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Lecture notes, cheat sheets
Infectious diseases. Acute and chronic viral hepatitis. Etiology, pathogenesis, clinical picture, differential diagnosis, treatment (lecture notes)
Directory / Lecture notes, cheat sheets Table of contents (expand) LECTURE № 16. Acute and chronic viral hepatitis. Etiology, pathogenesis, clinic, differential diagnosis, treatment 1. Viral hepatitis Viral hepatitis (Botkin's disease) is a disease of a viral nature that occurs with symptoms of general intoxication and a predominant lesion of the liver. These include viral hepatitis A, viral hepatitis B, hepatitis C, hepatitis D. Acute hepatitis is an inflammatory disease of the liver. The introduction of the hepatitis A virus occurs through the mucous membranes of the gastrointestinal tract. The hepatitis B virus enters the body during transfusion of blood or blood products (except for albumin and donor immunoglobulin), during medical manipulations, tattoos, contacts with blood (from surgeons, laboratory assistants); there is sexual transmission of the infection. Etiology. The hepatitis A virus is built from protein subunits that form a cavity in which a single-stranded RNA molecule with a diameter of 28 nm is tightly packed. The virus persists for a long time in water, soil and on household items. The virus is resistant to ether, acids, chlorine, sensitive to formaldehyde, and is inactivated by boiling within 5 minutes. It is excreted in feces from the end of the incubation period and during the pre-icteric period. With the onset of jaundice, the virus cannot be detected in the stool. Hepatitis B virus is a complex virus from a non-taxonomic group; a DNA-containing virus primarily affects liver cells. The virus has a double-stranded DNA polymerase, which is necessary for completing the internal DNA chain, and antigens (surface, core, infectious). The virus is stable in the external environment, persists at room temperature for up to 6 months, can withstand heating up to 60 °C for up to 10 hours. It loses the ability to cause infection at a temperature of 120 °C after 45 minutes, sterilization with dry steam at a temperature of 180 °C - within 60 min, boiling for 30 minutes. It is insensitive to acidic pH values, but is destroyed in an alkaline environment. Hydrogen peroxide, UV irradiation, chloramine, formalin, phenol have a detrimental effect on the virus; the virus is resistant to chemical factors. The virus can persist in the human body for several years. The most common acute liver injury in humans occurs with viral hepatitis. Acute hepatitis can be caused by enteroviruses, intestinal microbes, the causative agent of infectious mononucleosis, and septic bacterial infection. There are also acute toxic drug-induced hepatitis caused by MAO inhibitors, hydrazine derivatives, PAS, isonicotinic acid derivatives, male fern extract and other industrial poisons (phosphorus, organophosphorus insecticides, trinitrotoluene, etc.), mushroom poisons of inedible mushrooms (muscarine, aflatoxin, etc. .). Acute hepatitis can occur as a result of radiation injury, with extensive burns of the body, severe infectious diseases, and toxicosis of pregnant women. The pathogenesis consists in the direct impact of a damaging factor on the hepatic parenchyma or in immunological disorders that occur in response to a primary liver lesion, followed by cytolysis of affected and intact hepatocytes. In some cases, disturbances in blood flow in the liver and intrahepatic cholestasis are important. Clinic. The incubation period for viral hepatitis A can range from 7 to 50 days (usually 15-30 days), for hepatitis B - from 50 to 180 (usually 60-120 days). Viral hepatitis can have icteric, anicteric and subclinical forms. The duration of viral hepatitis is divided into acute (up to 3 months), protracted (3-6 months) and chronic (over 6 months). The development of the disease is gradual, the pre-icteric period lasts 1-2 weeks. There are influenza-like, dyspeptic, asthenovegetative and arthralgic variants of the pre-icteric period. At the end of it, the urine darkens, the feces become discolored, an enlargement of the spleen is observed, and the activity of liver enzymes increases, especially ALT. During the icteric period, patients experience general weakness, nausea, loss of appetite, dull pain in the liver area, and itchy skin. Jaundice may increase, but this is not a criterion for the severity of the disease; there may be severe forms with slight jaundice. The severity is determined by the severity of intoxication symptoms. Often not only the liver is enlarged, but also the spleen. With viral hepatitis A, the icteric period lasts 7-15 days, and recovery occurs within 1-2 months. Viral hepatitis B can have a protracted and chronic course. With hepatitis B, the development of acute liver failure (hepatic