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GANDAKI MEDICAL
     COLLEGE
CORRELATION SEMINAR
     GI SYSTEM




          PRESENTED BY:
         SAJANA BHANDARI
        SUDARSHAN ACHARYA
OBJECTIVE
   TO DESCRIBE THE MICROSCOPIC
    FEATURES OF DIFFERENT TYPES OF
    HEPATITIS
HEPATITIS
It is the inflammationof   liver .
Usually 2 types:

     VIRAL HEPATITIS


     NON-VIRAL HEPATITIS
VIRAL Hepatitis
Hepatitis A – Infectious hepatitis
Hepatitis B – Serum hepatitis

Hepatitis C – Non-A non-B or Post
    transfusion hepatitis
Hepatitis D – associated with Hep B

Hepatitis E - Epidemic hepatitis
NON-Viral hepatitis
   Staph aureus (toxic shock)

   Gram-Negative (Cholangitis)

   Parasitic (liver fluke)

   Amoeba (abscesses)

   AUTOIMMUNE

   ALCOHOLIC HEPATITIS
MORPHOLOGY OF ACUTE
 AND CHRONIC HEPATITIS
Acute Hepatitis
Hepatocyte injury

Hepatocyte necrosis

Regenerative changes

Sinusoidal cell reactive changes

Portal tracts changes
1.Hepatocyte injury

Diffused
swelling(balloonin
g degeneration)


Cholestasis:
canalicular bile
plug


HCV: Focal fatty
changes of
2.Hepatocyte necrosis

   Isolated cells
Cytolysis or
Apoptosis
Bridging
necrosis(portal-
portal , central –
central, portal –
portal)
Lobular
disarray: loss of
normal
architecture
5.Portal tracts:


 Mixture of
inflammator
y cells:
mainly
mononuclea
r


Interface
hepatitis
3.Regenerative changes:
                   hepatocyte proliferation

    4.Sinusoidal cell reactive changes:

   Accumulation of phagocytosed cellular debris in
                     kupffer cells

       Hypertrophy and hyperplasia of Kupffer cells
Chronic hepatitis

   Like acute hepatitis has similar;
      Hepatocyte injury,necrosis
    , regeneration, sinusoidal cell reactive changes

                   Portal tract changes



         Inflammatio                Fibrosis
              n
“Councilman” Bodies
FIBROSIS
       • Hallmark: deposition of fibrous
         tissue
   1

       • HBsAg: “Ground – glass
   2     hepatocytes”

       • HCV infection: Lymphoid
         aggregation and Bile duct damage
   3
Fibrosis of liver
Fulminant Hepatitis
Fulminant Hepatitis

 Hepatic insufficiency leading to hepatic
 encephalopathy
Histology: 2 forms
A) Submassive necrosis

                Orderly regeneration

             Partial necrosis usually in
             centrilobular and mid zone

            Collapsed reticulin framework
B)Massive necrosis



         • Necrosis of entire lobule
         • Loss of hepatic
           parenchyma

         • Collapsed and condensed
           reticulin framework


         • Disordered regeneration
         • Fibrosis doesn’t occur
ANY
      ….
           …..
                 …..
                       …..
                             …….
                                   Queries...?
THANK U !!!!!

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Hepatitis correlation2

  • 1. GANDAKI MEDICAL COLLEGE CORRELATION SEMINAR GI SYSTEM PRESENTED BY: SAJANA BHANDARI SUDARSHAN ACHARYA
  • 2. OBJECTIVE  TO DESCRIBE THE MICROSCOPIC FEATURES OF DIFFERENT TYPES OF HEPATITIS
  • 3. HEPATITIS It is the inflammationof liver . Usually 2 types: VIRAL HEPATITIS NON-VIRAL HEPATITIS
  • 4. VIRAL Hepatitis Hepatitis A – Infectious hepatitis Hepatitis B – Serum hepatitis Hepatitis C – Non-A non-B or Post transfusion hepatitis Hepatitis D – associated with Hep B Hepatitis E - Epidemic hepatitis
  • 5. NON-Viral hepatitis  Staph aureus (toxic shock)  Gram-Negative (Cholangitis)  Parasitic (liver fluke)  Amoeba (abscesses)  AUTOIMMUNE  ALCOHOLIC HEPATITIS
  • 6. MORPHOLOGY OF ACUTE AND CHRONIC HEPATITIS Acute Hepatitis Hepatocyte injury Hepatocyte necrosis Regenerative changes Sinusoidal cell reactive changes Portal tracts changes
  • 8. 2.Hepatocyte necrosis  Isolated cells Cytolysis or Apoptosis Bridging necrosis(portal- portal , central – central, portal – portal) Lobular disarray: loss of normal architecture
  • 9. 5.Portal tracts:  Mixture of inflammator y cells: mainly mononuclea r Interface hepatitis
  • 10. 3.Regenerative changes:  hepatocyte proliferation 4.Sinusoidal cell reactive changes:  Accumulation of phagocytosed cellular debris in kupffer cells  Hypertrophy and hyperplasia of Kupffer cells
  • 11. Chronic hepatitis  Like acute hepatitis has similar; Hepatocyte injury,necrosis , regeneration, sinusoidal cell reactive changes  Portal tract changes Inflammatio Fibrosis n
  • 13. FIBROSIS • Hallmark: deposition of fibrous tissue 1 • HBsAg: “Ground – glass 2 hepatocytes” • HCV infection: Lymphoid aggregation and Bile duct damage 3
  • 16. Fulminant Hepatitis Hepatic insufficiency leading to hepatic encephalopathy Histology: 2 forms A) Submassive necrosis Orderly regeneration Partial necrosis usually in centrilobular and mid zone Collapsed reticulin framework
  • 17. B)Massive necrosis • Necrosis of entire lobule • Loss of hepatic parenchyma • Collapsed and condensed reticulin framework • Disordered regeneration • Fibrosis doesn’t occur
  • 18. ANY …. ….. ….. ….. ……. Queries...?