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Upon completion of the chapter, the reader will be able to:

  1. Explain the pathophysiology of cirrhosis and portal hypertension.

  2. Outline the progression of liver damage from excessive alcohol intake.

  3. Identify signs and symptoms of liver disease in a given patient.

  4. Identify laboratory abnormalities that result from liver disease and describe the pathophysiology of each abnormality.

  5. Describe the consequences associated with decreased hepatic function.

  6. Create treatment goals for a patient with portal hypertension and its complications.

  7. Evaluate patient history and physical examination findings to determine the etiology of cirrhosis.

  8. Recommend a specific treatment regimen for a patient with cirrhosis that includes lifestyle changes, nonpharmacologic therapy, and pharmacologic therapy.




  • Image not available. Portal hypertension is the precipitating factor for many of the complications of cirrhosis. Lowering portal pressure can reduce the complications of cirrhosis and decrease morbidity and mortality.

  • Image not available. Chronic excessive ethanol intake causes progressive liver damage primarily because both ethanol and its metabolic products are direct hepatotoxins.

  • Image not available. Cirrhosis is irreversible; treatments are directed at limiting disease progression and minimizing complications.

  • Image not available. Nonselective β-blockers are first-line treatment for preventing variceal bleeding; they vasoconstrict the splanchnic bed through multiple mechanisms.

  • Image not available. The goals of treating ascites are to minimize acute discomfort, reequilibrate ascitic fluid, and prevent spontaneous bacterial peritonitis (SBP). Treatment should modify the underlying disease pathology; without directed therapy, fluid will rapidly reaccumulate.

  • Image not available. Cirrhosis is a high aldosterone state; spironolactone is a direct aldosterone antagonist and the primary treatment for ascites.

  • Image not available. Acute variceal hemorrhage is an emergency. It is crucial to control bleeding, decrease risk of rebleeding, and prevent SBP.

  • Image not available. Long-term antibiotic prophylaxis for SBP decreases mortality in patients with a history of SBP or low-protein ascites plus one of the following: serum creatinine (SCr) 1.5 mg/dL (133 μmol/L) or greater, blood urea nitrogen (BUN) 25 mg/dL (8.9 mmol/L) or greater, serum sodium 130 mEq/L (130 mmol/L) or less, or Child–Pugh score of at least 9, with bilirubin of at least 3 mg/dL (51.3 μmol/L).

  • Image not available. Lactulose is the foundation of pharmacotherapy to prevent and treat hepatic encephalopathy (HE). It binds ammonia in its ionic form in the gut and facilitates its excretion.




Cirrhosis is the progressive replacement of normal hepatic cells with fibrous scar tissue. This scarring is accompanied by the loss of viable hepatocytes, which are the functional cells of the liver. Image not available. Cirrhosis is irreversible and leads to portal hypertension, which is in turn responsible for many of the complications of advanced liver disease. Cirrhotic complications include (but are not limited to) ascites, spontaneous bacterial peritonitis (SBP), hepatic encephalopathy (HE), hepatorenal syndrome (HRS), and variceal bleeding.1




Cirrhosis is the result of long-term insult to the liver; damage is typically not evident clinically until the fourth decade of life. Chronic liver disease and cirrhosis combined were the 12th leading cause of death in the United States in ...

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