Study your flashcards anywhere!

Download the official Cram app for free >

  • 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

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/40

Click to flip

40 Cards in this Set

  • Front
  • Back
HEPATIC FAILURE - JENNINGS - WEDNESDAY FEB 7
what is acute hepatic failiure dominated by?
loss of function, as a consequence of loss of hepatocytes
what functions are lost in acute hepatic failure (4)?
1) excretory; 2) exocrine; 3) synthetic; 4) metabolic
whwhat occurs due to loss of excretory function?
hyperbilirubinemia
what occurs due to loss of exocrine function (4)?
1) hypercholesterolemia (cholesterol is not being consumed by making bile); 2) steatorrhea; 3) vitamin deficiencies (A, D, E, K); 4) pruritis due to accumulation of bile salts
what deficiencies may occur due to loss of synthetic function (6 - incomplete list)?
1) albumin; 2) transferrin; 3) ceruloplasmin; 4) haptoglobin; 5) complement factors; 6) coagulation factor deficiencies
what metabolic problems may occur in acute hepatic failure?
1) glucose metabolism; 2) glucose synthesis; 3) ketone body synthesis; 4) fatty acid synthesis; 5) drug metabolism; 6) estrogen metabolism
what is the picture of chronic hepatic failure like?
loss of normal hepatic lobular architecture with resulting increase in portal system pressures and decreased hepatic function
why is there decreased hepatic function?
loss of hepatocyte-sinusoid relationship
what are the consequences of portal hypertension (4)?
1) ascites; 2) splenomegaly; 3) edema; 4) porto-caval shunting
what leads to ascites?
increased sinusoidal pressure results in fluid transudation into hepatic interstitial space with eventual overflow into peritoneal third space
why is there protein in ascitic fluid?
because proteins may enter hepatic interstitial space through space of Disse - the capillaries let out the proteins into the space of Disse where liver has receptors to sense protein levels
what are consequences of splenomegaly from portal hypertension (2)?
1) anemia; 2) thrombocytopenia
why does edema result from portal hypertension?
due to hypo-albuminemia, salt and water retention - complex mechanisms
what problems does porto-caval shunting result in (5)?
1) esophageal varices; 2) abnormal glucose tolerance test; 3) spontaneous infection; 4) compromised hepatic perfusion; 5) GI bleeding
why is there spontaneous infection?
liver takes out bacteria, and shunt removes Kupffer cell effect - bacteria grow in ascitic fluid
what are two clinical syndromes seen in liver failure that we must know?
1) hepatic encephalopathy; 2) hepatorenal syndrome
what does hepatic encephalopathy start out as (3)?
1) confusion; 2) restlessness; 3) asterixis
what does it progress to (3)?
1) convulsion; 2) coma; 3) death
what are predisposing factors to hepatic encephalopathy (6)?
1) decreased hepatic function; 2) GI hemorrhage; 3) protein load; 4) infection; 5) sedatives; 6) constipation
what is true about all of these factors except sedatives?
they involve increased protein load
what happens in hepatorenal syndrome?
structurally normal kidneys with adequate vascular volume and cardiac function fail
what things are seen in the picture of hepatorenal failure (6)?
1) azotemia; 2) hyperkalemia; 3) acidosis; 4) oliguria; 5) concentrated urine; 6) very low sodium
what is true about the causes of both hepatorenal and hepatic encephalopathy?
they are metabolic syndromes - brain is ok, kidneys are ok
what is thought to be the cause of hepatorenal syndrome?
liver fails to metabolize an intra-renal vasoregulator
LIVER FUNCTION TESTING
what are the three categories of causes of jaundice?
1) pre-hepatic; 2) post-hepatic; 3) intra-hepatic
what will bilirubin be like in pre-hepatic, what will urobilinogen levels be like, and will there be anything else seen?
unconjugated, high urobilinogen
what will bilirubin be like in post-hepatic, what will urobilinogen levels be like, and will there be anything else seen?
conjugated bilirubin, low urobilinogen, with biliary enzymes
what will bilirubin be like in intra-hepatic, what will urobilinogen be like, and will there be anything else seen?
mixed conjugated and unconjugated, mixed urobilinogen, hepatocellular enzymes
what is a short term test of liver synthetic function?
coagulation factor VII (4-6 hour half life)
what is a long term test of liver synthetic function?
albumin (half life 21 days)
what else can be used to test liver synthetic function?
other plasma proteins
what are two types of hepatic injury that can be tested in lab?
1) hepatocellular; 2) biliary
levels of what substances will rise when there is hepatocellular injury (3)?
1) AST; 2) ALT; 3) LDH (isoform 5)
levels of what substances will rise when there is biliary injury (2)?
1) GGT; 2) alkaline phosphatase
what patterns of liver damage were mentioned (4)?
1) hepatocellular disease; 2) biliary disease; 3) pre-hepatic jaundice; 4) space occupying lesions