• Enteritis and enterocolitis symptoms

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    Enteritis and enterocolitis - pathology of the small intestine, which flow from the functional features of this segment of the intestinal tube.

    The motor function is defined by two border zones: proximally - the border with the gastroduodenal zone( plica duodenojejunalis), the distal - ileocecal valve. Both these border areas are active interoreceptors, sources of abundant reflex connections. So, the gastric contents, entering the jejunum, sends the first peristaltic wave, which, under the excitability of the nervous system, can reach the anus, causing immediate diarrhea. Rapid evacuation of the stomach generates, in addition, hypoglycemic reactions on the soil of accelerated absorption of carbohydrates, and is accompanied by a special "small intestine shock."Hypoglycemia and shock complicate numerous diseases of different organs and are directly related to the upper part of the small intestine.

    No less important is the absorption process, which is easily disturbed by the lesions of the above department. It is clear that any serious enteritis entails symptoms of deficiency of nutrients needed by the body in contrast to colitis, when even severe ulcerous lesions do not threaten the absorption processes. Therefore, the transition of the inflammatory process from the large intestine to a thin one, especially to its upper sections, is always a serious complication.

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    Secretory disorders of the small intestine play a lesser role in the overall digestive process due to the pronounced substituent role of pancreatic enzymes. However, with diffuse enteritis, the secretory and resorptive processes also suffer, and, consequently, the trophism of the organism.

    Inflammatory diseases of the small intestine are rarely found in isolated form. Much more often we are dealing with enterocolitis. However, the involvement of the small intestine is manifested very distinct signs. The predominance of the pathology of the small intestine, even with enterocolitis, imposes a bright imprint on the entire clinical picture. However, in a number of cases, the enteritis clinic is limited to individual symptoms, making up only one of the components of the common disease.

    An example is lambliasis enterocolitis, mesenteric lymphadenitis. Irritations of the small intestine are regularly accompanied and such diseases as anacid gastritis, cholecystitis, diseases of the operated stomach.

    But enteritis can also appear as an independent disease, most often in one of the following two forms.

    1. Ejonalnye diarrheas differ stormy urges on a chair soon after meal( on type ahilicheskih or giardiasis).Exercises have a greenish color, a liquid mushy consistency, contain mucus, closely mixed with feces, abundant saponified fat( crystals, clumps, needles of fatty acids).The abundance of fat can even make feces look discolored. This form is described as "soap dyspepsia"( Porges).Characteristic is the state of severe general weakness with a feeling of heat, trembling of hands and dizziness, until collapse, coming immediately after the stool and resembling a hypoglycemic coma. The mechanism of this "small intestinal shock" is explained differently. Some authors associate it with hypoglycemia on the basis of accelerated food transfer through the small intestine and rapid absorption of carbohydrates, which, with a general nervous instability, causes these symptoms. Others attribute the main role of hyperemia in the region of the celiac nerve with reflex hypotension. This explanation seems more likely to us when it comes to diseases of the small intestine, while hypoglycemia is more common in a number of gastric syndromes, for example, with achilles and after resection of the stomach.

    2. Chronic enteritis can last for many years. The onset of the disease is often anamnestically applies even to childhood. The course is usually mild, not progressive, but with a tendency to transition to enterocolitis.

    Chronic infections, including tuberculosis, stomach diseases( anacid gastritis, condition after stomach surgeries), chronic intoxications( lead), overloading of bulky and fatty foods play a role. Infection in the small intestine can be supported by a change in the bacterial flora( "dysbacteria"), when a decrease in the gastrointestinal barrier and alkaline reaction of inflammatory secrets promote the introduction and development of bacteria that acquire increased pathogenicity. This fact is proved experimentally by the method of intestinal cartridges.

