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Portal intrahepatic

Portal hypertension is a consequence of increased resistance to blood flow through the portal vein. Increased resistance is usually due to restructuring of intrahepatic tissue (sinusoidal damage) but may also be caused by presinusoidal damage such as portal vein occlusion from trauma, malignancy, or thrombosis. A third (and the least common) mechanism is outflow obstruction of the hepatic vein. This latter damage is posthepatic, and normal liver structure is maintained. This chapter will focus on portal hypertension caused by intrahepatic damage from cirrhosis. [Pg.324]

Increased intrahepatic resistance to portal flow increases pressure on the entire splanchnic bed an enlarged spleen (splenomegaly) is a common finding in cirrhotic patient and can result in thrombocytopenia due to splenic sequestration of the platelets. Portal hypertension mediates systemic and splanchnic arterial vasodilation through production of nitric oxide and other vasodilators in an attempt to counteract the increased pressure gradient. Nitric oxide causes a fall in systemic arterial pressure unfortunately, this activates both the renin-angiotensin-aldosterone and sympathetic nervous systems and... [Pg.325]

The resulting resistance to blood flow results in portal hypertension and the development of varices and ascites. Hepatocyte loss and intrahepatic shunting of blood results in diminished metabolic and synthetic function, which leads to hepatic encephalopathy (HE) and coagulopathy. [Pg.252]

Aliev MM (1991) Pathogenetic aspects of surgical treatment of intrahepatic blockage of portal blood circulation in children. MD Thesis (in Russian). Moscow, p 45... [Pg.239]

Portal hypertension most commonly occurs as a consequence of chronic liver disease. Portal hypertension Is caused by Increased blood flow within the portal venous system and increased resistance to portal flow within the liver. Splanchnic blood flow is increased in patients with cirrhosis due to low arteriolar resistance that is mediated by increased circulating vasodilators and decreased vascular sensitivity to vasoconstrictors. Intrahepatic vascular resistance is increased in cirrhosis due to fixed fibrosis within the spaces of Disse and hepatic veins as well as reversible vasoconstriction of hepatic sinusoids and venules. Among the consequences of portal hypertension are ascites, hepatic encephalopathy, and the development of portosystemic collaterals—especially gastric or esophageal varices. Varices can rupture, leading to massive upper gastrointestinal bleeding. [Pg.1330]

Liver cirrhosis is among the top 10 causes of death in the Western world. The disease occurs after chronic damage to hepatic cells, mainly hepatocytes, which can be caused by viral hepatitis, chronic alcohol abuse or toxic injury, biliary disease, and metabolic liver disorders [64], Liver cirrhosis is characterized by an abnormal deposition of connective tissue in the liver, which hampers the normal functions of the liver. Other features of the disease are general tissue damage, chronic inflammation, and the conversion of normal liver architecture into structurally abnormal nodules. Secondary to these anatomical changes are disturbances in the liver function and in the hemodynamics leading to portal hypertension and intrahepatic shunting [39, 64, 103],... [Pg.204]

A. Mallat, Hepatic stellate cells and intrahepatic modulation of portal pressure,... [Pg.232]

Stumpel F, Jungermann K (1997) Sensing by intrahepatic muscarinic nerves of a portal-arterial glucose concentration gradient as a signal for insulin-dependent glucose uptake in the perfused rat liver. FEBS Lett 406 119-122... [Pg.490]

Transjugular intrahepatic portosystemic shunt (TIPS) is a side-to-side non-selective portosystemic shunt that is frequently performed in cirrhosis to manage the complications of portal hypertension, such as variceal bleeding. The observation that the bioavailability of oral midazolam was significantly higher in cirrhotic patients with TIPS than in cirrhotic controls and healthy volunteers [57] may be due to reduced intestinal CYP3A activity or reduced contact with CYP3A in the entero-cyte due to increased splanchnic blood flow [57, 92]. [Pg.123]

Canaliculi enter canals of Hering in the portal triad and lead to intrahepatic bile ducts which coalesce to form the hepatic bile duct. The bile duct empties the bile into the gaU bladder which then is released into the duodenum. Bile that is excreted into the small intestine enhances nutrient uptake, protects enterocytes from oxidation, and facilitates excretion of xenobiotics and endogenous waste in the feces (Treinen-Moslen, 2001). [Pg.550]

Complex changes in blood flow occur with liver disease. Resistance to hepatic portal blood flow rises in cirrhosis, and portasystemic and intrahepatic shimts reduce drug delivery to hepatocytes. The pattern of change caused by disease relates to the manner in which the healthy liver treats a drug and there are two general classes ... [Pg.652]