coma, hepatic encephalopathy) may occur. Signs of increasing liver failure: memory impairment, increased general weakness, dizziness, agitation, increased jaundice, increased vomiting, decreased liver size, the appearance of hemorrhagic syndrome, ascites, fever, neutrophilic leukocytosis, decreased cholesterol levels (below 2,6 mmol/l, coefficient esterification below 0,2, sublimate titer less than 1,4, prothrombin index below 40%, fibrinogen below 2,93 µmol/l, platelets less than 10 x 106 µmol/l. In mild cases, acute hepatitis is practically asymptomatic, being detected only by chance examination. In more severe cases (with toxic hepatitis), clinical symptoms of the disease develop quickly, simultaneously with signs of general intoxication and toxic damage to other organs and systems. The height of the disease is characterized by icteric staining of the skin and mucous membranes, whitish-clay color of stool, deep dark color (beer-colored) urine, hemorrhagic phenomena, orange or saffron-colored skin. In mild cases, jaundice is visible only in daylight; icteric staining of the sclera and mucous membrane of the soft palate appears most early. Sometimes nosebleeds and petechiae appear. Patients are concerned about skin itching, bradycardia, depressed mental state, increased irritability, insomnia and other signs of damage to the central nervous system. Enlargement of the liver and spleen is slightly painful on palpation. Diagnostics. Based on clinical, epidemiological and laboratory data, hyperbilirubinemia (100-300 μmol / l or more), an increase in the activity of a number of serum enzymes (aldolase, aspartate aminotransferase and especially alanine aminotransferase (significantly above 40 units), lactate dehydrogenase), hypoalbuminemia, hyperglobulinemia are detected. Indicators of protein-sedimentary samples (thymol, sublimate, etc.) are deviated from the norm. One of the functions of the liver is disturbed - the production of fibrinogen, prothrombin, coagulation factors VII, V, as a result of which hemorrhagic manifestations appear. Laboratory confirmation of the diagnosis is an immunofluorescent method, by which antibodies to the hepatitis A virus are detected in the patient's blood serum. In hepatitis B, detection of the surface antigen of the hepatitis B virus or antibodies to it is of diagnostic importance. Differential diagnosis is carried out with liver damage in other infections (leptospirosis, infectious mononucleosis, pseudotuberculosis, salmonellosis, ornithosis, sepsis), with toxic hepatitis (poisoning with carbon tetrachloride, dichloroethane), drug-induced jaundice (from chlorpromazine, anti-tuberculosis drugs, etc.), hemolytic and mechanical jaundice, functional hyperbilirubinemia (Gilbert syndrome, Dubin-Johnson syndrome). Of great importance are a thorough history taking, identification of possible professional or domestic intoxications, the epidemiological situation when a disease is detected and its cause is identified. In unclear cases, the presence of viral hepatitis should be assumed. The determination of the so-called Australian antigen is a marker for serum hepatitis B (it is also detected in virus carriers). Mechanical (subhepatic) jaundice usually occurs with cholelithiasis as a result of blockage of the common bile duct by a stone. But in this case, before the appearance of jaundice, an attack of biliary colic occurs. Direct bilirubin is found in the blood, the stool is discolored. With hemolytic adrenal jaundice, free (indirect) bilirubin is present in the blood, the color of the stool is normal, and the osmotic resistance of red blood cells is usually reduced. With false jaundice (due to staining of the skin with carotene during prolonged and abundant consumption of oranges, pumpkins, carrots), the sclera are usually not stained, hyperbilirubinemia is absent. Treatment. Hospitalization in special departments of infectious diseases hospitals is mandatory, and sanitary and epidemiological measures are carried out at the source of infection. Prescribe bed rest, a gentle diet with limited fat and increased carbohydrate content, and a large amount of fruit juices. The basis of treatment is gentle treatment and nutrition (table No. 5). Liquid - up to 2-3 liters per day in the form of juices, alkaline mineral waters. A complex of vitamins is prescribed. For moderate forms, it is advisable to administer 5% glucose solution and Ringer-Locke solution 250-300 ml intravenously. In severe cases, hemodez or rheopolyglucin 200-400 ml are administered intravenously, and treatment continues in intensive care wards. A 10% glucose solution (up to 1 l/day), Lobari solution is administered intravenously (1 l of pyrogen-free water contains 1,2 g of potassium chloride, 0,8 g of magnesium sulfate, 0,4 g of calcium chloride and 100 g glucose) up to 1-1,5 l/day. In case of acute liver failure, prednisolone