Liver mass pathophysiology

Liver Mass Microchapters
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Iqra Qamar M.D.[2]

Gross Pathology

	Pathogeneis	Genetics	Associated conditions	Gross Pathology	Microscopic Pathology
Hepatocellular adenoma	Estrogens cause the transformation of hepatocytes via steroid receptors Results in generalized vascular ectasia	Transcription factor 1 gene (TCF1) Interleukin 6 signal transducer gene (IL6ST) β catenin-1 gene (CTNNB1)	Glycogen storage disease types Ia and III Fanconi anemia Thalassemia Familial adenomatous polyposis Familial diabetes mellitus Hurler disease Galactosemia	Well circumscribed Nonlobulated Smooth and soft White to yellow to brown lesions	Cords of hepatocytes that have a high glycogen and fat content Lack of normal hepatic parenchymal architecture Absence of portal tracts and hepatic veins
Focal nodular hyperplasia	Develop around a preexisting arterial malformation Hyperplastic growth response to parenchymal blood flow	β-catenin gene (CTNNB1) TP53 APC or HNF1α	Klippel-Trénaunay-Weber syndrome	Well-circumscribed Non-encapsulated Central fibrous scar	Hepatic parenchyma arranged in incomplete nodules Fibrous tissue with thick-walled vessels Bile ductular proliferation Cells of chronic inflammation
Intrahepatic bileduct cystadenoma
Hemangioma	Congenital disorder Vascular malformations that enlarge by ectasia  Estrogen and progesterone influence over tumor growth More common in females		Von Hippel Lindau disease	Well-circumscribed Appear red-brown Solitary nodules Less than 5cms	Large cystically dilated vessels Thin walls Intravascular thrombosis Calcifications
Lymphangioma
Lymphangiomatosis
Angiomyolipoma
Infantile Hemangioma
HCC
Cholangiocarcinoma
Hepatic abscess
Parasitic cysts