Chapter 9 - Liver Flashcards

1
Q

Trace the flow of blood through the liver.

A

Blood from the hepatic artery and portal vein enters the terminal portal vessels and sinusoids, exiting via the central veins which coalesce into L/R hepatic veins and the IVC.

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2
Q

Name the three main components of liver.

A

Hepatocytes, biliary system, and vessels

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3
Q

Describe the normal morphology of hepatocytes.

A

Large, pink polygonal cells with round nuclei (sometimes binucleate, or with nucleoli), arranged into plates lined with reticulin, separated by the sinusoids.

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4
Q

What are portal tracts, and what is their significance?

What is the lining of the bile canaliculi?

What is the limiting plate?

A

Portal tracts house the portal triad, and is the main focus of inflammatory processes.

Low cuboidal.

The hepatocytes immediately surrounding the portal tract.

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5
Q

What is the lobule?

What is the acinus?

A

A functional architectural unit with the central vein at the center and the portal tracts at the periphery.

A functional physiologic unit with the portal tract at its base and the portal vein at its tip. Divides into 3 zones!

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6
Q

Name some diseases of:

  1. Hepatocytes
  2. Biliary system
  3. Vessels
A
  1. Viral and autoimmune hepatitides, steatohepatitis, alcohol, drug toxicity
  2. Autoimmune biliary disease (PBC/PSC), obstruction, atresia, rejection, GHVD, drug toxicity
  3. Rejection, GVHD, systemic vasculitides
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7
Q

How do acute and chronic injury appear in the liver?

A

Same as in other organs;

Acute: Edema, inflammation, necrosis

Chronic: Mononuclear infiltrate, then cirrhosis.

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8
Q

Describe the appearance of portal inflammation

A

Inflammatory cells in the portal tract.

(usually mononuclear in autoimmune disease)

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9
Q

Describe the appearance of periportal hepatitis or interface activity.

A

Inflammation in the limiting plate, resembles portal inflammation spilling out.

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10
Q

Describe the appearance of lobular inflammation.

A

Chronic inflammation and necrosis of hepatocytes away from portal tracts.

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11
Q

Describe the appearance of vacuolar degeneration.

What about acidophilic bodies?

A

Swelling of cells with feathery and pale appearance.

Bright pink, rounded up, with pyknotic nuclei (similar to dyskeratosis).

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12
Q

Describe the appearance of steatosis and steatohepatitis.

A

Steatosis: Fat in the hepatocytes (30-60% moderate, >60% severe). Can be macrovesicular or microvesicular.

Steatohepatitis: Above with evidence of inflammation or injury (necrosis, fibrosis, balloon cells, mallory bodies)

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13
Q

What are Mallory bodies?

Megamitochondria?

A

Irregular pink blobs of condensed cytoskeleton, associated with alcoholic liver disease.

Markedly enlarged mitochondria which resemble RBCs.

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14
Q

Describe the appearance of cholestasis.

Of bile duct proliferation?

A

Backup of bile in the liver…results in bile duct injury. See other card.

>1-2 ducts per portal tract, which are often small and poorly formed. Also look for bile, edema, inflammation.

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15
Q

What diseases are typical of macrovesicular and microvesicular steatosis?

A

Macrovesicular: Alcoholic liver disease and NASH.

Microvesicular: Mitochondrial injury, eg Reye’s.

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16
Q

Describe the appearance of bile duct injury.

What is the end-stage?

A

Lymphocytes in the bile duct epithelium with vacuolization and dropout. Usually patchy.

Ends in ductopenia, in which <80% of tracts have a duct.

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17
Q

What is venulitis/endothelitis?

How does extramedullary hematopoiesis appear?

A

Damage to portal/central vessel endothelium, usually indicating GVHD.

Hematopoietic precursors appear in the sinusoids.

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18
Q

What three prognostic factors should be noted on any hepatitis biopsy signout?

A

Etiology (if known)

Grade (degree of inflammation/necrosis)

Stage (degree of fibrosis)

19
Q

Describe a typical staging of fibrosis.

