Enteritis is a group of inflammatory diseases of the small intestine.
Chronic enteritis is a disease of the small intestine, characterized by a violation of its functions (digestion and absorption) on the background of degenerative and regenerative (restorative) changes, culminating in the development of inflammation, atrophy and sclerosis of the mucous membrane of the small intestine.
Acute enteritis is an infectious disease that most often develops as a result of food poisoning and manifests itself clinically with gastroenteritis with symptoms of general intoxication, fever, severe diarrhea. The causative agents of acute gastroenteritis are: salmonella, typhoid paratyphoid group, cholera vibrio.
Causes and mechanisms of the disease
Chronic enteritis is a multi-causative disease.
The disease can be the outcome: acute inflammatory process; to be primarily chronic.
Perichina factor is considered – Yersinia, Helicobacter pylori, Proteus, Pseudomonas bacillus, rotaviruses, protozoa and helminths. No less important in the development of chronic enteritis are alimentary factors: overeating, eating a dry ration, the predominant use of carbohydrates, the abuse of spices, food allergies. Also promote the development of enteritis, some drugs – salicylates, indomethacin, corticosteroids, immunosuppressants, cytotoxic drugs, antibiotics for their long-term use.
Often, enteritis is associated with diffuse connective tissue diseases, tuberculosis, chronic pancreatitis, cirrhosis of the liver, and chronic renal failure. Congenital and acquired metabolic diseases, dysfunctions of the digestive glands and immunological homeostasis, changes in intestinal motility, and microcirculatory disorders of blood circulation contribute to functional and structural changes in the mucous membrane of the small intestine.
Of great importance in the mechanism of development of enteritis are changes in the intestinal microflora against the background of a decrease in local and general immunity. Changes in the immune status – reducing the content of secretory immunoglobulin A, increasing the level of IgE, reducing the reaction of lymphocyte blast-transformation, inhibiting the reaction of leukocyte migration lead to colonization of the small intestine by conditionally pathogenic microflora (Escherichia, Enterococcus, Staphylococcus), and a decrease in the normal anaerobic flora (microbes) (decrease of the normal anaerobic flora (microbes) (microbes), reduction of the normal anaerobic flora (microbes) (microbes), reduction of the normal anaerobic flora (microbes) in anoxic conditions). Bacterial colonization of the small intestine increases the intestinal secretion of epithelial cells (epithelial cells), which leads to an increase in intestinal permeability and ultimately to water-electrolyte disturbances. Under the influence of the microbial flora, the enterohepatic circulation of bile is disturbed. Under the influence of metabolic disorders of fat-soluble vitamins, the content of trace elements in the blood decreases. Prolonged dysbacteriosis promotes sensitization (increased sensitivity) to microbial food antigens, causes immunological inflammation of the mucous membrane. Increased permeability of the mucous barrier is accompanied by resorption (absorption) of non-cleaved protein macromolecules, which acquire the properties of allergens, they cause the release of biologically active substances (histamine, serotonin, prostaglandins), which alter the function of enterocytes, and the inhibition of the splitting carbohydrates (prostaglandins), which alter the function of enterocytes, and inhibit the production of carbohydrates (prostaglandins) and alter the function of enterocytes, and inhibit the production of carbohydrates (prostaglandins) and alter the function of enterocytes, and inhibit the production of biologically active substances (histamine, serotonin, prostaglandins) activity.
With dystrophic changes of epithelial cells (epithelial cells), synthesis of enzymes and sorption (settling) of them on epithelial cells membranes are reduced, which causes both membrane and cavitary digestion, which becomes the basis of malabsorption syndrome. Disorders of lipid metabolism (fats) associated with a decrease in fat absorption, loss of it with feces, changes in the intestinal phase of the enterogenous circulation of bile develop. Disruption of bile metabolism leads to disruption of lipid metabolism, changes in the structure and function of cell membranes, disrupts the synthesis of steroids (hormones) and the function of the endocrine glands. Morphologically chronic enteritis is manifested by inflammatory and dysregenerative changes in the mucous membrane of the small intestine, atrophy and sclerosis.
The phases of enteritis are aggravation and improvement. Complications: solarium (inflammation of the solar nerve plexus), nonspecific mesadenitis (inflammation of the inter-intestinal lymph nodes). The clinic consists of general and local manifestations. Local enteral syndrome is associated with impaired parietal (membrane) digestion and abdominal digestion (maldigestia).
Common enteral syndrome is associated with malabsorption, leading to the breakdown of all types of metabolism. In local enteral (small bowel) syndrome, patients complain of flatulence, pain in the middle of the abdomen, mainly in the navel, bloating in the form of a cap, loud rumbling, diarrhea, constipation, or their alternation. When palpation, pain in the mesogaster, on the left and above the navel (positive symptom of Porges), splashing noise in the cecum (Obraztsov symptom) is detected. The feces have a clayey appearance, characterized by polyfecalia (an increased amount of feces). Pathological changes (blood, pus) in the feces are absent. Intestinal manifestations often occur in the second half of the day at the height of the intestinal phase of digestion. Often, on the background of a feeling of distention in the abdomen, heart palpitations, pain in the region of the heart, and headaches appear. General enteral syndrome is manifested by impaired metabolism, primarily protein, which is accompanied by loss of body weight. Changes in carbohydrate metabolism are less pronounced (bloating, rumbling in the abdomen, increased diarrhea while taking dairy products). Changes in lipid metabolism are associated with metabolic disorders of fat-soluble vitamins.
Specific signs of calcium deficiency: a positive symptom of muscle muscle, convulsions, recurrent bone fractures, osteoporosis; swelling of the face, lips, glossitis, irritability, poor sleep. Disorders of water and electrolyte balance are clinically manifested by general weakness, physical inactivity, muscular hypotonia, nausea, vomiting, changes in the central nervous system.
Intestinal symptoms prevail in the mild form of chronic enteritis. The combination of local and general metabolic disorders with moderate and severe form is dominated by clear metabolic disorders with often irreversible changes in the functions of the internal organs. Symptoms of polyhypovitaminosis include bleeding gums, nosebleeds, bruises (vitamin C deficiency); accompanied by pallor of the skin, tongue inflammation, irritability, poor twilight vision, dry skin and mucous membranes – vitamin A deficiency, D, E, K, drowsiness, loss of appetite, dermatitis, impaired passage of food – vitamin B deficiency
In severe forms of chronic enteritis, there are symptoms of endocrine dysfunction, hypocorticism (decreased function of the adrenal cortex – hypotension – low blood pressure, arrhythmia, skin pigmentation).
In case of metabolic disorders, nonspecific reactive hepatitis develops – a feeling of heaviness in the right hypochondrium, there are disorders of the pigment metabolism, a moderate increase in the liver.