CHRONIC DIARRHEA SYNDROME MALABSORPTION At the core of
CHRONIC DIARRHEA SYNDROME MALABSORPTION
At the core of the development of chronic diarrhea syndrome is a violation of the processes of digestion and (or) absorption of nutrients in the gut The process of assimilation in the small intestine in three successive stages: Cavitary digestion - Membrane digestion - suction
Cindromom failure digestion (maldigestion) - understand cavitary digestion disorders, ie disorders of digestion of nutrients in the small intestine due to a lack of digestive enzymes. The term "malabsorption, " or "impaired intestinal absorption, " indicate malabsorption of nutrients in the small intestine
Form of the syndrome of insufficient digestion: • violation predominantly cavitary digestion • violation predominantly wall (membrane) digestion • dysfunction of transport proteins apical surface of enterocytes, responsible for the absorption of certain nutrients secondary violations - against the background of the small intestine atrophy CO) • violation of intracellular metabolism • violation of transit through the gastrointestinal tract • violation of the regulation of enterocyte • mixed forms
Violations cavitary digestion (dyspepsia) are due to uncompensated reduction of secretory function of the stomach, intestine, pancreas, bile Contribute to the emergence of dyspepsia • disorders of motor function of the gastrointestinal tract • stagnation due to spasm of the content stenosis or compression of the intestine rapid passage of food chyme, due to increased peristalsis solution the regulation of enterocyte mixed forms
Parietal (membrane digestion) is on the surface of enterocytes (in the brush border) by the enzyme synthesized by the intestinal cells, and pancreatic enzymes adsorbed apical brush border membrane of enterocytes
Lack of wall digestion develops in chronic diseases of the small intestine: • dystrophic and sclerotic changes in the mucous membrane of the small intestine • also change the structure of the villi and microvilli • decrease in their number per unit area of facilitating changes in the surface of the gut enzyme layer, resulting in impaired transport of nutrients from the gut cavity on the surface of enterocytes
Lack of intracellular digestion associated with primary or secondary enteropathy, which is based on genetically caused or acquired or disaccharide intolerance of certain proteins
Cindromom malabsorptionunderstand complex intestinal and extraintestinal symptoms due to inadequate absorption of nutrients in the small intestine
Pure forms of malabsorption: • celiac disease • malabsorption with food allergies • malabsorption of monosaccharides • Hereditary disorders of absorption of magnesium • enteropatichesky acrodermatitis (malabsorption of zinc)
Characteristics common enteric syndrome: • weight loss • Thrust anemic syndrome polyhypovitaminosis • hypoproteinemia with hypoalbuminemia, until the swelling • trophic disorders • severe weakness, hypotension, neuromuscular disorders
Diarrhea - frequent bowel movements or a single with the release of liquid stool. Diarrhea can be acute if its duration does not exceed 2 -3 weeks, and chronic if diarrhea persists for more than 3 weeks
Involved in the pathogenesis of diarrhea four mechanisms: • intestinal hypersecretion • increased osmotic pressure in the colon • violation of the transit of intestinal contents • E. giperekssudatsiya
Malabsorption syndrome (malabsorption) The basis of this syndrome is a series of factors: • morphological changes of the mucosa of the small intestine • change in enzyme systems, digestion of nutrients violation • disorder specific transport mechanisms • bowel bacteria overgrowth • impairments bowel
Gluten enteropathy (celiac disease) clinical manifestations: • unstable chair, on average, 5 -8 times per day, foulsmelling, loose, frothy; polifekaliya • weight loss with a relative increase in abdominal • abdominal pain (usually in the umbilical region) • changes in appetite - from its absence to a sharp increase; • lagging indicators of weight and height • constant fatigue • bone loss • manifestations of toxic encephalopathy • common allergic skin lesions - itching, dryness • expressed signs of hypovitaminosis A, B, C • manifestations of micronutrient deficiency
Whipple's disease Synonym of the disease - intestinal lipodystrophy. It is a disease of the small intestine with an infectious origin POLYSYSTEM lesions. Disease was first described in 1907 by Whipple
SYNDROME VIOLATION DIGESTION - MALDIGESTION Deficiency syndrome digestion (maldigestion) imply that the digestive cavity, ie, loss of digestion of nutrients in the small intestine due to a lack of digestive enzymes
VISCIDOSIS Cystic fibrosis - the disease caused by mutation of the CFTR gene (cystic fibrosis transmembrane regulator protein), characterized by lesions of the exocrine glands of the vital organs and systems. Probability of birth of the child patient, according to the European countries of 1: 2000 -2500 live births.
