Digestive Failure Syndrome - Causes

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. Thus, deficiency of protein, vitamins, microelements in the diet, unbalanced nutrition (amino acid imbalance, disturbance of the ratio between fatty acids, water-soluble and fat-soluble vitamins, mineral salts) can lead to persistent disorders of the digestive process. In addition, inhibition of the activity and biosynthesis of enzymes and protein can be caused by the toxic effect of some natural components of food or foreign impurities contaminating them. In certain food products (legumes, cereals, rice, eggs, etc.), heat-stable specific protein inhibitors have been found that form stable complexes with gastrointestinal tract proteinases and cause inhibition of their activity. As a result, the processes of digestion and assimilation of food protein are disrupted. The biosynthesis of some enzymes is disrupted due to insufficiency of coenzymes - water-soluble vitamins. This is due to the presence of antivitamins in food products, which destroy or replace vitamins in the structure of enzyme molecules, significantly reducing or completely suppressing the specific action of vitamins. The antagonist of nicotinic acid is a low-molecular compound - niacin and niacinogen, isolated from corn, and pyridoxine - linatin, contained in flax seeds. Freshwater fish contain the enzyme thiaminase, which catalyzes the hydrolytic breakdown of thiamine. The protein avidin found in raw eggs forms a stable complex with biotin in the gastrointestinal tract.

Contamination of food products with salts of heavy metals (mercury, arsenic), pesticides, mycotoxins (aflatoxins, trichothecene mycotoxins, etc.), which react with sulfhydryl groups of protein molecules, suppress protein biosynthesis, and inhibit enzymatic activity.

There are several forms of digestive insufficiency syndrome, manifested by disturbances of mainly cavity, parietal (membrane) and intracellular digestion. In addition, there are mixed forms of digestive insufficiency. All these varieties of forms are accompanied by diarrhea, flatulence and other dyspeptic disorders. At the same time, each of them has its own, first of all, pathogenetic features.

Disruption of predominantly cavity digestion (dyspepsia) occurs due to uncompensated decrease in the secretory function of the stomach, intestines, pancreas, and bile secretion. A significant role in its occurrence is played by disruption of the motor function of the gastrointestinal tract: stagnation of contents due to spasm, stenosis, or compression of the intestine, or accelerated passage of food chyme due to accelerated peristalsis. The occurrence of dyspepsia is facilitated by past intestinal infections, changes in intestinal microflora, when the number of bifidobacteria and E. coli decreases, the upper sections of the small intestine are populated by microorganisms, pathogenic flora is activated, causing fermentation and putrefaction processes in the large intestine. Dyspepsia is caused by alimentary disorders: overeating, unbalanced nutrition with the use of excessive amounts of carbohydrates, proteins, or fats, eating food lacking vitamins. Particularly dangerous is excessive food load in combination with mental and physical overstrain, overheating, hypothermia, i.e. with factors leading to inhibition of the secretory function of the digestive glands.

Dyspepsia is often observed when the stomach, intestines and other organs of the digestive system are affected. At present, the distinction between so-called functional dyspepsia is hardly justified, since it has been proven that each "functional" disease has its own morphological substrate.

In the pathogenesis of dyspepsia, an important role is played by incomplete breakdown of food substances by digestive enzymes, accelerated or slow passage of chyme through the gastrointestinal tract, and the occurrence of dysbacteriosis. Bacteria that appear in the upper sections of the small intestine secrete enzymes and take an active part in the breakdown of food substances. As a result of this process, toxic products such as indole, ammonia, low-molecular fatty acids are formed, which irritate the intestinal mucosa, increase its motor activity and, when absorbed, cause intoxication of the body. An increase in the enzymatic activity of microorganisms in the large intestine is accompanied by increased formation of these toxic products in the distal sections of the intestine.