LECTURE No. 12. Diseases of the digestive tract. Diseases of the intestines. Diseases of the small intestine. Chronic enteritis

Chronic enteritis is a disease of the small intestine, characterized by a violation of its functions (digestion and absorption) against the background of dystrophic and dysregenerative changes, culminating in the development of inflammation, atrophy and sclerosis of the mucous membrane of the small intestine.

Etiology and pathogenesis. This is a polyetiological disease that can be the result of acute inflammation of the small intestine or a primary chronic process.

In recent years, Yersinia, Helicobacteria, Proteus, Pseudomonas aeruginosa, rotaviruses, numerous representatives of protozoa and helminths (giardia, ascaris, tapeworms, opisthorchia, cryptosporidium) have been given great importance as an etiological factor in chronic enteritis.

Of great importance in the occurrence of chronic enteritis are alimentary factors - overeating, eating dry food, unbalanced, predominantly carbohydrate foods, abuse of spices. Enteritis is caused by ionizing radiation, exposure to toxic substances, and drugs. Among the common pathogenetic mechanisms of chronic diseases of the small intestine, there are changes in the intestinal microflora against the background of a decrease in local and general immunity.

Changes in the immune status - a decrease in the content of secretory IgA, an increase in the level of IgE, a decrease in blast transformation of lymphocytes and inhibition of leukocyte migration - lead to colonization of the small intestine by representatives of opportunistic microflora and a decrease in normal anaerobic flora.

Bacterial colonization of the small intestine enhances intestinal secretion due to the activation of epithelial cell cAMP, which increases intestinal permeability, enhances the production of electrolytes and water by cells. The secretion of water and electrolytes leads to a violation of water-salt metabolism. Under the influence of microbial flora, the enterohepatic circulation of bile is disturbed. Fatty acids bind calcium ions, forming sparingly soluble soaps that are excreted in the faeces. Violation of calcium metabolism is promoted by changes in the metabolism of vitamin D, which reduces the absorption of calcium. Under the influence of metabolic disorders of fat-soluble vitamins, the content of microelements in the blood decreases. Prolonged dysbiosis promotes sensitization to microbial and food antigens, causes immune inflammation of the mucous membrane, which results in the formation of tissue antigens. The increased permeability of the mucous barrier is accompanied by the resorption of unsplit protein macromolecules, which become allergens, and immunological reactivity is impaired. With allergies, biologically active substances are released that increase the permeability of the intestinal wall, change the functional properties of enterocytes. Violations of the microstructure of the enterocyte cytoplasmic membrane lead to inhibition of lactase activity first, and then maltase and sucrase activity. With dystrophic, dysregenerative changes in epitheliocytes, the synthesis of enzymes and their sorption on the membranes of epitheliocytes - disaccharidases, peptidases, enterokinase, alkaline phosphatase - are reduced, which causes disturbances in both membrane and cavity digestion. All this becomes the basis of the malabsorption syndrome. In the early stages of the disease, lipid metabolism disorders develop due to a decrease in fat absorption, its loss with feces, and changes in the intestinal phase of enterohepatic bile circulation.

Violation of bile metabolism, in turn, leads to a violation of lipid metabolism, which affects the structure and function of cell membranes. In connection with insufficient absorption of fat, a violation of the synthesis of steroids occurs, which induces a violation of the functions of the endocrine glands.

Morphologically, chronic enteritis is manifested by inflammatory and dysregenerative changes in the mucous membrane of the small intestine. If the process progresses, its atrophy and sclerosis are observed.

Classification (Zlatkina A. R., Frolkis A. V., 1985).

1) Etiology: intestinal infections, helminthic invasions, alimentary, physical and chemical factors, diseases of the stomach, pancreas, biliary tract.

2) Phases of the disease: exacerbation; remission.

3) Degree of severity: mild; moderate; heavy.

4) Current: monotonous; recurrent; continuously recurring; latent.

5) Character of morphological changes: eunit without atrophy; jeunitis with moderate partial villous atrophy; jeunitis with partial villous atrophy; eunit with total villous atrophy.

