the structure and function of enterocytes, their microvilli, as well as enzymes can destroy the protective barrier. This, in turn, leads to infection of the body, the development of intoxication, a disorder in the digestive process and the vital activity of the body as a whole.

DISEASES OF THE INTESTINE

Among intestinal diseases, inflammatory and neoplastic processes are of primary clinical importance. Inflammation of the small intestine is called enteritis , colon - colitis , all parts of the intestine - enterocolitis.

Enteritis.

Depending on the location of the process in the small intestine secrete:

inflammation of the duodenum - duodenitis;
inflammation of the jejunum - jejunitis;
inflammation of the ileum - ileitis.

Flow enteritis can be acute and chronic.

Acute enteritis. Its etiology:

infections (botulism, salmonellosis, cholera, typhoid fever, viral infections and so on.);
poisoning with poisons, poisonous mushrooms, etc.

Types and morphology of acute enteritis most commonly developed catarrhal enteritis. Mucous and submucosal membranes are impregnated with muco-serous exudate. In this case, degeneration of the epithelium and its desquamation occur, the number of goblet cells that produce mucus increases, and erosion sometimes appears.

fibrinous enteritis accompanied by necrosis of the mucous membrane (croupous enteritis) or mucous, submucosal and muscular layers of the wall (diffheritic enteritis); with rejection of fibrinous exudate, ulcers form in the intestine.

Purulent enteritis is less common and is characterized by impregnation of the intestinal wall with purulent exudate.

Necrotic ulcerative enteritis , in which either only solitary follicles undergo necrosis and ulceration (with typhoid fever), or ulcerative defects of the mucous membrane are common (with influenza, sepsis).

Regardless of the nature of the inflammation, hyperplasia of the lymphatic apparatus of the intestine and lymph nodes of the mesentery is noted.

Exodus. Usually, acute enteritis ends with the restoration of the intestinal mucosa after recovery from an intestinal disease, but can take a chronic course.

chronic enteritis.

Etiology diseases - infections, intoxications, the use of certain drugs, long-term errors in food, metabolic disorders.

Morphogenesis.

The basis of chronic enteritis is a violation of the processes of regeneration of the epithelium. Initially, chronic enteritis develops without mucosal atrophy. The inflammatory infiltrate is located in the mucosa and submucosa, and sometimes reaches the muscle layer. The main changes develop in the villi - vacuolar dystrophy is expressed in them, they are shortened, soldered together, and enzymatic activity decreases in them. Gradually, enteritis without atrophy turns into chronic atrophic enteritis, which is the next stage of chronic enteritis. It is characterized by even greater deformation, shortening, vacuolar dystrophy of the villi, cystic expansion of the crypts. The mucous membrane looks atrophic, the enzymatic activity of the epithelium is further reduced, and sometimes perverted, which prevents parietal digestion.

Complications of severe chronic enteritis - anemia, beriberi, osteoporosis.

Colitis- inflammation of the colon, which can develop in any one of its departments: typhlitis, transversitis, sigmoiditis, proctitis.

With the flow colitis can be acute or chronic.

Acute colitis.

Etiology diseases:

infections (dysentery, typhoid fever, tuberculosis, etc.);
intoxication (uremia, poisoning with sublimate or drugs, etc.).

Types and morphology of acute colitis:

catarrhal colitis , in which inflammation spreads to the mucous and submucosal membranes, there is a lot of mucus in the serous exudate:
fibrinous colitis that occurs with dysentery can be croupous and diphtheritic;
phlegmonous colitis characterized by purulent exudate, destructive changes intestinal walls, severe intoxication;
necrotizing colitis , in which tissue necrosis spreads to the mucous and submucosal layers of the intestine;
ulcerative colitis, arising from the rejection of necrotic masses, after which ulcers form, sometimes reaching the serous membrane of the intestine.

Complications:

bleeding , especially from ulcers;
ulcer perforation with the development of peritonitis;
paraproctitis - inflammation of the tissue around the rectum, often accompanied by the formation of pararectal fistulas.

Exodus . Acute colitis usually resolves upon recovery from the underlying disease.

Chronic colitis.

Morphogenesis. According to the mechanism of development, chronic colitis is also mainly a process that develops as a result of a violation of the regeneration of the epithelium, but inflammatory changes are also pronounced. Therefore, the intestine looks red, hyperemic, with hemorrhages, desquamation of the epithelium, an increase in the number of goblet cells, and shortening of the crypts are noted. Lymphocytes, eosinophils, plasma cells, neutrophilic leukocytes infiltrate the intestinal wall up to the muscle layer. Initially occurring colitis without mucosal atrophy is gradually replaced by atrophic colitis and ends with sclerosis of the mucous membrane, which leads to the cessation of its function. Chronic colitis may be accompanied by a violation mineral metabolism, occasionally there is an avitaminosis.

