1. Although the pathogens of the five types of viral hepatitis are different, there is a great deal of clinical similarity. However, the course of the disease is different, the course of the disease within 6 months for acute hepatitis, the course of the disease more than 6 months for chronic hepatitis, of which type A, type E viral hepatitis is only manifested as acute hepatitis type B, type C, type D viral hepatitis can be presented as acute hepatitis or chronic hepatitis performance, and there is a development of cirrhosis and hepatocellular carcinoma may be. It is important to note that due to the latent nature of viral infection, chronic hepatitis cannot be ruled out in viral hepatitis B, C, and D, even if the patient cannot provide a history of more than 6 months.
2, acute hepatitis: the patient in the recent past, continued for more than a few days, but there is no other reason to explain the symptoms, such as fatigue, loss of appetite, nausea and so on. Hepatomegaly with tenderness, tenderness to percussion in the liver area, and mild splenomegaly in some patients. Laboratory tests show elevated serum ALT and positive seropathology. If it is not accompanied by elevated bilirubin, it is acute non-jaundiced hepatitis; if it is accompanied by elevated bilirubin, it is acute jaundiced hepatitis.
3, chronic hepatitis: acute hepatitis disease duration of more than half a year, or the original hepatitis B, C, D or HBsAg carrier history, this time the same pathogen again due to hepatitis symptoms, signs and liver function abnormalities can be diagnosed as chronic hepatitis. Onset date is unknown or no history of hepatitis, but liver histopathology is consistent with chronic hepatitis, or according to the symptoms, signs, laboratory tests and ultrasound analysis, can also make the appropriate diagnosis.
4. According to China's 2000 viral hepatitis prevention and control program, chronic hepatitis can be clinically divided into: mild (clinical symptoms, signs and symptoms are mild or absent, liver function indexes are only 1 or 2 mild abnormalities), moderate (between mild and severe), and severe (there are obvious or persistent hepatitis symptoms, such as fatigue, fatigue, abdominal distension, yellow urine, loose stools, etc., accompanied by liver disease, liver palms, spider nevus, splenomegaly, and exclude other causes), and the diagnosis can be made accordingly. Splenomegaly and exclusion of other causes, and no signs of portal hypertension. Laboratory tests: repeated or persistent elevation of serum ALT and/or AST, lowered albumin or abnormal A/G ratio, significantly elevated gammaglobulin.) In addition to the above conditions, where the albumin?32g/L, bilirubin greater than 5 times the upper limit of normal value, prothrombin activity 60% to 40%, cholinesterase <2500U / L, one of the four tests to the extent of the above can be diagnosed as chronic hepatitis severe.
5, for most of the chronic hepatitis B, the whole course of the disease can be divided into immune tolerance, immune clearance, inactive and reactive period. The clinical regression of different periods is not the same.
Complications of hepatitis1, the pathogenesis of viral hepatitis is more complex, different types of viruses cause disease mechanism is not the same. Viral hepatitis A and E are caused by HAV and HEV infections respectively. After HAV/HEV enters the body through the mouth, it enters the bloodstream and reaches the liver through the intestinal tract, and is then excreted into the intestinal tract through the bile and appears in the feces.
2, the main organ invaded by the virus is the liver. the mechanism of HAV-induced hepatocellular damage is not yet clear, and it is generally believed that HAV does not directly cause hepatocellular lesions, and the liver damage is caused by the immunopathological reaction of HAV-infected hepatocytes; the inflammation of the liver in the early stage of hepatitis E is caused by the direct cytopathic lesions of HEV, whereas in the clearance period of the virus, hepatocellular lesions are mainly caused by HEV-induced immune reactions. The inflammation in the early stage of hepatitis E is mainly caused by HEV direct cytopathy, while the hepatocyte lesions in the viral clearance phase are mainly caused by HEV-induced immune response.
