Hepatitis

Question 1

Gross morhology of Acute hepatitis.

Answer 1

• Cut sectioon muddy-red, mushy with yellow or green discoloration due to jaundice.
• Involvement may be diffuse or patchy.
• Slightly enlarged & soft.

Question 2

Inflammatory cells in acute & chronic hepatitis.

Answer 2

T-Cells.

Question 3

In Acute inflammation, what is inflammation scattered throughout the hepatic lobule called?

Answer 3

Spotty necrosis or lobular hepatitis.

Question 4

Ballooning degeneration in Acute Hepatitis?

Answer 4

• Seen in mild injury.
• Swelling of hepatocytes.
• Empty and pale stained cytoplasm with clumping of cytoplasm around the nucleus.

Question 5

Explain these hepatocyte necrosis:

1. Dropout necrosis.
2. Acidophilic or apoptotic or councilman body.
3. Bridging necrosis.

Answer 5

1. Rupture of ballooned hepatocyte cell membrane > Cell death and focal loss of hepatocytes > Necrotic cell dropout > Collapse of sinusoidal collagen reticulin framework > Aggregates of macrophages around necrotic hepatocyte.
2. • Caused by antiviral cytotoxic T cells and may be surrounded by them.
     - Apoptotic hepatocytes shrink > Become intensely eosinophilic and have a densely staining pyknotic or fragmented nuclei.
     - Remnants of apoptotic hepatocytes may be extruded into the sinusoids > Appear as acidophilic or councilman bodies.
3. -Observed in severe acute hepatitis.
   - A band/zone of necrosis may extend from portal tract to portal tract, central vein to central vein, or portal to central regions of adjacent lobules.

Question 6

Interface hepatitis.

Answer 6

Occurs in acute and chronic hepatitis.

Question 7

Mononuclear inflammatory cells in acute hepatitis.

Answer 7

Lymphocytes and macrophages

Question 8

Lobular hepatitis.

Answer 8

The inflammation involving liver parenchyma away from portal tract (seen throughout the lobule)

Question 9

Kupffer cells in acute hepatitis.

Answer 9

• Show hypertrophy and hyperplasia.
• Contain lipofuscin pigment as a result of phagocytosis of hepatocellular debris.

Question 10

Cholestasis

Answer 10

A condition where bile cannot flow from the liver to the duodenum.

Question 11

Summary of microscopy of acute hepatitis.

Answer 11

1. Ballooning degeneration.
2. Dropout necrosis.
3. Councilman or acidophil body.
4. Bridging necrosis.
5. Inflammatory infiltrate.
6. Kupffer cell hyperplasia.
7. Cholestasis.
8. Regeneration.

Question 12

Hepatocellular injury is most marked in?

Answer 12

Zone 3/Centrilobular zone.

Question 13

HAV hepatitis in acute inflammation.

Answer 13

A panlobular involvement by heavy inflammatory infiltrate compared to other types.

Question 14

HCV hepatitis in acute inflammation.

Answer 14

• Causes milder necrosis with fatty change in hepatocytes.
• Shows presence of lymphoid aggregates in the portal triads.
• Degeneration of bile duct epithelium.

Question 15

Panlobular.

Answer 15

Involvement of entire acinus.

(An acinus refers to any cluster of cells that resembles a many-lobed “berry,” such as a raspberry.)

Question 16

Define chronic hepatitis.

Answer 16

Symptomatic, biochemical or serologic evidence of hepatic disease for more than 6 months.

Question 17

Viral causes of chronic hepatitis.

Answer 17

1. HCV- most common cause and mostly asymptomatic. (40 to 60 %)
2. HBV- if this infection occurs at a young age. -Maternal to infant transmission is a major risk factor. (90% of infected infants and 5% adults)
3. HDV+HBV- either superinfection or coinfection.

Question 18

Non-viral causes of chronic hepatitis.

Answer 18

1. Autoimmune hepatitis.
2. Grug induced chronic hepatitis.
3. Wilson’s disease.
4. Cryptogenic hepatitis (non-A-E hepatitis)
5. Alpha 1 antitrypsin deficiency.
6. Chronic alcoholism.

