Viral hepatitis is caused by a variety of different hepatitis viruses based infectious disease to liver damage according to the etiological diagnosis, at least five kinds of hepatitis virus A, B, C, D, hepatitis E virus, respectively,caused by a, b, C, D, E viral hepatitis, hepatitis a (hepatitis a), hepatitis B (hepatitis b), hepatitis C (hepatitis C), hepatitis D (hepatitis D) hepatitis Ehepatitis (hepatitis E). Another called the G viral hepatitis, and rare.
Viral hepatitis - symptoms
Viral diarrhea syndrome is caused by some virus. Viral hepatitis, mainly diarrhea, vomiting or fever, severe cases can cause dehydration, acidosis and electrolyte disturbances and even death. Widespread and popular throughout the world. Children and adults can get the disease, second only to respiratory tract infection common in children. Viral hepatitis, there are two kinds of ways, one is an outbreak occurred in older children or adults, another sporadically, occasionally epidemic, occurs mainly in infants and young children. Spread through contaminated water or food. The majority of acute onset. Seasonal in temperate zones, have occurred in the tropics throughout the year. Until the 1970s, the application of electron microscopy (referred to as electron microscopy) and immunological methods to detect some of the pathogenic cause of the disease: Rotavirus, Norwalk virus group of viruses, adenovirus, astrovirus, calicivirus, coronavirus , tiny respiratory orphan virus, tiny rotavirus, a small spherical virus, and some type of intestinal viruses. Different viruses cause disease in different seasons and different age groups. The diagnostic method is the direct application of electron microscopy in the detection of fecal virus particles, or specific immune diagnostic methods in the detection of viral antigens in the feces and serum.
Prevention and treatment of viral hepatitis antibodies. Viral hepatitis is currently no specific treatment is mainly symptomatic treatment. The application of oral rehydration therapy effective. Viral hepatitis prevention is to improve health conditions, diet and health, and trial vaccines.
Viral diarrhea syndrome is caused by some virus. Viral hepatitis, mainly diarrhea, vomiting or fever, severe cases can cause dehydration, acidosis and electrolyte disturbances and even death. Widespread and popular throughout the world. Children and adults can get the disease, second only to respiratory tract infection common in children. Viral hepatitis, there are two kinds of ways, one is an outbreak occurred in older children or adults, another sporadically, occasionally epidemic, occurs mainly in infants and young children. Spread through contaminated water or food. The majority of acute onset. Seasonal in temperate zones, have occurred in the tropics throughout the year. Until the 1970s, the application of electron microscopy (referred to as electron microscopy) and immunological methods to detect some of the pathogenic cause of the disease: Rotavirus, Norwalk virus group of viruses, adenovirus, astrovirus, calicivirus, coronavirus , tiny respiratory orphan virus, tiny rotavirus, a small spherical virus, and some type of intestinal viruses. Different viruses cause disease in different seasons and different age groups. The diagnostic method is the direct application of electron microscopy in the detection of fecal virus particles, or specific immune diagnostic methods in the detection of viral antigens in the feces and serum.
Prevention and treatment of viral hepatitis antibodies. Viral hepatitis is currently no specific treatment is mainly symptomatic treatment. The application of oral rehydration therapy effective. Viral hepatitis prevention is to improve health conditions, diet and health, and trial vaccines.
Viral hepatitis - clinical manifestationsThe incubation period of hepatitis of varying lengths. Hepatitis A is 2-6 weeks (an average of one month); hepatitis B for 6 weeks to 6 months (usually about three months); hepatitis C for 5 to 12 weeks (mean 7.8 weeks).
Acute hepatitisAcute jaundice hepatitis: the course can be divided into three stages.
Jaundice early (1): more than to the onset of fever, accompanied to the malaise, loss of appetite, tired of oil, nausea or even vomiting often abdominal discomfort, bloating, constipation or diarrhea; few cases, there may be respiratory symptoms, or rash, joint pain and other symptoms. Urine gradually deepened to the end of the urine samples Secheng tea. The liver may be mild swelling, with tenderness and percussion pain. Testing: urine bilirubin and urobilinogen positive, significantly elevated serum alanine aminotransferase (alanine aminotrans ferase, ALT). The period generally lasts 5 (3 ~ 7) days.
(2) deepening of jaundice urine, sclera and skin stained yellow and deepen day by day, more than a few days to 2 weeks up to the peak and then decreased gradually. In the emergence of yellow fever soon subsided, and gastrointestinal symptoms and malaise were seen in weight gain, but to before the jaundice is about to alleviate the rapid improvement. In obvious jaundice, itchy skin, stool color lighter, bradycardia and other symptoms. Children with mild jaundice, and a shorter duration. Current Issue hepatomegaly 1 ~ 3cm under the costal margin, there is obvious tenderness and percussion pain, and in some cases and mild splenomegaly. Liver function improved significantly. The issue lasted about six weeks.
(3) Recovery: jaundice, spirit and appetite improved. The enlargement of the liver gradually retracted, tenderness and percussion pain disappear. Liver function returned to normal. The period of about 1 to 2 months.
Two. Acute without jaundice hepatitis: the onset mostly bradycardia, mild clinical symptoms, only fatigue, loss of appetite, nausea, liver pain and bloating, loose stools and other symptoms, no more fever, do not develop jaundice. The liver often swollen with tenderness and percussion pain; a small number of splenomegaly. Changes in liver function elevated ALT. Many cases have no obvious symptoms, was found only in the census. Gradual return of more than three months. Part B and hepatitis C cases may develop chronic hepatitis.
Chronic hepatitisA. Chronic persistent hepatitis: acute hepatitis duration of more than six months, still showed a slight weakness, loss of appetite, abdominal distension, liver pain symptoms, and more without jaundice. Hepatomegaly with mild tenderness and percussion pain. Liver function test is a single elevated ALT. Moved healing of disease extension or repeated fluctuations of up to one year to several years, but the disease is relatively light.
