Gi #22: Liver Pathology 1

Front 1

What is the function of a stellate cell in the normal liver? What about in a state of injury (virus, alcohol, etc.)?

What are the "true" liver function markers?

Back 1

Normally, stellate cell= fat storage (vit A storage). In pathologic state, it produces collagen and is fibrogenic.

True = Bilirubin, Albumin, PT time/ coagulation factors (these all give an indication that liver is failing). AST, ALT are just markers of injury to cells.

Front 2

What histological finding is shown here? Is it specific to any condition?

Back 2

Ballooning Degeneration- swelling of hepatocytes with cytoplasmic pallor and irregularly clumped cytoplasmic organelles.

Non-specific--> Can be seen in alcoholic hepatitis, NASH, Wilson's disease, viral hepatitis.

Front 3

What is shown within the swollen cells? What condition is it most commonly associated with?

Back 3

Ballooned hepatocytes with MALLORY HYALINE (eosinophilic aggregates of keratin). These are intermediate filaments that resist degradation.

Associated with Alcoholic Hyaline (also seen in PBC, Wilson, chronic cholestasis, tumor, etc.)

Front 4

What type of liver change is seen here? What conditions is it seen in?

Back 4

Feather degeneration (swelling of individual hepatocytes). Looks similar to ballon degeneration but there is yellow discoloration.

Seen in cholestatic liver disease (retained biliary material)

Front 5

What type of stain would you use to diagnose Wilson's disease on a biopsy (shown above) ?

What about alpha1 antitrypsin deficiency?

Back 5

Wilson's disease --> Cu2+ deposits --> Rhodanine stain

a1AT deficiency --> PAS stain (for glycogen and glycoproteins). (shown above)

Front 6

What are the eosinophilic cells in this image called? What

Back 6

Counsilman Body (Acidophil Body) - they are apoptotic hepatocytes.

Front 7

What is another name for the type of necrosis shown above?

Back 7

Piecemeal necrosis = periportal inflammation = interface hepatitis

This is necrosis of limiting plate. Replacement of hepatocytes by inflammatory cells/fibrosis.

Front 8

What does the finding of "nutmeg liver" represent (shown above on gross image)?

If a patient had left sided heart failure, what zone would be most ischemic? Which zone would be most congested if the patient had right sided heart failure?

Back 8

Nutmeg liver = gross appearance of liver that has areas of hemorrhage and centrilobular necrosis

Left sided --> hypoperfusion --> Zone 3 most ischemic
Right sided --> retrograde congestion --> blood accumulates in Zone 3

Front 9

This person has overdosed on Acetaminophen and damaged their liver. What zone is most susceptible to necrosis?

Back 9

Centrilobular necrosis - from acetaminophen overdose. Tylenol is broken down by CYP450 enzymes and it's metabolites are released (causing damage).

CYP450 enzymes are most abundant in zone 3 (Note: usually toxins affect zone 1 because they are highest in concentration there).

Front 10

What is the predominant cell that comprises the mononuclear infiltrate seen in Acute Hepatitis?

What about in Autoimmune hepatitis? Alcoholic hepatitis? Drug induced hepatitis?

Back 10

Lymphocytes! Though acute, lymphocytes respond to the virus causing damage to hepatocytes.

Autoimmune --> Plasma cells
Alcoholic --> Neutrophils
Drug-induced --> Eosinophils

Front 11

What is the difference between liver regeneration after partial hepatectomy vs. submassive/massive hepatic necrosis?

What are the stem cells of the liver called?

Back 11

Partial hepatectomy --> compensatory hyperplasia and hepatocyte replication

Massive hepatic necrosis --> stem cell = oval cells (in the canal of Herring) , differentiate in hepatocytes and cholangiocytes

Front 12

T or F
Collagen Type IV is found in liver sinusoidal cells.

What stain is shown on the bottom image?

Back 12

False- they don't have basement membrane (no Col Type IV). Instead they have Col type 3 (stain positive with Reticulin).

Front 13

What are the most common causes of cirrhosis?

What are some characteristics of cirrhosis?

Back 13

1. Chronic alcoholism, 2. Hepatitis (B&C)

Characteristics =
- diffuse process (involves entire parenchyma)
- bridging fibrous septa
- parenchymal nodules that are encircled by fibrosis

Front 14

Does acute viral hepatitis cause portal or lobular inflammation? What about chronic viral hepatitis?

What are changes seen in Acute viral hepatitis (shown here)?

Back 14

ACUTE causes LOBULAR inflammation (chronic causes portal)

- ballooning degeneration
-acidophil bodies (apoptosis)
- lymphocyte predominance
- kupffer cell aggregates (phagocytosis of hepatocellular debris)
- LOBULAR disarray

Front 15

What is the definition of Chronic hepatitis? How does the distribution of inflammation in the liver differ from Acute hepatitis?

If someone is tested for Hep B and comes back with positive Anti-HBs, what does this indicate?

Back 15

Chronic - continuing/relapsing disease for > 6 months. Unlike acute, there is PORTAL/PERIPORTAL inflammation (with Interface hepatitis).

Anti-HBs --> either the person recovered from HBV infection (in which case, check Anti-HBc to check if positive), OR they were vaccinated (in which case HBsAg and HBc will be negative)

Front 16

What are the two major pathologic features of Chronic Hepatitis B, shown here?

Back 16

1. Ground glass hepatocytes (HBsAg in the cytoplasm)
2. Sanded nuclei (contain HBcAg- core antigen)

Front 17

What is the greatest risk factor for HCV infection? If someone is Anti-HCV positive, what does that mean about their immune status?

What are two ways in which a person can acquire hepatitis D virus?

Back 17

#1= IV drug abuse, #2= multiple sex partners
Presence of Antibodies DO NOT confer immunity (unlike HBV)

Hepatitis D:
1) via co-infection (with both hep C and hep B)
2) via superinfection (an HBV carrier can get superinfected with Hep D).

Front 18

What is the triad of findings you would see in CHRONIC hepatitis?

Back 18

1. Lymphoid aggregates in portal tracts
2. Mild steatosis of iver
3. Bile duct injury

Front 19

What cell type do you see in this predominate in this type of Hepatitis (hint: it is indistinguishable from chronic viral hepatitis)?

What type of labs would it be appropriate to check in these patients?

Back 19

Autoimmune Hepatitis: Prominent PLASMA cell and lymphocyte infiltrate. Otherwise, indistinguishable from chronic viral hepatitis.

Check autoantibodies (positive in 80% of cases) - ANA, Anti-smooth muscle, anti-liver kidney microsome)
*more predominant in females

Front 20

What is the causative agent of the abscess that you see in either image?

Back 20

Left= amebic abscess ("anchovy paste")
Right= ecchinococcus (can cause hydatid cyst that if it ruptures --> anaphylaxis)

Front 21

What are three forms of alcoholic liver disease? Which is shown above?

Which one(s) are(is) reversible?

Back 21

1. Hepatic steatosis (fatty liver)- reversible (shown in picture)

2. Alcoholic hepatitis- reversible
3. Cirrhosis --> IRREVERSIBLE

Front 22

What is this type of fibrosis (associated with alcoholic hepatitis) called?

Back 22

Chicken wire fence fibrosis (i.e. sinusoidal or pericellular fibrosis). From stellate cell activation and deposition of collagen.

Front 23

What condition is most commonly associated with the change seen on the left? What about the right?

Back 23

Left= Micronodular < 3 mm --> secondary to ETOH (can also be seen in Wilson's disease, hemochromatosis, PBC)

Right= Macronodular >3 mm--> most common cause is VIRAL hepatitis