Cirrhosis PP Week 4 Flashcards Preview

Primary Care 3 > Cirrhosis PP Week 4 > Flashcards

Flashcards in Cirrhosis PP Week 4 Deck (14)

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

1. increased in intrahepatic vascular resistance d/t the architectual distortion and deficiency of nitric oxide
2. portal htn from inc. intrhepatic resistance (decreased outflow and splanchnic arterial vasodilation (increased inflow)
3. 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)



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)