Two. Chronic active hepatitis: a history of hepatitis history, there are obvious symptoms of hepatitis such as fatigue, weakness, poor appetite, bloating, loose stools, liver area pain complexion is often dark, poor general health, labor loss. The hepatomegaly quality hard, accompanied by tenderness and percussion pain, enlargement of the spleen and more. Jaundice, spider naevi, liver palms and obvious acne. Long-term significantly abnormal liver function, ALT continues to rise or repeated fluctuations, decreased serum albumin, globulin, gamma globulin and IgG increased, prothrombin time, autoantibodies and rheumatoid factor positive, circulating immune complexes The material can be increased complement C3 and C4 can be reduced. Some cases the damage of the liver and other organs, such as chronic polyarthritis, chronic glomerulonephritis, chronic ulcerative colitis, nodular nodosa, Hashimoto's thyroiditis, etc..
Severe hepatitisA. Acute severe hepatitis, also known as fulminant hepatitis. Is characterized by: rapid onset, rapid progression of the disease, short course (usually not more than 10 days). Patients often have high fever, severe gastrointestinal symptoms (anorexia, nausea, frequent vomiting, drum intestines, etc.), extreme fatigue. Onset within a few days with neurological, psychiatric symptoms (such as personality changes, abnormal behavior, lethargy, irritability, etc.). Physical examination there is a flapping tremor. Liver smelly, can be abrupt development of hepatic coma. Jaundice appears, quickly deepened. Obvious bleeding tendency (epistaxis, bruising, vomiting, blood in the stool, etc.). The liver rapidly narrowing. Also appear swollen. Ascites and renal insufficiency. Laboratory tests: at the peripheral blood white blood cell count and increased neutrophils, thrombocytopenia; prolonged prothrombin time, decreased prothrombin activity, fibrinogen decreased. Decline in blood glucose; elevated blood ammonia; increase in serum bilirubin, ALT increased, but extensive necrosis of liver cells, ALT can decline rapidly, the formation of the enzyme bile separation "phenomenon. Urine can check to see protein and tube type, positive urine bilirubin.
Two. Sub-acute severe hepatitis, early onset of similar general acute jaundice hepatitis, but her condition aggravated, a highly fatigue, loss of appetite, frequent vomiting, jaundice deepened rapidly, serum bilirubin SITA the> 171.0μmol / L (10mg/dl) often liver smelly, intractable abdominal distension and ascites (complicated by peritonitis), bleeding tendency significantly, often nervous, psychiatric symptoms, late hepatorenal syndrome and death occurred complications of gastrointestinal bleeding, hepatic coma . Liver reduced or no significant narrowing. Duration up to several weeks to several months, the treatment of survivors, most of the development of post-necrotic cirrhosis. Laboratory tests: severe damage to liver function, speed of sound increase in serum bilirubin, ALT was significantly elevated, or ALT decreased with elevated bilirubin was liver enzyme separation; lower serum albumin, globulin, white, globulin ratio inversion, gamma globulin; significantly prolonged prothrombin time, decreased prothrombin activity; significantly reduced cholesterol ester and choline fat.
3. Chronic severe hepatitis deteriorated in the course of chronic active hepatitis or cirrhosis, the clinical manifestations of subacute severe hepatitis. Prognosis is poor.
Cholestatic hepatitisAlso known as capillary bile duct hepatitis or cholestatic hepatitis. Onset and clinical manifestations similar to acute hepatitis, jaundice, fatigue and loss of appetite, mild jaundice, weight and durable, obstructive jaundice, skin itching and other performance. Enlargement of the liver. Stool light color obstruction elevated GGT, alkaline phosphatase, and 5 - nucleotidase enzymes. ALT more than moderately elevated. Strongly positive urine bilirubin and urobilinogen negative.
Acute hepatitisAcute jaundice hepatitis: the course can be divided into three stages.
Jaundice early (1): more than to the onset of fever, accompanied to the malaise, loss of appetite, tired of oil, nausea or even vomiting often abdominal discomfort, bloating, constipation or diarrhea; few cases, there may be respiratory symptoms, or rash, joint pain and other symptoms. Urine gradually deepened to the end of the urine samples Secheng tea. The liver may be mild swelling, with tenderness and percussion pain. Testing: urine bilirubin and urobilinogen positive, significantly elevated serum alanine aminotransferase (alanine aminotrans ferase, ALT). The period generally lasts 5 (3 ~ 7) days.
(2) deepening of jaundice urine, sclera and skin stained yellow and deepen day by day, more than a few days to 2 weeks up to the peak and then decreased gradually. In the emergence of yellow fever soon subsided, and gastrointestinal symptoms and malaise were seen in weight gain, but to before the jaundice is about to alleviate the rapid improvement. In obvious jaundice, itchy skin, stool color lighter, bradycardia and other symptoms. Children with mild jaundice, and a shorter duration. Current Issue hepatomegaly 1 ~ 3cm under the costal margin, there is obvious tenderness and percussion pain, and in some cases and mild splenomegaly. Liver function improved significantly. The issue lasted about six weeks.
(3) Recovery: jaundice, spirit and appetite improved. The enlargement of the liver gradually retracted, tenderness and percussion pain disappear. Liver function returned to normal. The period of about 1 to 2 months.
Two. Acute without jaundice hepatitis: the onset mostly bradycardia, mild clinical symptoms, only fatigue, loss of appetite, nausea, liver pain and bloating, loose stools and other symptoms, no more fever, do not develop jaundice. The liver often swollen with tenderness and percussion pain; a small number of splenomegaly. Changes in liver function elevated ALT. Many cases have no obvious symptoms, was found only in the census. Gradual return of more than three months. Part B and hepatitis C cases may develop chronic hepatitis.
Chronic hepatitisA. Chronic persistent hepatitis: acute hepatitis duration of more than six months, still showed a slight weakness, loss of appetite, abdominal distension, liver pain symptoms, and more without jaundice. Hepatomegaly with mild tenderness and percussion pain. Liver function test is a single elevated ALT. Moved healing of disease extension or repeated fluctuations of up to one year to several years, but the disease is relatively light.