is administered (IV or IM 60-90 mg/day. A 20% sorbitol solution (250-500 ml/day), a 15% albumin solution (200-300 ml) is used. /day), 2-3 units of contrical (trasylol) are administered intravenously 10-000 times a day. To suppress opportunistic intestinal microflora, neomycin 30 g 000 times a day or kanamycin 1 is taken orally g 4 times a day. A siphon enema is done daily with a 0,5% sodium bicarbonate solution. An exchange blood transfusion is recommended. Hyperbaric oxygenation with a session regimen of 4 to 2 atm, lasting 1,5 minutes, as well as hemosorption using activated carbon. In severe cases, detoxification therapy is carried out. The prognosis is determined by the etiology of the disease, the severity of liver damage, and the timeliness of the treatment started. The prognosis for life is generally favorable. After the transfer of hepatitis B, in some cases, the development of chronic hepatitis and cirrhosis of the liver is possible. Prevention of acute hepatitis consists in observing the rules of personal hygiene, carrying out sanitary and epidemiological measures, ensuring appropriate sanitary and technical supervision at enterprises, which prevents the possibility of industrial poisoning with hepatotropic poisons. Do not eat unknown mushrooms. For the prevention of viral hepatitis B, it is necessary to examine donors (persons with the presence of an antigen to the hepatitis B virus or antibodies to it in the blood are excluded), careful processing of instruments is necessary. 2. Chronic hepatitis Chronic hepatitis is a polyetiological liver disease of a chronic nature, expressed in inflammatory-dystrophic changes with moderate fibrosis and generally preserved lobular structure of the liver, occurring without positive dynamics for at least 6 months. Clinically, chronic hepatitis is characterized by asthenovegetative, dyspeptic syndromes, an increase in liver size, impaired liver function, morphological persistence of necrosis, an inflammatory process, and the development of fibrosis while maintaining the overall structure of the liver. Etiology. The most important are the viral, toxic and toxic-allergic occurrence of liver damage. Pathogenesis. The direct impact of an etiological factor (virus, hepatotoxic substance) on the liver parenchyma causes degeneration and necrobiosis of hepatocytes and reactive proliferation of mesenchyme. One of the mechanisms for the transition of acute viral and toxic hepatitis into a chronic form and further progression of the process has an immunological specific nature. Clinic. Pain in the liver of a dull nature, constant. There is an increase in the liver, pain or a feeling of heaviness, fullness in the right hypochondrium, dyspepsia, less often jaundice, pruritus, low-grade fever are detected. Enlargement of the liver, enlargement of the spleen is absent (or it is slightly enlarged). Lethargy, fatigue, decreased appetite, belching, nausea, poor fat tolerance, flatulence, unstable stools, general weakness. The skin is pale, dryish, sometimes in some patients mild (subicteric sclera and palate) or moderate jaundice is detected. Diagnostics. Based on clinical and laboratory data, moderate hyperbilirubinemia is determined. Positive results of protein-sedimentary tests - thymol, sublimate, etc. In the blood serum of patients, the content of aminotransferases (ALAT, AST and LDH) is increased, with difficulty in the outflow of bile - alkaline phosphatase. Ultrasound of the liver and scanning of the liver can determine its size. In hepatitis, sometimes there is a reduced or uneven accumulation of the radioisotope in the liver tissue, in some cases there is an increased accumulation in the spleen. Methods of laparoscopy and puncture biopsy of the liver make it possible to more accurately differentiate these two forms of hepatitis and distinguish them from other liver diseases. Treatment. Compliance with a diet with the exception of hot, spicy seasonings, refractory animal fats, fried foods, excess meat dishes. It is recommended to use cottage cheese (daily up to 100-150 g), mild cheeses, boiled fish and meat, bread. With toxic and toxic-allergic hepatitis, it is extremely important to completely stop contact with the corresponding toxic substance. The use of hepatoprotectors (Karsila, Essentiale, etc.), cytostatics, antiviral drugs, immunocorrectors. Author: Gavrilova N.V. << Back: Adenoviral infection. R-s infection. Rhinovirus infection. Etiology, epidemiology, clinic, diagnosis, treatment (Adenovirus infection. R-s infection. Rhinovirus infection) >> Forward: Parasitic diseases. Epidemiology, clinic, treatment (Helminthiasis. Ascariasis. Alveococcosis. Hookworm disease (hookworm and necatoriasis). Diphyllobothriasis. Opisthorchiasis. Taeniasis. Trichocephalosis. Fascioliasis. Echinococcosis. Enterobiasis)
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