3. The mechanism of hepatitis B virus damage to the liver is complex, and most scholars believe that it is not direct, but through the immune response mediated hepatocyte necrosis and inflammation, in which cytotoxic T cells (CTL) cause liver lesions through cytolytic and non-cytolytic mechanisms; in fact, CTL directly cause hepatocyte damage only accounted for a small portion of the hepatic cytopathic lesions, and the cytokines such as TNF-? The activation of cytokines such as TNF-? and INF-? and apoptosis signaling Fas/FasL play a major role. TNF- and INF-? TNF-? and INF-? play an important role in immune clearance of the virus. In addition, the cytolytic mechanism of NK cells and NKT cells also plays a synergistic role.
4. The pathogenesis of viral hepatitis C is complex, and its occurrence, development and regression depend on the interaction between the virus and the immune system. Among them, HCV antigen-specific CTL plays an important role, apoptosis is one of the mechanisms of hepatitis C hepatocyte injury, in addition, regulatory T cells are also involved in the whole disease process.
Causes of hepatitis1. Viral hepatitis is a disease caused by hepatitis virus infection. At present, there are five kinds of hepatitis viruses: hepatitis A virus, hepatitis B virus, hepatitis C virus, hepatitis D virus and hepatitis E virus.
2, hepatitis A virus HAV is a member of the family of small RNA viruses, hepatophilic RNA viruses. HAV resistance is strong, can withstand 56 ℃ for 30 minutes, room temperature for a week. It can survive in dry feces at 25℃ for 30 days and in shellfish, sewage, freshwater, seawater and mud for months. This stability is favorable for HAV transmission through water and food. High-pressure steam (121 ℃, 20 minutes), boiling for five minutes, ultraviolet irradiation, formalin (1:4000, 37 ℃ for 72 hours), potassium permanganate (30 mg / L, 5 minutes), iodine (3 mg / L, 5 minutes), chlorine (free chlorine 2.0-2.5 mg / L, 15 minutes), 70% alcohol 25 ℃ for 3 minutes can be effective in inactivation of HAV.
Hepatitis B virus (HBV) can be inactivated in water and food. 3, Hepatitis B virus (HBV) belongs to hepatophilic DNA virus family (hepadnaviridae), genome length of about 3.2kb, for part of the double-stranded cyclic DNA. HBV resistance is strong, but 65 ℃ for 10h, boiled for 10min or high-pressure steam can be inactivated HBV. ethylene oxide, glutaraldehyde, peracetic acid and iodine vapors also have a better inactivation effect on HBV. After the invasion of HBV into hepatocytes, part of the double-stranded cyclic HBVDNA in the cell nucleus to extend the positive chain as a template for the negative chain DNA to repair the gap area in the positive chain to form *** valence closed loop DNA (cccDNA); then cccDNA as a template, transcribed into several different lengths of mRNA, respectively, as the pre-genomic RNA and encode a variety of antigens of HBV. cccDNA The cccDNA has a long half-life and is difficult to remove completely from the body.
4, hepatitis C virus is a RNA virus (HCVRNA), can be divided into six different genotypes and subtypes, such as 1a, 2b, 3c and so on. Genotype 1 has a global distribution and accounts for more than 70% of all HCV infections. Hepatitis C virus is sensitive to general chemical disinfectants, high temperature heating and formaldehyde fumigation can inactivate the virus.
5, hepatitis D virus (HDV) a defective virus, the completion of its biological cycle depends on the help of hepatitis B virus, so hepatitis D can not exist alone, must be in the presence of HBV in order to be infected and caused by the disease. HDV genome is a single-stranded RNA, the formation of a viral particles with a complete structure, the diameter of 35-37 nm, the shell of the hepatitis B surface antigen HBV. HDV genome is a single strand of RNA, forming a virus particle with a complete structure, diameter of 35-37nm, its shell for the hepatitis B surface antigen HBsAg, internal by HDAg and HDV-RNA conjugation, and HDV-RNA and HBV-DNA no homology, is not the host's RNA, but HDV genome, it is known that there is only one serotype of HDV, but HDV is prone to mutation, mutation of different strains of virulence are different, and most scholars believe that HDV infection can significantly inhibit the HBV-virus, the virus can be infected with the HBV-virus. Most scholars believe that HDV infection can significantly inhibit HBV-DNA synthesis.