    Main symptoms: rumbling and transfusion in the abdomen, swelling, pain shortly after the start of the meal, simulating early pain with high gastric ulcers. Insufficient attention is paid to the symptom of a vasomotor shock after a stool or meal. The reason for the latter, perhaps, lies in the violation of the barrier function of the epithelium of the small intestine as a regulator of the rhythm of food intake. Diarrhea can be absent for a long time. Acceleration of the passage through the small intestine is compensated by the slowing down of the passage along the thick intestine, where the feces have time to fully form, and the starch and fiber are digested by bacteria and enzymes. Disturbances of absorption are manifested by abundant remains of fat in the feces, which, with a large amount of fats taken, has a light color. This statoratoria should be distinguished from other similar disorders( with pancreatitis, tuberculosis of mesentery, sprue).

    Of the objective symptoms, the pain zone of cutaneous hyperesthesia in the area of ​​the rectus abdominis muscle and posterior to the left para-vertebral line from the last thoracic to the first lumbar vertebrae( Porges) should be noted. The painful point to the left of the navel coincides with that of the peptic ulcer of the small intestine. With regional ileitis, the pain point is in the ileocecal region, at the site of the infiltration. With mesenteric lymphadenitis, the pain zones correspond to the course of the mesentery( Sternberg's symptom).

    The characteristic coprological picture is reduced to the presence of a decorated feces, closely mixed with mucus, greenish or light yellow, with abundant content of saponified fats. Gastric secretion is often reduced to zero. Functional tests of the liver in case of complication with severe hepatitis are pathological. In urine, there is an increased indicator content, as in putrefactive dyspepsia.

    Radiographically, acceleration of passage through the small intestine is noted: after 2-3 hours, barium enters the large intestine. Sometimes with fluoroscopy after 2-3 hours, barium is in the stomach and the large intestine, while the small intestine is empty. In other cases, there are fluid levels in the loops of the small intestine with gas bubbles above them.

    Most often, the pathological process passes to the large intestine, causing a banal picture of enterocolitis. Violation of the absorption processes, of course, leads to dystrophy, beriberi and anemia. Damage to the intestinal epithelium supports chronic intoxication, which causes a number of toxic and allergic symptoms: urticaria, eczema, and Quincke's edema. Later the disease can be complicated by cholecystitis, hepatic colic, hypochromic anemia, glossitis, aphthous stomatitis, anaphylactic diarrhea. Possible lesions of the vessels of the abdominal cavity with the development of thrombophlebitic splenomegaly. As is known: in the history of patients with this disease of the spleen, there are indications either for a stomach injury or for chronic intestinal infections.

    When differentiating enteritis with other diseases, tuberculosis of the intestine, mesenteric lymphadenitis, sprue, chronic appendicitis should be excluded.

    Acute enteritis may be caused by any intestinal infection, perhaps by a virus or even by simple cooling.

    Treatment involves fractional meals in small portions, slow food and separate intake of dense food and liquids, in order to slow the evacuation and absorption of food. Prohibited coarse vegetable fiber and fat large meals. Meat is recommended in large quantities( up to 200 g per day) in chopped or softly boiled. With constipation appoint raw juices, compote, yogurt.

    Breakfast: soft-boiled egg, cocoa on water, dried white( or gray) bread and butter. Lunch: meat broth or vegetable soup with rice, meat cutlet, chicken or boiled low-fat fish with vegetable puree, fruit jelly. Early dinner: rice porridge on water with butter or cheese cakes. Before going to bed tea, biscuits, cookies.

    With diarrhea prescribed calcium carbonate of 1.0, tannalbine with bismuth nitrate in 0.5.With abundant gas formation, benzonaphthol is 0.5, infusion of dried herbs( chamomile, mint, dill, clover) 1/4 cup 3-4 times a day.

    In 1932 Cron, Gunzburg and Oppenheimer first described 13 cases of severe enteritis with diarrhea, abdominal pain, exhaustion, anemia, fever, infiltration in the ileocecal region complicated by stenosis and fistula. Half of the patients had scars after appendectomy. Later similar changes( granulomas) were described in the large intestine and even in the stomach.

