Digestive failure syndrome

Indigestion syndrome is a symptom complex associated with impaired digestion of nutrients due to a deficiency of digestive enzymes (enzymopathy).

The basis for the occurrence of digestive disorders is a genetically determined or acquired insufficient production of digestive enzymes in the small intestine. Moreover, either the absence of synthesis of one or several enzymes, or a decrease in their activity, or a change in biochemical reactions affecting enzymatic activity is observed.

Among congenital enzymopathies, the most common are deficiencies of disaccharidases (lactase, sucrase, isomaltase, etc.), peptidases (gluten enteropathy), and enterokinase. Acquired enzymopathies are observed in diseases (chronic enteritis, Crohn's disease, diverticulosis with diverticulitis, etc.) and resection of the small intestine, diseases of other digestive organs (pancreatitis, hepatitis, cirrhosis of the liver) and endocrine organs (diabetes mellitus, hyperthyroidism), as well as when taking certain medications (antibiotics, cytostatics, etc.) and irradiation. Among acquired enzymopathies, the most common is alimentary enzymopathies, in which disturbances in the production and activity of enzymes are associated with the nature of nutrition.

Causes of digestive insufficiency

In the clinical picture of dyspepsia, depending on the prevalence of signs of digestive disorders in various parts of the gastrointestinal tract, a distinction is made between gastric, intestinal, and sometimes pancreatogenic forms.

The occurrence of gastric dyspepsia is associated with atrophic gastritis, which is known to be characterized by secretory insufficiency, as well as with decompensated pyloric stenosis and gastric cancer. The clinical picture of this dyspepsia is characterized by loss of appetite, a feeling of heaviness, distension and pressure in the epigastric region after eating, belching air, food with a rotten smell, an unpleasant taste in the mouth, nausea, flatulence, and diarrhea. When examining gastric secretion, achylia or achlorhydria are detected.

Coprological examination most often reveals intestinal steatorrhea, when fatty acids, soaps, amylorrhea, creatorrhea, increased ammonia content, decreased stercobilin. Excretion of indican with urine is increased, the amount of bilirubin and bile acids in it is increased, and urobilin is decreased. X-ray examination of the upper digestive tract most often reveals accelerated passage of contrast agent through the small intestine.

Symptoms of digestive insufficiency

Treatment of dyspepsia primarily involves the impact on the underlying disease. Treatment of alimentary insufficiency of digestion is based on the additional introduction of missing substances into the diet - proteins, amino acids, vitamins, mineral salts in order to stimulate the biosynthesis of the protein or prosthetic part of enzymes.

Treatment of digestive insufficiency

Insufficiency of parietal digestion is a characteristic sign of chronic diseases of the small intestine, the morphological substrate of which are inflammatory, dystrophic and sclerotic changes in the mucous membrane, a decrease in the number and damage to the structure of villi and microvilli per unit surface. The occurrence of insufficiency of parietal digestion is facilitated by disturbances in the enzymatic layer of the intestinal surface and disorders of intestinal peristalsis, in which the transfer of nutrients from the intestinal cavity to the surface of enterocytes is disrupted. This syndrome is most often encountered in chronic enteritis, enteropathies, Whipple's disease, Crohn's disease and other diseases of the small intestine.

The clinical picture is similar to that observed in intestinal dyspepsia and malabsorption syndrome.

In order to clarify the diagnosis, enzyme activity (amylase, lipase) is determined by their sequential desorption in homogenates of biopsies of the small intestinal mucosa obtained by aspiration biopsy, which also helps to detect inflammatory and atrophic changes in the mucosa. In addition to determining enzymes, studying glycemic curves after per os loads of mono-, di- and polysaccharides helps to differentiate syndromes of parietal and cavitary digestion.

In therapy, the means and methods aimed at treating the underlying disease and eliminating the manifestations of malabsorption syndrome are essential. In this regard, it is advisable to prescribe a complete, protein-rich diet, excluding foods and dishes that irritate the intestines (diets No. 4, 46, 4v); astringents, carminatives, antispasmodics, as well as replacement therapy (enzyme and protein preparations, vitamins, anabolic steroids, iron preparations, calcium, etc.).

Insufficiency of intracellular digestion is a primary or secondary fermentopathy, which is based on genetically determined or acquired intolerance to disaccharides. Primary insufficiency of intracellular digestion, as a rule, develops at an early age with the introduction of an intolerant disaccharide into food. Acquired insufficiency is often a consequence of diseases of the small intestine: chronic enteritis, gluten enteropathy, exudative hypoproteinemic enteropathy, nonspecific ulcerative colitis, involvement of the small intestine in the pathological process in viral hepatitis, etc. In the pathogenesis of the syndrome, an increase in fermentation processes as a result of the entry of undigested disaccharides into the large intestine and activation of microbial flora is of significant importance.

The clinical picture of this form of deficiency is characterized by persistent diarrhea. The stool is liquid, abundant, foamy.

Coprological examination helps in diagnosis, which reveals a decrease in the pH of feces and an increase in the content of organic acids. The nature of intestinal disorders can be finally determined by determining the activity of disaccharidases in biopsies of the intestinal mucosa and studying glycemic curves after disaccharide loading. With a deficiency of disaccharidase, which breaks it down, the maximum increase in its content from the initial level does not exceed 0.2-0.25 g / l, and the glycemic curve looks flat.

The treatment of both genetically determined (primary) and secondary disaccharidase deficiency is based on the exclusion from the diet (permanent or temporary) of foods and dishes containing the intolerable disaccharide. In case of secondary deficiency, it is necessary to treat the underlying disease, which can lead to the restoration of tolerance to the corresponding disaccharide. In some cases, it is useful to prescribe falicor, phenobarbital, nerobol, folic acid, which stimulate the production of intestinal enzymes.

Preventive measures for insufficient digestion of alimentary origin should primarily include a balanced rational diet that provides the body's physiological needs for nutrients. Of significant importance is the appropriate culinary and technological processing of food products, which allows preserving vitamins and other nutrients, as well as inactivating or destroying harmful natural components (antivitamins, proteinase inhibitors, etc.).

Prevention of dyspepsia of toxic origin is based on compliance with hygienic standards concerning both the composition of food products and the prevention of the entry of foreign chemical and biological substances into them.