Two. Chronic active hepatitis: a history of hepatitis history, there are obvious symptoms of hepatitis such as fatigue, weakness, poor appetite, bloating, loose stools, liver area pain complexion is often dark, poor general health, labor loss. The hepatomegaly quality hard, accompanied by tenderness and percussion pain, enlargement of the spleen and more. Jaundice, spider naevi, liver palms and obvious acne. Long-term significantly abnormal liver function, ALT continues to rise or repeated fluctuations, decreased serum albumin, globulin, gamma globulin and IgG increased, prothrombin time, autoantibodies and rheumatoid factor positive, circulating immune complexes The material can be increased complement C3 and C4 can be reduced. Some cases the damage of the liver and other organs, such as chronic polyarthritis, chronic glomerulonephritis, chronic ulcerative colitis, nodular nodosa, Hashimoto's thyroiditis, etc..
Severe hepatitisA. Acute severe hepatitis, also known as fulminant hepatitis. Is characterized by: rapid onset, rapid progression of the disease, short course (usually not more than 10 days). Patients often have high fever, severe gastrointestinal symptoms (anorexia, nausea, frequent vomiting, drum intestines, etc.), extreme fatigue. Onset within a few days with neurological, psychiatric symptoms (such as personality changes, abnormal behavior, lethargy, irritability, etc.). Physical examination there is a flapping tremor. Liver smelly, can be abrupt development of hepatic coma. Jaundice appears, quickly deepened. Obvious bleeding tendency (epistaxis, bruising, vomiting, blood in the stool, etc.). The liver rapidly narrowing. Also appear swollen. Ascites and renal insufficiency. Laboratory tests: at the peripheral blood white blood cell count and increased neutrophils, thrombocytopenia; prolonged prothrombin time, decreased prothrombin activity, fibrinogen decreased. Decline in blood glucose; elevated blood ammonia; increase in serum bilirubin, ALT increased, but extensive necrosis of liver cells, ALT can decline rapidly, the formation of the enzyme bile separation "phenomenon. Urine can check to see protein and tube type, positive urine bilirubin.
Two. Sub-acute severe hepatitis, early onset of similar general acute jaundice hepatitis, but her condition aggravated, a highly fatigue, loss of appetite, frequent vomiting, jaundice deepened rapidly, serum bilirubin SITA the> 171.0μmol / L (10mg/dl) often liver smelly, intractable abdominal distension and ascites (complicated by peritonitis), bleeding tendency significantly, often nervous, psychiatric symptoms, late hepatorenal syndrome and death occurred complications of gastrointestinal bleeding, hepatic coma . Liver reduced or no significant narrowing. Duration up to several weeks to several months, the treatment of survivors, most of the development of post-necrotic cirrhosis. Laboratory tests: severe damage to liver function, speed of sound increase in serum bilirubin, ALT was significantly elevated, or ALT decreased with elevated bilirubin was liver enzyme separation; lower serum albumin, globulin, white, globulin ratio inversion, gamma globulin; significantly prolonged prothrombin time, decreased prothrombin activity; significantly reduced cholesterol ester and choline fat.
3. Chronic severe hepatitis deteriorated in the course of chronic active hepatitis or cirrhosis, the clinical manifestations of subacute severe hepatitis. Prognosis is poor.
Cholestatic hepatitisAlso known as capillary bile duct hepatitis or cholestatic hepatitis. Onset and clinical manifestations similar to acute hepatitis, jaundice, fatigue and loss of appetite, mild jaundice, weight and durable, obstructive jaundice, skin itching and other performance. Enlargement of the liver. Stool light color obstruction elevated GGT, alkaline phosphatase, and 5 - nucleotidase enzymes. ALT more than moderately elevated. Strongly positive urine bilirubin and urobilinogen negative.
Viral hepatitis - pathological changesHepatitis lesions are basically the same, liver cell degeneration, necrosis and apoptosis-based, accompanied by varying degrees of inflammatory cell infiltration, liver cell regeneration and proliferation of fibrous tissue.
A. Liver cell degeneration
(1) Water degeneration: very common in viral hepatitis. Intracellular water due to liver cell damage than normal due to the significantly increased. Microscopically, the enlargement of the liver cells, the cytoplasm loose reticular, translucent, and said the cytoplasm loose. Further development of the liver cells swollen spherical, the cytoplasm is almost completely transparent, known as ballooning. Sinusoidal pressure narrowed because of swelling of the liver cells. A high degree of ballooning degeneration of liver cells could eventually be dissolved necrosis (severe hepatitis, liver cell degeneration is often not obvious, and soon necrosis and disintegration).
Acute viral hepatitis: hepatocyte ballooning degeneration, and eosinophilic bodies (↑)
(2) eosinophilic degeneration and eosinophilic necrosis: mostly involved single or a few liver cells, scattered in the hepatic lobule within. Microscopically, the liver cell cytoplasm concentration, the particles disappeared, and was strongly eosinophilic. And then, in addition to the cytoplasm is more concentrated, the nuclei were also condensed and even disappear. The rest of the stain of crimson uniform circular body, known as eosinophilic bodies (acidophilic body, or Councillman body).
Eosinophilic bodies
(3) fatty degeneration: hepatic steatosis often occurs in hepatitis C
Two. Liver cell necrosis
According to the scope of liver cell necrosis, distribution characteristics and the morphology of necrosis necrosis of liver cells can be divided into the following four.
(1) punctate or focal necrosis (spotty necrosis): spotty necrosis of liver cells scattered in the hepatic lobule. Each necrosis involving only the 1 to a few liver cells, at the same time there with inflammatory cell infiltration.