    Pathological anatomy. The terminal loop of the ileum is most often affected, from where the process continues in the proximal direction, rarely caudally, passing to the large intestine, capturing the loops of the intestine, the richest in lymphatic elements. The affected segments are thickened, rigid, and the serous membrane is covered with fat and fibrinous effusion. The adjacent mesentery is edematic, thickened, the lymph nodes are enlarged. The process of the cecum is immersed in the adhesions. There are perforations of the intestine in the mesentery, with the formation of fistulas. On the resected loops of the intestine the wall is sharply thickened, the lumen is narrowed, there are ulcers, necrosis and hyperplasia of the mucosa. Histologically, nonspecific hyperplasia of the lymphatic tissue of the submucosal layer is noted. In the lymph nodes are giant cells without caseism and Koch bacilli. This lymphogranulomatous process is almost indistinguishable from tuberculosis.

    It has been hypothesized that this disease develops on the basis of tuberculosis of the intestine by bovine-type bacilli with good resistance of the macroorganism, with obstruction of the lymphatic vessels and secondary infection. It was also indicated anatomical similarity with Beck's sarcoidosis.

    It has been experimentally proved that it is possible to reproduce a similar process in the dog's intestines by injecting irritating substances( fine sand, talc) in the mesentery and lymph nodes that clog the milky paths. The subsequent intravenous introduction of bacteria strengthened the development of the process.

    Etiology and pathogenesis are reduced to a combination of an unknown infection with lymphatic obstruction.

    A history of appendicitis and bacterial dysentery, as well as poor nutrition conditions, is frequent.

    The clinical picture proceeds in the form of one of the following syndromes:

    The disease is complicated by abscesses, perforation, fistulas, stenoses.

    The flow is perennial, cyclical, with relapses of diarrhea, anemia, exhaustion, fever. Diarrhea is allergic, without the presence of certain food allergens.

    Objective research reveals infiltration in the terminal loop of the ileum, general exhaustion, edema, dermatitis, anemia, leukocytosis. X-ray signs are: "string symptom" in the region of narrowed loops and a nipple filling defect in the caecum.

    Differentiate regional ileitis with intestinal tuberculosis, lymphogranulomatosis, leukemia, lipodysgrophy, sarcomatosis.

    Treatment in severe cases is only surgical( resection, bypass surgery, opening of abscesses, suturing fistula).Conservative treatment is possible only in the initial stages without dystrophy and stenosis, when the inflammatory process is still partially reversible. Treatment is the same as in chronic ulcerative colitis: blood and plasma transfusion, nutrition, multivitamins, fresh yeast, high doses of calcium.

    Both diseases, in which one of the most severe symptoms are debilitating diarrhea, are considered avitaminosis. If vitamin deficiency does not serve as the sole cause of diarrhea, it still plays a major etiological role.

    In the etiology of pellagra, the main role is played by the deficit of nicotinic acid - exogenous, due to inadequate supply with food, or endogenous, on the basis of poor absorption or enhanced destruction of this vitamin. Some role is played by deficiency of vitamins C and B1.

    The common triad of symptoms - diarrhea, dermatitis and dementia( "three D") does not repeat so clearly in any other clinical syndrome. However, some elements of the same clinical picture( "pellagroide") occur in all kinds of severe eating disorders.

    Diarrhea, which began as a consequence of avitaminosis, is subsequently the cause of disease progression( according to the vicious circle mechanism).Watery stool contains many undigested food residues. The intestinal passage is accelerated throughout the tract. Skin changes( hyperkeratosis, hyperemia with the transition to brown pigmentation, peeling, wet bubbles), as well as neuropsychic disorders, are the result of profound dystrophic, often irreversible changes.

    The most effective therapeutic agent is nicotinic acid, administered subcutaneously or intravenously in 1% solution of 1-5 ml or by mouth at 0.05-0.1 g two to three times a day. At the same time, ascorbic acid and thiamine are injected in the same way in a 5% solution of 1-2 ml each.

    Sprue disease is known in two forms: tropical and endemic. It appears, like pellagra, a triad of clinical symptoms: diarrheas are combined with glossitis and anemia. The crimson-red tongue with the smoothed papillae resembles the Genter language in Burmese anemia. Diarrhea is accompanied by steatorrhea - abundant allocation of all fatty fractions, mainly neutral fats, as in pancreatic insufficiency, but without simultaneous creatorrhea.

