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Bowel disease

INTESTINAL DISEASES are quite frequent, but the true incidence is not exactly known, since the defeat of the intestine can be either an independent pathology or accompany other digestive tract diseases (for example, xR ° ptosis ™ ™ ™ No.> chronic pancreatitis). Accurate accounting of the frequency of the disease ™ ecch ™ is also difficult because the intestines react with the same type of reaction — diarrhea or constipation — for various pathological effects. Meanwhile, these symptoms can also be a manifestation of cu ^ b ° f ^ ™ 0 "local disorders and can also be determined by the nature of the patient’s nutrition.

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Currently, there is no single approach to the classification and diagnosis of intestinal diseases. The same suffering is often referred to in different terms. As an independent diagnosis, individual symptoms (constipation, diarrhea, dyspepsia) and syndromes appear, for example, malabsorption syndrome (malabsorption syndrome), digestive insufficiency syndrome, irritable bowel syndrome, bacteria overgrowth syndrome in the small intestine, intestinal lymphectasia, etc.

In domestic literature, the term "chronic enteritis" refers to a group of diseases that occur with long-term impaired intestinal digestion and absorption, although some authors do not recognize this definition. Nevertheless, in chronic enteritis, the main clinical signs are syndromes of malabsorption and impaired intestinal digestion, causing the appearance of the main symptom of chronic enteritis - small bowel diarrhea.

The term "chronic colitis" is also interpreted excessively broadly and mistakenly includes not only the inflammatory diseases of the colon itself, but also enzymatopathy, functional pathology, dysbiosis, dyspepsia (fermentative or putrefactive), non-infectious diarrhea. However, a number of authors do not recognize the existence of non-ulcer colitis, referring to inflammatory bowel diseases as non-specific ulcerative colitis (ULC) and granulomatous lesions of the colon (Crohn's disease). All this extremely complicates the work and does not contribute to a unified approach to intestinal diseases.

In this section, along with ulcerative colitis and Crohn's disease, chronic enteritis and irritable bowel syndrome are presented.

Chronic enteritis

Chronic enteritis (CE) is a chronic inflammatory and dystrophic disease of the small intestine, leading to morphological changes in the mucous membrane and impaired motor, secretory, absorption and other intestinal functions.

The disease is characterized by inflammatory changes in the mucous membrane (edema, mild infiltration of the mucous membrane by lymphocytes and plasma cells, erosion) with the subsequent development of atrophic processes. At the same time, the blood capillaries and lymphatic vessels of the intestine are affected, as well as the intraparietal nerve plexuses. Dystrophic changes are also found in the celiac plexus and border sympathetic trunks.

Etiology. The reasons for the development of CE are very diverse.

• Alimentary disorders, non-regime nutrition, alcoholism.

• Intoxication with drugs and chemicals.

• Exposure to penetrating radiation (as a rule, CE of this etiology is observed with x-ray irradiation or radiation therapy for tumors of various origins).

• Hereditary-constitutional factor; congenital deficiency of enzymes, in particular those involved in the breakdown of various carbohydrates.

• Diseases of the digestive tract - "secondary" enteritis. Pathogenesis. A number of pathological processes develop in the intestine,

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the severity of which depends on the characteristics of the leading etiol-

ghey factor. Thus, impaired motility of the small intestine and a decrease in the barrier function of the intestinal wall (due to a decrease in the production of immunoglobulins and lysozyme, as well as a violation of the integrity of the epithelium) indirectly lead to impaired digestion (maldigestion syndrome) and absorption (malabsorption syndrome in the narrow sense of the word). Both of these indromes are usually combined by the term “malabsorption” (in a broad sense). A significant role in the development of impaired absorption syndrome is played by dysbiosis - the appearance of a conditionally pathogenic or saprophytic flora in the small intestine and its abundant growth (the bacterial content in 1 ml is 105-107 or more). Some bacteria cause hydrolysis of bile acids and inhibit their conjugation. The hydrolysis products of bile acids have a toxic effect on the intestinal mucosa. In addition, the lack of bile acids prevents the formation of micelles (a combination of fatty acids and monoglycerides with bile acids), which disrupts the absorption of fats. Intestinal flora can intensely absorb vitamin B12, leading to a deficiency in the body. The secretion of their own enzymes is also disrupted, which leads to impaired absorption of carbohydrates and protein. Inflammatory changes in the intestinal wall also cause the exudation of the liquid part of the blood and electrolytes into the intestinal lumen (exudative enteropathy syndrome).

Classification. As mentioned earlier, there is no generally accepted classification of intestinal diseases (including the small intestine). Summarizing the available data, we can assume the following classification:

1. By etiology (discussed above).

2. According to the clinical course: lung, moderate, severe.

3. By the nature of functional disorders of the small intestine: a) digestive insufficiency syndrome; b) malabsorption syndrome; c) exudative enteropathy syndrome.

4. With the flow: the phase of remission, the phase of exacerbation.

The clinical picture. At the first stage of the diagnostic search, first of all, it is possible to identify the features of the onset of the disease, as well as the manifestations of the main syndromes. A slow, gradual onset is more characteristic of chronic nutritional etiology. Information about occupational hazards, drug abuse (especially laxatives against the background of constant constipation), episodes of radiation therapy, intolerance to certain types of food should help establish the etiology of the disease.

Patients' complaints are determined by the severity of dyskinetic, dyspeptic and asthenoneurotic syndromes.

