Acute Parenchymal Disease of Liver Acute Hepatitis Inflammation

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

Drugs – Paracetamol, Isoniazide, Rifampicin l Alcohol Others l Pregnancy l Circulatory Insufficiency l Autoimmune Hepatitis l Wilson’s Disease l 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 2

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 l is defined as the presence of persistent (at least 6 months) necroinflammatory injury that can lead to cirrhosis. l (Symptomatic, biochemical, serological & histological evidence of continuing or relapsing hepatic disease for more than 6 months) l Dr S Chakradhar 3

HAV l Is a benign self limited, disease with an incubation period of 2 wks to 6 wks. l Does not cause chronic hepatitis (5% Fulminant hepatitis) l Clinical disease tends to be mild or asymptomatic and rare after childhood l 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 4

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

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

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

8 Dr S Chakradhar

9 Dr S Chakradhar

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

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

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

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

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

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

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

Points Virus type Antigen HAV RNA HA Ag Antibodies Anti-HAV HBV DNA HBs Ag, HBc, Ag, HBe Ag. Anti-HBs, Anti. HBc, Anti HBe Mode of transmission Blood Uncommon Yes Faecal – oral Yes No route Sexual Contact No Yes HCV RNA HCAg HDV RNA HDAg HEV RNA HEAg Anti HCV Anti HDV Anti HEV Yes No No Yes Uncommon Yes ? No 3 -8 wks Any No No Vertical No Incubation Period 2 -6 wks Yes 2 -6 months Uncommon 2 -26 wks Yes 6 -9 wks Age Chronicity Liver cancer Young No No Any Yes (5 -10%) Yes Any Yes Yes Prevention Vaccine Hygiene Vaccine No As in HBV Dr S Chakradhar No Hygie ne 18

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

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

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

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

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

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

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

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

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

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