1. Acute Parenchymal Disease of Liver Acute Hepatitis Inflammation of liver caused by various agents Viral infections Viral infections Hepatitis A Virus Hepatitis A Virus Hepatitis B Virus Hepatitis B Virus Hepatitis C Virus Hepatotrophic virus Hepatitis C Virus Hepatotrophic virus Hepatitis D Virus Hepatitis D Virus Hepatitis E Virus Hepatitis E Virus Cytomegalovirus Cytomegalovirus Epstein Barr virus Epstein Barr virus Herpes simplex virus Herpes simplex virus 1 Dr S Chakradhar

2. Drugs – Paracetamol, Isoniazide, Rifampicin Drugs – Paracetamol, Isoniazide, Rifampicin Alcohol AlcoholOthers Pregnancy Pregnancy Circulatory Insufficiency Circulatory Insufficiency Autoimmune Hepatitis Autoimmune Hepatitis Wilson’s Disease Wilson’s Disease Viral hepatitis by hepatitis viruses which are hepatotrophic i.e. have a particular affinity for the liver Systemic viral infections involving the Liver 2 Dr S Chakradhar

3. Definitions Definitions Acute viral hepatitis is defined by the sudden onset of significant aminotransferase elevation as a consequence of diffuse necroinflammatory liver injury. is defined by the sudden onset of significant aminotransferase elevation as a consequence of diffuse necroinflammatory liver injury. Chronic viral hepatitis is defined as the presence of persistent (at least 6 months) necroinflammatory injury that can lead to cirrhosis. is defined as the presence of persistent (at least 6 months) necroinflammatory injury that can lead to cirrhosis. (Symptomatic, biochemical, serological & histological evidence of continuing or relapsing hepatic disease for more than 6 months) (Symptomatic, biochemical, serological & histological evidence of continuing or relapsing hepatic disease for more than 6 months) 3 Dr S Chakradhar

4. HAV Is a benign self limited, disease with an incubation period of 2 wks to 6wks. Is a benign self limited, disease with an incubation period of 2 wks to 6wks. Does not cause chronic hepatitis (5% Fulminant hepatitis) Does not cause chronic hepatitis (5% Fulminant hepatitis) Clinical disease tends to be mild or asymptomatic and rare after childhood Clinical disease tends to be mild or asymptomatic and rare after childhood Spread by ingestion of contaminated water and food and shed in stool for 2-3 wks before and 1 week after onset of jaundice. Spread by ingestion of contaminated water and food and shed in stool for 2-3 wks before and 1 week after onset of jaundice. 4 Dr S Chakradhar

5. Fate of Acute Type A Hepatitis 95% patient totally cure 95% patient totally cure 5% patient may develop Fulminant hepatitis 5% patient may develop Fulminant hepatitis 5 Dr S Chakradhar

6. Diagnosis – Serum markers for HAV The diagnosis of acute HAV is made by the detection of IgM anti- HAV antibody. (appears at onset of symptoms) The diagnosis of acute HAV is made by the detection of IgM anti- HAV antibody. (appears at onset of symptoms) The recovery phase and immunity phase are characterized by IgG anti-HAV antibody. The recovery phase and immunity phase are characterized by IgG anti-HAV antibody. 6 Dr S Chakradhar

7. HBV HBV may be asymptomatic, acute hepatitis, chronic hepatitis & hepatocellular carcinoma HBV may be asymptomatic, acute hepatitis, chronic hepatitis & hepatocellular carcinoma Incubation period is 1-6 months Incubation period is 1-6 months Spread principally by transfusion of blood and blood products Spread principally by transfusion of blood and blood products Sexual contact Sexual contact Vertical transmission Vertical transmission Use of contamination needles – drug addicts etc Use of contamination needles – drug addicts etc 7 Dr S Chakradhar

