Cirrhosis PP Week 4 Flashcards
what is cirrhosis
Late stage of progressive hepatic fibrosis: characterized by distortion of the hepatic architecture
– formation of regenerative nodules
– considered to be irreversible in its advanced stages, at
which point the only option may be liver transplantation
In earlier stages of cirrhosis
specific treatments aimed at the underlying cause of liver disease may improve or even reverse cirrhosis
major complications of decompensated cirrhosis
Variceal hemorrhage, Ascites, Spontaneous
bacterial peritonitis, Hepatic encephalopathy, Hepatocellular carcinoma, Hepatorenalsyndrome, Hepatopulmonarysyndrome
Risk factors for decompensation include
bleeding, alcohol intake, infection, medications, dehydration, constipation, obesity, portal vein thrombosis, cardiomyopathy (**= these complications alone are not considered to have decompensated cirrhosis)
many of the complications of cirrhosis are the result of portal hypertension, which
increased pressure within the venous portal system. It can lead to the formation of: venous
collaterals (varices), Circulatory abnormalities, Vascular abnormalities, Functional abnormalities biochemical
abnormalities (All contribute to the pathogenesis of ascites and other complications)
stages of hepatic encephalopathy
stage 1- personality changes
stage 2- lethargy, tremors, muscle twitching
stage 3- combative, violent
stage 4- coma
how does liver disease lead to varices
- increased in intrahepatic vascular resistance d/t the architectual distortion and deficiency of nitric oxide
- portal htn from inc. intrhepatic resistance (decreased outflow and splanchnic arterial vasodilation (increased inflow)
- varices form in the esophagus and stomach by dilation of preexisting vessels and by active angiogenesis. they increase in size with severity of portal htn and can rupture and bleed when the pressure exceeds a maximal point
spontaneous bacterial peritonitis evaluation
do a tap- look at PMN, if greater than 250 assume bacterial peritonitis- start broad spectrum such as cefoxatime and also give albumin (on day 1 and day 3 if serum creatinine is greater than 1 and BUN greater than 30)
SBP
common but treatable complication of decompensated cirrhosis, its the translocation of bacteria and endotoxins from GI tract to peritoneal fluid, facilitated by impaired defensive mechanisms in cirrhotic patients
hepatorenal syndrome caused by
cirrhosis–> portal hypertension–> severe renal constriction–> hepatorenal syndorome.
hepatorenal syndrome easily recognized features
low mean arterial BP less than 80, hyponatremia, urinary sodium retention (low urinary sodium concentration), oliguria
treatment for hepatorenal syndrome
IV albumin, vasocontrictors i.e. midodrine plus octreotide, IV terlipressin
portal htn gastropathy
effects of portal htn- hematemesis/ melena (from esophogeal variceles), dilated abdominal veins (caput medusa), splenomegaly, ascites
hepatic hydrothorax
transudative pleural effusion usually greater than 500ml, aims of therapy is relieve sx and to prevent pulmonary complications (tx- duretics, lasix/ spironolactone)