Patients who continue to bleed despite the above measures require surgery (ligation or transection of varices) or placement of a stent between intrahepatic branches of the portal and (systemic) hepatic veins under radiological control. The latter is now the technique of choice for the 10-15% of patients with acute bleeding resistant to conventional treatment, and also for long-term management of patients who are difficult to help by other methods (see below). [Pg.655]

ERASISTRATUS OF KEOS (ca. 300-250 BC) Coined the term "parenchyma (i.e. poured out beside) for liver tissue, based on the belief that it was formed by coagulation of the blood released from the hepatic vessels. For him, however, liver parenchyma was a completely useless structure. He also described for the first time the "choledochos , which he believed absorbed the redundant and rather harmful bile (transported into the liver with the portal vein blood) from the intrahepatic bile ducts, and conducted it away. This separation of bile from blood in the liver was allegedly effected by the different viscosities of the two fluids and the different diameters of the adjacent ( ) intrahepatic bile ducts and blood vessels. Stoppage of the bile flow would lead to jaundice (obstructive icterus ) and inflammation of the liver. He attributed the dropsy commonly associated with liver disease to a hardening of the liver, which he termed "skirros this compressed the intrahepatic vessels, diverting the flow of the watery fluid into the abdomen. Based on this surmise, he rejected the practice of... [Pg.7]

LEONARDO DA VINCI (1452-1519) Can be regarded as the greatest universal genius in the history of mankind. In the field of hepatology, he studied the portal vein system, the intrahepatic vessels and the bile-duct system in an excellent manner. He did not publish his first-rate observations, which therefore remained unknown for a long time. [Pg.9]

Detection of portal hypertension (see chapter 14) is of crucial importance in the diagnosis of cirrhosis. The sensitivity is 76-80% and the specificity 100%. The following findings may be present (7.) dilation of the portal vein (> 1.5 cm), (2.) calibre leap between the extra-and intrahepatic segments of the portal vein in the porta hepatis (so-called portal vein amputation), (3.) dilation of the splenic vein (>1.5 cm), (4.) widening of the hep-... [Pg.130]

Fig. 6.16 HepatocelMar carcinoma (subcostal section) with extended hypoechoic carcinoma (small arrows). Infiltration of the portal vein (intrahepatic) (large arrow) as a pathognomonic sign of liver cell carcinoma (- )... Fig. 6.16 HepatocelMar carcinoma (subcostal section) with extended hypoechoic carcinoma (small arrows). Infiltration of the portal vein (intrahepatic) (large arrow) as a pathognomonic sign of liver cell carcinoma (- )...
Portal veins There are reports on MRI visualization of large intrahepatic portovenous shunts (59), collaterals in the portal vein (92, 115) and VOD staging. (88)... [Pg.178]

Percutaneous splenoportography has lost its importance. Should a direct procedure be indicated, laparoscopic splenoportography is a possible alternative. Recently, a new technique has been described. (134) The percutaneous splenic puncture is performed using a thin needle under screen control, with the needle directed at the splenic hilus. The pressure of the splenic pulp can be measured directly in order to estimate the portal vein pressure. Contrast medium is injected manually or by a special device. From this depot in the red pulp, the splenic vein, the portal vein and the intrahepatic branches of the portal vein are contrasted within a few seconds, (s. fig. 8.12) Complications resulting from percutaneous splenoportography include afterbleeding from the spleen, bilateral rupture of the spleen, arterial aneurysms and a.v. shunts — these complications are serious in nature, but rare. Contraindications for the procedure should be carefully observed, (s. tab. 8.6)... [Pg.181]

Araki, T., Ohtomo, K., Kachi, K., Monzawa, S., Hihara, T., Ohba, H., Ainoda, T., Kumagai, H., Uchiyama, G. Magnetic resonance imaging of macroscopic intrahepatic portal-hepatic venous shunts. Gastrointest. Radiol. 1991 16 221-224... [Pg.188]

Eosinophilic infiltrations in the portal fields generally point to intrahepatic cholestasis. By contrast, ductular changes with bile cylinders, ballooning, acidophilia of the liver cells at the lobular centres, bile infarcts, increase in the copper content, etc. are usually signs of extrahepatic cholestasis, (s. fig. 13.5) (s. tab. 13.10)... [Pg.238]

Non-parenchymatous portal hypertension 1. Prehepatic portal hypertension 2. Intrahepatic portal hypertension ... [Pg.245]


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See also in sourсe #XX -- [ Pg.246 ]




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