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Liver, Biliary Tract and Pancreatic Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Budd–Chiari syndrome results from thrombosis of the hepatic veins. Causes include hypercoagulable states (polycythaemia, protein C or S deficiency, lupus anticoagulant, factor V Leiden mutation, malignancy, cysts, congenital webs, trauma, drugs (especially oral contraceptives) and idiopathic mechanisms.
Systemic Veins of the Thorax.
Published in Fred W Wright, Radiology of the Chest and Related Conditions, 2022
The Budd-Chiari syndrome is a rare disorder of the hepatic veins, or impaired hepatic venous drainage due to anomalies of the IVC. There are two types: Primary due to congenital obstruction of the hepatic veins or hepatic portion of the IVC by webs or diaphragms, andSecondary due to tumour (especially a hepatoma), thrombosis or trauma.
Answers
Published in Samar Razaq, Difficult Cases in Primary Care, 2021
Alagille’s syndrome is an autosomal dominant disorder in which there is paucity of the intrahepatic bile ducts. The resultant chronic cholestasis causes jaundice, pruritis and hypercholesterolemia. Dysmorphic faces, cardiac anomalies, vertebral anomalies, failure to thrive and developmental delay are features of the syndrome. Budd–Chiari’s syndrome is a rare condition in which there is obstruction of the hepatic veins. Gilbert’s syndrome is a usually harmless condition in which reduced levels of a particular enzyme (uridine-diphosphate glucuronosyltransferase) in the liver results in slightly raised serum bilirubin levels. Criggler–Najjar’s syndrome is a rare disorder in which a defective enzyme results in defective breakdown of bile, causing its levels to rise.
Indications and methods for measuring portal hypertension in cirrhosis
Published in Scandinavian Journal of Gastroenterology, 2022
Helle Kristensen, Nina Kimer, Søren Møller
Measuring HVPG is performed in local anesthesia where for example a Swan-Ganz balloon catheter is placed within the liver through the internal jugular, the femoral or the brachial veins. The hepatic vein is catheterized under x-ray control, visualizing the anatomic placement by infusing contrast. The catheter is connected to a pressure monitor and the FVHP is measured within the liver vein. By insufflation a balloon occluding the liver vein, the WHVP can be measured. When the hepatic vein is occluded the hepatic venous outflow is blocked it forms a continuous column of fluid between the catheter and the sinusoids equal to the sinusoidal pressure and the WHVP (see Figure 2). The connections between the sinusoids are decreased in cirrhosis, meaning there will be no dissipation of the pressure, and the static column of blood in the hepatic vein where the catheter is placed, extends all the way to the portal vein [38].
Cirrhosis and partial portal thrombosis leading to severe variceal bleeding, an unusual presentation of sarcoidosis
Published in Acta Clinica Belgica, 2022
Marco Moretti, Pierre Lefesvre, Joop Jonckheer
It has been hypothesized that several mechanisms may increase intrahepatic resistances and could lead to portal hypertension. Maddrey et al. hypothesized that primary vascular injury drives to portal hypertension and sequentially to cirrhosis without affection of the bile ducts [4]. Arterial-venous shunts within hepatic granulomas may increase the portal blood flow. Modification and/or destruction of hepatic sinusoids due to granulomas may augment hepatic flow resistances. Moreover, thrombosis of portal and hepatic veins may cause respectively hepatic ischemia and congestion, with the rise of blood flow resistances [3,4]. However, there is disagreement on whether hepatic sarcoidosis might cause progressive destruction of the bile ducts, through the portal and periportal granulomas, and might evolve in biliary cirrhosis [5]. Considering this last speculation, the presence of suppurative bile duct destruction could help to differentiate between sarcoidosis and primary biliary cholangitis (PBC). However, in our opinion, it would still be arduous to differentiate between the two. Further studies are needed to better understand the mechanism causing portal hypertension in sarcoidosis.
Variations in the vascular and biliary structures of the liver: a comprehensive anatomical study
Published in Acta Chirurgica Belgica, 2018
Burak Veli Ülger, Eyüp Savaş Hatipoğlu, Özgür Ertuğrul, Mehmet Cudi Tuncer, Cihan Akgül Özmen, Mesut Gül
Blood is supplied to the liver by the proper hepatic artery and drained from the liver by the hepatic portal vein. Other hepatic veins also provide venous drainage. The branches of the proper hepatic artery, hepatic portal vein, and common hepatic duct constitute the portal triad. The right portal triad exhibits a short course (1–1.5 cm) before entering the porta hepatis (a deep fissure on the inferior surface of the liver through which all neurovascular structures—except the hepatic veins—and the hepatic ducts enter or exit the liver). After entering the right lobe, the portal triad divides into anterior and posterior branches that supply the paramedian (V and VIII) and the lateral (VI and VII) segments [4]. The left portal triad continues to the top of the hepatoduodenal ligament and then moves 3–4 cm to the left to run under the quadrate lobe. The triad then turns forward, accessing segments II, III, and IV from the ligamentum venosum fissure [5,6]. The caudate lobe has a left portion of fixed size and a right portion that varies individually in size. Both the right and left portal triads drain blood from the caudate lobe and also drain bile. The caudate process, which is on the right, delivers venous blood to branches from the fork of the hepatic portal vein and the right branch of that vein; the left part of the caudate lobe delivers blood only to the left branch of the hepatic portal vein. The combined venous blood from the caudate lobe drains into the inferior vena cava via a single vein [7].