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Book - Molavi > Chapter 9 - Liver > Flashcards

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
Q

Describe several mass lesions affecting:

  1. Hepatocytes
  2. Biliary tract
  3. Vessels
A
  1. FNH, adenoma, HCC (& variants)
  2. Bile duct hamartoma, adenoma, cholangiocarcinoma
  3. Cavernous hemangiomas, epithelioid hemangiomas, angiosarcomas.
26
Q

What is focal nodular hyperplasia and how does it appear?

A

A small island of cirrhosis in a noncirrhotic background. Central scar but no capsule; nodules divided by bands of fibrosis & thick vessels.

27
Q

What is hepatic adenoma and how does it appear?

A

A benign clonal neoplasm associated with OCP use. Circumscribed, partially encapsulated. Bland-looking with no veins or bile ducts.

28
Q

What is hepatocellular carcinoma and how does it appear?

A

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
Q

How can poorly differentiated HCC be identified?

What is fibrolamellar HCC?

A

Look for bile.

Well-differentiated variant in young patients. Features oncocytic cells with prominent nucleoli in a dense fibrotic stroma.

30
Q

What is bile duct adenoma​ and how does it appear?

A

<1 cm and subcapsular lesion comprised of small simple tubules without inflammation. May produce mucin but not bile.

31
Q

What is bile duct hamartoma and how does it appear?

A

<1cm and subcapsular lesion with dilated/angulated tubules that produce bile.

32
Q

How does cholangiocarcinoma appear?

A

A nondescript adenocarcinoma in the liver that does not produce bile. Note also an intense desmoplastic response.

33
Q

Recall and summarize 3 vascular lesions and their significance.

A

Cavernous hemangiomas are benign vascular lesions.

Epithelioid hemangioendotheliomas have low malignant potential.

Angiosarcomas are malignant.

34
Q
A

Top: Portal tract

  1. Limiting plate
  2. Hepatic artery
  3. Bile ductule
  4. Portal vein

Bottom: Central vein

35
Q
A

Portal inflammation

Arrow: Spillage of lymphocytes into the limiting plate

36
Q
A

Cirrhosis in a biopsy (trichrome)

Blue: Collagen

37
Q
A

Steatohepatitis

  1. Adjacent portal tract with minimal inflammation
  2. Macrovesicular steatosis
    Arrows: Neutrophils
38
Q
A

Mallory bodies

Arrow: Pink refractile worm-like structure in a background of steatosis and inflammation

39
Q
A

Bile stasis

  1. Acute inflammation
  2. Proliferation of poorly formed ducts
  3. Fibrosis (end-stage)
40
Q
A

Acute liver rejection

Arrow: Duct epithelium invaded by lymphocytes

41
Q
A

Primary biliary cirrhosis

Arrow: Granulomatous inflammation with destruction of a bile duct

42
Q
A

Well-differentiated HCC. Note golden bile, absence of portal tracts.

43
Q
A

Bile duct adenoma

Benign tangle of proliferative bile ducts surrounded by edema. No bile or atypia.

44
Q
A

Cholangiocarcinoma

Arrow: Intense desmoplastic response

Book - Molavi (29 decks)

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