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Pathology - Cirrhosis
Definition • Irreversible substitution of normal liver structure with fibrous tissue bands that segregate nodules of regenerating hepatocytes.
Epidemiology • Prevalent and rising in frequency attributable to alcohol consumption and obesity.
Aetiology
Alcohol, chronic viral hepatitis, and non-alcoholic fatty liver disease (NAFLD) are the predominant etiological factors. • Less frequently, primary biliary cholangitis (PBC), primary sclerosing cholangitis (PSC), autoimmune hepatitis (AIH), Wilson's disease, and hemochromatosis. • In certain instances, the etiology remains ambiguous (cryptogenic cirrhosis).
Pathogenesis
Persistent liver damage prompts Kupffer cells within the vascular sinusoids to secrete cytokines that activate hepatic stellate (Ito) cells. Activated stellate cells undergo proliferation and release substantial amounts of thick collagen, resulting in permanent liver fibrosis and hepatocyte depletion. Cirrhosis induces several functional impairments: diminished synthesis of coagulation factors; decreased glycogen reserves; impaired clearance of pathogens by Kupffer cells; portal hypertension accompanied by hypersplenism and esophageal varices; splanchnic vasodilation; reduced renal blood flow; secondary hyperaldosteronism; and ascites.
Presentation • Atypical symptoms of fatigue and general discomfort. Clinical examination typically reveals signs of chronic liver disease, and liver function tests are generally abnormal. Patients frequently exhibit complications associated with cirrhosis, such as upper gastrointestinal hemorrhage.
Macroscopy • The liver may present as normal in size, hypertrophied, or atrophied. • The sliced surface exhibits a firm texture and displays diffuse nodularity.
Histopathology • The liver is entirely substituted by nodules of regenerating hepatocytes encircled by fibrous bands. • The fibrous bands exhibit a heterogeneous inflammatory infiltrate and reactive bile ductular proliferation. • In certain instances, the characteristics may indicate a specific cause.
Prognosis • Generally unfavorable, with a substantial risk of considerable complications including infections (notably bacterial peritonitis), upper gastrointestinal hemorrhage, renal failure, and hepatocellular cancer.The emergence of comorbidities may lead the patient to terminal liver failure, marked by profound jaundice, significant coagulopathy, hepatic encephalopathy, and an elevated risk of mortality.
Definition • Irreversible substitution of normal liver structure with fibrous tissue bands that segregate nodules of regenerating hepatocytes.
Epidemiology • Prevalent and rising in frequency attributable to alcohol consumption and obesity.
Aetiology
Alcohol, chronic viral hepatitis, and non-alcoholic fatty liver disease (NAFLD) are the predominant etiological factors. • Less frequently, primary biliary cholangitis (PBC), primary sclerosing cholangitis (PSC), autoimmune hepatitis (AIH), Wilson's disease, and hemochromatosis. • In certain instances, the etiology remains ambiguous (cryptogenic cirrhosis).
Pathogenesis
Persistent liver damage prompts Kupffer cells within the vascular sinusoids to secrete cytokines that activate hepatic stellate (Ito) cells. Activated stellate cells undergo proliferation and release substantial amounts of thick collagen, resulting in permanent liver fibrosis and hepatocyte depletion. Cirrhosis induces several functional impairments: diminished synthesis of coagulation factors; decreased glycogen reserves; impaired clearance of pathogens by Kupffer cells; portal hypertension accompanied by hypersplenism and esophageal varices; splanchnic vasodilation; reduced renal blood flow; secondary hyperaldosteronism; and ascites.
Presentation • Atypical symptoms of fatigue and general discomfort. Clinical examination typically reveals signs of chronic liver disease, and liver function tests are generally abnormal. Patients frequently exhibit complications associated with cirrhosis, such as upper gastrointestinal hemorrhage.
Macroscopy • The liver may present as normal in size, hypertrophied, or atrophied. • The sliced surface exhibits a firm texture and displays diffuse nodularity.
Histopathology • The liver is entirely substituted by nodules of regenerating hepatocytes encircled by fibrous bands. • The fibrous bands exhibit a heterogeneous inflammatory infiltrate and reactive bile ductular proliferation. • In certain instances, the characteristics may indicate a specific cause.
Prognosis • Generally unfavorable, with a substantial risk of considerable complications including infections (notably bacterial peritonitis), upper gastrointestinal hemorrhage, renal failure, and hepatocellular cancer.The emergence of comorbidities may lead the patient to terminal liver failure, marked by profound jaundice, significant coagulopathy, hepatic encephalopathy, and an elevated risk of mortality.
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