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Diagnosis of hepatitis, cholecystitis, liver cirrhosis. Chronic hepatitis polyetiological chronic liver inflammatorydestructive nature with moderate fibrosis and preserved lobular structure, lasting more than 6 months. Etiology: the onset and progression of infectious and noninfectious nature is crucial defective immune response to damage liver tissue. Hepatitis viral, toxic and alcoholic lesions developed not only as a result of damages which the agent, but also as a result of an immune reaction cell type against hepatocytes. Damage liver hepatotoxic viruses emerging area of immune cytolysis of hepatocytes in which the virus persists and there are its markers - surface antigens of viruses. Induces immune cytolysis: antibodies fixed on the surface of hepatocytes exhibit a cytotoxic effect and induce cytotoxic T-lymphocytes against liver cells. At the same cells transformed with K-cells (killer), sensitized to hepatocytes caused by migration of cells formed inflammatory infiltrate, composed in viral hepatitis include lymphocytes, macrophages, fibroblasts. Clinical manifestations of hepatitis and cirrhosis of the liver: Asthenic syndrome. Asthenic phenomena accompany most liver diseases are often the first signs of illness. Characterized by weakness, decreased performance, increased fatigue, loss of previous interests reduction initiatives. Changing emotional background of the man - depressed mood, depression, irritability episodes Diarrheal syndrome Dyspeptic symptoms, early signs of liver damage. Dry and bitter taste in the mouth - most often met symptoms. Nausea, vomiting, belching. Discomfort right subcostal area - a characteristic feature. The equivalent symptom is a feeling of heaviness in the epigastrium, constant bloating. Decreased appetite combined with intolerance of many products. Constipation particularly pronounced in portal hypertension. Diarrhea alternating with constipation. There slimming down to cachexia. Abdominal pain. The most easy option - a feeling of heaviness, pressure in the upper abdomen. Monotone pain in the right upper quadrant due to stretching of the fibrous membrane of the liver, most often appear after eating. Pain can be long or sharp. Sometimes the pain is located in the right subcostal area , and under the breasts. Cholestatic syndrome. Manifested persistent or intermittent ochrodermia, skin itching, dark urine, feces lightening. Vehetodystonic syndrome. Psycho-emotional instability, insomnia, headache, cardialgia, fluctuations in blood pressure, sweating. Febrile syndrome. Unexplained fever, prolonged or recurrent, most often seen in chronic active hepatitis, in the active stage of liver cirrhosis. The reason could be severe overgrowth of endogenous intoxication, periodic bacteremia. In 2/3 patients with cirrhosis due to fever associated infectious lesions pneumonia, ascites - peritonitis. Articular syndrome. Joint pain, prolonged or intermittent, without deformation accompanying reactive hepatitis and cirrhosis of the liver. Hemorrhagic syndrome. Bleeding from the nose and gums, subcutaneous hemorrhage, menorrhagia, bloody vomiting, tarric excrements. Edematous-ascitic syndrome. Fluid retention, increasing the size of the abdomen, swelling of the legs. Entsefalopatyc syndrome. Memory loss, drowsiness, dyzoriyentation in time and space, inappropriate behavior. Classification I. Etiology: viral alcoholic autoimmune toxic drug (toxic-allergic) nonspecific reactive Secondary biliary hepatitis with hepatic cholestasis outside II. The morphological changes: 1. Persystic 2. Lobular 3. Activities: a) with moderate activity; b) a high degree of activity. 4. Cholestatic Classification III. The clinical course: Phase of aggravation Phase of remission IV. For the functional state of the liver: compensated decompensated Physical examination: -Skin - greyish-pale, can be local or diffuse hyperpigmentation (melasma). -Jaundice - develops when hyperbilirubinemia above 30 mmol / l, expressed in bilirubin more than 120 mmol / l. -Originally jaundice appears on the palate and sclera, sometimes there is only partial ochrodermia nasolabial triangle, forehead, palms. Itching and traces solutions, caused an increase in the skin of bile acids. -Teleangiectasia, or star-shaped angiomas on the neck, face, shoulders, back , racemes. Their expression is reduced in the fall of blood pressure, bleeding. Xanthoma - internally yellow skin plaques that form in severe hyperlipidemia. Hemorrhage into the skin - pinpoint hemorrhages develop in protracted course of hepatitis. For chronic liver disease characterized by painless superficial hemorrhages in the skin and mucous membranes, bleeding from the gums, nose, uterine bleeding. Palmar