(2) piecemeal necrosis (piecemeal necrosis): often occurs in the hepatic lobule of the community board. Microscope, a small group of liver cell degeneration and necrosis, infiltration of lymphocytes and plasma cells, proliferation of fibrous tissue inserted into the hepatic lobule around and separated by a single or small group of liver cells. Piecemeal necrosis is the main lesion in the active stage of chronic hepatitis.(3) bridging necrosis (bridging necrosis): refers to necrosis was the cord-like ducts constitute the central vein between the bridge-like connection between the portal area or central vein and portal District. Necrotic accompanied by irregular regeneration of liver cells and fibrous tissue hyperplasia, and late fibrous septa separated the lobules. Common in moderate to severe chronic hepatitis.
(4) sub-massive necrosis and massive necrosis: characterized by extensive necrosis of liver cells, can affect the liver acinus I, II, III. Such as the survival time of only a very small number of liver cells known as massive necrosis; When the residue of the region Ⅰ more island-like arrangement of liver cells known as the sub-massive necrosis. Common in acute severe viral hepatitis.
3. Liver cell apoptosis:
4. Inflammatory cell infiltration in hepatitis, often varying degrees of inflammatory cell infiltration in the portal area or within the hepatic lobule. Infiltration of inflammatory cells, mainly lymphocytes, monocytes, and sometimes see a small amount of plasma cells and neutrophils.
5 Regeneration and proliferation of viral hepatitis, degeneration and necrosis is the main pathological changes. To tide over the acute phase, in particular, chronic hepatitis, are also common to have the change of regeneration and proliferation. Regenerative hyperplasia belongs to the repair reaction, but sometimes more complex condition, such as cirrhosis. Mainly as viral hepatitis regeneration and hyperplasia are several.
(1) liver regeneration: hepatic necrosis, adjacent liver cells through direct or indirect split regeneration and repair. Is more obvious in the recovery of hepatitis or chronic stage. Regeneration of liver cell volume is large, large nuclei and deeply stained, and some may have a dual-core. Chronic cases of hyperplasia of small bile ducts in the portal area is still visible.
(2) of Kupffer cell hypertrophy: This is the inflammatory response of the intrahepatic mononuclear phagocyte system. Proliferation of the cells were spindle or polygonal, abundant cytoplasm, prominent in the sinus wall or into the sinus to become a self-wall off the migration of phagocytic cells.
(3) of mesenchymal cells and the proliferation of fibroblasts: mesenchymal cells with multilineage differentiation potential, present in the liver interstitial hepatitis differentiate into tissue cells. Recurrent severe necrosis cases, fibrous tissue hyperplasia can develop into liver fibrosis and cirrhosis.
Hepatitis lesions, liver cell cytoplasm loose and the balloon-like change, has a relatively characteristic punctate necrosis and eosinophilic bodies formed for the diagnosis of common hepatitis; large areas of necrosis of liver cells, collapse of severe hepatitis Characteristics of the main lesion.
A. Liver cell degeneration
(1) Water degeneration: very common in viral hepatitis. Intracellular water due to liver cell damage than normal due to the significantly increased. Microscopically, the enlargement of the liver cells, the cytoplasm loose reticular, translucent, and said the cytoplasm loose. Further development of the liver cells swollen spherical, the cytoplasm is almost completely transparent, known as ballooning. Sinusoidal pressure narrowed because of swelling of the liver cells. A high degree of ballooning degeneration of liver cells could eventually be dissolved necrosis (severe hepatitis, liver cell degeneration is often not obvious, and soon necrosis and disintegration).
Acute viral hepatitis: hepatocyte ballooning degeneration, and eosinophilic bodies (↑)
(2) eosinophilic degeneration and eosinophilic necrosis: mostly involved single or a few liver cells, scattered in the hepatic lobule within. Microscopically, the liver cell cytoplasm concentration, the particles disappeared, and was strongly eosinophilic. And then, in addition to the cytoplasm is more concentrated, the nuclei were also condensed and even disappear. The rest of the stain of crimson uniform circular body, known as eosinophilic bodies (acidophilic body, or Councillman body).
Eosinophilic bodies
(3) fatty degeneration: hepatic steatosis often occurs in hepatitis C
Two. Liver cell necrosis
According to the scope of liver cell necrosis, distribution characteristics and the morphology of necrosis necrosis of liver cells can be divided into the following four.
(1) punctate or focal necrosis (spotty necrosis): spotty necrosis of liver cells scattered in the hepatic lobule. Each necrosis involving only the 1 to a few liver cells, at the same time there with inflammatory cell infiltration.
(2) piecemeal necrosis (piecemeal necrosis): often occurs in the hepatic lobule of the community board. Microscope, a small group of liver cell degeneration and necrosis, infiltration of lymphocytes and plasma cells, proliferation of fibrous tissue inserted into the hepatic lobule around and separated by a single or small group of liver cells. Piecemeal necrosis is the main lesion in the active stage of chronic hepatitis.(3) bridging necrosis (bridging necrosis): refers to necrosis was the cord-like ducts constitute the central vein between the bridge-like connection between the portal area or central vein and portal District. Necrotic accompanied by irregular regeneration of liver cells and fibrous tissue hyperplasia, and late fibrous septa separated the lobules. Common in moderate to severe chronic hepatitis.
(4) sub-massive necrosis and massive necrosis: characterized by extensive necrosis of liver cells, can affect the liver acinus I, II, III. Such as the survival time of only a very small number of liver cells known as massive necrosis; When the residue of the region Ⅰ more island-like arrangement of liver cells known as the sub-massive necrosis. Common in acute severe viral hepatitis.
3. Liver cell apoptosis:
4. Inflammatory cell infiltration in hepatitis, often varying degrees of inflammatory cell infiltration in the portal area or within the hepatic lobule. Infiltration of inflammatory cells, mainly lymphocytes, monocytes, and sometimes see a small amount of plasma cells and neutrophils.
