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The exact cause is not always known, but it may occur in patients with a long and mobile colon (dolichocolon), chronic lung disease such as emphysema, or liver problems such as cirrhosis and ascites. Chilaiditi's sign is generally not associated with symptoms, and is most commonly an incidental finding in normal individuals.
The dense MCA sign may be the first and only sign of MCA occlusion within the first 1–2 hours of symptom onset, even before parenchymal hypodensity develops. Early recognition enables rapid initiation of treatment, such as intravenous thrombolysis (e.g., tissue plasminogen activator, tPA) or endovascular thrombectomy. [4]
The hepatopulmonary syndrome results from the formation of microscopic intrapulmonary arteriovenous dilatations in patients with both chronic, and far less commonly acute liver failure. The mechanism is unknown but is thought to be due to increased liver production or decreased liver clearance of vasodilators, possibly involving nitric oxide. [1]
The treatment of hepatic encephalopathy depends on the suspected underlying cause (types A, B, or C) and the presence or absence of underlying causes. If encephalopathy develops in acute liver failure (type A), even in a mild form (grade 1–2), it indicates that a liver transplant may be required, and transfer to a specialist centre is advised ...
No single mechanism leading to steatosis exists; rather, a varied multitude of pathologies disrupt normal lipid movement through the cell and cause accumulation. [7] These mechanisms can be separated based on whether they ultimately cause an oversupply of lipid which can not be removed quickly enough (i.e., too much in), or whether they cause a failure in lipid breakdown (i.e., not enough used).
In the majority of acute liver failure (ALF) there is widespread hepatocellular necrosis beginning in the centrizonal distribution and progressing towards portal tracts. The degree of parenchymal inflammation is variable and is proportional to duration of disease. [7] [20] [21] Zone 1 (periportal) occurs in phosphorus poisoning or eclampsia.
Two morphologic patterns of hepatic peliosis were described by Yanoff and Rawson. [14] In the phlebectatic type, the blood-filled spaces are lined with endothelium and are associated with aneurysmal dilatation of the central vein; in the parenchymal type, the spaces have no endothelial lining and they usually are associated with haemorrhagic ...
Symptoms are typically related to the brain and liver. Liver-related symptoms include vomiting, weakness, fluid build-up in the abdomen, swelling of the legs, yellowish skin, and itchiness. Brain-related symptoms include tremors, muscle stiffness, trouble in speaking, personality changes, anxiety, and psychosis. [1]