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GROUP 3A
What is Cirrhosis?
Cirrhosis facts
Progressive, leads to liver failure.
Insidious, prolonged course.
9th leading cause of death in U.S.
Twice as common in men.
Highest incidence between ages 40 and 60.
Types of cirrhosis
Alcoholic
Post-necrotic
Biliary/obstructive
Cardiac
Alcoholic cirrhosis
Complication of:
viral infections
toxicity
autoimmune hepatitis
Biliary cirrhosis
Associated with chronic biliary obstruction and/or infection.
Primary sclerosing cholangitis
Diffuse fibrosis of liver.
Jaundice is main feature.
Cardiac cirrhosis
Pathophysiology
Hepatic fibrosis.
Insulin, glucagon, and patterns of intrahepatic blood flow determine how and where
nodules develop.
Angiogenesis produces new vessels within the fibrous sheath that surrounds
nodules. These vessels connect the hepatic artery and portal vein to hepatic
venules, restoring the intrahepatic circulatory pathways. Such interconnecting
vessels provide relatively low-volume, high-pressure venous drainage that cannot
accommodate as much blood volume as normal.
As a result, portal vein pressure increases. Such distortions in blood flow contribute
to portal hypertension, which increases because the regenerating nodules compress
hepatic venules.
The progression rate from fibrosis to cirrhosis and the morphology of cirrhosis vary
from person to person. Presumably, the reason for such variation is the extent of
exposure to the injurious stimulus and the individual's response.
Diagnostic Studies
Decrease in:
total protein.
Albumin.
Increase in:
serum bilirubin.
globulin levels.
Anorexia
Diarrhea or constipation
Pain
Fever
Weight loss
Later Manifestations
Jaundice
Skin Lesions/Spider angiomas.
Palmer erythema.
Thrombocytopenia, Leukopenia, Anemia .
Coagulation disorders.
Endocrine disturbance.
Peripheral neuropathy & peripheral edema.
Hematologic Problems
Thrombocytopenia
Leukopenia
Anemia
Vitamin K deficiency
Endocrine Problems
Hyperaldosteronism.
Complications
Portal Hypertension
Esophageal & Gastric Varices
Peripheral Edema & Ascites
Hepatic Encephalopathy
Hepatic encephalopathy
What is Hepatic encephalopathy?
Ammonia
Pathogenesis
urea in the blood is emitted into intestinal lumen and degraded by urease
in bacteria to produce ammonia.
Alteration of neurotransmitters
phenylalanine phenylethanolamine.
tyrosine octopamine.
Lactulose
Liver transplantation.