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Digestion disorders in the gastrointestinal tract
Protein digestion disorders can occur at the stage of gastric, intestinal, parietal digestion.
In the stomach, peptide hydrolases cleave peptide bonds between aromatic and dicarboxylic amino acids. Protein digestion sharply slows down in hypoacid conditions, especially with achilia and total gastric resection (if the pH does not reach at least 5.0 units). Without hydrochloric acid, the swelling of protein-containing substances, the activation of pepsinogen and pepsin are disrupted. With the weakening of the activity of pepsin as the most powerful collagenase in the digestive system, the undigested collagen layers of meat shield muscle fibers from further breakdown. Lack of gastric digestion reduces the release and absorption rate of tryptophan and tyrosine, which leads to a slowdown in the absorption of amino acids and protein synthesis by hepatocytes. Aminoacidemia and aminoaciduria develop.
Pancreatic juice is active in the small intestine, containing proenzymes trypsinogen, chymotrypsinogen, proelastase, procarboxypeptidases A and B. Intestinal enterokinase converts trypsinogen into active trypsin, which triggers a cascade reaction of activation of the remaining proenzymes. At the stage of intestinal digestion, the hydrolysis of peptide bonds of basic amino acids occurs. So, trypsin breaks down bonds involving arginine and lysine, chymotrypsin - tyrosine, tryptophan, phenylalanine, and elastase - neutral amino acids. Even with the complete absence of gastric digestion, the intestinal stage of protein digestion does not stop if there is no pancreatic insufficiency. Significant inhibition of the intestinal stage of protein digestion is not compensated and gives symptoms of creatorrhea (the presence of undigested cylindrical muscle fibers in the feces).
It should be noted that creatorrhea can also occur in conditions of accelerated gastric evacuation of the chyme, for example, with resection of the stomach, increased intestinal peristalsis, pancreatic insufficiency. There are differential signs of the origin of creatorrhea. Pancreatic creatorrhea is accompanied by a predominance of undigested fibers (cylindrical with right angles and preserved striation), gastric - semi-digested fibers (cylindrical with rounded edges with partially preserved striation). With intestinal creatoreia, significant inhibition of the intestinal intestinal stage of protein digestion is not observed, and digested muscle fibers are found in the feces, which look like yellowish clumps. Severe insufficiency of gastric and pancreatic digestion is characterized by the appearance of symptoms of lientorrhea - the presence in the stool of large lumps of undigested chyme components.
At the next stage of parietal digestion, dipeptidases of the brush border cleave short peptides to amino acids. These enzymes are adsorbed from pancreatic juice (for example, carbopeptidases A and B), from intestinal juice (aminopeptidases M and N) and are secreted by enterocytes in the mode of intracellular digestion. Disturbances of parietal digestion, depending on the reasons, can be primary, including hereditary, and secondary.
The causes of a secondary violation of the intestinal stage of parietal digestion include:
• primary or secondary pancreatic insufficiency (pancreatitis, cystic fibrosis, blockage of the Wirsung duct in cholelithiasis);
• rapid evacuation of acidic gastric chyme and its inactivation of pancreatic enzymes acting in an alkaline environment of intestinal contents (Zollinger-Ellison syndrome);
• protein-free diet;
• soy and bean diet (these products contain peptide hydrolase inhibitors);
• accelerated intestinal motility;
• accelerated motility of the stomach.
In pathology, combined disorders of parietal digestion and absorption of proteins and amino acids are often observed.
Among the causes of the primary violation of the parietal stage of digestion and absorption of proteins and amino acids are called:
• immunopathological enteritis (non-tropical sprue or celiac disease - celiac enteropathy);
• ulcerative colitis;
• Crohn's disease;
• hereditary defects of enterokinases and specific transmembrane transporters of amino acids into cells - permease systems (five basic permeases have been described to date).
We will explain in more detail the causes of the primary violation of parietal digestion (maldigestion) and absorption (malabsorption) of proteins and amino acids.
Non-tropical sprue, or celiac disease (celiac enteropathy), occurs with a frequency of 1 / 2000-1 / 3000 in Caucasians and Negroids.
The pathogenesis of the disease is autoimmune enteritis with lymphoid mucosal infiltration, deposition of gliadin, a water-insoluble composite of gluten and avenine, wheat, rye, oats, barley; atrophy of villi and impaired parietal digestion and malabsorption with intolerance to cereals.
Among the pathogenetic factors affecting the development of autoimmune celiac disease, the following are recognized:
• constitutional features - up to 90% of patients have the gene of the main histocompatibility complex (HCH) DR3, DR7 or B8, DQW2;
• primary defect of enterocyte peptidase enzymes - undigested peptides can cause cross sensitization; lectin-like properties of cereal proteins act as polyclonal immunostimulants, including autoreactive lymphocyte clones;
• Adenovirus infection of the 12th serotype, carrying the Elb peptide, cross-reacting with the gliadin peptide.
In the pathogenesis of a tropical form, an infectious agent is a provoking factor.
Stress inhibits parietal membrane digestion of peptides and absorption of amino acids.
Fever is accompanied by inhibition of peptide hydrolase inhibition by pyrogenic cytokines.
With a primary hereditary defect of enterokinases, the activation of pepsin and other proteases of intestinal juice is disrupted at the stage of cavity digestion. A picture of endogenous protein starvation with oncotic edema is developing.
Hereditary defects of specific transmembrane transporters of amino acids (permease systems) are discussed in the section “Disorders of transmembrane transport of amino acids and aminoacidopathy”.
Both primary and secondary disorders of the parietal stage of digestion and absorption of proteins form the clinical syndrome of maldigestion and malabsorption of proteins. By manifestations, it can be selective and complex, combined with other malabsorption syndromes (for carbohydrates, fats, iron, etc.). Like all forms of malabsorption, the syndrome includes osmotic diarrhea, dysbiosis (like putrefactive dyspepsia) and auto-intoxication by the products of bacterial destruction of amino acids (intestinal auto-toxic syndrome).
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Digestion disorders in the gastrointestinal tract
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Carbohydrates enter the body in the form of poly-, di- and monosaccharides. Their splitting mainly occurs in the duodenum and small intestine, the juices of which contain active amylolytic enzymes (amylase, maltase, sucrase, lactase, invertase, etc.). Carbohydrates are broken down to monosaccharides and absorbed. The breakdown and absorption of carbohydrates is disturbed in various pathological
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