eritema (liver palms) - symmetric splotchy red palms and soles. Spots become pale with pressing and again blush at the termination of pressure. "Crimson, the cardinal's tongue" - and no sinergy of papillae of the tongue to the degree of "patent" surface. Atrophy of the shoulder musculature due to violation of protein metabolismand hormonal imbalance. There is thickening of the distal phalanges of the fingers of the type "drumsticks“ Gynecomastia - female type hair on the body develops as a result of increased estrogen levels. Possible loss of pubic hair, axillary areas, testicular atrophy. Syndrome most often occurs in alcoholic hepatitis. Leg swelling, lymphadenopathy - arises in severe hypoalbuminemia. Enlargement of the liver - a characteristic sign of its parenchyma. Reducing the size of the liver is rare, in the later stages of cirrhosis of the liver is a bad prognostic sign. On palpation the liver during severe pathological process activity observed liver tenderness. Liver tissue is sealed, the edge can be condensed, the pointed, hilly. Splenomegaly is not typical for most cases of hepatitis Diagnostic tests. -Zag en. blood - anemia, leykopeniya. Acute alcoholic hepatitis occurs with leukocytosis, a sharp increase in ESR, stab shift. -Tjtal urine test - a possible micro hematuria, mild proteinuria -biochem. of blood - an increase of ALT and AST, hlutamat dehidrohenaze, lactate dehydrogenase, iron, vitamin B12, an alkaline phosphatase linked (direct) bilirubin, total bilirubin, cholesterol, reduced albumin, protein, prothrombin complex. -Sonography of liver: increased in size, increased density heterogeneity of ehostruktures. -Radionuclide study of liver. Used radiopharmaceutical Bengal pink for study of liver function. - Morphological study of the liver - punctures on biopsy. Treatment depends on the etiology, process activity severity. A during acute process. Bedrest Diet 5 Drugs that improve metabolism in liver cells - ATP, Vit. B group, Glutamic acid. Hepatoprotectors: Essenciale forte, Gepabene, Sealy boron, Vitohepat. Glucocorticoids: Prednisolone, Methyl Prednisolone (at high process activity). Amino quinoline drugs: Delahil, Plakvenil, immunosuppressive drugs: Azathioprine, Cyclosporine. when viral hepatitis B, C, D - interferons α, β, γ. Detoxification Therapy - Gemodez, Glucose, Sodium Thiosulfate, enzyme preparations. Adsorbents bile acids - Bilihnin, Cholestyramine, Activated carbon with vitamins A, D, E, K, Enterodez, Ursofalk. Oxygen therapy, herbal medicine Bile - Yarrow, Immortelle, Hypericum, Rose, Dandelion roots. Cirrhosis This is a progressive, diffuse, polyetiological disease characterized by a significant decrease in the mass of functioning hepatocytes, fibrosis with impaired hepatic lobule structure and vasculature liver. Etiology 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. Alcoholic Virus (HBV, HVC, HBV + HDV) Primary biliary cirrhosis Secondary biliary cirrhosis Violation of venous outflow from the liver Metabolic Toxic Nutritional Cryptogenic Parasitic diseases Shunt surgery for intestinal Diagnosis. Main symptoms and syndromes: Astenovegetative, edematous syndrome, endotoxemia, hyperbilirubinemia, diarrhea, intrahepatic cholestasis, portokavalnoho bypass, hepatomegaly, splenomegaly, mesenchymalinflammatory, cytolytic, bleeding, hepatocellular failure, portal hypertension, malabsorption, anemia, hormonal imbalance. Physical data Resized and seal liver Palpable spleen determined Spider veins on the upper trunk and face Palmar erythema Gynecomastia and testicular atrophy Veins on the anterior abdominal wall Ascites jaundice Laboratory parameters Hematologic: concentration of Hb, # of leukocytes and platelets, Coagulation, blood type, Rh factor, prothrombin index. Biochemical: bilirubin, albumin, globulin, chloride, urea, creatinine, K, Na, copper, iron, Ig in the serum activity of ALT, AST, alkaline phosphatase. Immunological indices serum HBsAg, anti-HVC, antibodies to smooth muscle, to soluble liver antigen, α-feto-protein. Instrumental research Esophagogastroduodenoscopy Doppler-ultrasound liver Computed tomography of the liver Krizshkirna needle biopsy Radioisotope scanning of the liver Fluoroscopy esophagus and stomach Treatment of cirrhosis Regieme - depending on the stage of cirrhosis. Diet № 5 in portal hypertension - bezso Levu, in hepatic coma - Protein-free. Detoxification therapy: Neogemodez, Glucose. Anti-inflammatory therapy: steroids, antibiotics, immunosuppressants, hepatoprotectors, adsorbents bile acids, drugs that improve metabolism in hepatocytes, pancreatic enzymes "The main symptoms and syndromes in diseases of the hepato-biliary system. Methods of clinical, laboratory and instrumental examination. ' Chronic non-calculous (bilestone free) cholecystitis (sholecystitis chronica) - a chronic inflammatory disease. Polyetiological gall bladder, which is combined with motor-tonic disorders (dyskinesia), biliary tract and changes in physico-chemical properties and biochemical composition of bile (dysholia). Etiology. 