Chronic Enteritis

Chronic enteritis.

Definition: Chronic enteritis – polietiolohichne disease, based on a dystrophic process in the small intestine that leads to destruction ¬ ing barrier function, digesting and absorption, settling its upper large number of microorganisms are recycled ¬ metabolic and immune disorders, disorders function of the nervous system. (Pathophysiologic basis of symptoms and signs of malabsorption syndromes and the classification given in the annex).

Etiology. Chronic enteritis (CE) – polietiolohichne disease. Moreover, it can be as a result of acute and independent disease. Among the etiologic factors of enteritis: moved dyzen ¬ Terry, mikrosporidioz, tsyklospory, salmonellosis, staphylococcal infection, iyersyniyi, kampilobakteriyi, but Ps.aeruginosa, viruses (rotavirusy, enteral adenoidal pharyngeal conjunctival virus), protozoan and hlystni invasion (lyambliyi, opistorhiyi kryptosporydiyi, ascaris, stronhiloyidy , wide lentets).

The second cause of enteritis is alimentary factors – unhealthy diet with the predominant use of carbon food, overeating, poor food vitamins suhoyidinnya.

Surely among the causes of enteritis is ionizing radiation (radiation of strontium, cesium), toxic effects of lead, phosphorus, arsenic, herbicides, medications (salicylates, nonsteroidal anti-inflammatory mullion, corticosteroids, cytostatics, anti) mullion, immunosuppressant.

CE develops after hastrektomiyi, gastric resection, vagotomy, imposing hastroenteroanastomozu in patients with tuberculosis, rheumatism, psoriasis, eczema, chronic pancreatitis, hepatitis, liver cirrhosis, against a background of chronic renal, pulmonary, cardiovascular ¬ not sufficiency.

Among the reasons Hae liquid can intestinal wall ischemia on a background of atherosclerosis, vasculitis mesenteric vascular disturbances of the immune homeostasis.

Pathogenesis. The basis of virulence of pathogens enteritis is a combination of pathogens and intestinal enterocytes, resulting in forming pilus bacteria, increasing contact with the epithelial membrane. We ¬ tupnym part is sticking. Bacterial adhezyny (lektynopodibni and lectin molecule), which is on the surface of microorganisms interact with specific binding of carbon places mikrovorsynkah epithelial cells on the principle of ligand-receptor interaction. This mechanism is typical for esherihy, Campylobacter. An important role is temperature-stable toxin, which is typical for products iersyniyi, shihel. Inhibition of growth of normal flora under the influence of antibiotics on subsequent reproduction klostrydium difitsile and allocating them toxin and underlies the development of pseudomembranous enteritis. In the development of infectious diarrhea, but these toxins, taking an active part endogenous stimulants water and electrolyte secretion in the small intestine. This is particularly serotonin (5-HT). It connects to the 5-NT3-receptor neurons afferentyyh intramural nervous arc, which controls water and electrolyte secretion. As a result of this process increases water and electrolyte flow. Another endogenous stimulator of this secretion is intestinalyyy Vasoactive peptide (V1P). He interacts with VIP receptors bazolateralnoyi membrane of intestinal epithelial cells, induces water and electrolyte secretion and inhibited intestinalnu absorption of electrolytes and neurotransmitters are a group of nerve endings pidslyzovoho plexus. Strengthen an important role in intestinal secretion of prostaglandins play, in which hyperproduction kryptosporoyidalniy invasion causes shortening of intestinal villi, crypt deepening, inhibition of sodium and fluid absorption.

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