Acute Parenchymal Disease of Liver Acute Hepatitis Inflammation of liver caused by various agents Viral infections Hep

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

2. Drugs – Paracetamol, Isoniazide, Rifampicin • Alcohol Others • Pregnancy • Circulatory Insufficiency • Autoimmune Hepatitis • 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 Dr S Chakradhar

3. Definitions Acute viral hepatitis • 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. • (Symptomatic, biochemical, serological & histological evidence of continuing or relapsing hepatic disease for more than 6 months) Dr S Chakradhar

4. HAV • Is a benign self limited, disease with an incubation period of 2 wks to 6wks. • Does not cause chronic hepatitis (5% Fulminant hepatitis) • 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. Dr S Chakradhar

5. Fate of Acute Type A Hepatitis • 95% patient totally cure • 5% patient may develop Fulminant hepatitis 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 recovery phase and immunity phase are characterized by IgG anti-HAV antibody. Dr S Chakradhar

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

8. Dr S Chakradhar

9. Dr S Chakradhar

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

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

13. Dr S Chakradhar

14. HBV - Serum markers of HBV are: • Antibodies against HCV (anti-HCV) may be undetectable for the first 8 weeks after infection. • 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. • The antibody does not confer immunity. • It determines the presence of actual virus and ongoing infection. Dr S Chakradhar

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

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

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

18. Dr S Chakradhar

19. Dr S Chakradhar

20. Pathogenesis of Infective Hepatitis • Direct cytopathic effect • 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. 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) • Fever on and off • Anorexia, nausea, vomiting, diarrhoea • Weakness, headache, fatigue • Upper abdominal pain   Dr S Chakradhar

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

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

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

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

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

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

28. Chronic Viral Hepatitis /Chronic hepatitis Classification – according to extent of inflammation • Chronic persistent hepatitis – confined to portal tract • 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

29. Dr S Chakradhar