5 Regeneration and proliferation of viral hepatitis, degeneration and necrosis is the main pathological changes. To tide over the acute phase, in particular, chronic hepatitis, are also common to have the change of regeneration and proliferation. Regenerative hyperplasia belongs to the repair reaction, but sometimes more complex condition, such as cirrhosis. Mainly as viral hepatitis regeneration and hyperplasia are several.
(1) liver regeneration: hepatic necrosis, adjacent liver cells through direct or indirect split regeneration and repair. Is more obvious in the recovery of hepatitis or chronic stage. Regeneration of liver cell volume is large, large nuclei and deeply stained, and some may have a dual-core. Chronic cases of hyperplasia of small bile ducts in the portal area is still visible.
(2) of Kupffer cell hypertrophy: This is the inflammatory response of the intrahepatic mononuclear phagocyte system. Proliferation of the cells were spindle or polygonal, abundant cytoplasm, prominent in the sinus wall or into the sinus to become a self-wall off the migration of phagocytic cells.
(3) of mesenchymal cells and the proliferation of fibroblasts: mesenchymal cells with multilineage differentiation potential, present in the liver interstitial hepatitis differentiate into tissue cells. Recurrent severe necrosis cases, fibrous tissue hyperplasia can develop into liver fibrosis and cirrhosis.
Hepatitis lesions, liver cell cytoplasm loose and the balloon-like change, has a relatively characteristic punctate necrosis and eosinophilic bodies formed for the diagnosis of common hepatitis; large areas of necrosis of liver cells, collapse of severe hepatitis Characteristics of the main lesion.
Viral hepatitis - diagnostic criteria1 suspected case
① the hepatitis history of exposure, or history of eating unclean (hepatitis A), blood transfusion or application of the history of blood products (hepatitis B, C, D).
② the recent loss of appetite, nausea, tired of the oil, weakness, yellow sclera, dark urine, liver enlargement, liver area pain, can not except other diseases.
③ serum ALT repeated increases can not be explained by other reasons.
2 confirmed cases of etiology or the positive results of serological tests help confirm the diagnosis.
Viral Hepatitis - impact factor(A) AgeA. Children's cases the condition is generally lighter, shorter duration recovered completely. Milk less than 1 year old juvenile suffering from hepatitis serious condition, prone to severe hepatitis or cirrhosis.Two. Old age: elderly people suffering from hepatitis and more jaundice, cholestasis is more common, and longer duration; the high incidence of severe hepatitis, the mortality is also higher.
(B) of pregnancy, pregnancy, women with hepatitis are often jaundice, the disease is generally heavier; in late pregnancy, viral hepatitis is prone to severe hepatitis and high mortality, and could easily cause premature birth, stillbirth, neonatal asphyxia, fetal congenital deformities such as; labor and postnatal prone to bleeding.
Viral Hepatitis - complicationsNerve (a), the spirit of system: cranial nerve involvement, meningoencephalitis, acute multiple nerve root inflammation, mental changes.(B) heart damage: arrhythmia, myocarditis, pericarditis, etc..(C) of the blood system: pancytopenia, aplastic anemia, acute hemolytic anemia, hepatitis, hyperbilirubinemia, and so on.(D) of the digestive system: cholangitis, cholecystitis, hepatitis, fatty liver and so on.(E) one hepatocellular liver cancer: HBV and (or) HCV chronic infection is the occurrence of primary hepatocellular carcinoma an important factor.
Viral hepatitis - assistant examination(A) The blood WBC count was normal or slightly lower, the relative increase in lymphocytes, occasional abnormal lymphocytes. Severe hepatitis leukocytes and neutrophils can be increased. Platelets can be reduced in some chronic hepatitis patients.
(B) liver function tests Liver function tests are many kinds, should be selected depending on the circumstances.
Jaundice index the bilirubin quantitative test jaundice hepatitis these indicators can be increased. Urinalysis bilirubin, urobilinogen and bile in the urine were increased.Two serum enzymes commonly used in the alanine aminotransferase (ALT) and aspartate aminotransferase (AST), serum transaminases in hepatitis incubation period, the early onset of latent infection can be increased, it is useful for early diagnosis.Cholesterol, cholesteryl ester, choline esterase determination of liver cell damage in blood total cholesterol decreased, obstructive jaundice, cholesterol increased. Severe hepatitis in patients with cholesterol, cholesteryl ester, choline lipase can be significantly decreased, suggesting a poor prognosis.4 serum proteins and amino acids to patients with chronic active hepatitis, protein electrophoresis showed gamma-globulin often> 26%, cirrhosis of the liver, γ-globulin> 30%. Schistosomiasis cirrhosis, autoimmune disease, myeloma, sarcoidosis, γ-globulin percentage can be increased. The ratio of plasma branched chain amino acids (BCAA) and aromatic amino acids (AAA), such as the ratio decreased or inverted, which reflects the liver parenchymal dysfunction, reference to the efficacy of the judge the prognosis of severe hepatitis and assessment of branched-chain amino acids.Serum collagen III (P III P) Determination of serum P Ⅲ P value increased, suggesting that intrahepatic fibrosis will be formed may be reported in the literature that the sensitivity was 31.4%, specificity of 75.0%. Normal P Ⅲ P <175μg / L.
(C) immunological studies determination of anti-HAV-IgM hepatitis A have early diagnostic value of HBV mark (HBsAg, HBEAg, HBCAg and anti-HBs, anti-HBe, anti-HBc) in determining whether the hepatitis B infection of great significance. Of HBV-DNA, DNA-P and PHSA receptor determination, determine whether the hepatitis B patients in vivo HBV replication of great value. High titers of anti - HBc-IgM positive and conducive to the diagnosis of acute hepatitis B.
Hepatitis C often Lai queuing influenza, hepatitis B, hepatitis E and other viruses (CMV, EBV) and diagnosis, serum anti of HCV-IgM and / or HCV-RNA positive can be confirmed.Serological diagnosis of hepatitis D depends on the serum anti-HDV-IgM positive or HDAg or HDV cDNA hybridization positive; HDAg-positive liver cells or the HDV of cDNA hybridization-positive can be confirmed.The diagnosis of hepatitis E relies on serum anti-HEV-IgM positive or immune electron microscopy to see 30 ~ 32nm virus particles in the stool.