8. 8

9. 9

10. HBV - Serum markers of HBV are: Antigens HBsAg - Done routinely. It appears before the onset of symptoms & peaks during overt disease in 3 – 6 months it is usually undetectable HBsAg - Done routinely. It appears before the onset of symptoms & peaks during overt disease in 3 – 6 months it is usually undetectable HBcAg is not found in serum HBcAg is not found in serum HBeAg appears shortly after HBsAg in the serum Rises early & declines rapidly Its persistence is indicative of Chronic liver disease HBeAg appears shortly after HBsAg in the serum Rises early & declines rapidly Its persistence is indicative of Chronic liver disease 10 Dr S Chakradhar

11. Antibodies Anti -HBs (IgG) appears after the disappearance of HBsAg (3-6 months) and after vaccination. Persists for many years or perhaps permanently. Anti-HBs implies either a previous infection Anti -HBs (IgG) appears after the disappearance of HBsAg (3-6 months) and after vaccination. Persists for many years or perhaps permanently. Anti-HBs implies either a previous infection Anti - HBcAg (IgM anti-HBc) - appears early and rapidly reaches a high titre which then subsides gradually. Anti-HBc is initially of IgM type with IgG appearing later. Suggests an acute & continuing viral replication Anti - HBcAg (IgM anti-HBc) - appears early and rapidly reaches a high titre which then subsides gradually. Anti-HBc is initially of IgM type with IgG appearing later. Suggests an acute & continuing viral replication Anti-HBe usually indicates low-level replication and a lower degree of infectivity. Anti-HBe usually indicates low-level replication and a lower degree of infectivity. 11 Dr S Chakradhar

12. HCV Is responsible for 90-95% causes of transfusion associated hepatitis. Is responsible for 90-95% causes of transfusion associated hepatitis. Incubation period 2-26 wks Incubation period 2-26 wks HCV has high rate of progression to chronic disease & eventually cirrhosis HCV has high rate of progression to chronic disease & eventually cirrhosis 12 Dr S Chakradhar

13. 13

14. HBV - Serum markers of HBV are: Antibodies against HCV (anti-HCV) may be undetectable for the first 8 weeks after infection. Antibodies against HCV (anti-HCV) may be undetectable for the first 8 weeks after infection. HCV RNA can be detected serum 1-3 weeks. HCV RNA can be detected serum 1-3 weeks. Positive tests are usually diagnostic in patients with elevated liver enzymes and with risk factors for the infection. Positive tests are usually diagnostic in patients with elevated liver enzymes and with risk factors for the infection. The antibody does not confer immunity. The antibody does not confer immunity. It determines the presence of actual virus and ongoing infection. It determines the presence of actual virus and ongoing infection. 14 Dr S Chakradhar

15. HDV It co-infects with HBV as it requires help from HBV for its replication and expression. It co-infects with HBV as it requires help from HBV for its replication and expression. Mode of transmission is similar to HBV. Mode of transmission is similar to HBV. Incubation period – 6-9 wks Incubation period – 6-9 wks 15 Dr S Chakradhar

16. Diagnosis Is made by finding HDV RNA or HDV antigen in serum or liver Is made by finding HDV RNA or HDV antigen in serum or liver And by detecting antibody to the HDV antigen. And by detecting antibody to the HDV antigen. 16 Dr S Chakradhar

17. HEV Transmitted through Faecal-oral route Transmitted through Faecal-oral route Does not cause chronic hepatitis Does not cause chronic hepatitis Incubation Period 3-8 weeks Incubation Period 3-8 weeks 17 Dr S Chakradhar

18. 18 Dr S Chakradhar PointsHAVHBVHCVHDVHEV Virus typeRNADNARNA AntigenHA AgHBs Ag, HBc, Ag, HBe Ag. HCAgHDAgHEAg AntibodiesAnti-HAVAnti-HBs, Anti- HBc, Anti HBe Anti HCVAnti HDVAnti HEV Mode of transmission  Blood UncommonYes No  Faecal – oral route YesNo Yes  Sexual Contact NoYesUncommonYes? VerticalNoYesUncommon YesNo Incubation Period2-6 wks2-6 months2-26 wks6-9 wks3-8 wks AgeYoungAny ChronicityNo Yes (5-10%)Yes No Liver cancerNoYes No PreventionVaccine Hygiene VaccineNoAs in HBVNo Hygie ne