1. 2. 3. 4. 5. Bacterial infections Parasitic infestation Duodenobiliar reflux Allergies Chronic inflammatory disease of the digestive system. 6. Acute cholecystitis. Predisposing factors 1. Stagnation of bile. 2. Reflex effects from abdominal organs during development in their overall process. 3. Intestinal dysbiosis. 4. Metabolic disorders contributing to changes in physico-chemical properties and composition of bile (obesity, diabetes, gout). 5. Hereditary with respect to XX. The main pathogenic factors: 1. 2. 3. 4. 5. Neurodegenerative changes ZHM wall. Neuroendocrine disorders. Stagnation and dysholiya bile. Violation of the wall ZHM. Factors: Allergic reactions and Immunoinflammatory. Classification of chronic cholecystitis 1. 2. 3. 4. Etiology: kolibatcilic, enterokokcial, strepto-, stafilo-, pneumococcal, Salmonella, typhoid, dysentery, brutselozal, paratyphoid and others. The degree of severity: mild, moderate, severe. The nature of the course: recurring, monotonous, intermittent. During phases: pointed, decreasing exacerbation, stable remission, unstable remission. In the presence of complications, uncomplicated, complicated periholecistitis. Clinical Subjective symptoms: -Pain at HBH localized in the area of right hypochondrium, sometimes in the epigastrium, radiating to the right shoulder blade, sometimes - in the collarbone. -Dyspeptic symptoms: nausea, vomiting, a feeling of bitterness in the mouth, belching bitter. Due to the development of secondary gastritis, pancreatitis, enteritis appear heartburn, belching rotten, flatulence, loss of appetite, diarrhea. Itchy skin. -Fever. -Psycho-emotional disorders: depression, weakness, fatigue, irritability, emotional lability. Physical examination . Review. Most patients say overweight. In some patients there subictericity of scleras and skin. Palpation marked tenderness in the region of the gallbladder. May show some positive signs: Symptom Zakharyin - pain when pressing the point ZHM. S-m of Vasilenko - when tapped at the point ZHM at the height of inspiration there is a sharp pain. S-m of Obraztsov-Murphy - after clicking on the area offered ZHM patient to breathe, while the patient "intercepts" breath of pain in the ZHM. S-m of Ker - pain on vdosi during palpation right hypochondrium. S-m of Ortner - pain when tapped his hand on the edge of right costal arch. S-m of Myusi cardiology - pain at the point of the phrenic nerve (frenikus-symptom). Pain point at disease gall bladder: 1 - cystic point 2 - epigastric area 3 - choledochitis-pancreatic area 4 - zone in the area of proc. acromion 5 - point n. phrenici 6 - spade point 7 - point at the end of the 12th rib 8 - point about 8 - 11 thoracic vertebrae 9 - point to the right of 12 thoracic vertebrae Laboratory and instrumental methods 1. 2. 3. 4. Total blood: moderate leukocytosis, left shift with increasing stab leukocytes, ESR acceleration. Biochemical analysis of blood: an exacerbation of increased content of sialic acids seromucoid, fibrin, alpha 2-globulin, possibly gamma globulin. Imunolohiche blood research: reduced number of B and T lymphocytes and IgA. Fractional duodenal intubation: Changes of duodenal intubation (portions "B"), typical of chronic cholecystitis: - The presence of large numbers of leukocytes, especially their clusters. - Detection by visual inspection bile pronounced turbidity, flakes of mucus. - Established in bile of a large number of cells columnar epithelium. - The appearance of cholesterol crystals and calcium bilirubinate. - Reduction of relative density and pH of gallbladder bile. - Changes in biochemical composition of bile (increased # of mucins substances reduced content of bile acids, cholate-cholesterol ratio, lipid complex) - Bacteriological study: the number of bacteria than 100,000 in 1 ml of bile. 5. ultrasound: Echo signs of Mts. cholecystitis ZHM wall thickening greater than 2 mm; sealing wall, especially with thickening; unevenness and deformation path bladder, increase or decrease the size, adhesions; reduction or absence of motion ZHM breathing; nonhomogenouse content of "gall precipitate." Ultrasound of the liver and gall bladder 6. Ro-study ZHM: Cholecystography: Signs HNH - Impaired concentration ability and motor function ZHM (sharp slowdown emptying ZHM); - ZHM deformity (inequality contours due pereholecystitis). 