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Diseases of the intestine are quite frequent, however, the true incidence is not precisely known, since the ischemic lesion can be both an independent pathology and can accompany other diseases of the digestive tract (for example, xR ° ptas ™ ^ ™ J№> chronic pancreatitis). Exact accounting of the incidence of disease ™ is also difficult because of the various pathological effects of the intestine rather than a similar reaction - diarrhea or constipation. In the meantime, these symptoms can be manifestations of SU ^ b ° F ^ ™ 0 nal disorders and can also be determined by the nature of the patient’s diet.
Currently, there is no single approach to the classification and diagnosis of intestinal diseases. The same suffering is often denoted by different terms. Separate symptoms (constipation, diarrhea, dyspepsia) and syndromes, such as malabsorption syndrome, malabsorption syndrome, digestive insufficiency syndrome, irritable bowel syndrome, bacterial overgrowth syndrome in the small intestine, intestinal lymphoectasia, etc., appear as an independent diagnosis.
In the domestic literature, the term "chronic enteritis" refers to a group of diseases that occur with many years of impaired intestinal digestion and absorption, although some authors do not recognize this definition. However, in chronic enteritis, the main clinical signs are the syndromes of malabsorption and impaired intestinal digestion, which cause the appearance of the main symptom of chronic enteritis - small bowel diarrhea.
The term “chronic colitis” is also interpreted excessively widely and mistakenly includes not only the inflammatory diseases of the colon itself, but also fermentative pathologies, functional pathology, dysbacteriosis, dyspepsia (fermentation or putrefaction), non-infectious diarrhea. However, a number of authors do not recognize the existence of non-ulcerative colitis, referring to inflammatory bowel disease only as ulcerative colitis (UC) and granulomatous lesion of the colon (Crohn's disease). All this makes work extremely difficult 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 (ChE) is a chronic inflammatory-dystrophic disease of the small intestine, leading to morphological changes in the mucosa and impaired motor, secretory, absorption and other functions of the intestine.
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 subsequent development of atrophic processes. At the same time, blood capillaries and intestinal lymphatic vessels are affected, as well as intrahepatic nerve plexuses. Dystrophic changes are also found in the celiac plexus and border sympathetic trunks.
Etiology. The causes of ChE are very diverse.
• Alimentary disorders, modeless nutrition, alcoholism.
• Intoxication with drugs and chemicals.
• Impact of penetrating radiation (as a rule, CE of such etiology is observed during X-ray irradiation or radiation therapy for tumors of various origin).
• Hereditary constitutional factor; congenital deficiency of enzymes, in particular, participating in the breakdown of various carbohydrates.
• Diseases of the digestive tract - "secondary" enteritis. Pathogenesis. A number of pathological processes develop in the intestine,
severity of which depends on the characteristics of the leading etiology
gychesky factor. Thus, impaired motility of the small intestine and a decrease in the barrier function of the intestinal wall (due to decreased production of immunoglobulins and lysozyme, as well as impaired integrity of the epithelium) indirectly lead to impaired digestion (maldigestia syndrome) and absorption (malabsorption syndrome in the narrow sense of the word). Both of these INDromes are usually combined with the term "malabsorption" (in a broad sense). Dysbacteriosis plays a significant role in the development of impaired absorption syndrome - the appearance in the small intestine of conditionally pathogenic or saprophytic flora and its abundant growth (the bacteria content in 1 ml is 105-107 or more). Some bacteria cause hydrolysis of bile acids and prevent their conjugation. The products of hydrolysis of bile acids have a toxic effect on the mucous membrane of the intestine. In addition, the lack of bile acids prevents the formation of micelles (the combination of fatty acids and monoglycerides with bile acids), which disrupts the absorption of fats. The intestinal flora can vigorously absorb vitamin B12, leading to its deficiency in the body. The release of its own enzymes is also impaired, which leads to a breakdown in the 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 (syndrome of exudative enteropathy).
Classification. As mentioned earlier, the generally accepted classification of intestinal diseases (including the small intestine) does not exist. Summarizing the available data, we can assume the following classification:
1. According to etiology (discussed above).
2. According to the clinical course: mild, moderate, severe.
3. By the nature of the functional disorders of the small intestine: a) digestive insufficiency syndrome; b) syndrome of insufficiency of absorption; c) syndrome of exudative enteropathy.
4. Downstream: the phase of remission, the phase of aggravation.
Clinical picture. At stage I of the diagnostic search, first of all, it is possible to reveal the features of the onset of the disease, as well as the manifestations of the main syndromes. Slow, gradual onset is more characteristic for CE of alimentary etiology. Information about occupational hazards, drug abuse (especially laxatives on the background of persistent constipation), episodes of radiation therapy, intolerance to certain types of food should help in establishing the etiology of the disease.
Complaints of patients are determined by the severity of dyskinetic, dyspeptic and asthenoneurotic syndromes.
Most often, patients complain of impaired function disorder, which manifests itself mainly in the form of diarrhea. Diarrhea (diarrhea) is characterized by frequent emptying of the intestines and the release of unformed feces. Diarrhea with CE has all the properties of the so-called small bowel diarrhea: the stool is usually 2-3 times a day, plentiful, since a violation of digestion and absorption in the small intestine leads to a significant increase in the amount of undigested food entering the large intestine. Since the reservoir function of the colon is preserved, bowel movements occur only a few times a day, but with a large amount of feces released.