Most often, patients complain of a dysfunction of the emptying function, which manifests itself mainly in the form of diarrhea. Diarrhea (diarrhea) is characterized by frequent bowel movements and the release of unformed feces. Diarrhea with CE has all the properties of the so-called small bowel diarrhea: stools are usually 2-3 times a day, plentiful, since the violation of digestion and absorption in the small intestine leads to a significant increase in the amount of undigested food entering the colon. Since the reservoir function of the colon is preserved, defecation occurs only several times a day, but with the release of a large amount of feces.
The absence of inflammatory changes in the left half of the colon and rectum excludes tenesmus, as well as the presence of blood in the feces. With CE, the urge to Defecate occurs 20-30 minutes after eating and accompanied by

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given by strong rumbling and transfusion in the stomach. Milk intolerance is often noted. Acute eating is also aggravated by overeating, writing, containing a large amount of fat and carbohydrates. Patients pay attention to a peculiar yellowish (golden) color of feces, due to the presence of unreduced bilirubin and a large amount of fat in them.

Dyskinetic syndrome is also manifested by pain. When the small intestine is affected, the pains are more often localized near the navel, are dull, bursting, do not radiate, appear 3-4 hours after eating, are accompanied by bloating, transfusion in the abdomen, and calm down after warming the abdomen.

In patients with CE, flatulence is often noted - bloating due to increased gas formation. For the predominance of fermentation processes, a large outflow of odorless gases is typical. With a prolonged course of CE, especially severe form, asthenoneurotic syndrome is pronounced: patients note weakness, increased physical and mental fatigue.

When the small intestine is damaged due to malabsorption of the products of the breakdown of proteins, vitamins, and lipids, the body weight decreases, while this symptom is not typical for the primary lesion of the colon. However, in the latter case, weight loss is possible due to the patient's voluntary refusal to eat due to fear of pain and impaired bowel function.

Thus, after stage I, an impression of bowel disease is formed.

At stage II of the diagnostic search, the amount of information is less. However, this information is also important for the diagnosis, since the failure to detect a number of symptoms with an undoubted assumption of the presence of CE will indicate a milder course of the disease, the absence of complications.

Thus, the data of stage II will be largely determined by involvement in the pathological process of the intestine, as well as by the reaction from the remaining organs of the digestive system. CE, being in some cases a complication of a number of diseases, contributes to damage to the liver, bile ducts, stomach, pancreas.

With severe damage to the small intestine, signs of malabsorption syndrome appear: weight loss, trophic changes in the skin (dryness, peeling, thinning) and its derivatives (hair loss, brittle nails). Hypovitaminosis B2 is manifested by cheilitis, angular stomatitis; hypovitaminosis PP - glossitis, hypovitaminosis C - bleeding gums.

In case of impaired absorption of calcium in the intestine, pathological fragility of the bones occurs, as well as signs of hypoparathyroidism (positive symptoms of Hvostek and Trusso, in severe cases - convulsions).

With the development of adrenal insufficiency, signs of addisonism appear - hyperpigmentation of the skin, especially skin folds of the palms, oral mucosa, arterial and muscle hypotension. Dysfunction of the gonads in men is manifested by impotence, in women - amenorrhea. However, these endocrine disorders occur quietly in severe CE, when malabsorption syndrome is pronounced.

On palpation of the abdomen, pain is observed in the navel - in the young Porges (pain in palpation of the abdomen and severe pressure

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slightly to the left and above the navel), Hertz's symptom (splashing noise on the palpus - !! and the cecum due to the rapid passage of chyme through the small intestine and the intake of undigested and non-absorbed liquid contents and intestinal gas into the cecum).

At the III stage of the diagnostic search, it is first necessary to confirm the assumption of intestinal damage. This is aided by the results of feces, endoscopy and the radiological method.

Analysis of feces involves microscopy, chemical and bacteriological studies. Based on the results of these studies, typical coprological syndromes are distinguished.

• Small bowel digestion syndrome:

a) liquid yellow feces of an alkaline reaction;

b) a large number of muscle fibers, a little connective tissue, neutral fat and iodophilic microflora;

c) a significant amount of fatty acids and soaps;

d) a very high content of starch and digestible fiber.

• Syndrome of accelerated evacuation from the small intestine:

a) liquid yellow or light brown feces of a slightly alkaline reaction;

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one

6) a significant amount of muscle fibers, fatty acids and soaps, a little connective tissue; c) a lot of neutral fat, starch and digestible cage. Of particular importance is the study of the bacterial microflora of feces to detect dysbiosis, the presence of which contributes to the development of enteritis and further supports its chronic course. In patients with CE, the number of bifidobacteria and lactobacilli was reduced, the number of hemolytic and lactose-negative Escherichia, pathogenic staphylococcus, protea, hemolytic streptococcus was increased. Restoring normal bacterial flora in the intestine is a pretty good criterion for successful treatment. In CE with a predominant lesion of the small intestine, the concentration of enterokinase and alkaline phosphatase (enzymes involved in the absorption of protein and fatty acids) increases significantly in all its departments and in the feces. The increase in the concentration of enzymes in the small intestine is explained by a compensatory increase in their production and increased desquamation of the intestinal epithelium containing these enzymes. The increase in the number of enzymes in feces is due to increased intestinal motility and disruption of enzyme deactivation processes in the distal intestines due to activation of the bacterial flora. To detect malabsorption, a test with D-xylose and vitamin Bp is used (Schilling test). To test with D-xylose, 5 g of D-xylose, a monosaccharide absorbed from the upper small intestine without preliminary cleavage, is given inward. In case of malabsorption only from the upper parts of the small intestine, the excretion of D-xylose with urine decreases in the first 2 hours, and with more extensive lesions, also with urine in 5 hours. If the excretion of D-xylose is disturbed only in the first 2 hours, and during the next 5 hours proceeds normally, then malabsorption in the upper part of the small intestine is compensated by absorption in its distal parts. With damage to the mucous membrane of the small intestine, the absorption of vitamin B12 is impaired. Schilling's test is as follows: pain-
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