Liver Pathology - Dunn Flashcards
(36 cards)
Describe the prototypical patient that develops primary biliary cirrhosis.
How is this patient’s outlook?
Generally a slightly older woman (think: Autoimmune!)
Not great; average survival is 10-12yrs as cirrhosis and portal HTN develop.
What physical exam or lab findings can be found in PBC?
How is it treated?
Pruritus, xanthomata, and jaundice.
Cholestatic liver panel, elevated cholesterol/bilirubin, and AMAs. “Florid ductal inflammation” on histology.
UDCA, Cholestyramine, Diphenhydramine. Transplant to cure.
What is secondary biliary cirrhosis, and what can cause it?
(hint: Different for adults and children)
Disease caused by extrahepatic biliary obstruction.
Adults: Stones, tumors, strictures.
Children: Biliary atresia, CF, cysts.
Describe the prototypical patient that develops primary sclerosing cholangitis.
How is its outlook?
Usually a young (~30yo) man.
Outlook is poor; fibrosis/portalHTN develop and risk of cholangiocarcinoma is increased.
What lab and exam findings can be seen in PSC?
What major association is relevant here?
Cholestatic liver panels, ANCA+. Biopsy shows “onion-skin/pearls” around bile duct which may be collapsed.
The majority of PSC patients also have an inflammatory bowel disease (eg ulcerative colitis)
Liver infarcts are rare, but when they do occur, where are they seen?
What are some causes for intrahepatic vascular obstruction?
Subcapsular.
Cirrhosis, SCD, DIC, and peliosis hepatis (sinusoidal dilation causing blood sequestration).
What are some causes for extrahepatic portal vein obstruction?
Hepatic vein obstruction?
Sepsis, pancreatitis, thrombosis, tumor invasion…
(known as Budd-Chiari** Syndrome**) Polycythemia vera, increased estrogen, HCC.
What is centrilobular hemorrhagic necrosis?
What causes it, and what does it look like?
Ischemic necrosis of the centrilobular (ZONE 3) space.
Main cause is R-sided heart failure, looks like nutmeg liver.
What is sinusoidal obstructive syndrome?
Who develops it, and when?
How is the outlook?
Damaged endothelial cells create thromboemboli resulting in hepatic vein fibrosis.
Post-BM transplant patients (and Jamaican bush tea drinkers…)
Most patients recover spontaneously. 15-30% death.
Who gets FNH?
What does it look like?
Symptoms and outlook?
Young to middle-aged adults, usually female.
Central stellate scar! (and surrounding hyperplasia)
Fullness, discomfort (mass effect only; outlook is good!)
What are macroregenerative nodules?
Are they dangerous?
Very large nodules found in cirrhotic livers.
No risk of malignancy.
Many hepatocellular carcinomas initially develop from dysplastic nodules. Which are high-grade, and which are low-grade?
(Also, match to A/B dysplasia)
High-grade are small-cell (B), large-cell (A) are low-grade and carry less risk of malignant transformation.
What are cavernous hemangiomas, and what problems can they cause?
Very common benign neoplasm of endothelium (blood filled).
Subcapsular; these may rupture (bleeding) or cause pain (if innervated).
Who gets hepatic adenomas?
What risks do they carry?
Women on oral contraceptives.
May rupture (especially in pregnancy), b-catenin+ has risk of malignant transformation.
Describe the epidemiology and 2 subtypes of hepatoblastoma.
Most common malignant liver tumor of childhood.
Epithelial resembles normal liver, mixed (epithelial and mesenchymal) has a worse prognosis.
What are the (Sattar approved!) exposure risk factors for angiosarcoma and cholangiosarcoma?
What is Aflatoxin a risk for?
Angiosarcoma: Vinyl chloride, arsenic, thorotrast
Cholangiosarcoma: Thorotrast
Aflatoxin is a risk factor for hepatocellular carcinoma.
HCC in the US is (more/less) common than in asia and africa, affects (older/younger) patients and is (more/less) associated with cirrhosis.
Less common, older patients, more cirrhosis.
Name 3 major etiologies of HCC.
Is cirrhosis a requirement?
Viral infection, chronic alcoholism, aflatoxins.
No, but it strongly correlates.
Why is vascularization an indication of malignancy?
What vessels is relevant here?
Only malignant tumors promote angiogenesis; HCCs do so to get increased blood supply from the hepatic artery.
What are the key features of HCC?
Major causes of death?
Hepatomegaly, ascites, fever & pain. Alpha-fetoprotein…
Cachexia, bleeding, liver failure, tumor rupture.
How does HCC appear on histology?
“Rosettes”, look almost like secretory acini.
What is the name given to the HCC variant seen in younger patients and is not associated with HBV or cirrhosis?
How is its outlook?
“Fibrolamellar” variant.
Better prognosis.
What is notable about the liver’s blood supply?
It has a dual blood supply. This makes liver infarcation rare.
Portal vein - 60-70%
Hepatic artery - 30-40%
In terms of liver microanatomy:
What is a classic lobule?
What is a portal lobule?
Classic: Unit drained by one central vein
Portal: Unit supplied by one portal triad
