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BY-
RAMYA DEEPTHI
VIJAY MARIE COLLGE OF NURSING
Definition
Chronic hepatitis is defined as continuing or relapsing
hepatic disease for more than 6 months, with presence
of symptoms and other diagnostic parameters-
serology, biochemical and histopathology.
Etiology
 Usually due to hepatitis B, C, or a combined hepatitis B, D
 Non viral causes-
1. Wilson disease
2. Antitrypsin deficiency
3. Chronic alcoholism
4. Impaired immunity
5. Extremes of age
 Chronic hepatitis is a carrier state where the individual
harbors and replicates virus, hence can transmit the
organism.
Clinical features
 Common features are-
Fatigue
Loss of appetite
Mild jaundice
Raised serum transaminases
Lab findings reveal liver cell injury
Morphology
MICROSCOPY: histological features of chronic hepatitis ranges
from mild to severe.
1. PIECEMEAL NECROSIS:
 piece by piece necrosis around the portal tract, infiltration
of lymphocytes, plasma cells and macrophages.
2. INTRALOBULAR LESION:
Focal area of necrosis and inflammation are seen in adjacent
areas of liver parenchyma called interface hepatitis.
These have scattered acidophilic body and kupffer cell
hyperplasia.
3. BRIDGING FIBROSIS:
Initially portal tract and later periportal areas exhibit fibrosis
followed by linking fibrous septa between lobules causing
disarray of the architecture.
Activity score
 Evolved to assess the activity of chronic hepatitis based on
the histomorphology as follows.
a. Necrosis: periportal bridging- score ranges from 0-10
0- no necrosis
10- multilobular necrosis
b. Inflammation: depth/ extent. Score ranges from 0-4
0- no inflammation
4-marked portal inflammation
c. fibrosis: density/ extent. Score ranges form 0-4
0- no fibrosis
4- resembles cirrhosis
Based on activity score chronic
hepatitis is further classified into -
 Chronic persistent hepatitis- mild activity
 Chronic lobular hepatitis- mild to moderate fibrosis
 Chronic active hepatitis- moderate to severe fibrosis.
IV. CARRIER STATE
 Individual with out symptoms but harboring infection with
hepatotrophic virus and is capable of transmitting
infection to others is called carrier state.
 Hepatitis A and E do no produce carrier state.
 Hepatitis B is mostly responsible for all carrier cases in the
world.
 It is detected by HBsAg in the serum.
 Morphology:
 Carrier on biopsy do not show any changes on liver.
 They show granular ground glass eosinophilic cytoplasm as
evidenced by HBsAg.
V. FULMINANT HEPATITIS
 It is most severe form of acute hepatitis seen within 2-3
weeks of onset of symptoms and progress to fulminate
hepatic failure.
 2 patters are seen-
1. Sub fulminate- has a less rapid course, and 3extends
up to 3months
2. Fulminate type: it has 2 etiological agents-
a. Viral- usually HBV, HAV, HCV and rarely HBV HDV.

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Chronic Hepatitis: Definition, Etiology, Clinical Features, Morphology, Activity Score, Carrier State, and Fulminant Hepatitis

  • 1. BY- RAMYA DEEPTHI VIJAY MARIE COLLGE OF NURSING
  • 2. Definition Chronic hepatitis is defined as continuing or relapsing hepatic disease for more than 6 months, with presence of symptoms and other diagnostic parameters- serology, biochemical and histopathology.
  • 3. Etiology  Usually due to hepatitis B, C, or a combined hepatitis B, D  Non viral causes- 1. Wilson disease 2. Antitrypsin deficiency 3. Chronic alcoholism 4. Impaired immunity 5. Extremes of age  Chronic hepatitis is a carrier state where the individual harbors and replicates virus, hence can transmit the organism.
  • 4. Clinical features  Common features are- Fatigue Loss of appetite Mild jaundice Raised serum transaminases Lab findings reveal liver cell injury
  • 5. Morphology MICROSCOPY: histological features of chronic hepatitis ranges from mild to severe. 1. PIECEMEAL NECROSIS:  piece by piece necrosis around the portal tract, infiltration of lymphocytes, plasma cells and macrophages.
  • 6. 2. INTRALOBULAR LESION: Focal area of necrosis and inflammation are seen in adjacent areas of liver parenchyma called interface hepatitis. These have scattered acidophilic body and kupffer cell hyperplasia.
  • 7. 3. BRIDGING FIBROSIS: Initially portal tract and later periportal areas exhibit fibrosis followed by linking fibrous septa between lobules causing disarray of the architecture.
  • 8. Activity score  Evolved to assess the activity of chronic hepatitis based on the histomorphology as follows. a. Necrosis: periportal bridging- score ranges from 0-10 0- no necrosis 10- multilobular necrosis b. Inflammation: depth/ extent. Score ranges from 0-4 0- no inflammation 4-marked portal inflammation c. fibrosis: density/ extent. Score ranges form 0-4 0- no fibrosis 4- resembles cirrhosis
  • 9. Based on activity score chronic hepatitis is further classified into -  Chronic persistent hepatitis- mild activity  Chronic lobular hepatitis- mild to moderate fibrosis  Chronic active hepatitis- moderate to severe fibrosis.
  • 10. IV. CARRIER STATE  Individual with out symptoms but harboring infection with hepatotrophic virus and is capable of transmitting infection to others is called carrier state.  Hepatitis A and E do no produce carrier state.  Hepatitis B is mostly responsible for all carrier cases in the world.  It is detected by HBsAg in the serum.  Morphology:  Carrier on biopsy do not show any changes on liver.  They show granular ground glass eosinophilic cytoplasm as evidenced by HBsAg.
  • 11. V. FULMINANT HEPATITIS  It is most severe form of acute hepatitis seen within 2-3 weeks of onset of symptoms and progress to fulminate hepatic failure.  2 patters are seen- 1. Sub fulminate- has a less rapid course, and 3extends up to 3months 2. Fulminate type: it has 2 etiological agents- a. Viral- usually HBV, HAV, HCV and rarely HBV HDV.