    Regular allocation of fatty stools is described under the terms "idiolatic steatorrhoea", endemic( non-tropical) sprue, "white diarrhea", Herter's disease or "celiac disease" of childhood. This disease can not be confused with various forms of symptomatic steatorrhea due to pancreatic disease or lipodystrophy( tuberculosis of the mesentery vessels of the mesentery - Whipple's disease).

    Pathological changes are expressed in lymph and plasmacytic infiltration of the wall of the small intestine, atrophy, less often in ulceration of the mucosa and submucosal fibrosis. The same changes, expressed weaker, are also noted in the large intestine. In the adrenal gland, there is a certain atrophy and a decrease in the content of lipoids.

    Along with the essential forms of sprue, symptomatic, secondary, on the ground lymphosarcomas of mesentery and Hirschsprung's diseases are noted.

    The pathogenesis of the sprue is not fully understood and, apparently, is not unified. Biochemical disorders are reduced to a violation of absorption of dietary fats and the process of phosphorylation, which occurs with the participation of hormones of the adrenal cortex. It is possible that the lack of secretion of bile acids in the liver plays a role. Recently, a known role is attributed to the lack of folic acid. The whole syndrome therefore appears as a hormone-vitamin-deficiency. However, some authors do not exclude the role of infection in the form of tuberculosis lesions of the lymphatic system of mesentery or typhoid fever suffered in early childhood.

    The main etiological factor is the inferiority of food, one-sided, excess nutrition of carbohydrates, which, especially in hot climates, promotes the development of fermentation dyspepsia. As an accompanying factor, the role of endocrine insufficiency plays, in particular in the period of pregnancy and lactation.

    According to other authors, in the etiology and pathogenesis of the sprue, the main role is played by the deficiency of the external or internal factor of the Castle, as well as the damage to the absorption capacity of the small intestines after severe infections( dysentery, typhoid, tuberculosis).

    Fermentation( "gas") dyspepsia in these patients leads to impaired absorption of fats, calcium, vitamins and anti-anemic substances in the affected small intestine. Hence, it is easy to explain all the main symptoms of the disease: fatty diarrhea, hypocalcemia with osteoporosis, anemia and a number of avitaminous phenomena( cheilosis, glossitis, hemeralopia, polyneuritis).

    Clinical picture. In the first place, diarrhea with -shaped grayish-yellow dough or liquid stool, acidic or putrid odor. Cal contains 45-70% of the consumed fat( instead of 6% with normal digestion), mainly in the form of fatty acids and soaps. Isolation of nitrogenous slags is not increased. Regular symptom in the period of exacerbation is anemia, the nature of which is variable: in the period of exacerbation - hyperchromatic-macrocytic, in the period of remission - hypochromic. With severe dehydration, anemia can be masked by a thickening of the blood. Glotissus of the genetics type, stomatitis and cheilosis are regular signs of avitaminosis. Symptoms of polyneuritis such as beriberi and funicular myelosis are less regular. When cutting diarrhea, there are symptoms of deficiency of all other vitamins.

    Hypocalcemia is accompanied by symptoms of osteoporosis and muscle spasms with normal calcium content in the urine. The main exchange is usually elevated. Despite the abundant diarrhea, there is polyuria with a low specific gravity of urine refractory to pituitrin and adiurecrinum, i.e., not of pituitary origin, but of insufficient reabsorption in tubules on the soil. The content of proteins, residual nitrogen, cholesterol and sugar in the blood is lowered. Functional liver samples are normal. Rectoscopy does not reveal anything characteristic. Radiologic examination shows a smoothness of the contours of the small intestines, a persistent delay in the barium in the individual loops of the jejunum( the "dummy symptom"), spotting and cicateness of the relief, sometimes a megacolon picture. The spotting of the relief depends, apparently, on the accumulation of small clumps of mucus in the small intestine, which can explain the disturbance of the absorption processes.

