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Titlebook: Vascular Disorders of the Liver; VALDIG‘s Guide to Ma Dominique Valla,Juan Carlos Garcia-Pagan,Pierre-Em Book 2022 Springer Nature Switzerl

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41#
發(fā)表于 2025-3-28 14:41:21 | 只看該作者
42#
發(fā)表于 2025-3-28 18:44:09 | 只看該作者
43#
發(fā)表于 2025-3-28 23:08:52 | 只看該作者
Budd-Chiari Syndrome: Hepatic Venous Outflow Tract Obstructionll hepatic veins to the junction of the inferior vena cava and the right atrium..Underlying disorders including hereditary and acquired hypercoagulable states can be found in about 75% of patients with BCS, being most frequently myeloproliferative neoplasms..Obstruction of the hepatic venous outflow
44#
發(fā)表于 2025-3-29 04:02:28 | 只看該作者
Extrahepatic Portal Vein Obstruction: Recent Portal Vein Thrombosis and Portal Cavernoma in the Absec or splenic veins, the obstruction being complete or partial. This chapter will focus on EHPVO, unrelated to a malignant invasion (and thus corresponding to thrombosis) in the absence of cirrhosis. After a recent occlusion of the portal venous lumen, a network of porto-portal collaterals develop wh
45#
發(fā)表于 2025-3-29 10:29:05 | 只看該作者
46#
發(fā)表于 2025-3-29 14:47:20 | 只看該作者
Porto-Sinusoidal Vascular Disorderhe portal venules and sinusoid, with or without signs of portal hypertension. This group of entities was previously known largely as idiopathic non-cirrhotic portal hypertension. Liver histopathology is fundamental for diagnosis. Specific histopathologic findings include nodular regenerative hyperpl
47#
發(fā)表于 2025-3-29 18:55:32 | 只看該作者
Sinusoidal Obstruction Syndrome/Hepatic Veno-Occlusive Diseasefter myeloablative hematopoietic cell transplantation (5–10% of adults and 20–30% of children post-transplant) or high-dose chemotherapy. Damage to the sinusoidal endothelial cells and hepatocytes and ensuing hemodynamic events combine to cause progressive post-sinusoidal portal hypertension, worsen
48#
發(fā)表于 2025-3-29 20:24:39 | 只看該作者
49#
發(fā)表于 2025-3-30 03:49:44 | 只看該作者
50#
發(fā)表于 2025-3-30 07:45:51 | 只看該作者
Congestive Cardiac Hepatopathyhypertension and decreased cardiac output. In most adults with chronic heart failure, liver biochemical test abnormalities are usually the only alterations found. However, among patients with complex congenital cardiac defects who have undergone palliative procedures such as Fontan surgery, severe h
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