7. Computed tomography ZHM. 8. Radioisotope studies of biliary tract: Symptoms: - persistent infringement speed filling and emptying ZHM; increase or decrease its size; seal lying ZHM. 9. Thermography: observed local temperature increase of 0,3 -2 ° C, zone ZHM looks bright. Cholelithiasis (CT scan) 1 - chronic cholecystitis (thickening of the walls of the gall bladder), 2 - calcium-containing stones in area neck of the gallbladder Treatment 1. 2. 3. 4. 5. 6. In acute patient lax recommend bed rest for 7-10 days, 1-2 days a warm drink. Diet № 5, frequent meals (5-6 times / day)) in small portions. Purchasing pain m anticholinergics: Atropine Sulfate, Methacin, Platifillin Gidrotartrata, Gastrotsepin; antispasmodics: Papaverine, Nospanum; Analgesics: Proteins, Baralgin, Droperiodol. Antibiotic therapy in acute. Appointed when thinking about the nature of the bacterial disease have clinical and laboratory data confirming the activity of the inflammatory process in ZHM (Erythromycin, Ampicillin, Oxacillin, Lincomycin, Furazolizon, Penicillin, Tetracycline, Blacks, Taryvid, Cephalosporin antibiotics). Detoxification therapy in very severe exacerbation of symptoms of intoxication: broths hips, alkaline mineral water / drip - gemodez, polidez, 5% glucose isotonic district. 7. Bile means. Rational choice bile depends on the phase of chronic cholecystitis and concomitant type dyskinesia. 1) drugs that stimulate the formation of liver bile - Bile true (choleretic): preparations containing bile acids (Hologon, Deholin, Alahol, Festal, Holenzim, Liobil); synthetic choleretic (Nikodin, Tsykvalon, Oksafenamid); vegetable (Immortelle, Corn Silk, Flamini, Peppermint, Holosas, Parsley); hidroholiretyky (water type "NAFTA"); 2) drugs that stimulate bile (holekinetiki): Xylitol, Sorbitol, MgSO4, Tansy. 8. Normalization function of the autonomic NS: sedativ, minor tranquilizers. 9. Immunomodulatory therapy: Timalin, Taktyvhin, Sodium Nukleinat, Adaptogens (Ginseng, Pantocrinum, Siberian ginseng). 10. Physiotherapy treatment. 11. When stihanii acute phenomena inductothermy, UHF, microwave, SMT, UST, electrophoresis of novocaine, MgSO4, applications paraffin wax, ORT, balneotherapy. 12. Treatment of mineral water. 13. Spa treatment in remission (Truskavets Gusyatin, Satan, Essentuki, Borjomi). Chronic calculous cholecystitis (sholecystitis chronica calculosa, cholelithiasis) - a disease characterized by the formation of stones in the gallbladder, at least - in the bile ducts. In the development of gallstones are important metabolic disorders, infection and bile stasis. There are three stages of gallstone disease. The first stage (physical and chemical). The second stage (latent) is characterized by changes in lithogenic bile to form gallstones. The third stage of cholelithiasis - clinical (calculous cholecystitis). Clinical Subjective symptoms: The most characteristic feature of the disease is a liver or biliary colic. Intense pain localized in the right upper quadrant and epigastric, radiating to the back, chest thing, right shoulder, shoulder, arm. Join nausea, repeated vomiting, which does not facilitate pain, bloating, delayed stool. With prolonged fit of itching appears. Physical examination. On examination can detect jaundice (the second day), xanthoma. There bloating, muscle tension and local tenderness in the right upper quadrant. Positive gallmihurni symptoms and areas of hyperesthesia (lower angle shoulder, shoulder area, paravertebral right from VIII to IX thoracic vertebra). Xanthelasma of the upper eyelid Laboratory and instrumental methods In the biochemical analysis of blood observed increase in cholesterol levels, increasing the activity of alkaline phosphatase. Ultrasound. The smallest size of stones that can diagnose = 1-2 mm. Often unable to determine sediment (sand) in ZHM. Cholecystography. Stones in the bile ducts and ZHM seen as a zone of enlightenment. Treatment. First stage: diet number 5, eat lots of vegetables, fruits, regularly engage in physical activity, obesity be prevented. Second stage: to dissolve cholesterol (x-RAY negative) gallstones prescribe (Henohol, Henofalk) and urodyzoksyholevoyi (Ursofalk, Urso - 100) acids. In the third stage of the disease, during an attack of bilious colic, the patient admitted to the surgical department. Assign antispasmodics, analgesics, if necessary - to operate. Cholangitis (angiocholitis - cholaengitis) inflammation of the bile ducts. There are acute and chronic cholangitis. Chronic cholangitis may be latent, recurrent and prolonged septic component of the course. Clinical The feeling of heaviness or dull pain in the right upper quadrant, which occurs in violation diet bumpy ride, physical work. The pain spread to the right shoulder and shoulder. Diarrheal syndrome: a bitter taste in the mouth, aversion to fatty foods, nausea when inhaled the smell of this dish. Itching of the skin that can