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CHAPTER SUMMARY FROM THE PHARMACOTHERAPY HANDBOOK

For the chapter in the Wells Handbook, please go to Chapter 21. Cirrhosis and Portal Hypertension.

KEY CONCEPTS

KEY CONCEPTS

  • Image not available. Cirrhosis is a severe, chronic, irreversible disease associated with significant morbidity and mortality. However, the progression of cirrhosis secondary to alcohol abuse can be interrupted by abstinence. It is therefore imperative for the clinician to educate and support abstinence from alcohol as part of the overall treatment strategy of the underlying liver disease.

  • Image not available. Patients with cirrhosis should receive endoscopic screening for varices, and certain patients with varices should receive primary prophylaxis with nonselective β-adrenergic blockade therapy to prevent variceal hemorrhage.

  • Image not available. When nonselective β-adrenergic blocker therapy is used to prevent rebleeding, therapy can be titrated to achieve a goal heart rate of 55 to 60 beats/min or the maximal tolerated dose.

  • Image not available. Octreotide is the preferred vasoactive agent for the medical management of variceal bleeding. Endoscopic band ligation is the primary therapeutic tool for the management of acute variceal bleeding.

  • Image not available. The combination of spironolactone and furosemide is the recommended initial diuretic therapy for patients with ascites.

  • Image not available. All patients who have survived an episode of spontaneous bacterial peritonitis (SBP) should receive long-term antibiotic prophylaxis.

  • Image not available. The mainstay of therapy of hepatic encephalopathy (HE) involves therapy to lower blood ammonia concentrations and includes diet therapy, lactulose, and antibiotics alone or in combination with lactulose.

Chronic liver injury causes damage to normal liver tissue resulting in the development of regenerative nodules surrounded by fibrous bands.1 Cirrhosis is an advanced stage of liver fibrosis that leads to shunting of the portal and arterial blood supply directly into hepatic outflow through the central veins with compromised exchange between hepatic sinusoids and hepatocytes. Clinical consequences of cirrhosis include impaired hepatocyte function, the increased intrahepatic resistance of portal hypertension, and hepatocellular carcinoma. Circulatory irregularities, such as splanchnic vasodilation, vasoconstriction and hypoperfusion of the kidneys, water and salt retention, and increased cardiac output, also occur. The word cirrhosis is derived from the Greek kirrhos, meaning orange-yellow, and refers to the color of the cirrhotic liver as seen on autopsy or during surgery.2

Image not available. While cirrhosis has many causes (Table 37-1), in the Western world, excessive alcohol intake and hepatitis C are the most common causes.1,3 Nonalcoholic steatohepatitis is also an important cause of cirrhosis in the end diagnosis of cirrhosis without an apparent cause occurs infrequently today.1 This chapter elucidates the pathophysiology of cirrhosis and the resultant effects on human anatomy and physiology. Treatment strategies for managing the most commonly encountered clinical complications of cirrhosis are discussed.

TABLE 37-1Etiology of Cirrhosis

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