6) The nature of functional disorders: disorders of membrane digestion (disaccharidase deficiency), malabsorption of water, electrolytes, trace elements, vitamins, proteins, fats, carbohydrates.

7) Complications: solaritis, nonspecific mesadenitis.

clinical picture. The clinical picture of chronic enteritis consists of local and general enteric syndromes. The first is caused by a violation of the processes of parietal (membrane) and cavity digestion (maldigestion). Patients complain of flatulence, pain in the paraumbilical area, cap-shaped bloating, loud rumbling, diarrhea, and, less commonly, constipation. Palpation reveals pain in the mesogastrium, as well as to the left and above the navel (positive Porges sign), splashing noise in the area of ​​the cecum (Obraztsov sign). The feces take on a clayey appearance, and polyfecal matter is characteristic.

General enteral syndrome is associated with impaired absorption of food ingredients (malabsorption), resulting in disorders of all types of metabolism, changes in homeostasis. Characterized by multifaceted metabolic disorders, primarily protein, which is manifested by a progressive loss of body weight. Changes in carbohydrate metabolism are less pronounced, which is manifested by bloating, rumbling in the abdomen and increased diarrhea while taking dairy products. To a large extent, the deficiency of body weight in patients is due not only to protein, but also to lipid imbalance. Changes in lipid metabolism are closely related to metabolic disorders of fat-soluble vitamins and minerals (calcium, magnesium, phosphorus). The characteristic signs of calcium deficiency are a positive symptom of the muscle roller, convulsions, recurrent "unmotivated" bone fractures, osteoporosis, osteomalacia. There are also swelling of the face, cyanosis of the lips, glossitis, irritability, poor sleep. Violations of the water and electrolyte balance are manifested by general weakness, physical inactivity, muscle hypotension, nausea, vomiting, and changes in the central nervous system.

Symptoms of polyhypovitaminosis become typical for chronic enteritis of moderate and severe severity. Hypovitaminosis C is clinically manifested by bleeding gums, repeated nasal, uterine bleeding, bruising on the skin. Hypovitaminosis B is accompanied by pallor of the skin, glossitis, angular stomatitis (cheilez). Signs of deficiency of fat-soluble vitamins (A, O, E, K): poor twilight vision, dry skin and mucous membranes, increased bleeding of the gums.

Severe forms of chronic enteritis occur with symptoms of endocrine dysfunction (pluriglandular insufficiency). Hypocorticism is manifested by arterial hypotension, cardiac arrhythmias, anorexia, and skin pigmentation. A decrease in the activity of the gonads is accompanied by ovarian dysfunction, menstrual disorders, in men - impotence, gynecomastia, hair loss.

Thyroid dysfunction is characterized by general weakness, dry skin, bradycardia, decreased performance, and intellectual-mnestic disorders.

Diagnosis and differential diagnosis. A general blood test reveals micro- and macrocytic anemia, an increase in ESR, and in severe cases - lympho- and eosinopenia. If the disease is of parasitic origin, lymphocytosis and eosinophilia may be observed in the blood.

A scatological examination reveals an intestinal type of steatorrhea due to fatty acids and soaps, creatorrhea, amylorrhea. The content of enterokinase and alkaline phosphatase in feces increases. The daily mass of feces increases significantly.

Bacteriological analysis of feces reveals dysbacteriosis of varying degrees. There is a decrease in lacto- and bifidobacteria, enterococci, strains of Escherichia coli with altered enzymatic properties appear.

In the general analysis of urine in severe form of chronic enteritis, microalbuminuria and migrohematuria are noted.

In a biochemical blood test, hypoproteinemia, hypoalbuminemia, hypoglobulinemia, hypocalcemia, a decrease in the level of magnesium, phosphorus, and other microelements, electrolyte metabolism disorders in the form of a decrease in the level of sodium and potassium are detected. Lipid metabolism disorders are accompanied by changes in the lipid spectrum: the level of cholesterol, phospholipids decreases, and the spectrum of bile acids, phospholipids and triglycerides also changes.

