Cirrhosis is a diffuse injury to the liver characterized by fibrosis and a conversion of the normal hepatic architecture into structurally abnormal nodules. The end result is destruction of hepatocytes and their replacement by fibrous tissue.
The resulting resistance to blood flow results in portal hypertension and the development of varices and ascites. Hepatocyte loss and intrahepatic shunting of blood result in diminished metabolic and synthetic function, which leads to hepatic encephalopathy (HE) and coagulopathy.
Cirrhosis has many causes (Table 21–1). In the United States, excessive alcohol intake and chronic viral hepatitis (types B and C) are the most common causes.
Cirrhosis results in elevation of portal blood pressure because of fibrotic changes within the hepatic sinusoids, changes in the levels of vasodilatory and vasoconstrictor mediators, and an increase in blood flow to the splanchnic vasculature. The pathophysiologic abnormalities that cause it result in the commonly encountered problems of ascites, portal hypertension and esophageal varices, HE, and coagulation disorders.
Portal hypertension is noted by elevated pressure gradient between the portal and central venous pressure and is characterized by hypervolemia, increased cardiac index, hypotension, and decreased systemic vascular resistance.
Ascites is the pathologic accumulation of fluid within the peritoneal cavity. It is one of the earliest and most common presentations of cirrhosis.
The development of ascites is related to systemic arterial vasodilation mediated by nitric oxide that leads to the activation of the baroreceptors in the kidney and an activation of the renin–angiotensin–aldosterone system, activation of the sympathetic nervous system, and release of antidiuretic hormone in response to the arterial hypotension. These changes cause sodium and water retention.
TABLE 21–1Etiology of Cirrhosis |Favorite Table|Download (.pdf) TABLE 21–1 Etiology of Cirrhosis
Chronic alcohol consumption
Chronic viral hepatitis (types B and C)
Metabolic liver disease
Nonalcoholic steatohepatitis (“fatty liver”)
Primary biliary cirrhosis
Isoniazid, methyldopa, amiodarone, amoxicillin-clavulanate, nitrofurantoin, diclofenac, methotrexate, nevirapine, propylthiouracil, valproate
PORTAL HYPERTENSION AND VARICES
The most important sequelae of portal hypertension are the development of varices and alternative routes of blood flow resulting in acute variceal bleeding. Portal hypertension is defined by the presence of a gradient of greater than 5 mm Hg (0.7 kPa) between the portal and central venous pressures.
Progression to bleeding can be predicted by Child-Pugh score, size of varices, and the presence of red wale markings on the varices. First variceal hemorrhage occurs at an annual rate of about 15% and carries a mortality of 7% to 15%.
Hepatic encephalopathy (HE) is a metabolically induced functional disturbance of the brain that is potentially reversible.
The symptoms of HE are thought to result from an accumulation of gut-derived nitrogenous substances in the systemic circulation as a consequence of shunting through portosystemic collaterals ...
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