occur to limit the area. Astenodepresyvnyy syndrome: weakness. Long periods of unwarranted subfebrile with periodic fever. When viewed subikteryc mucous. They exhibit a larger soft, tender liver. Laboratory and instrumental methods Complete blood count: leukocytosis, left shift, accelerated ESR, anemia. Biochemical analysis of blood: increased bilirubin, alpha 2 and γ-globulin, transaminases, alkaline phosphatase, γhlyutamiltranspeptydazy, sialic acid, fibrin. Urine lab. the possible emergence of protein cylinders bilirubin. Fractional duodenal intubation. Portion B - a large number of shallow cylindrical epithelium. Portion C - bacterial flora, leukocytes, increase in sialic acid, fibrin, enzymes. Ultrasound - expanding intrahepatic bile ducts, liver enlargement. Intra / a cholangiography or endoscopic retrograde pankreatoholangiohraphy exhibit advanced bile duct. Treatment Diet number 5a; antibacterial; bile med-s. if necessary - surgery. Hepatorenal syndrome. About hepatorenal syndrome talking when along with marked and anatomically proven liver and biliary tract revealed signs of kidney damage. It is most commonly observed in liver cirrhosis. Cholestatic syndrome. (Cholestasis syndrome). It is characterized by dark, like brown skin, intense itching, which precedes the appearance of jaundice. On the palms in the corners of the eyes, the outer surface of the elbows, knees flat formation appear yellow due to hypercholesterolemia xanthelasma. In some cases there may be fever, chills. In blood levels of conjugated bilirubin, cholesterol, β-lipoprotein, hemahlyutamintransferazy. Urine is dark in color, like color of beer, feces may be bright. The syndrome of hepatic failure (insuffitientia hepatitis) - is a violation of the liver, accompanied by severe disorders of homeostasis and violation of the internal organs, especially the central nervous system. Diarrheal syndrome is characterized by nausea, spitting, heartburn, vomiting, appetite disturbance. Pain in the right upper quadrant. Chronic autoimmune hepatitis More common in girls and young women aged 10-30 years, at least women in menopause. According to the literature, the ratio of women and men in this disease 3-1. Beginning disease can manifest weakness, anorexia, dark urine, jaundice prior. Chance of a extrahepatic manifestations: fever, joint damage that gives rise to the diagnosis of rheumatic fever, lupus. In later stages: fever to subfebrile digits combined with arthralgia. The process involved large joints of the upper and lower extremities, occasionally spine. Configuration joints varies mainly due peryartykulyar inflammation and tendon-muscle syndrome. Chronic autoimmune hepatitis is a systemic disease with lesions of the skin, mucous membranes and internal organs. It is characterized by the presence of pleuritis, myocarditis, pericarditis, ulcerative colitis, glomerulonephritis. Described Cushing's syndrome, diabetes, generalized lymphadenopathy, hemolytic anemia The disease has a continuous flow. In the study revealed an increase in blood levels of bilirubin, aminotransferases. Hypergammaglobulinemia occurs so often that one of the names of this form of the disease is "progressive hyperhammaglobulinemic hepatitis." Typical hypoalbuminemia, significant deviations thymol and a sharp slowdown allocation of bromsulfaleyin. Possible signs of hypersplenismus (platelets and leukopenia). Often there are positive LE-cell phenomenon, antinuclear factor, complement fixation, high (1:160, 1:320 and higher) titer of antibodies to tissue smooth muscle (the latter is a pathognomonic sign of liver damage). Pain in the right upper quadrant, constantly aching, often intense, sharply intensified after exercise. This pain associated with inflammatory infiltration in the connective tissue in the liver capsule. In some patients the equivalent is the feeling of heaviness and fullness in the right upper quadrant. Diarrheal syndrome appears distorted taste of food, constant nausea, which increases after meals and medication depends on the violation of decontaminating the liver and reactive pancreatitis. Syndrome "small" liver failure, which manifested drowsiness, severe bleeding, transient jaundice and ascites occurs in patients with severe necrotic changes in hepatocytes. For cholestasis syndrome characterized by itching, increased bilirubin, cholesterol, alkaline phosphatase, gammahlutamiltransferazy serum Hepatomegaly is found in all cases HVH. In acute liver disease stands at 5-7 cm from the edge of the arc, it is moderately dense, tapered edge, palpation is painful. Remission accompanied by a marked decrease in liver. The spleen is enlarged slightly. Blood analysis revealed during acute hypergammaglobulinemia, hypoalbuminemia, increased thymol and