Pathology of Viral Hepatitis

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Nearly all men can stand adversity, but if you
want to test a man's character, give him
power  Abraham Lincoln
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Pathology of Hepatitis
Dr. Venkatesh M. Shashidhar. Associate Professor
of Pathology Fiji School of Medicine
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Normal Liver
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• 1.5 kg, wedge shape
• 4 lobes, Right, left, Caudate, Quadrate.
• Double blood supply
• Hepatic arteries
• Portal Venous blood
• Acini / Portal triad.
• Lobules central. V

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Normal Liver - Infant
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CT Scan Normal Abdomen
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Structure of Liver Lobule
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Normal Liver - Microscopy
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Liver Functions

• Metabolism Carbohydrate, Fat Protein
• Secretory bile - Bile acids, salts pigments
• Excretory Bilirubin, drugs, toxins
• Synthesis Albumin, coagulation factors
• Storage Vitamins, carbohydrates etc.
• Detoxification toxins, ammonia, etc.

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Hepatic Injury

• The liver is vulnerable to a variety of toxic,
  metabolic, infectious, circulatory, and
  neoplastic insults, both primary and secondary
• The liver has a limited number of responses to
  an infinite number of insults inflammation,
  degeneration, necrosis, fibrosis, cirrhosis.

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Introduction

• Hepatitis Inflammation of Liver
• Hepatocyte Necrosis liver func jaundice.
• Viral, Alcohol, immune, Drugs Toxins
• Biliary obstruction gall stones.
• Acute, Chronic Fulminant - types
• Viral Hepatitis
• Specific Heptitis A, B, C, D, E, other
• Systemic - CMV, EBV, other.

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Pattern of Viral Hepatitis

• Carrier state / Asymptomatic phase
• Acute hepatitis
• Chronic Hepatitis
• Chronic Persistent Hepatitis (CPH)
• Chronic Active Hepatitis (CAH)
• Fulminant hepatitis
• Cirrhosis
• Hepatocellular Carcinoma

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Acute Hepatitis

• Cell Swelling and hydropic/fatty change
• Portal inflammation and Cholestasis
• Necrosis
• Piecemeal, Bridging, panacinar Apoptosis.
• Inflammation lymphocytes, Macrophages
• Ground glass hepatocytes HBV
• Mild fatty change HCV

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Pattern of Liver Damage

• Zonal Toxin/Hypoxia
• Bridging Viral severe
• Interface Immune
• Apoptotic - Viral

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Chronic Hepatitis

• Persistent Active types. CPH/CAH
• Lymphoid aggregates
• Periportal fibrosis
• Necrosis with fibrosis bridging fibrosis.
• Cirrhosis regenerating nodules.

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Acute - Hepatitis - Chronic
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Acute viral Hepatitis
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Liver Biopsy - CAH
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Acute viral Hepatitis
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Acute viral Hepatitis C
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Liver Biopsy CPH
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Chronic Active viral Hepatitis
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Bridging Fibrosis
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Fulminant Hepatitis

• Hepatic failure with in 2-3 weeks.
• Reactivation of chronic or acute hepatitis
• Massive necrosis, shrinkage, wrinkled
• Collapsed reticulin network
• Only portal tracts visible
• Little or massive inflammation time
• More than a week regenerative activity
• Complete recovery or - cirrhosis.

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Liver Biopsy Cirrhosis
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Liver Biopsy Cirrhosis
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Viral Hepatitis Microbiology
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Alcoholic Liver Injury
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Alcoholic Liver Injury

• Ethyl alcohol Common cause of acute/Chronic
  liver disease
• Alcoholic Liver disease - Patterns
• Fatty change,
• Acute hepatitis (Mallory Hyalin)
• Chronic hepatitis with Portal fibrosis
• Cirrhosis, Chronic Liver failure
• All reversible except cirrhosis stage.

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Alcoholic Liver Injury Pathogenesis

• Acetaldehyde metabolite hepatotoxic
• Diversion of metabolism to alcohol
• Fat storage fatty change. Cell swelling..
• Rupture ?Fat necrosis ? severe inflammation ?
  fibrosis.
• Alcohol stimulates collagen synthesis
• Inflammation, Portal bridging fibrosis
• Micronodular cirrhosis.

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Alcoholic Liver Damage
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Alcoholic Fatty Liver
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Alcoholic Fatty Liver
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Alcoholic Fatty Liver
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Micronodular cirrhosis
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Liver Function Tests
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Bilirubin

• Direct Bilirubin
• Conjugated
• Soluble in H2O
• 0-20 in plasma

• Indirect Bilirubin
• Unconjugated
• Insoluble in H2O
• 80-100 in plasma

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Three Categories of Jaundice
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Liver Function Tests

• Synthesis ?
• Total protein albumin on low side PT abnormal
• Obstruction ?
• Alk Phos Bilirubin are up
• Hepatocyte Direct Injury
• ALT AST are DRAMATICALLY increased.
• Alk Phos moderately increased.

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Case 2

• 47 yrF presents with Acute abdominal pain.
  Initially intermittant, but now is constant
  increasing in intensity.
• PE Abdominal tenderness, No organomegaly. Mild
  Scleral icterus
• Labs ALT 50 (N 8-33 U/L)
• AST 62 (N 4-36 U/L)
• Alk Phos 1800 (N 20-130 u/L)
• Bilirubin 2.9 (N 0.1-1.2 mg/dL)
• T Protein 6.8 (N 6.0-7.8 g/dL)
• Albumin 3.5 (N 3.2-4.5 g/dl)
• PT 12 sec (N 11-14.7 sec )

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Case 2

• Synthesis? (Total protein, albumin PT normal.)
  is OK
• Obstruction Bilirubin Clearance ? (Alk Phos is
  up QUITE DRAMATICALLY Bilirubin up modestly)
• PROBABLY A PRIMARY OBSTRUCTIVE PROCESS.
• Hepatocyte Direct Injury ALT AST are up a
  bit, but not dramatically.
• THE PRIMARY PROCESS IS OBSTRUCTIVE !!!
• Could be
• common bile duct obstruction pancreatic cancer
  (esp. in head of pancreas)

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