Pathoma: Liver Cirrhosis and Tumors Flashcards
The classic description of cirrhosis on histologic exam is ________________.
broad bands of fibrosis with regenerative nodules in between
Fibrosis in the liver is mediated by which cell type?
The stellate cells –also called Ito cells –that secrete TGFbeta
What is hypersplenism?
Congestion of the spleen (from ascites) can lead to an overactive spleen that destroys more RBCs than it should.
The liver plays a key role in removing __________ from the blood. As such, liver disease can lead to gynecomastia, palmar erythema, and spider angiomata from too much of this substance.
estrogen
What pathologic changes will you see in someone with fatty liver disease?
A heavy, greasy liver
_____________ can lead to acute hepatitis from excess acetaldehyde.
Binge drinking
What can cause accumulation of pink/red inclusions in hepatocytes? What are these?
Acute binge drinking (the stem describes Mallory bodies, also called acidophilic bodies); these are damaged intermediate filaments
What presentation is characteristic of acute hepatitis from alcohol?
Painful hepatomegaly with AST greater than ALT
True or false: all alcohols will eventually develop cirrhosis.
False. Only about 20%
How would you diagnose NASH?
Non-alcoholic steatohepatitis resembles alcohol-induced liver disease, but it occurs in the absence of drinking. It is more common in obese people, and ALT will be greater than AST.
Differentiate hemochromatosis and hemosiderosis.
Hemosiderosis is the deposition of iron in tissues, and hemochromatosis is the symptomatic presentation of the disease.
What is the most common genetic cause of primary hemochromatosis?
C282Y defect in the HFE gene –resulting in increased iron absorption from the duodenum
What normally regulates iron absorption? How is this disrupted in hemochromatosis?
Enterocytes normally absorb all the iron in the gut and hold it within their cytoplasm; they use HFE to detect when the blood iron level drops, and then they release iron into the blood. Defective HFE thus leads to all the iron being absorbed.
What is the classic triad of hemochromatosis? When does this usually present?
Cirrhosis, secondary diabetes, and bronze skin
Late adulthood
What lab findings are indicative of iron overload?
Increased ferritin
Decreased TIBC
Increased serum iron
Increased iron saturation
What is lipofuscin? How can you distinguish between this and iron?
A “wear-and-tear protein” within hepatocytes from peroxidized lipids; the Prussian blue stain
What genetic cause is most often implicated in Wilson’s disease?
Defect in the ATP7B gene that pumps iron into bile
What liver disease can present with Parkinson’s or chorea?
Wilson’s
Three non-genetic tests can help diagnose Wilson’s disease: _______________.
(1) increased urinary copper, (2) decreased serum ceruloplasmin, and (3) copper deposition in a liver biopsy
________________ presents as granulomatous destruction of intrahepatic bile ducts.
Primary biliary cholangitis
True or false: primary sclerosing cholangitis only affects the extrahepatic bile ducts.
False. It affects both the intrahepatic and extrahepatic bile ducts.
What lab value is often positive in those with PSC?
p-ANCA (just like UC!)
What cellular dysfunction is involved in Reye syndrome?
Mitochondrial damage
What is the classic presentation of a child with Reye syndrome?
Nausea and vomiting
Hypoglycemia
Elevated liver enzymes
What liver neoplasm is associated with OCP use?
Hepatocellular adenoma
Three big risk factors are associated with increased risk of hepatocellular carcinoma: __________________.
(1) chronic hepatitis
(2) cirrhosis
(3) aflatoxins from Aspergillus
True or false: Budd-Chiari presents with thrombosis in the portal vein.
False. It is the hepatic vein.
HCC presents with elevation of what serum marker?
Alpha-fetoprotein