Upon completion of the chapter, the reader will be able to:
Explain the pathophysiology of cirrhosis and portal hypertension.
Identify signs and symptoms of liver disease in a given patient.
Identify laboratory abnormalities that result from liver disease and describe the pathophysiology of each abnormality.
Describe the consequences associated with decreased hepatic function.
Create treatment goals for a patient with portal hypertension and its complications.
Evaluate patient history and physical examination findings to determine the etiology of cirrhosis.
Recommend a specific treatment regimen for a patient with cirrhosis that includes lifestyle changes, nonpharmacologic therapy, and pharmacologic therapy.
Cirrhosis involves replacement of normal hepatic cells with fibrous scar tissue and progressive deterioration of liver function. Scarring is accompanied by loss of viable hepatocytes, the functional cells of the liver. KEY CONCEPT Cirrhosis is irreversible and leads to portal hypertension, which in turn is responsible for the complications of advanced liver disease. Complications of cirrhosis include ascites, spontaneous bacterial peritonitis (SBP), hepatic encephalopathy (HE), hepatorenal syndrome (HRS), and variceal bleeding.1 These complications carry high mortality rates and are associated with disease progression.
EPIDEMIOLOGY AND ETIOLOGY
Cirrhosis is the 12th leading cause of death in the United States. It also 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.
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. Alcohol ingestion and viral hepatitis C infection are the most common causes of cirrhosis in the United States, whereas hepatitis B accounts for the majority of cases worldwide.2
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.3 Differences in metabolism may account for this gender disparity; women metabolize less alcohol in the gastrointestinal (GI) tract, allowing delivery of more ethanol (which is directly hepatotoxic) to the liver.4 Genetic factors also play a role in disease progression; some patients develop cirrhosis with much less cumulative alcohol intake than is typical (either fewer drinks per day or faster disease onset), but others with much greater intake never develop cirrhosis.
Infection with one or more strains of viral hepatitis causes acute, potentially reversible, hepatic inflammation, whereas chronic infection with hepatitis B or C can lead to cirrhosis. Both hepatitis B and C infections are transmitted through IV drug use, but sexual contact is the more common route of hepatitis B transmission.5 See ...