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Pathophysiology of Liver Cirrhosis

Laennecs cirrhosis Biliary cirrhosis


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

Bile duct Decrease bile in the


Liver parynchymal Functional obstruction intestine
Fibrosis stimulation Failure to
destruction hepetocytes
Death conjugate bilirubin
Cholestatic Light colored feces
Foci of regeneration jaundice
Fibrous repair tissue Hyperbilirubinemia
formed
Scarring Bile salts Decreased bile salts
Fibrosis Macro &micro nodules formation Hepatocellular accumulate in in the liver
jaundice the blood
Diminished fat
Liver cirrhosis Steatorrhea
emulsification and
Bile salts carries absorption
Impaired Faulty urea Faulty protein Faulty Hormone Vascular Increase arterial Hepatorenal into tissues
detoxification synthesis synthesis inactivation compression loading syndrome
activity Increase gastrin in the Decreased vit. K Weight loss
blood Pruritus absorption
Increase Hypoalbuminemia Increase Increase resistance Increase flow Destruction of
Toxin ammonia circulating of blood flow through hepatic live
exaggeration in the Excessive stimulation through the liver vasoconstrictor Decrease clotting General
of stomach parietal artery weakness
Tissue exposure to factor synthesis
cells
Increase Hepatic estrogen Decrease blood Increase blood Increase
susceptibility encephalopathy Oversecretion of acid flow to hepatic volume in sinusoid vasoconstrictor Clotting defects
to infection veins and veins in circulation
Gynecomastia Palmar
erythem Ulcer formation DIC
Agitation, Asterixis a Portal Congestion Interference in Kidney
lethargy & (liver Flap) congestion kidney blood damage
stupor
Increase pressure in capillary Portal hypertension flow
Coma beds
Diversion of blood to
Splenomegaly Hepatic shunting collateral channel
Increase capillary Decrease venous return
permeability
Decrease leukopenia Hypersplenism thrombocytopenia Blood bypasses
colloidal Fluid shift to extravascular Decrease BP the liver
osmotic pressure compartment
Susceptibility Excessive RBC Anemia
Release of renin to infection lysis Increase portal flow
By: Romeo Q. Rivera Jr. 09282434418 Ascites Hemoglobin
release Engorgement
Reference: Joyce Black: Medical-Surgical
dyspnea Conversion of angiotensin 1 to
angiotensin 2 & to angiotensin 3
Nursing
Increase bilirubin
Carol Porth: Pathophysiology,High vascular pressure
Concepts Esophageal varices Hemorrhoids
formation
Abdominal
vessel congestion
of Altered Health States Secretion of Vasoconstriction
aldosterone
Lemone & Burke: Medical-Surgical
Organisms gain access Hemolytic
to peritoneal cavity Increase BP jaundice Protrusion in Caput
esophageal lumen medusae
Na & H2O
retention
Rapid proliferation
Blood in stool
Edema Hematemesis Erosion, rupture

Spontaneous bacterial
peritonitis
Bleeding

Death

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