Dyspepsia - Causes and Pathogenesis

The main causes of alimentary dyspepsia are violation of the regime, nature and quality of nutrition, long-term unbalanced nutrition with a deficit of food ingredients necessary for the body's vital functions (proteins, fats, vitamins, microelements, 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 mucous membrane and significant daily losses of various substances with rejected cells. In this regard, the amount of nutritional products necessary to ensure the normal structure of the mucous membrane of the small intestine is very large. The renewal period of the epithelium of its mucous membrane is 2-3 days, and up to 300 g of cellular mass is 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. In order to restore the normal structure of the small intestine mucosa, in addition to proteins and fats, other food ingredients are also needed - vitamins B ₁₂, D, folic acid. The high proportion of alimentary dyspepsia, which occurs due to malnutrition, becomes understandable.

At the same time, excessive food load with proteins or carbohydrates, 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, violation of the regime and rhythm of nutrition, systematic use of large amounts of coarse plant fiber (with prolonged use of fiber, a functional and morphological restructuring of the small intestine occurs). Thus, in vegetarians and healthy people living in tropical countries, the villi of the mucous membrane of the jejunum become wide, branched, sometimes fused, i.e. a picture is observed characteristic of chronic enteritis with intestinal dyspepsia syndrome. For normal development of villi, it is necessary to introduce pectin, not cellulose, which was established in an experiment.

In the pathogenesis of alimentary dyspepsia, a significant 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. Food of a more acidic reaction, not fully digested by enzymes, enters the small intestine, which inhibits the production and secretion of intestinal enzymes. Under these conditions, the motor function of the small intestine is impaired: food chyme is retained in its upper sections, which promotes the migration of bacteria from the lower sections of the intestine to those located above, as well as an increase in their enzymatic activity. Activation of flora that is not typical for the intestine leads to the occurrence of putrefaction and fermentation in the intestine, while the predominance of putrefactive or fermentation processes is due not only to the type of bacteria, but also to the quality of food.

Stasis of the contents in the proximal sections promotes decomposition of food in both the large and small intestines. A large number of toxic products of the breakdown of food substances (indole, skatole, hydrogen sulfide, ammonia, low-molecular fatty acids, etc.) are formed, which irritate the receptors of the intestinal mucosa, affect its motility, and cause diarrhea. In turn, the accelerated passage of food masses prevents normal digestion. Lime salts (soaps) formed during dyspepsia inhibit the growth of bifidobacteria - normal representatives of the intestinal microflora, which aggravates the disruption of digestion processes.

The digestion disorders that result in diarrhea are joined over time by malabsorption syndrome. This includes thinning of the small intestinal mucosa, loss of brush border disaccharidases, impaired absorption of simple sugars, decreased digestion and absorption of proteins and fats, an even more pronounced increase in the passage time of contents through the intestine, and a more significant colonization of the small intestine by bacteria. Structural reorganization of the small intestine occurs - flattening of the epithelium of its mucosa and changes in the brush border, which are considered the most characteristic, atrophy of the villi, the development of which is associated with dysbacteriosis and the effect of unconjugated bile acids on the mucosa. Electron microscopic examination reveals an increase and deformation of the villi, accumulation of lipids in the epithelium, changes in regenerative processes in the form of impaired formation, maturation, and migration of cells. Thus, the so-called functional nature of alimentary dyspepsia is refuted by morphological findings, which support the position put forward by domestic pathologists about the unity of structure and function.

Morphological changes in the small intestinal mucosa underlie the syndrome of intestinal absorption insufficiency. The absorption of carbohydrates is significantly affected by the disorder of the surface hydrolysis process, which can be judged by the decrease in the activity of disaccharidases in the "brush" border, as well as by the disruption of their absorption and utilization. The activity of intestinal dipeptidases decreases in the most severe manifestations of malnutrition and diarrhea, playing a certain role in the disruption of protein digestion. Pathogenetic factors of lipid digestion disorder in the form of steatorrhea include decreased secretion of pancreatic lipase, disorder of the process of emulsification of fats by bile acids, intestinal dysbacteriosis, and changes in the mucous membrane, which leads to a decrease in fat absorption.

Protein-energy deficiency aggravates motor disorders in the form of slow evacuation from the stomach and passage through the intestines, promotes further colonization of the proximal small intestine by microorganisms and the associated disruption of vitamin B12 absorption _. Protein deficiency is combined with a deficiency of nicotinic acid with a disorder of the digestion and absorption processes.

Severe protein-energy deficiency causes hypophosphatemia, which in turn affects hematopoiesis processes, immunological status, and reduces the regenerative capacity of epithelial cells. Zinc deficiency often leads to digestive disorders and diarrhea, and a relationship has been found between the zinc content in feces and their mass. At the same time, pathological bodies are detected in enterocytes with acidophilic granules in biopsies of the small intestinal mucosa, which are regarded as altered secretory granules and proliferating lysosomes. The connection of these changes with zinc deficiency is confirmed by their disappearance after long-term treatment with zinc preparations.

Thus, the small intestine is very sensitive to the deficiency and excess of certain food ingredients and reacts to them with “functional” and morphological changes.

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