Nonspecific ulcerative colitis- a disease whose cause is not clear. Young women are more often ill.

It is believed that allergies play a leading role in the occurrence of this disease. associated with intestinal flora and autoimmunization. The disease flows acutely and chronically.

Acute nonspecific ulcerative colitis characterized by defeat individual sections or the entire colon. The leading symptom is inflammation of the intestinal wall with the formation of foci of mucosal necrosis and multiple ulcers (Fig. 65). At the same time, islands of the mucous membrane resembling polyps remain in the ulcers. Ulcers penetrate into muscle layer where fibrinoid changes in the interstitial tissue, vessel walls and hemorrhages are observed. In part of the ulcers, granulation tissue and integumentary epithelium grow excessively, forming polypoid outgrowths. There is a diffuse inflammatory infiltrate in the intestinal wall.

Complications.

In the acute course of the disease, perforation of the intestinal wall in the area of ulcers and bleeding is possible.

Chronic nonspecific ulcerative colitis characterized by a productive inflammatory reaction and sclerotic changes in the intestinal wall. There is scarring of ulcers, but the scars are almost not covered with epithelium, which grows around the scars, forming pseudopolyps. The intestinal wall becomes thick, loses elasticity, the intestinal lumen narrows diffusely or segmentally. Abscesses often develop in crypts (crypt abscesses). Vessels are sclerosed, their lumens are reduced or completely overgrown, which maintains the hypoxic state of intestinal tissues.

Appendicitis- inflammation of the appendix of the caecum. This is a widespread disease of unknown etiology.

Along the course, appendicitis can be acute and chronic.

Rice. 65. Nonspecific ulcerative colitis. Multiple ulcers and hemorrhages in the intestinal wall.

Acute appendicitis has the following morphological forms. which are also the phases of inflammation:

simple;
surface;
destructive, which has several stages:
- - phlegmonous;
- - phlegmonous-ulcerative.
gangrenous.

Morphogenesis.

Within a few hours from the onset of an attack, a simple one occurs, which is characterized by circulatory disorders in the wall of the process - stasis in the capillaries, vessels, edema, and sometimes perivascular hemorrhages. Then serous inflammation develops and a site of destruction of the mucous membrane appears - the primary affect. It marks the development acute superficial appendicitis . The process swells, becomes dull, the vessels of the membrane are full-blooded. By the end of the day develops destructive , which has several stages. The inflammation acquires a purulent character, the exudate diffusely infiltrates the entire thickness of the process wall. This type of appendicitis is called phlegmonous (Fig. 66). If at the same time ulceration of the mucous membrane occurs, they speak of phlegmonous-ulcerative appendicitis. Sometimes purulent inflammation spreads to the mesentery of the process and to the wall of the appendicular artery, which leads to its thrombosis. In this case, it develops gangrenous appendicitis: the process is thickened, dirty green, covered with purulent-fibrinous deposits, there is pus in its lumen.

Rice. 66. Phlegmonous appendicitis. A - purulent exudate diffusely impregnates all layers of the wall of the appendix. The mucous membrane is necrotic; b - the same, a large increase.

Rice. 67. Colon cancer. a - polypous, b - polypous with pronounced secondary changes (necrosis, inflammation); c - mushroom-shaped with ulceration; g - circular.

Complications of acute appendicitis.

The most common is perforation of the appendix and peritonitis develops. At gangrenous appendicitis self-amputation of the process may occur and peritonitis also develops. If the inflammation spreads to the tissues surrounding the process, sometimes purulent thrombophlebitis of the mesenteric vessels develops, which spreads to the branches portal vein - pipephlebitis . In such cases, thrombobacterial embolism of vein branches and the formation of pylephlebitic liver abscesses are possible.

Chronic appendicitis occurs after acute appendicitis and is characterized mainly by sclerotic and atrophic changes in the appendix wall. However, against this background, exacerbations of the disease may occur with the development of phlegmon and even gangrene of the appendix.

bowel cancer develops both in the small and in the large intestine, especially often in the rectum and sigmoid colon (Fig. 67). In the duodenum, it occurs only as adenocarcinoma or undifferentiated cancer of the duodenal papilla. and in this case, one of the first manifestations of this cancer is subhepatic jaundice (see chapter 17).

Precancerous diseases:

ulcerative colitis;
polyposis:
fistulas of the rectum.

According to the appearance and nature of growth, there are:

exophytic cancer:

polyposis:
mushroom;
saucer-shaped;
cancerous ulcers.

endophytic cancer:

diffuse-infiltrating cancer, in which the tumor circularly covers the intestine in one direction or another.

Histologically exophytically growing cancerous tumors are usually more differentiated, have the structure of papillary or tubular adenocarcinoma. In endophytically growing tumors, cancer often has a solid or fibrous structure (skirr).

Metastasis.

Colon cancer metastasizes lymphogenously to regional lymph nodes, but sometimes hematogenously, usually to the liver.