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Source: Sease JM. Portal Hypertension and Cirrhosis. In: DiPiro JT, Talbert RL, Yee GR, Wells BG, Posey LM. Pharmacotherapy: A Pathophysiologic Approach. 8th edition. http://accesspharmacy.com/content.aspx?aid=7979093. Accessed April 27, 2012.

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  • Diffuse injury to liver characterized by destruction of hepatocytes and their replacement by fibrous tissue.

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  • Most common causes are excessive alcohol intake and chronic viral hepatitis (types B and C, Table 1).

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Table Graphic Jump Location
Table 1. Etiology of Cirrhosis
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  • Elevation of portal blood pressure because of fibrotic changes within hepatic sinusoids, changes in levels of vasodilatory and vasoconstrictor mediators, and increase in blood flow to splanchnic vasculature.
  • Resistance to blood flow contributes to portal hypertension and the development of varices, ascites, hepatic encephalopathy (HE), and coagulopathy.
  • Portal hypertension characterized by:
    • Hypervolemia
    • Increased cardiac index
    • Hypotension
    • Decreased systemic vascular resistance

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  • Ranges from asymptomatic, with abnormal laboratory or radiographic tests, to decompensated with ascites, spontaneous bacterial peritonitis, HE, or variceal bleeding.

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Signs and Symptoms

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  • Anorexia
  • Malaise
  • Weight loss
  • Pruritus
  • Jaundice
  • Palmar erythema
  • Spider angiomata
  • Hyperpigmentation
  • Hepatomegaly
  • Splenomegaly
  • Ascites
  • Edema
  • Pleural effusion
  • Respiratory difficulties
  • Coagulopathy
  • Mental status changes

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Means of Confirmation and Diagnosis

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Laboratory Tests

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  • No laboratory or radiographic tests of hepatic function can accurately diagnose cirrhosis.
  • Routine liver function tests include alkaline phosphatase, bilirubin, aspartate transaminase (AST), alanine aminotransferase (ALT), and γ-glutamyl transpeptidase (GGT).
  • Albumin and prothrombin time (PT)
  • Complete blood count (CBC): Thrombocytopenia relatively common feature in chronic liver disease; found in 15–70% of cirrhotic patients.

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  • Clinical improvement or resolution of acute complications
    • Resolution of hemodynamic instability
  • Prevention of complications
    • Adequate lowering of portal pressure with medical therapy
    • Support of abstinence from alcohol

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  • Identify and eliminate causes of cirrhosis (e.g., alcohol abuse).
  • Assess risk for variceal bleeding and begin pharmacologic prophylaxis where indicated, reserving endoscopic therapy for high-risk patients or acute bleeding episodes.
  • Evaluate for clinical signs of ascites and manage with pharmacologic treatment (e.g., diuretics) and paracentesis. Careful monitoring for spontaneous bacterial peritonitis (SBP) in patients with ascites who undergo acute deterioration.
  • HE is common complication of cirrhosis and requires clinical vigilance and treatment with dietary ...

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