    Disease usually lasts for many years. The first dyspeptic symptoms( diarrhea, bloating) are often observed from childhood. Women are sick more often than men. The flow is always cyclical: prolonged exacerbations are replaced by more or less light intervals, when all the symptoms subsided, even steatorria disappears against a defatted diet. Anemia does not completely pass, but takes a hypochromic character.

    For cyclical course, sprue is characterized by a change in symptoms during periods of exacerbations and remissions: the onset of remission may be accompanied by the appearance of glossitis, cheilosis and angular stomatitis. Glossitis is observed in 90% of cases and serves as a kind of transitional symptom( from relapse to remission and back).It is not cured by diet, nicotinic acid and riboflavin, but it can occur spontaneously or under the influence of hepatic therapy. Anemia is also subject to dynamic fluctuations, occurs with the onset of remission through the phases of macrocytic anemia, pure macrocytosis without anemia with the transition to normalization of red blood. Outcome is often aplastic anemia.

    One of the causes of anemia and cachexia is sodium deficiency, to a lesser extent - chlorides on the basis of electrolyte loss with feces.

    In differential diagnosis, a number of related diseases should be considered. Pancreatic lesions( severe pancreatitis, cystic fibrosis) occur with a normal content of nitrogen in the stool, neutral fats prevail, diastasis of urine is increased. Pancreatic cancer is characterized by sharp pain and weight loss. Important for pulmonary tuberculosis is pulmonary history, lung damage and the presence of bacilli in feces. With addison's disease, skin pigmentation, hypotension, flattened sugar curve after loading are observed. Tropical sprue flows with a stagnant hyperchromic anemia, otherwise it is difficult to distinguish from an endemic sprue and is treated by the same methods.

    Pellagra does not give hyperchromic anemia even in the period of exacerbation, but differs in characteristic dermatitis and changes in the psyche. Birmer's anemia occurs with more severe hemolysis, normally stained feces, stagnant gastric achilles, without cachexia. Among the changes in the nervous system, there is often a funicular myelosis, rather than polyneuritis, as in the sprue.

    Treatment. In the foreground is a diet designed to affect two major digestive disorders - steatorrhoea and fermentation dyspepsia.

    Individual authors solve this problem by recommending a sharp restriction of carbohydrates and increased intake of fats, which should make up for their loss with feces( 10-15 eggs and 50 grams of butter per day).However, most doctors put forward another principle of the diet, which seems more justified to us: a sharp restriction of fats with a slightly lowered supply of carbohydrates, which, as experience shows, are better tolerated against a defatted diet. Of carbohydrates most shown products with loose fiber( fruits, berries) with the limitation of starchy foods( bread, potatoes), enhancing the fermentation processes in the intestine. During periods of exacerbation, sugar is sharply limited. It is necessary to increase the supply of proteins to 1.5-2 g per 1 kg of weight to combat fermental dyspepsia and hypoproteinemia. Calcium is prescribed in large quantities in the form of acidic dairy products, and as a medicine: 5% calcium chloride intravenously and gluconate and calcium carbonate inside. To increase its assimilation, daily injections of 1 ml of parathyreocrine are indicated.

    Anemia is affected by iron and vitamin B 2.Liver drugs are effective only with parenteral administration, in contrast to Burmese anemia, when internal techniques also help. Treatment of vitamin deficiency requires the use of all vitamins.

    The effect of folic and folinic acid( 10-15 times more effective than folic acid), as well as vitamin B12, was studied mainly in tropical sprue. An increase in reticulocytosis and an improvement in the composition of red blood in a number of patients treated in the remission period were noted. Folic acid potentiates the hematopoietic action of vitamin B12.Plasma transfusions help normalize the protein level of the blood. The use of pancreatin in doses up to 3.0 per day is shown. As a general stimulant, cortico-hormone and ultraviolet irradiation are recommended.

    Complete recovery of sprue is hardly possible. However, long-term remissions allow for a long time to restore relative ability to work. For illustration, we quote excerpts from the case histories.

