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For instructor materials including Power Points, Answers to Clinical Encounter Questions, please contact userservices@mhprofessional.com.
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LEARNING OBJECTIVES
Upon completion of the chapter, the reader will be able to:
Explain the pathophysiology of cirrhosis and portal hypertension.
Identify signs and symptoms of cirrhosis.
Identify laboratory abnormalities that result from liver disease and describe the associated pathophysiology.
Describe the consequences associated with decreased hepatic function.
Identify treatment goals for a patient with complications of cirrhosis.
Recommend a specific treatment regimen for a patient with cirrhosis that includes lifestyle changes, nonpharmacologic measures, and pharmacologic therapy.
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Cirrhosis involves replacement of normal hepatic architecture with fibrous scar tissue. Scarring is accompanied by loss of viable hepatocytes, which are the functional cells of the liver. Cirrhosis is characterized by progressive damage and deterioration of liver function, but even with extensive scarring some patients remain asymptomatic. 
Advanced cirrhosis is irreversible and leads to portal hypertension, which in turn is responsible for the complications that define decompensated cirrhosis. Complications of cirrhosis include ascites, spontaneous bacterial peritonitis (SBP), hepatic encephalopathy (HE), hepatorenal syndrome (HRS), and variceal bleeding.1 These complications all carry high mortality rates and are signs of disease progression.
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EPIDEMIOLOGY AND ETIOLOGY
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Cirrhosis is the 12th leading cause of death in the United States. It places an enormous economic and social burden on society from hospitalizations, lost wages, decreased productivity, and emotional strain of the disease on both patients and their families.
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Cirrhosis is the result of long-term insult to the liver, and damage usually doesn’t become clinically evident until the fourth decade of life. Infection with one or more strains of viral hepatitis causes acute, potentially reversible hepatic inflammation, whereas chronic infection with hepatitis B (HBV) or C (HCV) can lead to cirrhosis. Alcohol ingestion and HCV are the most common causes of cirrhosis in the United States, whereas HBV accounts for the majority of cases worldwide.2 HCV therapies that provide sustained virologic response (SVR) essentially cure the disease, and are expected to dramatically decrease new cases of cirrhosis. Even patients who have already developed HCV cirrhosis can benefit from antiviral therapy, and recent guidelines recommend treatment for nearly all patients (see Chapter 24, Viral Hepatitis, for more details).3
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Alcoholic cirrhosis usually develops only after decades of heavy drinking. It develops more quickly in women than men, even after taking body weight into account. Estimates vary, but alcoholic cirrhosis can develop after as few as two to three daily drinks in women and three to four drinks in men, although five to eight daily drinks is more typical.4 Differences in metabolism may account for the gender disparity; women metabolize less alcohol in the gastrointestinal (GI) tract, allowing delivery of more ethanol (which is directly hepatotoxic) to the liver.5 Genetic factors also play a role in disease ...