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Liver cirrhosis occurs when the regenerative capacity of the liver is overwhelmed by alcohol consumption, drug or chemical damage, long-term infection brought upon by infection or extra hepatic bile obstruction. Numerous infiltrating inflammatory cells stimulate fibrosis in response to such massive destruction. It will then result in an ever increasing scarring until sheets of fibrous repair tissue form throughout the liver. These are diffusely distributed thereby isolating areas of the liver that still retains their regenerative capacity. These detached areas are called nodules and are readily apparent in the liver’s surface. This condition of nodularity and fibrosis is called cirrhosis.

Cirrhosis is a non-specific end-stage disease towards which various pathologic consequences converge. The differing degrees of functional loss of the hepatocytes results in variable signs and symptoms. In certain instances, the liver is able to compensate for necrosis that none or minimal symptoms appear. This situation leads to an unnoticed and unresolved destruction of hepatocytes until adequate function can no longer be maintained and reserves are completely depleted leading to liver failure.

Liver cirrhosis is defined by two principal factors: Portal Hypertension and Hepatic Dysfunction. Portal hypertension is the result of restricted flow of blood through the liver to the hepatic veins and then to the inferior vena cava. The resulting portal congestion increases portal pressures and decreases blood flow to the liver. With reduced blood flowing to the cirrhotic liver, the hepatocytes have minimal accessed to blood, severely hampering their capacity to detoxify harmful chemicals. As a result, toxins become more concentrated in the blood producing damaging effects particularly the production of ammonia (from amino acid breakdown). Instead of being excreted, ammonia stays in the blood causing hepatic encephalopathy and a noticeable foul breath. Furthermore, the hepatocytes continue to die leading to a progressive deterioration of the liver’s regulatory capabilities resulting in hypocoagulation and hypoalbuminemia. Congestion in the hepatic portal system causes blood to be diverted to the collateral vessels forcing them to accommodate larger volumes. This engorgement causes the veins to bulge producing easily visible hemorrhoids. Another consequence of this diversion is the dilation of the thin-walled esophagus causing esophageal varices. Esophageal varices are subjected to trauma as food is swallowed and expose to gastric reflux. This poses a potential threat of rupture and bleeding. When the varices rupture it is usually asymptomatic and sudden, bringing forth a large scale blood loss. Compounded by a prolonged bleeding time, esophageal varices is a very serious complication of liver cirrhosis.

Portal hypertension in liver cirrhosis also causes ascites (accumulation of fluid in the peritoneal cavity) and splenomegaly. Ascites is caused by hampered albumin production, the osmotic pressure decreases reducing the return of fluid to the blood from the tissues. It results in a significant and pronounced abdominal distention, compressing the abdomen and compromising breathing.

Splenomegaly is the enlargement of the spleen as a result of the inability of the veins that drain the spleen to empty into a congested portal system. The enlarged spleen increasingly takes up and hold formed elements of the blood causing thrombocytopenia and anemia.

Signs and Symptoms

  • Edema
  • Ascites
  • Anemia
  • Bleeding
  • Foul breath
  • Jaundice
  • Fatigue
  • Pain
  • High Grade Fever
  • Loss of appetite

Types of Cirrhosis

  • Alcoholic- involves the production of high levels of metabolites.
  • Post-necrotic- severe necrosis linked to viral or toxic damage most commonly as a result of hepatitis B or C.
  • Biliary Cirrhosis- Chronic autoimmune destruction of the inter-hepatic bile ducts.

Pathophysiology of Liver Cirrhosis & Schematic Diagram

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