    This result, on the one hand, confirmed the correctness of the initial treatment of the disease as an erased form of sprue, which gradually acquired all the signs of this syndrome. On the other hand, the role of tuberculosis has been reduced to the effect of a secondary aggravating factor, which has stratified on the primary background of vitamin deficiency. Factors of vitamin deficiency, dystrophy and secondary infection were closely intertwined, which made it difficult to identify the leading factor in pathogenesis and etiology, and only dynamic observation made it possible to clarify the sequence and ratio of individual elements of this complex eating disorder.

    The terms "colitis" and "enterocolitis" refer primarily to inflammatory processes in the intestine, in contrast to purely functional states. Naturally, the line between functional and organic suffering can sometimes be erased, for example, in the complication of functional constipation with inflammatory reactions with the development of "stop colitis."The feedback of functional disorders on the soil of the primary organic process is also understandable, that is, colitis can proceed with constipation, when both states are burdened by each other, according to the mechanism of the "vicious circle".And yet, with all the closeness of organic and functional diseases, they can be studied separately for the purpose of clearest understanding of the pathogenesis of intestinal diseases.

    An attempt by some authors to distinguish between two pathogenetic groups of colitis - infectious and alimentary - has not been widely recognized, since the first group can be considered as colitis dysentery, postdisenteria, protozoal, etc., and the second - as intestinal dyspepsia and dystrophic enterocolitis.

    Completely unusable from a clinical point of view is the widely known term "spastic colitis."Under this mask are concealed a variety of conditions: a reflex colpospasm for certain diseases of the abdominal organs, vegetative reactions on the basis of general neurosis, as well as any form of colitis accompanied by intestinal spasms. In each individual case, a detailed examination will be required to clarify the etiology. The diagnosis of "spastic colitis" is usually only a forced designation for all kinds of unclear intestinal diseases.

    The clinic of numerous intestinal diseases can be schematized several times in a series of definite syndromes that affect the picture of the disease:

    The listed syndromes, although not associated with a specific etiology, give a typical pathogenetic imprint of the disease and help in the selection of differentiated therapy.

    Great attention is paid to the study of the causes of chronicity of colitis. Most chronic colitis develops from acute forms, and this transition occurs either directly, without apparent recovery, or unnoticeably, after an intermediate latent stage of apparent, false recovery. The latter forms are more difficult to recognize, their etiological roots can remain hidden for a long time.

    But there are also forms with such an inconspicuous tendency to a gradual, stubborn flow that gives the impression of primary chronic colitis proceeding in the manner of chronic appendicitis. This includes many cases of intestinal lambliasis and trichomoniasis, and possibly other chronic infections, even bacterial dysentery, when the onset of the disease is anamnesticheski not specified, the disease occurs cyclically with a change in exacerbations and remissions for a number of years.

    The cause of chronicity can often be accurately established. In bacterial dysentery, it usually consists of delayed recognition, late onset of treatment, and inadequate radicality and duration of therapy with too weak doses that promote the development of sulfonamide-resistant strains of bacteria. In other cases, for example, when lamblia and amoeba are invaded, there is an incest of these protozoa, disappearance from the intestinal lumen;they take refuge in the submucosa or deep pockets and become inaccessible to specific drugs.

    Finally, in a number of cases, the chronicity of the defeat is supported by a weak resistance of the organism, beriberi, anemia, dystrophy, which for a long time delays the fight against infestation and prevents recovery. The instability to infection can precede or develop as a result of the disease itself. In such cases, specific therapy is usually impotent and should be replaced with restorative means of action on the macroorganism, for example blood transfusions, glucose with vitamins, enhanced nutrition, climatic treatment.

    The old subdivision for colitis "superficial" and "deep"( : in other terminology - heavy, ulcerative, parietal) does not cover the entire amount of morphological changes occurring in the intestinal wall with enterocolitis. In addition, the morphological sign does not always serve as an indicator of the severity of the disease. Only with the most severe, irreversible forms of colitis( amoeba, tuberculosis, dysentery) we are dealing with deep lesions of all layers of the intestinal tube, up to penetrating and perforating ulcers, fistulas, stenoses, reticulosis, granulosa, tumor-like infiltrates.