The absence of inflammatory changes in the left half of the colon and rectum eliminates tenesmus, as well as the presence of blood in the stools. With CE, the urge to Defecate occurs 20–30 minutes after a meal and is accompanied by
given by a strong rumbling and transfusion in the stomach. Milk intolerance is often noted. Spicy food is also exacerbated by overeating, writing, containing large amounts of fats and carbohydrates. Patients pay attention to the peculiar yellowish (golden) color of feces caused by the presence of unrestored bilirubin and a large amount of fat in them.
Diskinetic syndrome is also manifested by pain. With the defeat of the small intestine, pain is more often localized near the navel, is dull, arching, does not radiate, appears 3-4 hours after a meal, is accompanied by bloating, transfusion in the abdomen, subsides after warming the abdomen.
In patients with CE, meteorism is often noted - bloating due to increased gas formation. For the prevalence of fermentation processes, a large amount of odorless gases are typical. With a prolonged course of CE, especially of a severe form, the asthenoneurotic syndrome is clearly pronounced: patients note weakness, increased physical and mental fatigue.
With the defeat of the small intestine due to impaired absorption of the products of the breakdown of proteins, vitamins, lipids, body weight is reduced, whereas for the primary lesion of the colon, this symptom is not typical. However, in the latter case, weight loss is possible due to the patient's voluntary refusal to eat because of fear of pain and bowel function disorder.
Thus, after stage I, an impression of intestinal disease appears.
At stage II of the diagnostic search, the amount of information is less. However, this information is also important for diagnosis, since failure to detect a number of symptoms with the undoubted assumption 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 the involvement of the intestine in the pathological process, as well as the reaction of the rest of the digestive system organs. CE, being in some cases itself a complication of the course of a number of diseases, contributes to the damage to the liver, biliary tract, 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). Vitamin A hypovitaminosis is manifested by cheilitis, an angular stomatitis; hypovitaminosis PP - glossitis, hypovitaminosis C - bleeding gums.
When calcium absorption is impaired in the intestine, pathological bone fragility occurs, as well as signs of hypoparathyroidism (positive symptoms of Khvostek and Trusso, in severe cases - convulsions).
With the development of adrenal insufficiency, signs of addisonism appear - hyperpigmentation of the skin, especially the skin folds of the palms, the oral mucosa, arterial and muscular hypotension. Impaired function of the gonads in men is manifested by impotence, in women - by amenorrhea. However, these endocrine disorders occur quietly with severe CE, when malabsorption syndrome is pronounced.
On palpation of the abdomen, tenderness in the navel is noted - in the young Porghes (tenderness on palpation of the abdomen and strong pressure
slightly to the left and above the navel), Hertz symptom (splashing sound on palp - and the cecum due to the rapid passage of chyme through the small intestine and the receipt of undigested and non-absorbed liquid contents and intestinal gas in the cecum).
At stage III of the diagnostic search, it is first necessary to confirm the assumption of intestinal damage. This is assisted by the results of fecal examination, endoscopy and X-ray method.
Stool analysis involves microscopy, chemical and bacteriological examination. Based on the results of these studies, typical scatological syndromes are distinguished.
• Digestive insufficiency syndrome in the small intestine:
a) liquid yellow alkaline feces;
b) a large amount of muscle fibers, some 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.
• Accelerated evacuation syndrome from the small intestine:
a) liquid yellow or light brown feces of weakly alkaline reaction;
6) a significant amount of muscle fibers, fatty acids and soaps, some connective tissue; c) a lot of neutral fat, starch and digestible cell-specific. The study of bacterial microflora of feces is of particular importance for the detection of dysbacteriosis, 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 is reduced, the number of hemolytic and lactose-negative escherychias, pathogenic staphylococcus, Proteus, and hemolytic streptococcus is increased. The restoration of normal bacterial flora in the intestines is a fairly good criterion for successful treatment. With CE, with predominant damage to 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 feces. The increased concentration of enzymes in the small intestine is due to a compensatory increase in their production and enhanced desquamation of the intestinal epithelium containing these enzymes. The increase in the number of enzymes in feces is due to increased intestinal motility and impaired enzyme deactivation processes in the distal intestine due to the activation of the bacterial flora. For detection of malabsorption using the test with D-xylose and vitamin B (Schilling test). For the test with D-xylose, 5 g of D-xylose, a monosaccharide absorbed from the upper small intestine without prior cleavage, is obtained. In case of violation of absorption only from the upper parts of the small intestine, D-xylose is excreted in the urine in the first 2 hours, and in case of more extensive lesions, also in the urine in 5 hours. If the release of D-xylose is disturbed only in the first 2 hours, and during the next 5 hours proceeds normally, the violation of absorption in the upper part of the small intestine is compensated by absorption in its distal parts. If the mucous membrane of the small intestine is damaged, the absorption of vitamin B12 is impaired. The Schilling test is as follows:
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