(D) The pathological examinations of great value to the diagnosis of hepatitis by electron microscopy of liver tissue, immunohistochemical detection and observation of HAI Knodell scoring system of the pathogen of chronic hepatitis, etiology, degree of inflammatory activity and fibrosis The degree of all to get the correct data, clinical diagnosis and differential diagnosis.
① the hepatitis history of exposure, or history of eating unclean (hepatitis A), blood transfusion or application of the history of blood products (hepatitis B, C, D).
② the recent loss of appetite, nausea, tired of the oil, weakness, yellow sclera, dark urine, liver enlargement, liver area pain, can not except other diseases.
③ serum ALT repeated increases can not be explained by other reasons.
2 confirmed cases of etiology or the positive results of serological tests help confirm the diagnosis.
Viral Hepatitis - impact factor(A) AgeA. Children's cases the condition is generally lighter, shorter duration recovered completely. Milk less than 1 year old juvenile suffering from hepatitis serious condition, prone to severe hepatitis or cirrhosis.Two. Old age: elderly people suffering from hepatitis and more jaundice, cholestasis is more common, and longer duration; the high incidence of severe hepatitis, the mortality is also higher.
(B) of pregnancy, pregnancy, women with hepatitis are often jaundice, the disease is generally heavier; in late pregnancy, viral hepatitis is prone to severe hepatitis and high mortality, and could easily cause premature birth, stillbirth, neonatal asphyxia, fetal congenital deformities such as; labor and postnatal prone to bleeding.
Viral Hepatitis - complicationsNerve (a), the spirit of system: cranial nerve involvement, meningoencephalitis, acute multiple nerve root inflammation, mental changes.(B) heart damage: arrhythmia, myocarditis, pericarditis, etc..(C) of the blood system: pancytopenia, aplastic anemia, acute hemolytic anemia, hepatitis, hyperbilirubinemia, and so on.(D) of the digestive system: cholangitis, cholecystitis, hepatitis, fatty liver and so on.(E) one hepatocellular liver cancer: HBV and (or) HCV chronic infection is the occurrence of primary hepatocellular carcinoma an important factor.
Viral hepatitis - assistant examination(A) The blood WBC count was normal or slightly lower, the relative increase in lymphocytes, occasional abnormal lymphocytes. Severe hepatitis leukocytes and neutrophils can be increased. Platelets can be reduced in some chronic hepatitis patients.
(B) liver function tests Liver function tests are many kinds, should be selected depending on the circumstances.
Jaundice index the bilirubin quantitative test jaundice hepatitis these indicators can be increased. Urinalysis bilirubin, urobilinogen and bile in the urine were increased.Two serum enzymes commonly used in the alanine aminotransferase (ALT) and aspartate aminotransferase (AST), serum transaminases in hepatitis incubation period, the early onset of latent infection can be increased, it is useful for early diagnosis.Cholesterol, cholesteryl ester, choline esterase determination of liver cell damage in blood total cholesterol decreased, obstructive jaundice, cholesterol increased. Severe hepatitis in patients with cholesterol, cholesteryl ester, choline lipase can be significantly decreased, suggesting a poor prognosis.4 serum proteins and amino acids to patients with chronic active hepatitis, protein electrophoresis showed gamma-globulin often> 26%, cirrhosis of the liver, γ-globulin> 30%. Schistosomiasis cirrhosis, autoimmune disease, myeloma, sarcoidosis, γ-globulin percentage can be increased. The ratio of plasma branched chain amino acids (BCAA) and aromatic amino acids (AAA), such as the ratio decreased or inverted, which reflects the liver parenchymal dysfunction, reference to the efficacy of the judge the prognosis of severe hepatitis and assessment of branched-chain amino acids.Serum collagen III (P III P) Determination of serum P Ⅲ P value increased, suggesting that intrahepatic fibrosis will be formed may be reported in the literature that the sensitivity was 31.4%, specificity of 75.0%. Normal P Ⅲ P <175μg / L.
(C) immunological studies determination of anti-HAV-IgM hepatitis A have early diagnostic value of HBV mark (HBsAg, HBEAg, HBCAg and anti-HBs, anti-HBe, anti-HBc) in determining whether the hepatitis B infection of great significance. Of HBV-DNA, DNA-P and PHSA receptor determination, determine whether the hepatitis B patients in vivo HBV replication of great value. High titers of anti - HBc-IgM positive and conducive to the diagnosis of acute hepatitis B.
Hepatitis C often Lai queuing influenza, hepatitis B, hepatitis E and other viruses (CMV, EBV) and diagnosis, serum anti of HCV-IgM and / or HCV-RNA positive can be confirmed.Serological diagnosis of hepatitis D depends on the serum anti-HDV-IgM positive or HDAg or HDV cDNA hybridization positive; HDAg-positive liver cells or the HDV of cDNA hybridization-positive can be confirmed.The diagnosis of hepatitis E relies on serum anti-HEV-IgM positive or immune electron microscopy to see 30 ~ 32nm virus particles in the stool.
(D) The pathological examinations of great value to the diagnosis of hepatitis by electron microscopy of liver tissue, immunohistochemical detection and observation of HAI Knodell scoring system of the pathogen of chronic hepatitis, etiology, degree of inflammatory activity and fibrosis The degree of all to get the correct data, clinical diagnosis and differential diagnosis.
Viral hepatitis - treatment:
Viral hepatitis is currently no reliable and satisfactory antiviral therapy. Commonly used combination therapy, proper rest and reasonable nutrition, according to the different conditions given appropriate drug treatments, while avoiding the drink spilled, and the use of hepatotoxic drugs and its liver adverse factors.
(A) acute hepatitis is mostly self-limiting disease. If timely rest in the early, proper nutrition, and general supportive therapy, most cases in clinical cure in three to six months.