19. Dr S Chakradhar 19

20. Pathogenesis of Infective Hepatitis Direct cytopathic effect Direct cytopathic effect Induction of immune responses against viral antigen that damage virally infected hepatocytes. Induction of immune responses against viral antigen that damage virally infected hepatocytes. Alteration of liver cell antigens and the initiation of an auto immune reaction. Alteration of liver cell antigens and the initiation of an auto immune reaction. 20 Dr S Chakradhar

21. C/F - H/O should elicit risk factors Symptoms Infection begins with a incubation period A) Pre Icteric phase (few days to 2 wks) A) Pre Icteric phase (few days to 2 wks) Fever on and off Fever on and off Anorexia, nausea, vomiting, diarrhoea Anorexia, nausea, vomiting, diarrhoea Weakness, headache, fatigue Weakness, headache, fatigue Upper abdominal pain Upper abdominal pain 21 Dr S Chakradhar

22. C) Icteric phase Jaundice Jaundice Stool become paler Stool become paler Urine darker Urine darker Tenderness Tenderness C) Post Icteric (Recovery phase) Disappearance of jaundice Disappearance of jaundice Urine and stool becomes normal Urine and stool becomes normal Appetite improves and GI symptoms subside Appetite improves and GI symptoms subside 22 Dr S Chakradhar

23. Signs Jaundice Jaundice Tender hepatomegaly Tender hepatomegaly Enlarged cervical nodes (occasionally) Enlarged cervical nodes (occasionally) (Generally recovery occurs within 3-6 wks) 23 Dr S Chakradhar

24. Investigations TC, DC, ESR, Hb TC, DC, ESR, Hb LFT LFT Serum Bilirubin - raised Serum Bilirubin - raised Serum Aminotransferase – Very high Serum Aminotransferase – Very high Serum Alkaline Phosphatase increased Serum Alkaline Phosphatase increased Prolonged Prothrombin time Prolonged Prothrombin time Viral markers – Anti HAV, HBs Ag Viral markers – Anti HAV, HBs Ag 24 Dr S Chakradhar

25. Treatment No specific treatment, only severely affected patient require hospitalization No specific treatment, only severely affected patient require hospitalization Bed rest (till jaundice subside) Bed rest (till jaundice subside) Diet – Nutrition diet (Glucose water, sugar fruit juice, soup) with slight fat restriction. Diet – Nutrition diet (Glucose water, sugar fruit juice, soup) with slight fat restriction. Paracetamol is preferred anti pyretic & analgesics in low doses Paracetamol is preferred anti pyretic & analgesics in low doses Avoid drugs as far as possible especially sedatives & hypnotics Avoid drugs as far as possible especially sedatives & hypnotics Educate patient about personal Hygiene. Educate patient about personal Hygiene. Vitamin B-complex Vitamin B-complex 25 Dr S Chakradhar

26. Complications Chronic hepatitis Chronic hepatitis Cirrhosis of liver Cirrhosis of liver Fulminant hepatic failure Fulminant hepatic failure Hepatic coma. Hepatic coma. Hepatocellular Carcinoma Hepatocellular Carcinoma Bleeding Disorders Bleeding Disorders 26 Dr S Chakradhar

27. Prevention of Hepatitis B Prevention depends on avoiding risk factors such as Prevention depends on avoiding risk factors such as Sharing needles Sharing needles Multiple sexual partners Multiple sexual partners Blood & blood products Blood & blood products 2. Immunization by hepatitis B vaccine 2. Immunization by hepatitis B vaccine 27 Dr S Chakradhar

28. Chronic Viral Hepatitis /Chronic hepatitis Classification – according to extent of inflammation Chronic persistent hepatitis – confined to portal tract Chronic persistent hepatitis – confined to portal tract Chronic active hepatitis – spills into the parenchyma & surrounds regions of necrotic Hepatocytes Chronic active hepatitis – spills into the parenchyma & surrounds regions of necrotic Hepatocytes Chronic lobular hepatitis – persistent inflammation is confined to the lobule Dr S Chakradhar 28

29. Dr S Chakradhar 29