The results of an x-ray study allow us to clarify the motor function of the small intestine and the relief of the mucosa, dystonic and dyskinetic changes in the form of a slowdown or acceleration of the passage of a suspension of barium sulfate through the small intestine, and the relief of the mucosa changes in the form of uneven thickening, deformation and smoothing of the folds. Gastroduodenoscopy reveals atrophic gastritis and duodenitis.

The morphological picture of a mild form of chronic enteritis is characterized by thickening of the villi, their deformation, a decrease in the depth of the notches, a decrease in the tone of smooth muscles, subepithelial edema, degenerative changes in the surface of the epithelium, thinning of the brush border of cells, a decrease in the number of goblet cells in the region of the villi, an increase in the number of crypts, infiltration of the own layer mucosa with lymphoplasmacytic elements, a decrease in Paneth cells in the area of ​​the bottom of the crypts.

For the moderate form, partial atrophy of the villi, a decrease in the number of crypts, thinning of the mucous membrane, a decrease in the brush border, and lymphoplasmacytic infiltration of the submucosal and muscular layers are typical. The severe form of the disease is characterized by progressive villous atrophy, diagnosed by histological, histochemical, and morphometric criteria. The process of proliferation of enterocytes prevails over their differentiation, an abundance of immature, defective cells appears.

Differential diagnosis in chronic enteritis is carried out with celiac enteropathy, Crohn's disease, Whipple's disease, intestinal amyloidosis, diverticular disease, lymphoma, tumors of the small intestine. Common to all these conditions are clinical syndromes of indigestion, absorption and dysbacteriosis. The final diagnosis is confirmed by morphological examination of the mucous membrane of the small intestine.

So, for celiac enteropathy, an anamnestic indication of the relationship of exacerbations of the disease with the use of gliadin-containing products is typical. The clinic of celiac enteropathy resembles chronic enteritis. Most often, the upper intestines are affected and there are no changes in the ileum. The optimal site for taking biopsy specimens is the area of ​​the mucous membrane near the ligament of Treitz. Morphological examination reveals a decrease in the number of goblet cells and an increase in the number of interepithelial lymphocytes, subtotal villous atrophy, and inflammatory cell infiltration of its own layer. With celiac enteropathy, morphological changes on the background of a gluten-free diet are reversible, in contrast to banal chronic enteritis, in which morphological changes are irreversible.

In Crohn's disease, clinical polymorphism is noted, due to the autoimmune genesis of the disease and its characteristic systemic manifestations (such as autoimmune thyroiditis, polyarthritis, iritis, hepatitis, frequent combination of enteritis and distal colitis). Endoscopic and morphological tests have a high resolution in the verification of Crohn's disease, revealing the mosaic nature of the intestinal lesion, typical changes of the "cobblestone pavement" type, which alternate with areas of intact mucosa. X-ray, endoscopic examination can detect intestinal strictures, sometimes intestinal fistulas are formed. Morphological diagnostics states inflammatory cell infiltration of all layers of the intestinal wall with maximum damage to the submucosal layer and minimal changes in the mucosa. In the submucosal layer, lymphocytic sarcoid-like granulomas, pathognomonic for this disease, are found.

For Whipple's disease, in addition to signs of enteritis, extraintestinal manifestations in the form of fever, arthritis, lymphadenopathy, arterial hypotension, and skin pigmentation are characteristic. The most informative morphological criteria of the disease. Biopsy specimens taken from the small intestine reveal intracellular and extracellular fat accumulation in the small intestinal mucosa and mesenteric lymph nodes; infiltration of its own layer by large microphages containing CHIC-positive fat-free granules, and the presence of bacilli in the mucosa.

Treatment. Treatment of chronic enteritis should be comprehensive, including agents that affect etiological factors, pathogenetic mechanisms, as well as local and general symptoms of the disease.

