Pathophysiology of Liver Cirrhosis

Right sided heart failure Hepatotoxic drugs Chemical toxins Hepa a virus Mild acute injury Liver regeneration Recovery Chronic persistent hepatitis Post hepatic/ post necrotic cirrhosis Viral infection Laennecs cirrhosis Excessive alcohol ingestion Hepatitis B virus & hepatitis c virus Continued or repeated infection Chronic active hepatitis Exaggerated detoxification Inflammato ry cell infiltration Destructive metabolites Cell protein Fat accumulation in hepatocytes steatosis Biliary cirrhosis 1 biliary cirrhosis Intrahepatic obstruction Blockage of bile excretion Autoimmune liver cell destruction 2ndary biliary cirrhosis Extrahepatic obstruction Accumulation of bile hepatomegaly

Massive liver necrosis

in the

Formation of stasis Bile duct obstruction Cholestatic jaundice Bile salts accumulate in the blood Bile salts carries into tissues Pruritus Decrease bile in the intestine Light colored feces

Fibrosis stimulation Death Fibrous repair tissue

Liver parynchymal destruction

Functional hepetocytes Foci of regeneration formed

Failure to conjugate bilirubin Hyperbilirubinemia Hepatocellular jaundice



Macro &micro nodules formation

Decreased bile salts in the liver Diminished fat emulsification and absorption Decreased vit. K absorption Decrease clotting factor synthesis Clotting defects DIC Steatorrhea

Liver cirrhosis Impaired detoxification activity Toxin exaggeration Increase susceptibility to infection Faulty urea synthesis Increase ammonia in the Hepatic encephalopathy Faulty protein synthesis Hypoalbuminemia Faulty Hormone inactivation Increase circulating Tissue exposure to estrogen Gynecomastia Asterixis (liver Flap) Coma Palmar erythem a Vascular compression Increase resistance of blood flow through the liver Decrease blood flow to hepatic veins Portal congestion Increase arterial loading Increase flow through hepatic artery Increase blood volume in sinusoid and veins Congestion Hepatorenal syndrome Destruction of live vasoconstrictor Increase vasoconstrictor in circulation Interference in kidney blood flow Kidney damage

Increase gastrin in the blood Excessive stimulation of stomach parietal cells Oversecretion of acid Ulcer formation

Weight loss

General weakness

Agitation, lethargy & stupor

Increase pressure in capillary beds Increase capillary permeability Fluid shift to extravascular compartment Decrease venous return Decrease BP Release of renin

Portal hypertension Splenomegaly leukopenia Susceptibility to infection Hypersplenism Excessive RBC lysis

Hepatic shunting thrombocytopenia Anemia

Diversion of blood to collateral channel Blood bypasses the liver Increase portal flow

Decrease colloidal osmotic pressure

By: Romeo Q. Rivera Jr. 09282434418 Ascites dyspnea Reference: Joyce Black: Medical-Surgical Nursing Carol Porth: Pathophysiology,High vascular pressure Concepts of Altered Health States Lemone & Burke: Medical-Surgical gain access Organisms
to peritoneal cavity

Conversion of angiotensin 1 to angiotensin 2 & to angiotensin 3

Hemoglobin release


Increase bilirubin Secretion of aldosterone Vasoconstriction Increase BP Na & H2O retention Edema Hemolytic jaundice

Esophageal varices

Hemorrhoids formation

Abdominal vessel congestion

Protrusion in esophageal lumen

Caput medusae

Rapid proliferation

Blood in stool Hematemesis Erosion, rupture Spontaneous bacterial peritonitis