• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/20

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

20 Cards in this Set

  • Front
  • Back
prothrombin time
assess amount of circulating clotting factors - indirectly asses liver function
acetomenophen toxicity
most acetamenophen is glucuronidated to nontoxic form

10% is turned into toxic intermediates - if there isn't enough glutathion available for conjugation (due to alcohol, etc) -> accumulation of toxin will cause hepatocyte necrosis

certain drugs can induce CYP2E1 and CYP3A4 to increase formation of toxin
N-acetyl cysteine
treatment for acetomenophen overdose

increases amount of glutathione for conjugation with toxic intermediates
signs of chronic liver failure
spider angiomata, ascities, caput madusa, splenomegaly, low platelet, low clotting factors, shrunken nodular liver, signs of cirrhosis
aminita phyllodies, aminita verna
poisonous mushroom

alpha-amatoxin inhibits protein synthesis -> hepatocyte death

phalloidin interfere with actin and dmg enteric cell membranes
drug induced acute liver failure
phenytoin, acetaminophen, valproic acid, HAART agents, isoniazid

amidarone - steatohepatitis
most common viral cause of fulminent hepatic failure
Hepatitis B

dude to overactive immune response to clear virus
most common virus to cause symptomatic acute infection of liver
Hepatitis C - doesnt cause acute liver failure often
Hepatitis D
requires concurrent HBV infection since it uses HBV machinery to bud
Hepatitis E mortality is high in this group of paitents
20% mortality in pregnant women
fulminant hepatic failure
encephalopathy within 8 weeks of jaundice

cerebral edema
childs pugh score (5 factors)
looks at 5 factors: encephalopathy, ascites, bilirubin, albumin, PT prolongation
wedged/free HV pressures
wedged hepatic vein pressure = WHVP

free hepatic vein pressure = FHVP

gradient = WHVP - FHVP

normal <5
Portal HTN > 10

varices bleed WHVP > 12
hepatic encephalopathy
metabolic failure of liver causes ammonia to go unmetabolized

constructional apraxia, asterixis

begins as slow mentation, mood changes -> lethargy -> suporus/obtunded -> comatose
causes of hepatic encephalopathy
GUSDICK

GI bleeding
uremia
sedatives
dietary indiscretion
infection
constipation
hypokalemia
serum albumen-ascites gradient
differentiate portal HTN from nonportal HTN

serum albumen - ascites albumen

>1.1 = Portal HTN
cirrhosis caused portal HTN vs noncirrhotic
cirrhosis casuses closure of sinusiod fenstration means ascites low in total protein

noncirrhotic (cardiac, budd chirari) the sinusoids are patent, protein leaks
infected ascites
see with ascitic fluid protein < 1 - usually ecoli infection
spontaneous bacteria peritonitis (ascites infection) vs Peritonitis
SBP is monomicrobial, has less total protein, more glucose, and low LDH
hepatorenal syndrome
liver failure causes kidney failure

no actual damage to kidney, its a functional renal failure due to the liver failure (unknown mech)