activity of aminotransferases (ALT, AST more). Increasing total protein and bilirubin in serum. In remission, these figures are improving, but do not reach the standards. Ultrasound shows moderate hepatomegaly with a rounded bottom edge of both particles liver. Prolonged disease decreases sound conductivity and elasticity of the liver. Some diagnostic value has nuclear scans. Chronic hepatitis B (chronic viral hepatitis B) in 10-20% of cases are due to acute process. Major antigenic and serological markers of viral replication - HBV DNA, DNA polymerase, HbeAg, anti-Ig NBc class M. They are found in patients with chronic disease and they are an indicator of activity of the process. The presence of NVs-Ag in serum is a sign of viral persistence. Chronic hepatitis C (HVHS) occupies a special place among HVH because 20-50% of cases transformed into cirrhosis. HCV virus is heterogeneous, is not less than 6 of its types, which differ both in the degree of pathogenicity, and the sensitivity to interferon. Feature of HCV is that its replication can occur not only in the liver tissue, but also in mononuclear cells. This explains poliorhannist damage in HCV. The basis of extrahepatic manifestations (idiopathic thrombocytopenia, aplastic anemia, uveitis, lesions of the thyroid gland, systemic vasculitis, etc.). Lie as a direct effect of the virus, and autoimmune reactions. Chronic hepatitis D (XVHD) runs as a mixed infection because replication of the virus (NDV) is required HbsAg hepatitis B virus (HBV). Chronic drug-induced hepatitis (HMH) - drug liver damage - is an urgent problem due to the increasing number of different medications, uncontrolled use, widespread polypharmacy. HMH is up to 5% of all chronic heptytiv. Damaging factors can be realized in the form of autoimmune and toxic reactions. Hepatotoxic agents can cause necrosis already in high doses and their toxicity increases with dose (chloroform, muscarinic et al.). Effects of other drugs due to idiosyncrasy and is independent of dose (chlorpromazine, ftorotan, isoniazid, erythromycin, tetracycline, anabolic steroids, oral contraceptives, and others.) May manifest metabolic or immunological disorders. Chronic cryptogenic (idiopathic) hepatitis. This group includes chronic hepatitis without identified etiology, which may be due to insufficient sensitivity of existing serological tests, especially to certain subtypes faith hepatitis B, C or D, their mutations and other causes. In addition, it is expected that other types of hepatitis viruses are not identified so far. In establishing the diagnosis of chronic hepatitis B should reflect the etiology, pathogenesis, level of activity and stage of disease. The degree of activity (weight process) for chronic hepatitis determined by enzyme laboratory tests and morphological study of liver biopsy. From laboratory signs is to identify the most informative alanine aminotransferase (ALT) increasing its level of 3-5 reflects the minimum of 5-10 times moderate, more than 10 times - a high degree of activity. In the morphological study using semi-quantitative analysis of the index of histological activity (ISSAR) - "index Knodel". Step hCG reflects prebih disease and is characterized by the degree of liver fibrosis until the development of cirrhotic changes. There fibrosis: portal, periportal, peryhepatotselyulyarnyy. Weather. In chronic hepatitis mostly favorable, especially after the elimination of etiological factors. Prevention of chronic hepatitis includes early diagnosis, adequate treatment of acute viral hepatitis, clinical supervision for him, to prevent exposure to various industrial, medical and consumer intoxication others. Treatment of chronic viral hepatitis. Should exclude all hepatotoxic effects (contact with hepatotropic poisons the workplace, alcohol). Obmezhuyetsya heavy physical work. Not intended medication slowly neutralized liver (tranquilizers, sedatives, analgesics) are contraindicated physiotherapy on the plot liver balneotherapy. In acute disease surgery performed only for health indications. Recommended diet number 5. Food consumed 4-5 times a day in small portions. Drug therapy involves the use of immunostimulants (levalizol, timalin, T-activin) and antiviral drugs (interferon ademin-arabinoside). The main treatment for patients with chronic viral hepatitis is interferon (IF). It inhibits virus replication and stimulates the production of endogenous ineterferonu. Treatments IF long enough: at least 4-6 months with HVH type B (510 million IU 3 times a week subcutaneously or intramuscularly), up to 18 months at HVH type C (3 million IU 3 times per week), and 12 months at HVH type D (10 million IU 3 times a week). Possible combinations of IF with antioxidants dezoksyholevoyu acid and