A. Rest early onset must stay in bed to alleviate the symptoms, jaundice, liver function was significantly improved, gradually increase the volume of activity, does not cause fatigue and liver function fluctuations for the degree. Symptoms, normal liver function, and then a three month break observed, can gradually return to work. But should be regularly reviewed by 1 to 2 years.
Two. The early onset of nutrition should be to easy to digest, for patients with taste bland diet, but should note that the contains the right amount of calories, protein and vitamin and supplement vitamin C and B vitamins. If the patient is loss of appetite, eating too little, by intravenous glucose and vitamin C. Appetite improved, should give contain enough protein, carbohydrates and moderate fat diet, do not emphasize the high-sugar low-fat diet, and should not be overfed.
3. Chinese medicine treatment can be adapted to local conditions, the use of Chinese herbal medicine treatment or Chinese Herbs dialectical treatment. The treatment of acute hepatitis should be heat and dampness, aromatic Huazhuo, regulating qi and blood circulation. Emphasis the available Yinchenhao soup, hot the gardenia Bo Pi decoction, or gentian, Isatidis, money grass, honeysuckle decoction; wet emphasis the available Yinchen four Ling San, San Ren Tang addition and subtraction. Cholestatic hepatitis with hot and humid cholestatic hepatobiliary loss of vent related Qingrejiedu dampness on the basis of reuse eliminate silt choleretic law, such as red peony, Dai alum, saltpetre and alum scattered.
(B) of chronic hepatitis: Integrative Medicine.
A. Rest should be appropriate in the disease activity of bed rest; condition improved should be noted that combining static and dynamic; to the stationary phase can be engaged in light work; symptoms, liver function returned to normal more than three months, return to normal work, but should avoid fatigue and subject to periodic review.
Two. Nutrition should be into the high-protein diet; calorie intake should not be too high to prevent the occurrence of fatty liver; not Yishi excessive sugar, so as not to lead to diabetes.
3. Antiviral therapy
(1) alpha-interferon (InterferonIFNα) can prevent virus replication in the host liver cells, and immunomodulatory effects. Therapeutic doses daily should not be less than 1 million U, subcutaneously or intramuscularly daily, some every other day injection times. Course of 3 to 6 months. Can make about 1/3 of serum HBV DNA negative, HBeAg positive to anti-HBe positive, HBV DNA polymerase activity decreased HCV RNA negative, but in some cases after discontinuation serum markers reversed. Early high-dose, long course of interferon therapy can increase efficacy. Have fever, hypotension, nausea, diarrhea, myalgia, fatigue and other side effects, and may appear early in treatment, can also be temporary hair loss, neutropenia, thrombocytopenia, anemia, but the rapid recovery after discontinuation.
(2) The interferon inducer poly inosinic acid: poly inosinic acid (poly Peoly I: C) in vivo can induce interferon and block virus replication, but less ability to induce interferon. The general dosage is 2 ~ 4mg intramuscularly, twice a week, 3 to 6 months for a course; also used large doses (each 10 to 40) static Swimming infusion, 2 times a week. HbeAg recent negative rate seems. No side effects. So near and yet synthesis of new drug Ampligen (Poly I: C. 12U) is a role than the Polyinosinic powerful interferon inducer.
(3) A adenosine (Ara-A) and monophosphoryl vidarabine (Ara-AMP), mainly to the inhibition of viral DNA polymerase and ribonucleotide reductase activity, thereby blocking the replication of HBV, antiviral stronger but more short-lived after discontinuation rebound. Ara-A is not soluble in water, the commonly used dose of 10 ~ 15mg / kg, diluted grape liquid 1000ml slow intravenous infusion of 12 hours, once every two to eight weeks, the side effects of fever, malaise, anorexia, nausea, vomiting muscles and joint pain, bloating, blood sticky drop.
Monophosphate Vidarabine soluble in water, commonly used dose of 10 mg / kg per day, two times intramuscularly for 3 to 5 weeks, or daily 5mg / kg, 2 times intramuscularly for eight consecutive weeks. Allows serum HBV the DAN negative DNA polymerase negative, HBsAg titer decreased, HBeAg converted to anti-HBe. This product may also be vein infusion. Large doses may produce fever, malaise, lower limb muscle spasm pain, thrombocytopenia and other side effects.
(4) acyclovir (acyclovir) and 6 - deoxy acyclovir selective inhibition of viral DNA polymerase, there is a strong antiviral activity, low toxicity of the body. Dose of the daily 10 ~ 45mg / kg static Swimming infusion, 7 to 14 days for a course of treatment. Some inhibition of viral replication role. Large doses can cause kidney damage, phlebitis, lethargy, delirium, rashes, the ALT increased.
6 - deoxy acyclovir oral absorption can be long-term use.
(5) other antiviral drugs ribavirin (ribavirin in) phosphine A salts, tenofovir, both in the trial.
(6) the joint use of the combination therapy of antiviral drugs such as alpha-interferon and Ara-adenosine, a synergistic antiviral effect, may increase efficacy, but toxicity is also increased, alpha-interferon and acyclovir, plastic oxygen-free acyclovir, or r-interferon in combination, can enhance the efficacy.
(7) alpha-interferon to strengthen loose shock therapy before the interferon treatment, the first to give short (six weeks), prednisone, can improve the sensitivity of patients to antiviral therapy, thereby enhancing efficacy. However, the sudden withdrawal stop of strong pine, stimulate the risk of severe liver necrosis.
(8) nucleoside drug lamivudine (lamivudine), adefovir dipivoxil (Geoffrey force, on behalf of small, Forrest Gump given, Adi cents, excellent He d), ex entecavir (Bo Lu be), plain V (telbivudine).
Viral hepatitis is currently no reliable and satisfactory antiviral therapy. Commonly used combination therapy, proper rest and reasonable nutrition, according to the different conditions given appropriate drug treatments, while avoiding the drink spilled, and the use of hepatotoxic drugs and its liver adverse factors.