A

0 - None

1 - Portal fibrosis

2 - Periportal fibrosis

3 - Bridging fibrosis

4 - Cirrhosis

20
Q

Compare & contrast the appearance of liver rejection and GVHD

A

They are highly analogous, with the latter taking place in context of a bone marrow transplant.

21
Q

Distinguish the features of acute and chronic rejection.

A

Acute: Mixed inflammation, venulitis, bile duct inflammation & change.

Chronic: Ductopenia and fibrosis.

22
Q

Try to summarize the defining features of primary biliary cirrhosis.

A

Occurs mainly in women. Associated with AMA.

Intrahepatic cholangitis.

Begins with inflammation and bile duct injury (granulomatous!) and progresses to ductopenia / cirrhosis.

23
Q

Try to summarize the defining features of sclerosing cholangitis.

A

Occurs mainly in men. Associated with IBD & p-ANCA.

Extrahepatic cholangitis (also affects large intrahepatic ducts).

Nonspecific pattern with ductular proliferation. Leads to patchy stricturing lesions.

24
Q

What is the most common mass lesion in liver?

A

Metastasis.

25
Describe several mass lesions affecting: 1. Hepatocytes 2. Biliary tract 3. Vessels
1. FNH, adenoma, HCC (& variants) 2. Bile duct hamartoma, adenoma, cholangiocarcinoma 3. Cavernous hemangiomas, epithelioid hemangiomas, angiosarcomas.
26
What is *focal nodular hyperplasia* and how does it appear?
A small island of cirrhosis in a noncirrhotic background. Central scar but no capsule; nodules divided by bands of fibrosis & thick vessels.
27
What is *hepatic adenoma* and how does it appear?
A benign clonal neoplasm associated with OCP use. Circumscribed, partially encapsulated. Bland-looking with **no veins or bile ducts**.
28
What is *hepatocellular carcinoma* and how does it appear?
Resembles an adenoma, also with no veins or bile ducts. Nuclei can look atypical. Look at the *reticulin stain;* \>3 cell thickness indicate malignancy rather than adenoma.
29
How can poorly differentiated HCC be identified? What is fibrolamellar HCC?
Look for bile. Well-differentiated variant in young patients. Features oncocytic cells with prominent nucleoli in a dense fibrotic stroma.
30
What is *bile duct adenoma*​ and how does it appear?
\<1 cm and subcapsular lesion comprised of small simple tubules without inflammation. May produce **mucin** but not bile.
31
What is *bile duct hamartoma* and how does it appear?
\<1cm and subcapsular lesion with dilated/angulated tubules that produce **bile**.
32
How does cholangiocarcinoma appear?
A nondescript adenocarcinoma in the liver that **does not produce bile**. Note also an intense desmoplastic response.
33
Recall and summarize 3 vascular lesions and their significance.
Cavernous hemangiomas are benign vascular lesions. Epithelioid hemangioendotheliomas have low malignant potential. Angiosarcomas are malignant.
34
Top: Portal tract 1. Limiting plate 2. Hepatic artery 3. Bile ductule 4. Portal vein Bottom: Central vein
35
Portal inflammation Arrow: Spillage of lymphocytes into the limiting plate
36
Cirrhosis in a biopsy (trichrome) Blue: Collagen
37
Steatohepatitis 1. Adjacent portal tract with minimal inflammation 2. Macrovesicular steatosis Arrows: Neutrophils
38
Mallory bodies Arrow: Pink refractile worm-like structure in a background of steatosis and inflammation
39
Bile stasis 1. Acute inflammation 2. Proliferation of poorly formed ducts 3. Fibrosis (end-stage)
40
Acute liver rejection Arrow: Duct epithelium invaded by lymphocytes
41
Primary biliary cirrhosis Arrow: Granulomatous inflammation with destruction of a bile duct
42
Well-differentiated HCC. Note golden bile, absence of portal tracts.
43
Bile duct adenoma Benign tangle of proliferative bile ducts surrounded by edema. **No bile or atypia**.
44
Cholangiocarcinoma Arrow: Intense desmoplastic response