Dyspepsia: causes and pathogenesis

The main causes of alimentary dyspepsia are a violation of the regime, the nature and quality of nutrition, a long unbalanced diet with a deficiency of food ingredients necessary for the life of the organism (proteins, fats, vitamins, trace elements, etc.). It should be remembered that the small intestine is very sensitive to insufficient intake of certain nutrients, which is primarily due to the rapid rate of renewal of its mucosa and significant daily losses of various substances with tearing off cells. In this regard, the amount of nutrients needed to ensure the normal structure of the small intestine mucosa is very large. The period of epithelial renewal of its mucous membrane is 2-3 days, with 300 g of cell mass being rejected daily, which is approximately 95% of the "cellular loss" of the entire digestive tract - up to 20 g of proteins and fats, although some of them are reabsorbed. To restore the normal structure of the mucous membrane of the small intestine, in addition to proteins and fats, other food ingredients - vitamins B ₁₂, D, folic acid - are needed . It becomes clear the high specific gravity of alimentary dyspepsia, which arises from malnutrition.

At the same time, excessive protein or carbohydrate loading, especially in combination with factors that inhibit the secretory function of the digestive glands (overheating, hypothermia, physical and mental overstrain), often also leads to the appearance of alimentary dyspepsia. Its development is facilitated by the abuse of spicy dishes and seasonings, the disturbance of the regime and the rhythm of nutrition, the systematic use of a large amount of coarse plant fiber (with long-term use of fiber there is a functional and morphological alteration of the small intestine). Thus, for vegetarians and healthy individuals living in tropical countries, the villi of the jejunal mucosa become broad, branched, sometimes fused, ie, a pattern characteristic of chronic enteritis with intestinal dyspepsia syndrome is observed. For the normal development of villi, the introduction of pectin, rather than cellulose, which is established in the experiment.

In the pathogenesis of alimentary dyspepsia, an important role is played by the disorder of not only the secretory and motor functions of the stomach, which at first often increase and then decrease, but also the exocrine function of the pancreas and bile secretion. In the small intestine, the food of a more acidic reaction is not cleaved by enzymes, which inhibits production and the release of intestinal enzymes. In these conditions, the motor function of the small intestine is disrupted: food chyme is retained in its upper parts, which facilitates the migration of bacteria from the lower intestine to the above, and also increases their enzymatic activity. Activation of flora uncharacteristic of the intestines leads to the appearance of putrefaction and fermentation in the intestine, with the predominance of putrefactive or fermenting processes due to not only the type of bacteria, but also the quality of food.

The stasis of the contents in the proximal regions promotes the decomposition of food in both the thick and small intestine. A large number of toxic products of degradation of nutrients (indole, skatole, hydrogen sulphide, ammonia, low-molecular fatty acids, etc.), which irritate the receptors of the intestinal mucosa, affect its motility, cause diarrhea. In turn, the accelerated passage of food masses prevents normal digestion. Formed with dyspepsia, calcareous salts (soaps) inhibit the growth of bifidobacteria - normal representatives of the intestinal microflora, which aggravates the violation of digestion processes.

To violations of digestion, the consequence of which is diarrhea, with the passage of time, the syndrome of impaired absorption is added. In this case, thinning of the mucous membrane of the small intestine, loss of brush border disaccharidases, impaired absorption of simple sugars, decreased digestion and absorption of proteins and fats, an even more pronounced increase in passage time of the contents in the gut and a more significant colonization of small intestine bacteria. There is a structural rearrangement of the small intestine - a flattening of the epithelium of its mucous membrane and changes in the brush border, which are considered to be the most characteristic, atrophy of the villi, the development of which is associated with dysbiosis and action on the mucosa of unconjugated bile acids. In electron microscope research, the villus is enlarged and deformed, the accumulation of lipids in the epithelium, changes in regenerative processes in the form of impaired education, maturation and migration of cells. Thus, the so-called functional character of alimentary dyspepsia is refuted by morphological findings, which testify to the position put forward by domestic pathologists about the unity of structure and function.

Morphological changes in the mucous membrane of the small intestine underlie the syndrome of intestinal absorption failure. The digestion of carbohydrates is significantly affected by the breakdown of the process of surface hydrolysis, which can be judged by the decrease in the activity of disaccharidases in the brush border, as well as by the violation of their absorption and utilization. Activity of intestinal dipeptidases decreases with the most severe manifestations of malnutrition and diarrhea, playing a role in the violation of protein digestion. Pathogenetic factors of lipid digestion disorders in the form of steatorrhoea include reduced secretion of pancreatic lipase, disorder of emulsification of bile acids, intestinal dysbacteriosis, and changes in the mucous membrane, which leads to reduced absorption of fats.

Protein-energy insufficiency aggravates motor disorders in the form of retardation of evacuation from the stomach and passage through the intestine, facilitates the further colonization of the proximal small intestine by microorganisms and the associated impairment of absorption of vitamin B ₁₂. Protein deficiency is combined with a deficiency of nicotinic acid in the disorder of digestion and absorption processes.

With severe protein-energy deficiency, hypophosphatemia occurs, which in turn affects the processes of hematopoiesis, immunological status, reduces the regenerative capacity of epithelial cells. Zinc deficiency often leads to digestion and diarrhea, and a relationship between zinc content in feces and their mass is found. In the biopsy specimens of the small intestine mucosa in enterocytes with acidophilic granules, pathological bodies are identified, which are regarded as altered secretory granules and proliferating lysosomes. The association of these changes with zinc deficiency is confirmed by their disappearance after prolonged treatment with zinc preparations.

Thus, the small intestine is very sensitive to the lack and excess of these or other food ingredients and reacts to them by "functional" and morphological changes.

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