Chapter 9 - Liver Flashcards
Trace the flow of blood through the liver.
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.
Name the three main components of liver.
Hepatocytes, biliary system, and vessels
Describe the normal morphology of hepatocytes.
Large, pink polygonal cells with round nuclei (sometimes binucleate, or with nucleoli), arranged into plates lined with reticulin, separated by the sinusoids.
What are portal tracts, and what is their significance?
What is the lining of the bile canaliculi?
What is the limiting plate?
Portal tracts house the portal triad, and is the main focus of inflammatory processes.
Low cuboidal.
The hepatocytes immediately surrounding the portal tract.
What is the lobule?
What is the acinus?
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!
Name some diseases of:
- Hepatocytes
- Biliary system
- Vessels
- Viral and autoimmune hepatitides, steatohepatitis, alcohol, drug toxicity
- Autoimmune biliary disease (PBC/PSC), obstruction, atresia, rejection, GHVD, drug toxicity
- Rejection, GVHD, systemic vasculitides
How do acute and chronic injury appear in the liver?
Same as in other organs;
Acute: Edema, inflammation, necrosis
Chronic: Mononuclear infiltrate, then cirrhosis.
Describe the appearance of portal inflammation
Inflammatory cells in the portal tract.
(usually mononuclear in autoimmune disease)
Describe the appearance of periportal hepatitis or interface activity.
Inflammation in the limiting plate, resembles portal inflammation spilling out.
Describe the appearance of lobular inflammation.
Chronic inflammation and necrosis of hepatocytes away from portal tracts.
Describe the appearance of vacuolar degeneration.
What about acidophilic bodies?
Swelling of cells with feathery and pale appearance.
Bright pink, rounded up, with pyknotic nuclei (similar to dyskeratosis).
Describe the appearance of steatosis and steatohepatitis.
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)
What are Mallory bodies?
Megamitochondria?
Irregular pink blobs of condensed cytoskeleton, associated with alcoholic liver disease.
Markedly enlarged mitochondria which resemble RBCs.
Describe the appearance of cholestasis.
Of bile duct proliferation?
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.
What diseases are typical of macrovesicular and microvesicular steatosis?
Macrovesicular: Alcoholic liver disease and NASH.
Microvesicular: Mitochondrial injury, eg Reye’s.
Describe the appearance of bile duct injury.
What is the end-stage?
Lymphocytes in the bile duct epithelium with vacuolization and dropout. Usually patchy.
Ends in ductopenia, in which <80% of tracts have a duct.
What is venulitis/endothelitis?
How does extramedullary hematopoiesis appear?
Damage to portal/central vessel endothelium, usually indicating GVHD.
Hematopoietic precursors appear in the sinusoids.
What three prognostic factors should be noted on any hepatitis biopsy signout?
Etiology (if known)
Grade (degree of inflammation/necrosis)
Stage (degree of fibrosis)
Describe a typical staging of fibrosis.
0 - None
1 - Portal fibrosis
2 - Periportal fibrosis
3 - Bridging fibrosis
4 - Cirrhosis
Compare & contrast the appearance of liver rejection and GVHD
They are highly analogous, with the latter taking place in context of a bone marrow transplant.
Distinguish the features of acute and chronic rejection.
Acute: Mixed inflammation, venulitis, bile duct inflammation & change.
Chronic: Ductopenia and fibrosis.
Try to summarize the defining features of primary biliary cirrhosis.
Occurs mainly in women. Associated with AMA.
Intrahepatic cholangitis.
Begins with inflammation and bile duct injury (granulomatous!) and progresses to ductopenia / cirrhosis.
Try to summarize the defining features of sclerosing cholangitis.
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.
What is the most common mass lesion in liver?
Metastasis.
Describe several mass lesions affecting:
- Hepatocytes
- Biliary tract
- Vessels
- FNH, adenoma, HCC (& variants)
- Bile duct hamartoma, adenoma, cholangiocarcinoma
- Cavernous hemangiomas, epithelioid hemangiomas, angiosarcomas.
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.
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.
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.
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.
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.
What is bile duct hamartoma and how does it appear?
<1cm and subcapsular lesion with dilated/angulated tubules that produce bile.
How does cholangiocarcinoma appear?
A nondescript adenocarcinoma in the liver that does not produce bile. Note also an intense desmoplastic response.
Recall and summarize 3 vascular lesions and their significance.
Cavernous hemangiomas are benign vascular lesions.
Epithelioid hemangioendotheliomas have low malignant potential.
Angiosarcomas are malignant.
Top: Portal tract
- Limiting plate
- Hepatic artery
- Bile ductule
- Portal vein
Bottom: Central vein
Portal inflammation
Arrow: Spillage of lymphocytes into the limiting plate
Cirrhosis in a biopsy (trichrome)
Blue: Collagen
Steatohepatitis
- Adjacent portal tract with minimal inflammation
- Macrovesicular steatosis
Arrows: Neutrophils
Mallory bodies
Arrow: Pink refractile worm-like structure in a background of steatosis and inflammation
Bile stasis
- Acute inflammation
- Proliferation of poorly formed ducts
- Fibrosis (end-stage)
Acute liver rejection
Arrow: Duct epithelium invaded by lymphocytes
Primary biliary cirrhosis
Arrow: Granulomatous inflammation with destruction of a bile duct
Well-differentiated HCC. Note golden bile, absence of portal tracts.
Bile duct adenoma
Benign tangle of proliferative bile ducts surrounded by edema. No bile or atypia.
Cholangiocarcinoma
Arrow: Intense desmoplastic response
