128. Circulatory disorders and tumors of the liver & gall bladder Flashcards
Impaired blood flow into the liver
- hepatic artery obstruction
- cause: embolism, neoplasia, inflammation (ex:
polyarteritis nodosa) - portal vein obstruction
- extrahepatic portal vein, feature: portal HTN, cause:
thrombosis, hypercoagulable state, inflammation,
trauma - intrahepatic portal vein, feature: infract of zahn,
cause: schistosomiasis; acute thrombosis
- extrahepatic portal vein, feature: portal HTN, cause:
Impaired blood flow through the liver
features: necrosis of hepatocytes
cause: cirrhosis, DIC, intrasinusoidal metastasis and eclampsia
hepatic venous outflow obstruction
sinusoidal obstruction syndrome: obstruction of small intrahepatic veins due to thrombosis
- cause: 3 weeks after HSC transplantation,
chemotherapy
- patho: damage to sinusoidal cell –> inflammation –>
congestion
Budd-Chiari syndrome: obstruction of more than 1 hepatic vein –> hepatosplenomegaly, pain, ascites
- cause: thrombosis or hepatocellular carcinoma
- morph: centrilobular congestion and necrosis
Nutmeg liver
centrilobular hemorrhagic necrosis
- right heart failure –> centrilobular congestion (due to retrograde congestion)
- left heart failure –> centrilobular necrosis (due to hypoperfusion and hypoxia)
Benign tumors of liver
focal nodular hyperplasia
-hypoperfused parenchyma collapses to produce septa while
hyperperfused regions undergo hyperplasia
cavernous hemangioma
- benign blood vessel neoplasm
- most common benign liver tumor
hepatocellular adenomas
- benign tumor
- arise from: hepatocytes
- cause: hella sex hormones (oral contraceptives)
- malignant potential: depending on molecular classification
- complications: rupture and bleeding
Malignant carcinomas of liver
Hepatocellular carcinoma
- most common primary malignant tumor in the liver
- risk group: male
- pathogenesis: synergic effect when the following factors are combined
- chronic liver disease is the most common setting for emergence of HCC
- viral infection: HBV and HCV
- toxic injury: alfatoxins and alcohol
- hereditary liver disease (hemochromatosis, alpha-1 AT deficiency, Wilson disease)
- NAFLD
- genetic mutation: HCC is induced by acquiring driver mutations
- driver mutations: Beta-catenin (gain of function due to genomic instability) and p-53 (loss of function,
associated with aflatoxin effect)
- premalignant lesions can give rise to HCC
- hepatic adenoma (carries beta-catenin activating mutations)
- dysplastic nodules ( are found in any stage of chronic liver disease)
- the high grade dysplastic nodules are found to lead to HCC
- metastasis to the lungs
- diagnosis:imaging, serology (alpha-fetoprotein
- clinical features: same as cirrhosis
- complications: cachexia, GI or esophageal varices, liver failure, tumor rupture and bleeding
Cholangiocarcinoma
- second most common
- arise: intra/extrahepatic bile duct epithel (cholangiocytes)
- pathogenesis: chronic inflammation and cholestasis
- liver fluke:
- primary sclerosing cholangitis (associated with ulcerative colitis)
- HBV and HCV
- NAFLD - morph: mucin secreting adenocarcinoma and desmoplastic reaction is dominant
Gall bladder carcinoma
most common malignant tumor of the extrahepatic biliary tract
older women are in the risk group
risk factors: chronic inflammation with gallstones (cholecystitis); primary sclerosing cholangitis