Cirrhosis Blog

The liver supports almost every organ in the body and is vital for survival. Because of its strategic location and multidimensional functions, the liver is also prone to many diseases.

The most common include: Infections such as hepatitis A, B, C, E, alcohol damage, fatty liver, cirrhosis, cancer, drug damage (especially acetaminophen (also known as paracetamol) and cancer drugs)

Many diseases of the liver are accompanied by jaundice caused by increased levels of bilirubin in the system. The bilirubin results from the breakup of the Hemoglobin of dead red blood cells; normally, the liver removes bilirubin from the blood and excretes it through bile.

There are also many pediatric liver diseases including biliary atresia, alpha-1 antitrypsin deficiency, alagille syndrome, progressive familial intrahepatic cholestasis, and Langerhans cell histiocytosis, to name but a few.

Diseases that interfere with liver function will lead to derangement of these processes. However, the liver has a great capacity to regenerate and has a large reserve capacity. In most cases, the liver only produces symptoms after extensive damage.

Liver diseases may be diagnosed by liver function tests, for example, by production of acute phase proteins.

The term biliary tree is derived from the arboreal branches of the bile ducts. The bile produced in the liver is collected in bile canaliculi, which merge to form bile ducts. Within the liver, these ducts are called intrahepatic (within the liver) bile ducts, and once they exit the liver they are considered extrahepatic (outside the liver). The intrahepatic ducts eventually drain into the right and left hepatic ducts, which merge to form the common hepatic duct. The cystic duct from the gallbladder joins with the common hepatic duct to form the common bile duct.

Bile can either drain directly into the duodenum via the common bile duct, or be temporarily stored in the gallbladder via the cystic duct. The common bile duct and the pancreatic duct enter the second part of the duodenum together at the ampulla of Vater.

The liver receives a dual blood supply from the hepatic portal vein and hepatic arteries. Supplying approximately 75% of the liver’s blood supply, the hepatic portal vein carries venous blood drained from the spleen, gastrointestinal tract, and its associated organs. The hepatic arteries supply arterial blood to the liver, accounting for the remainder of its blood flow. Oxygen is provided from both sources; approximately half of the liver’s oxygen demand is met by the hepatic portal vein, and half is met by the hepatic arteries.
Blood flows through the sinusoids and empties into the central vein of each lobule. The central veins coalesce into hepatic veins, which leave the liver and empty into the inferior vena cava.

Amitrano L, Guardascione MA, Ames PR.
Gastroenterology Unit, A. Cardarelli Hospital, Naples, Italy. luamitra@tin.it

The liver has a central role in the clotting process and an altered haemostasis is common in advanced liver disease. Nevertheless, recent studies have questioned the historical belief that impaired haemostasis in liver disease means an increased risk of bleeding.
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Coagulation and anticoagulation mechanisms are still balanced but are set at a lower level. Platelet function and number also play a role. The prevalence of thrombotic events is similar in both cirrhotic patients and in the general population but the cirrhotic patients have an increased risk for thrombosis in the splanchnic area. Portal blood flow stasis is the main underlying change favouring thrombosis even if other local, systemic, congenital and acquired factors are present. The onset of portal vein thrombosis strongly affects the prognosis of liver cirrhosis, worsening both portal hypertension and liver function. Some of the known risk factors for venous thrombosis–G20210A mutation of prothrombin, factor V Leiden, endoscopic treatment of esophageal varices and abdominal surgery–have a specific role in the development of splanchnic thrombosis in cirrhotic patients. The knowledge of the pathophysiological aspects of portal vein thrombosis and clotting alterations in liver disease will allow determination of the indication, duration and timing of anticoagulation therapy.