(A) acute hepatitis is mostly self-limiting disease. If timely rest in the early, proper nutrition, and general supportive therapy, most cases in clinical cure in three to six months.
A. Rest early onset must stay in bed to alleviate the symptoms, jaundice, liver function was significantly improved, gradually increase the volume of activity, does not cause fatigue and liver function fluctuations for the degree. Symptoms, normal liver function, and then a three month break observed, can gradually return to work. But should be regularly reviewed by 1 to 2 years.
Two. The early onset of nutrition should be to easy to digest, for patients with taste bland diet, but should note that the contains the right amount of calories, protein and vitamin and supplement vitamin C and B vitamins. If the patient is loss of appetite, eating too little, by intravenous glucose and vitamin C. Appetite improved, should give contain enough protein, carbohydrates and moderate fat diet, do not emphasize the high-sugar low-fat diet, and should not be overfed.
3. Chinese medicine treatment can be adapted to local conditions, the use of Chinese herbal medicine treatment or Chinese Herbs dialectical treatment. The treatment of acute hepatitis should be heat and dampness, aromatic Huazhuo, regulating qi and blood circulation. Emphasis the available Yinchenhao soup, hot the gardenia Bo Pi decoction, or gentian, Isatidis, money grass, honeysuckle decoction; wet emphasis the available Yinchen four Ling San, San Ren Tang addition and subtraction. Cholestatic hepatitis with hot and humid cholestatic hepatobiliary loss of vent related Qingrejiedu dampness on the basis of reuse eliminate silt choleretic law, such as red peony, Dai alum, saltpetre and alum scattered.
(B) of chronic hepatitis: Integrative Medicine.
A. Rest should be appropriate in the disease activity of bed rest; condition improved should be noted that combining static and dynamic; to the stationary phase can be engaged in light work; symptoms, liver function returned to normal more than three months, return to normal work, but should avoid fatigue and subject to periodic review.
Two. Nutrition should be into the high-protein diet; calorie intake should not be too high to prevent the occurrence of fatty liver; not Yishi excessive sugar, so as not to lead to diabetes.
3. Antiviral therapy
(1) alpha-interferon (InterferonIFNα) can prevent virus replication in the host liver cells, and immunomodulatory effects. Therapeutic doses daily should not be less than 1 million U, subcutaneously or intramuscularly daily, some every other day injection times. Course of 3 to 6 months. Can make about 1/3 of serum HBV DNA negative, HBeAg positive to anti-HBe positive, HBV DNA polymerase activity decreased HCV RNA negative, but in some cases after discontinuation serum markers reversed. Early high-dose, long course of interferon therapy can increase efficacy. Have fever, hypotension, nausea, diarrhea, myalgia, fatigue and other side effects, and may appear early in treatment, can also be temporary hair loss, neutropenia, thrombocytopenia, anemia, but the rapid recovery after discontinuation.
(2) The interferon inducer poly inosinic acid: poly inosinic acid (poly Peoly I: C) in vivo can induce interferon and block virus replication, but less ability to induce interferon. The general dosage is 2 ~ 4mg intramuscularly, twice a week, 3 to 6 months for a course; also used large doses (each 10 to 40) static Swimming infusion, 2 times a week. HbeAg recent negative rate seems. No side effects. So near and yet synthesis of new drug Ampligen (Poly I: C. 12U) is a role than the Polyinosinic powerful interferon inducer.
(3) A adenosine (Ara-A) and monophosphoryl vidarabine (Ara-AMP), mainly to the inhibition of viral DNA polymerase and ribonucleotide reductase activity, thereby blocking the replication of HBV, antiviral stronger but more short-lived after discontinuation rebound. Ara-A is not soluble in water, the commonly used dose of 10 ~ 15mg / kg, diluted grape liquid 1000ml slow intravenous infusion of 12 hours, once every two to eight weeks, the side effects of fever, malaise, anorexia, nausea, vomiting muscles and joint pain, bloating, blood sticky drop.
Monophosphate Vidarabine soluble in water, commonly used dose of 10 mg / kg per day, two times intramuscularly for 3 to 5 weeks, or daily 5mg / kg, 2 times intramuscularly for eight consecutive weeks. Allows serum HBV the DAN negative DNA polymerase negative, HBsAg titer decreased, HBeAg converted to anti-HBe. This product may also be vein infusion. Large doses may produce fever, malaise, lower limb muscle spasm pain, thrombocytopenia and other side effects.
(4) acyclovir (acyclovir) and 6 - deoxy acyclovir selective inhibition of viral DNA polymerase, there is a strong antiviral activity, low toxicity of the body. Dose of the daily 10 ~ 45mg / kg static Swimming infusion, 7 to 14 days for a course of treatment. Some inhibition of viral replication role. Large doses can cause kidney damage, phlebitis, lethargy, delirium, rashes, the ALT increased.
6 - deoxy acyclovir oral absorption can be long-term use.
(5) other antiviral drugs ribavirin (ribavirin in) phosphine A salts, tenofovir, both in the trial.
(6) the joint use of the combination therapy of antiviral drugs such as alpha-interferon and Ara-adenosine, a synergistic antiviral effect, may increase efficacy, but toxicity is also increased, alpha-interferon and acyclovir, plastic oxygen-free acyclovir, or r-interferon in combination, can enhance the efficacy.
(7) alpha-interferon to strengthen loose shock therapy before the interferon treatment, the first to give short (six weeks), prednisone, can improve the sensitivity of patients to antiviral therapy, thereby enhancing efficacy. However, the sudden withdrawal stop of strong pine, stimulate the risk of severe liver necrosis.
(8) nucleoside drug lamivudine (lamivudine), adefovir dipivoxil (Geoffrey force, on behalf of small, Forrest Gump given, Adi cents, excellent He d), ex entecavir (Bo Lu be), plain V (telbivudine).