The basis is dietary nutrition, which helps to reduce the increased osmotic pressure in the intestinal cavity, reduces secretion, and normalizes the passage of intestinal contents. Exclude products containing coarse vegetable fiber (raw vegetables, fruits, rye bread, nuts, pastry, canned food, spices, spicy dishes, whole milk, beer, kvass, carbonated and alcoholic drinks). The use of table salt is limited. Fractional meals are needed, up to 5-6 times a day. During the period of remission, some vegetables and fruits are introduced into the diet, up to 100-200 g per day. Assign lettuce, ripe peeled tomatoes, soft pears, sweet apples, oranges, tangerines, raspberries, strawberries, wild strawberries. Food should be boiled or steamed.

Drug therapy should be etiotropic, pathogenetic and symptomatic. Etiotropic treatment: for grade II-IV dysbiosis, antibacterial drugs are prescribed: metronidazole (0,5 g 3 times a day), clindamycin (0,5 g 4 times a day), cephalexin (0,5 g 2 times a day). day), biseptol (0,48 g 2 times a day), sulgin (1 g 3-4 times a day), furazolidone (0,1 g 4 times a day). After using antibacterial drugs, eubiotics are prescribed - bifidumbacterin or bificol 5 doses 3 times a day 30 minutes before meals, coli-bacterin or lactobacterin 3 doses 3 times a day before meals, hilakforte 40 drops 3 times a day before meals. Treatment with bacterial preparations is carried out for a long time: 3 courses of 3 months each year. For staphylococcal dysbacteriosis, an antistaphylococcal bacteriophage is prescribed (20 ml 3 times a day for 15-20 days), for proteus dysbacteriosis - coliprotean bacteriophage orally, 20 ml 3 times a day, the course of treatment is 2-3 weeks.

As an antidiarrheal symptomatic agent, imodium (loperamide) is prescribed 1 capsule 2-3 times a day before meals for 3-5 days.

To improve the digestion process, enzymes are recommended: pancreatin, panzinorm forte, festal, digestal, pankurmen, mezim forte, trienzyme, the doses of which are selected individually (from 1 tablet 3 times a day to 3-4 tablets 4 times a day) and which are prescribed directly before or during meals for 2-3 months. If necessary, enzyme replacement therapy is continued for a longer time.

To normalize the general condition of patients with enteritis and eliminate metabolic disorders, substitution therapy is indicated. In order to compensate for the deficiency of vitamins, vitamins B and B are prescribed for 4-5 weeks.₆ 50 mg each, PP - 10-30 mg, C - 500 mg each. For steatorrhea, parenteral administration of vitamin B is indicated.₂ (100-200 mcg) in combination with fat-soluble vitamins.

Riboflavin 0,02 g, folic acid 0,003 g once a day, vitamin E 3300 IU 2 times a day are prescribed inside. In chronic enteritis occurring with severe protein deficiency, along with a diet, parenteral administration of plasma, 150-200 ml of protein hydrolysates and mixtures of amino acids (aminopeptide, alvesin, polyamine, intrafusin, 250-500 ml intravenously for 20 days) in combination with anabolic hormones (retabolil 2,0 ml 1 time in 7-10 days for 3-4 weeks) and fatty mixtures such as intralipid.

The appointment of steroids is indicated only with significant protein deficiency, hypoproteinemia, the presence of adrenal insufficiency.

To correct water and electrolyte disorders, intravenous administration of panangin 20-30 ml, calcium gluconate 10% 10-20 ml in 200-400 ml of isotonic solution or glucose solution, polyionic solutions "Disol", "Trisol", "Quartasol" are indicated. Electrolyte solutions are administered intravenously for 10-20 days under the control of the acid-base state and the level of blood electrolytes.

Prognosis and prevention. The prognosis for life and ability to work is favorable in most cases. Prognostically unfavorable signs are a continuously relapsing course of the disease, sudden significant weight loss, anemia, endocrine disorder syndrome (decreased libido, dysmenorrhea, infertility).

Prevention of chronic enteritis consists in the timely treatment of acute intestinal infections and concomitant diseases of the gastroduodenal zone, in observing the diet, in the prophylactic administration of bacterial preparations during X-ray and radiotherapy.

Author: Mostovaya O.S.

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