    In acute and subacute processes, the most common common inflammatory changes( swelling, hyperemia, increased secretion of mucus, easy vulnerability and bleeding).Inflammatory exudate can contain leukocytes, plasmocytes, erythrocytes, cells of the desquamated epithelium, soluble protein. In clinical conditions, these inflammatory changes are detected with the help of laboratory and rectoscopy studies and in part according to the X-ray study of the relief.

    In chronic processes, deeper lesions( stiffness of the wall, adhesive fusion, stenosis and intestinal loops deformations) are established during life mainly by roentgenologic. These intravital diagnostic methods allow, along with physical examination of the abdomen, to follow the dynamics of anatomical changes, partially reversible against the background of treatment.

    The autopsy report also shows the most varied morphological changes in the intestinal wall in colitis. The anatomical process in some cases proceeds diffusely, in the form of a penis and ta, spreading frequently to the small intestine. In other cases, it has a nesting, focal character, localizing in some parts of the intestinal tube. The specific topography is characterized by the infiltrative-ulcerative form of intestinal tuberculosis with its beloved localization in the caecum, with a tumor-like infiltrate and caseous decay. Regional ileitis produces similar gross morphological changes in the terminal ileum, but without the involvement of the bacillary factor.

    The histology of orthosis and colitis is distinguished by an exceptional variety, an abundance of cytological variants( proliferation of lymphocytic, plasmocyte, reticulo-endothelial elements according to the type of reticulocytosis).Various layers of the intestinal wall are also affected differently: from hypertrophic and polyposic changes to complete atrophy, when the intestine turns into a thin-walled tube with almost complete disappearance of all parenchymal elements, by analogy with atrophic gastritis. In contrast to the pathology of the stomach, when in chronic gastritis inflammatory processes alternate or combine with degenerative restructuring of the epithelium. In colitis, inflammatory changes predominate. It is noteworthy, however, that in a number of cases there is a striking discrepancy between the clinical picture of dystrophy and the nature of the anatomical process, when instead of the expected thinning of the intestinal wall, hypertrophy and swelling of the mucosal folds are detected.

    The main anatomical forms of enterocolitis( catarrhal, follicular, diphtheritic and ulcerative-necrotic) do not exhaust the whole variety of morphological changes in the intestinal wall. For tuberculosis is characterized by caseous decay, for amebiasis, the formation of a granule( "amoeba") with the possibility of malignancy, which is not characteristic of bacterial dysentery.

    Ulcerative processes in the intestine often reflect the specific etiology of the disease. So, ulcers in dysentery, amebiasis, tuberculosis, lymphogranulomatosis and cancer, regional ileitis and ulcerative colitis have a morphological imprint, characteristic for this etiologic factor. But there are also uncharacteristic changes characteristic of any chronic inflammatory process.

    In bacterial dysentery, three morphological stages are described: catarrhal-diphtheritic, ulcerative and regenerative. As with all anatomical processes, changes in the peripheral autonomic nervous system are of great importance in the intestine, especially in ulcerative lesions. Undoubtedly, the defeat of nerve endings and plexuses( Auebakhov, Meissner, solar, aortal) takes place not only with ulcer forms, but with all other serious bowel diseases, and possibly with functional dyspepsia, dyskinesia and anatomical abnormalities such as megacolon and dolichosigma, in which there are observed denervirovanie parts of the distal part of the colon, explaining motor disorders with the expansion of intestinal loops.

    Peripheral nervous system disorders best explain trophic, vascular and motor disorders in all forms of colitis and serve as a link between functional and organic diseases.

    Important lesions of lymphatic vessels and mesentery nodes, causing severe disorders of fat absorption. This applies to various forms of mesenteric lymphadenitis( tuberculosis, etc.), the so-called intestinal lipodystrophy( Whipple's disease), regional ileitis( Crohn's disease), celiac disease( Herter's disease), etc.