CLASSIFICATION OF CYSTIC FIBROSIS • Mixed form (lung and intestine) - 75 -80% • Predominantly pulmonary form - 15 -20% • Mainly intestinal form of 5% • Meconium ileus 5 -10% • Abortive and erased form 1 -4%
Dysbacteriosis Dysbiosis in the last two decades to become one of the most popular diagnoses, especially among pediatricians. His pose, from birth, the first violation chair, so called. diathesis, allergy, skin diseases, infectious giporezistentnosti. Analysis of dysbiosis, easily prescribed by the doctor, is one of the most expensive laboratory DYSBIOSIS - IS AN IMBALANCE BETWEEN MACROORGANISM AND ITS SYMBIOTIC MICROFLORA
The composition of the intestinal microflora in the norm Microorganisms Content is normal in 1 g of feces pathogenic enterobacteria 0 The total number of E. coli 10^6 – 10^7 Lactosonegative E. coli 0 Hemolytic E. coli 0 Opportunistic enterobacteria 0 – less 10^3 enterococci 10^3 – 10^6 streptococci 10^3 Staphylococci: golden, koagulozonegativny 0 lactobacilli 10^6 Bifidobakterin 10^3 Fungi Cadida 0 yeast-like fungi 0 anaerobic spore- 10^3
Differential diagnosis of acute intestinal infections and dysbiosis - Acute onset of illness - Is the source of infection (patient AII or faulty product) - Identify pathogen - The increase in antibody titer to the causal factor of 2 -4 - the first 2 weeks of the disease, reducing the titer of antibodies - to 3 weeks after the elimination of the pathogen
Dysbiosis: - Not an acute onset of the disease - No source of infection - Discover opportunistic pathogens (Klebsiella, Proteus, Citrobakter) - No increase in antibody titer to the pathogen
Intestinal dysbiosis promote prolonged, relapsing course of the disease and the development of complications. Reduction of bifidoflora accompanied tendency to flatulence, constipation, weight flattening of the curve.
TREATMENT syndrome of digestion and absorption Combined therapy includes: • clinical nutrition (diet with restriction or exception intolerable, indigestible and irritating bowel products) • the use of means to stimulate the hydrolysis of membrane processes in the small intestine • correction of metabolic disorders • the use of tools to improve the processes of digestion (enzyme preparations) • detoxification • the use of antidiarrheal • use of normalizing the composition of the intestinal flora (dysbiosis correction) • immunocorrection • use of symptomatic agents
POLYENZYME DRUGS
preparation Amylase Proteaza Lipaza other components Panzunorm 7500 2000 6000 bile Panzinorm forte 7500 450 (трипсин) 1500 (химеотрипси н) 6000 Холевая к-та, пепсин, гидрохлориды аминокислот Pankreatin 12000 100 Mezim forte 4200 250 3500 Pankurmen 1000 63 1000 Кукурма (8 мг) Digestal 6000 100 Гемицеллюлоза (50 мг), желчь (25 мг) Solizim 20000 липолитически й фермент Festal 4500 300 6000 Threeferment 4 18 6 Kreon 9000 450 800 Kreon 25000 18000 1000 25000 Likreaza 14000 660 12000 Enzistal 4500 300 600 Pansitrat 9000 500 10000 Гемицеллюлоза (30 мг), желчь (25 мг) Гемицеллюлоза (50 мг), желчь (25 мг)
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