Question 19

Gross morphology of chronic hepatitis.

Answer 19

Early stage- Liver may appear normal.
Later stage- Liver feels firm because of increased fibrosis > may progress to macronodular cirrhosis.

Question 20

Interface hepatitis in chronic inflammation. (Piecemeal necrosis/periportal necrosis)

Answer 20

An important feature characterized by spillover of inflammatory cells (lymphocytes and plasma cells) from portal tracts into the adjacent parenchyma at the limiting plate > associated with degenerating and apoptosis of periportal hepatocytes.

Question 21

Fibrosis in chronic inflammation.

Answer 21

Initially- Seen only in portal tracts.
Later- Periportal septal fibrosis occurs > followed by bridging/linking of fibrous septa (bridging fibrosis) between adjacent fibrotic portal tracts.

Question 22

Microscopy of chronic inflammation.

Answer 22

1. Piecemeal necrosis.
2. Portal tract lesions.
3. Intralobular lesions.
4. Bridging fibrosis.

Question 23

Physical findings in chronic inflammation.

Answer 23

1. Spider angiomas (a type of telangiectasis (swollen blood vessels) found slightly beneath the skin surface, often containing a central red spot and deep reddish extensions (see Blood color) which radiate outwards like a spider’s web or a spider’s legs)
2. Palmar erythema (reddening of the palm)
3. Hepatic tenderness.
4. Mild splenomegaly. (A condition where the size of the spleen is increased. This may cause pain in the upper abdomen, frequent infections and easy bruising)

Question 24

Lab findings in chronic inflammation.

Answer 24

1. Increased bilirubin and urobilinogen in urine.
2. Raised serum transaminase.
3. Prolonged prothrombin time.
4. Hyperbilirubinemia.
5. Mild elevation of alkaline phosphatase level.

Question 25

Causes of post necrotic cirrhosis.

Answer 25

• Viral hepatitis.
• Autoimmune hepatitis.
• Hepatotoxins like carbon tetrachloride, mushroom poisoning.
• Drugs like Acetaminophen and alpha-methyldopa
• Rarely also alcohol.

Question 26

Gross morphology of fulminant hepatic failure.

Answer 26

1. Liver shrinks to 500-700 g.
2. Wrinkled capsule.
3. Massive necrosis of hepatocytes.
4. Minimal inflammatory reaction.

Question 27

Causes of fulminant hepatic failure.

Answer 27

1. HBV and HAV.
2. Occasionally HCV.
3. Acetaminophen toxicity.

Question 28

Fulminant Hepatitis or hepatic failure.

Answer 28

Most severe form of acute hepatitis in which there are rapidly progressing hepatic failure.
Has two recognizable patterns.

Question 29

What are the two stages or recognizable patterns of Fulminant hepatitis.

Answer 29

1. Submassive necrosis.
2. Massive necrosis.

Question 30

Submassive necrosis.

Answer 30

Large groups of hepatocytes in zone 3 (centrilobular zone) and zone 2 (mid zone) are wiped out leading to a collapsed reticulin framework.
Extends up to 3 months.

Regeneration here is more orderly and may result in restoration of normal architecture.

Question 31

Massive necrosis.

Answer 31

Entire liver lobules are necrotic.
As a result of loss of hepatic parenchyma, all that is left is the collapsed and condensed reticulin framework and portal tracts with proliferated bile ductules plugged with bile.
Occurs in 2-3 weeks.

Question 32

Features of Hepatitis viruses.

Answer 32

Question 33

Carrier State in HBV

Answer 33

A “carrier” is an individual who harbors and can transmit an organism (HBV), but does not manifest symptoms.

Question 34

Inactive carriers (healthy carriers)

Answer 34

1. They carry one of the viruses but have no liver disease.
2. They have normal or only mildly raised serum aminotransferase values without HBeAg, but show anti-HBe.
3. Majority do not progress to liver disease.

Question 35

Active carriers.

Answer 35

1. They harbor the viruses and have non-progressive liver damage.
2. They are usually asymptomatic, but show intermittent or persistent elevation of serum aminotransferase levels.
   - HBsAg+
   - HBeAg+
   - HBV-DNA+
   - IgG anti-HBc+