DR. ROOPAM JAIN PROFESSOR & HEAD DEPT. OF PATHOLOGY & BLOOD BANK

1. LIVER
& GALLBLADDER -
VIRAL HEPATITIS
DR ROOPAM JAIN
PROFESSOR & HEAD, PATHOLOGY

2. Infectious Disorders
VIRAL
HEPATITIS

3. CLINICOPATHOLOGIC
SPECTRUM
• The various clinical patterns and pathologic consequences of different
hepatotropic viruses can be considered under the following headings:
• i) Carrier state
• ii) Asymptomatic infection
• iii) Acute hepatitis
• iv) Chronic hepatitis
• v) Fulminant hepatitis (Submassive to massive necrosis)

4. 1. Carrier State
• An asymptomatic individual without manifest disease, harbouring
infection with hepatotropic virus and capable of transmitting it is called
carrier state.
• There can be 2 types of carriers:
• 1. An ‘asymptomatic healthy carrier’ who does not suffer from ill-eff ects
of the virus infection but is capable of transmitting.
• 2. An ‘asymptomatic carrier with chronic disease’ capable of transmitting
the organisms.

5. 2. Asymptomatic Infection
• These are cases who are detected incidentally to have infection with
one of the hepatitis viruses
• raised serum transaminases
• detection of the presence of antibodies but are otherwise
asymptomatic.

6. 3. Acute Hepatitis
The most common consequence of all hepatotropic viruses is acute
inflammatory involvement of the entire liver.
Clinically, acute hepatitis is categorised into 4 phases:
incubation period, pre-icteric phase, icteric phase and posticteric phase

7. 3. Acute Hepatitis
MORPHOLOGIC FEATURES
• Grossly - liver is slightly enlarged, soft and greenish.
• Histologically, (Fig):
• 1. Hepatocellular injury - liver cell injury but it is most marked in zone
3 (centrilobular zone):
• ballooning degeneration
• Councilman body or acidophil body
• dropout hepatocellular necrosis
• Bridging necrosis is a more severe form of hepatocellular injury in
acute viral hepatitis and may progress to fulminant hepatitis or
chronic hepatitis

8. • 2. Inflammatory infiltrate - There is infiltration by mononuclear
inflammatory cells, usually in the portal tracts, but may permeate into the
lobules.
• 3. Kupffer cell hyperplasia - There is reactive hyperplasia of Kupffer
cells
• 4. Cholestasis - Biliary stasis is usually not severe in viral hepatitis
• 5. Regeneration - As a result of necrosis of hepatocytes,

9. Acute viral hepatitis
The predominant histologic changes are: variable degree of necrosis of
hepatocytes, most marked in zone 3 (centrilobular); & mononuclear cellular
infiltrate in the lobule.
Mild degree of liver cell necrosis is seen as ballooning degeneration while
acidophilic Councilman bodies (inbox) are indicative of more severe liver cell injury.

10. 4. Chronic viral hepatitis:
• Symptomatic, biochemical or serologic evidence of continuing or relapsing
disease for > 6 months with histologic documentation of inflammation and
necrosis.
• Majority of cases of chronic hepatitis are the result of infection with hepato
tropic viruses
• hepatitis B,
• hepatitis C &
• combined hepatitis B and hepatitis D infection.
• some non-viral causes of chronic hepatitis include:
• Wilson’s disease,
• alpha-1-antitrypsin deficiency,
• chronic alcoholism,
• drug-induced injury
• autoimmune diseases

11. 4. Chronic viral hepatitis:
• Chronic hepatitis constitutes a “Carrier State”.
• Healthy carriers are individuals having the virus without adverse effects.
• Vertical transmission with HBV produces carrier in 90-95% cases.
• The most common symptom is fatigue;
• less common symptoms are malaise, loss of appetite, and occasionally
mild jaundice.

13. The portal tract is expanded due to increased lymphomononuclear
inflammatory cells which are seen to breach the limiting plate
(i.e. hepatocytes at the interface of portal tract and lobule are destroyed)

14. 4. Chronic viral hepatitis:
MORPHOLOGIC FEATURES
• The pathologic features are common to both HBV and HCV infection
• 1. Piecemeal necrosis
• i) Necrosed hepatocytes
• ii) infiltration of lymphocytes, plasma cells and macrophages
• 2. Portal tract lesions
• i) Inflammatory cell infiltration by lymphocytes, plasma cells and
macrophages (triaditis).
• ii) Proliferated bile ductules in the expanded portal tracts.

15. 4. Chronic viral hepatitis:
MORPHOLOGIC FEATURES
• 3. Intralobular lesions
• i) focal areas of necrosis & inflammation within the hepatic parenchyma.
• ii) Scattered acidophilic bodies in the lobule.
• iii) Kupffer cell hyperplasia.
• iv) bridging necrosis
• v) Regenerative changes
• 4. Bridging fibrosis

16. 4. Chronic viral hepatitis:
• A histologic grading of chronic hepatitis:
A. Necroinflammatory activity:
Periportal necrosis
Intralobular necrosis, focal or confluent
Extent and depth of portal inflammation
B. Stage of fibrosis:
• Extent and density of fibrosis (ranging from score 0 as ‘no fibrosis’ to
score 6 as ‘cirrhosis’).

17. 4. Chronic viral hepatitis:
CLINICAL FEATURES
• The clinical features of chronic hepatitis are quite variable ranging from
mild disease to fullblown picture of cirrhosis.
• i) Mild chronic hepatitis shows only slight but persistent elevation of
transaminases (‘transaminitis’) with fatigue, malaise and loss of appetite.
• ii) mild hepatomegaly, hepatic tenderness and mild splenomegaly.
• iii) Laboratory fi ndings - prolonged prothrombin time,
hyperbilirubinaemia, hyperglobulinaemia and markedly elevated alkaline
phosphatase.

18. 5. Fulminant Hepatitis
(Submassive to Massive Necrosis)
• Fulminant hepatitis is the most severe form of acute hepatitis in which
there is rapidly progressive hepatocellular failure.
• Two patterns are recognised
• submassive necrosis having a less rapid course extending up to 3
months
• massive necrosis in which the liver failure is rapid and fulminant
occurring in 2-3 weeks

19. Fulminant hepatitis
wiping out of liver lobules with only collapsed reticulin framework

20. Clinicopathologic course of HBV and HCV infection