Pathophysiology Of Liver Cirrhosis

Pathophysiology of Liver Cirrhosis Right sided heart failure

Hepatotoxic drugs

Hepa a virus

Hepatitis B virus & hepatitis c virus

Mild acute injury

Continued or repeated infection Chronic persistent hepatitis

Liver regeneration

Biliary cirrhosis

Excessive alcohol ingestion

Viral infection

Chemical toxins

Massive liver necrosis

Laennecs cirrhosis

Post hepatic/ post necrotic cirrhosis

Inflammato ry cell infiltration

Fat accumulation in hepatocytes

protein

hepatomegaly

Autoimmune liver cell destruction

steatosis

Functional

Failure to

hepetocytes

conjugate bilirubin

Foci of regeneration formed Scarring

Blockage of bile excretion

2ndary biliary cirrhosis Extrahepatic obstruction Accumulation of bile

Liver parynchymal destruction

Fibrous repair tissue

Fibrosis

Cell

Exaggerated detoxification

Recovery

Fibrosis stimulation

Intrahepatic obstruction

Destructive metabolites

Chronic active hepatitis

Death

1 biliary cirrhosis

Hyperbilirubinemia Hepatocellular jaundice

Macro µ nodules formation

in the

Formation of stasis Bile duct obstruction

Decrease bile in the intestine

Cholestatic jaundice

Light colored feces

Bile salts accumulate in the blood

Decreased bile salts in the liver

Liver cirrhosis Impaired detoxification activity

Faulty urea synthesis Increase ammonia in the

Toxin exaggeration Increase susceptibility to infection

Faulty protein synthesis

Faulty Hormone inactivation Increase circulating

Hypoalbuminemia

Tissue exposure to estrogen

Hepatic encephalopathy

Gynecomastia

Agitation, lethargy & stupor

Asterixis (liver Flap)

Palmar erythem a

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

Increase pressure in capillary beds

Coma

Decrease colloidal osmotic pressure

Vascular compression Increase resistance of blood flow through the liver Decrease blood flow to hepatic veins Portal congestion

Increase arterial loading Increase flow

Decrease venous return

Fluid shift to extravascular compartment

Decrease BP Release of renin

Destruction of live vasoconstrictor

through hepatic artery Increase blood volume in sinusoid and veins

Increase vasoconstrictor in circulation

Congestion

Interference in

Portal hypertension

Increase capillary permeability

Hepatorenal syndrome

Splenomegaly

kidney blood flow

Hepatic shunting

leukopenia

Hypersplenism

thrombocytopenia

Susceptibility to infection

Excessive RBC lysis

Anemia

Bile salts carries into tissues Pruritus

Diminished fat emulsification and absorption Decreased vit. K absorption

Weight loss

Decrease clotting factor synthesis

General weakness

Clotting defects

Kidney damage

Steatorrhea

DIC

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

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

Conversion of angiotensin 1 to angiotensin 2 & to angiotensin 3

Increase bilirubin Secretion of aldosterone

Na & H2O retention

Engorgement

Esophageal varices

Vasoconstriction Increase BP

to peritoneal cavity

Rapid proliferation

Hemoglobin release

Hemolytic jaundice

Hemorrhoids formation

Protrusion in esophageal lumen

Abdominal vessel congestion

Caput medusae

Blood in stool Edema Spontaneous bacterial peritonitis

Hematemesis

Erosion, rupture

Bleeding

Death