drugs from the group hepatoprotetoriv (essentiale, vitamins B, C, etc.).. In chronic autoimmune hepatitis commonly used steroids in combination with immunosuppressive drugs. cirrhosis Cirrhosis (sirrhosis hepatis) - Polyetiological chronic progressive disease with severe symptoms in varying degrees of functional liver failure and portal hypertension, the main feature of which is the significant growth of connective tissue. The morphological structure distinguish large-, MKD, mixed and biliary (primary and secondary) liver. Mixed (macro-mikronodulyarnu) form is diagnosed when a number of small and large sites about equally. Large-(makronodulyarnyy, postnekrotychnyy) cirrhosis is characterized by the formation of nodes of various sizes over 3mm in diameter. Some units reach 5 cm size liver may be normal, increased and decreased sharply. The initial clinical manifestations of large-cirrhosis is often dyspeptic syndrome (loss of appetite, flatulence), asthenia (decreased performance, irritability, hipohondriya), pain or a feeling of heaviness in the upper abdomen. On examination revealed liver enlargement with thickening and deformation of the surface, the liver edge sharpened. Initially, there is a uniform increase in both particle unsharp liver. Subsequently often dominates the increase of the left lobe. Portal hypertension in the initial stage shows moderate splenomegaly. In the expanded stage of the disease early and persistent symptoms, regardless of etiological and morphological types is a pain in the right upper quadrant and hepatolienal syndrome. This can be detected signs hipersplenizmu (leukopenia, thrombocytopenia, anemia). diarrheal syndrome skin changes Fever lasted Hemorrhagic syndrome The syndrome of gastrointestinal tract Hepatopankreatic syndrome intestinal lesion Syndrome of endocrine disorders Toxic encephalopathy syndrome Syndrome of cardiovascular changes Clinically distinguish light, medium and severe hepatocellular failure: light - general weakness, degradation, loss of appetite, nausea; medium - jaundice, drowsiness, decreased mental abilities, "liver palms" appearance of vascular "stars" on the body, hemorrhagic syndrome (bleeding from the nose, with esophageal varices, hemorrhoids veins, hemorrhage); severe - impaired consciousness until its complete loss, muscle twitching, they cramp, periodic excitation. Reflexes fade, lowers blood pressure, increases respiration rate, and so on. MKD (mikronodulyar, portal) cirrhosis - units of the same size, with a diameter of 1-3 mm. Liver of normal size or enlarged. This form of cirrhosis is often observed in alcoholism, bile duct obstruction, breach of venous outflow, hemochromatosis. The initial stage (diarrheal) vascular and parenchymal compensation. The clinic is dominated dyspeptic, astenovegetative syndromes. Standing is a sign of a moderate increase in the liver. Extensive stage (ascites) accompanied by manifestations of primary parenchymal and portal decompensation. In the initial stage of clinical signs attached portal hypertension (Fig. 3), hemorrhagic syndrome, endocrine disorders, jaundice, "hepatic features", weight loss and atrophy of skeletal muscles. During acute increases body temperature. The liver is enlarged, firm, often rough, rounded edge. Increased spleen. In general blood test show signs of moderate anemia, leukopenia, thrombocytopenia, and increased ESR. Phase of severe parenchymal and portal failure (kahektychna). Pronounced symptoms of the second stage. Typical is with cholestatic jaundice component severe hemorrhagic syndrome (nosebleeds, distributed or pislyain'yektsiyni spontaneous ecchymosis), hepatic encephalopathy. Severe signs of portal hypertension: ascites, dilatation of abdominal wall ("Head of Medusa") (Fig. 5), right pleural effusion, umbilical hernia, bleeding from hemorrhoidal veins of esophageal varices and gastric. Can a progressive decrease in the size of liver. In general blood test show signs hypersplenizmus, accelerated ESR. In biochemical analysis of blood - reducing total protein, albumin, cholesterol, prothrombin, increased ALT, bilirubin, indicators of thymol. In the analysis of urine - proteinuria, microhematuria, cylindruria. Ultrasound examination of the liver reveals hepatosplenomegaly, diffuse lesions, ascites, sudden expansion of portal vein, absence of respiratory fluctuations lumen of portal vein. In Radionuclide imaging the liver are hepatomegaly, diffuse lesions, diffuse weakening hatching, uneven intensity figure. Biliary cirrhosis is divided into primary and secondary. The basis of primary biliary cirrhosis is an autoimmune disease that begins as a chronic nonsuppurative destructive cholangitis. Long time no severe symptoms. More common in women over 35 years. The most