Portal hypertension arises when there is diminished flow through the portal venous system, which may occur because of obstruction at the prehepatic, intrahepatic, or posthepatic level. While it can occur in acute live failure, portal hypertension is more commonly seen with chronic liver failure and is discussed later. In acute liver failure, the obstruction is usually intrahepatic and the major clinical consequences are ascites and hepatic encephalopathy. In chronic liver disease, portal hypertension develops over months to years, and its effects are more complex and widespread (see later).
• Hepatorenal syndrome is a form of renal failure occurring in individuals with liver failure in whom there are no intrinsic morphologic or functional causes for kidney dysfunction. Sodium retention, impaired free-water excretion, and decreased renal perfusion and glomerular filtration rate are the main renal functional abnormalities. There is decreased renal perfusion pressure due to systemic vasodilation, activation of the renal sympathetic nervous system and vasoconstriction of the afferent renal arterioles, and increased activation of the renin-angiotensin axis, causing vasoconstriction that further decreases glomerular filtration. The syndrome’s onset begins with a decrease in urine output and rising blood urea nitrogen and creatinine levels.
Cirrhosis is the morphologic change most often associated with chronic liver disease; it refers to the diffuse transformation of the liver into regenerative parenchymal nodules surrounded by fibrous bands (
Fig. 16.5 ). The leading causes of chronic liver failure worldwide include chronic hepatitis B, chronic hepatitis C, non-alcoholic fatty liver disease (NAFLD), and alcoholic liver disease. While cirrhosis is a common feature of a number of chronic liver diseases, it is not a specific entity, and it is important to recognize that not all chronic liver disease terminates in cirrhosis, and that not all cirrhosis leads to end-stage liver disease. For example, chronic biliary tract diseases often do not give rise to cirrhosis even at end stage, whereas patients with treated autoimmune hepatitis or cured hepatitis C may have adequate liver function in the face of cirrhosis. Even in diseases that are likely to give rise to cirrhosis, such as untreated viral hepatitis, alcoholic liver disease, NAFLD, and metabolic diseases, the morphology and pathophysiology of cirrhosis in each may be different.
Fig. 16.5 Cirrhosisresultingfromchronicviralhepatitis.Notethebroadscarsseparatingbulgingregenerativenodulesovertheliversurface.
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MORPHOLOGYLiverfailureinchronic liverdiseaseismostoftenassociatedwithcirrhosis,whichismarkedbythediffusetransformationoftheentireliverintoregenerative parenchymal nodules surrounded by fibrous bands.Thenodularnatureoftheprocessisreadilyevidentbothgrossly(
Fig.16.5
Fig.16.6,A ).Thesizeofthenodules,thepatternofscarring(linkingofportaltractstoeachothervs.linkingofportaltractstocentralveins),thedegreeofparenchymalloss,andthefrequencyofvascularthrombosis(particularlyoftheportalvein)allvarybetweendiseasesandeven,insomecases,betweenindividualswiththesamedisease.
Asmentionedearlier,stemcellactivationanddifferentiationgivesrisetoduct-likestructures,thesocalledductularreactions.In chronic liver disease, ductular reactions increase with disease progression and are usually most prominent in cirrhosis. Ductularreactionsmayincitesomeofthescarringinchronicliverdiseaseandthusmayhaveanegativeeffectonprogressiveliverdisease.