common and most constant symptom is itchy skin. Inconsistent initially it for years ahead of jaundice, which gives rise to long-term treatment of "skin disease". Subsequently itch becomes a constant, increasing after a warm bath at night. There is a dark brown pigmentation of the skin in the area of the blades, jaundice cholestatic type xanthelasma. Rarely is expressed mild hepatomegaly. Extensive stage disease is characterized by the increase of jaundice, fever to febrile digits depletion until cachexia due to malabsorption in the intestines. Often there is redness of her hands, sometimes with a yellowish tinge ("liver palms"). In some cases, changing as nails watch glass. Thickening of distal phalanges ("drumsticks") In end-stage (terminal) itchy skin decreases. Pigmented skin thickens, coarsens, it can manifest as swelling in scleroderma. A violation occurs secretion of bile malabsorption of fatsoluble vitamins, osteoporosis. MKD (mikronodulyar, portal) cirrhosis - units of the same size, with a diameter of 1-3 mm. Liver of normal size or enlarged. This form of cirrhosis is often observed in alcoholism, bile duct obstruction, breach of venous outflow, hemochromatosis. The initial stage (diarrheal) vascular and parenchymal compensation. The clinic is dominated dyspeptic, astenovegetativnogo syndromes. Standing is a sign of a moderate increase in the liver. Extensive stage (ascites) accompanied by manifestations of primary parenchymal and portal decompensation. In the initial stage of clinical signs attached portal hypertension (Fig. 3), hemorrhagic syndrome, endocrine disorders, jaundice, "hepatic features", weight loss and atrophy of skeletal muscles. During acute increases body temperature. The liver is enlarged, firm, often rough, rounded edge. Increased spleen. In general blood test show signs of moderate anemia, leukopenia, thrombocytopenia, and increased ESR. Blood analysis increases the activity of enzymes of cholestasis: alkaline phosphatase, leytsynaminopeptydazy, gamma hlyutamiltranspeptydazy. Increased bilirubin slow and occurs in the later stages. Increasing the concentration of bile acids and copper content in serum and iron levels decreased. Typical is hyperlipidemia with increasing concentrations of cholesterol, beta-lipoproteins, phospholipids. The level of circulating immune complexes, exhibit kriohlobuliny, antimitochondrial antibodies. Ultrasound detects unchanged bile duct, liver biopsy in the study are nonsuppurative destructive cholangitis intrahepatic in the early stages of the disease, then biliary cirrhosis. Secondary biliary cirrhosis is caused by prolonged violation vidtikannya bile at large intrahepatic ducts, due to strictures, stones, primary metastatic tumors. Clinic determined the primary disease. It is dominated by such signs as jaundice, diffuse hyperpigmentation of the skin, its dryness, thickening and itching. Sometimes the forefront aholiya, steatorrhea. Almost always there is pain. Characterized by hyperthermia, sweating. More pronounced than in primary biliary cirrhosis, avitaminosis fat-soluble vitamins A, C, and D. The blood found neutrophilic leukocytosis, accelerated erythrocyte sedimentation rate. Treatment for cirrhosis of the liver Assign diet number 5 (with Pevsner). If the patient shows signs of hepatocellular failure, then limit the protein, with edema - salt. Drug therapy includes drip of 5% Glucose solution, Dextran, Alvezin, Reohlyumanu with detoxification effect, improves microcirculation. In addition, the tools that affect the liver cell membrane (Essenciale, Lipostabil, Kars, Hoftiol, Riboksin). In portal hypertension, ascites using Potassium-sparing diuretics (Veroshpiron, Triamterene), which can be combined with Saluretics (Furosemide, Urehit, Oksodomin), beta-blockers. The use of diuretics requires periodic prescribing potassium (Asparcam, Panangin). Assign vitamins A, D, E, C, B vitamins to reduce itching - Cholestyramine, Carbon and Silicon sorbents. When symptoms of encephalopathy apply glutamic acid, Ornitsetyn, Hoftiol, Purslane, Antibacterials, Plazmaforez, Hemosorbtion. When ascites intravenously administered native plasma albumin, which increase the osmotic pressure of the plasma, improve metabolism in liver cells. During resistant ascites, which defies adequate therapy accession hepatorenal syndrome threats abdominal bleeding apply parantsentez (removed no more than three liters of fluid). Unfavorable prognosis. The average life span of patients with cirrhosis 4-6 years. It remains the longest performance with biliary cirrhosis, less - in portal and postnekrotyc cirrhosis. Prevention. First elimination or limitation of etiological factors, timely diagnosis and treatment of chronic hepatitis and liver. Thanks for your attention!