Hepatic Physiology Flashcards
what happens if you remove part of liver?
hepatocytes proliferate to replace lost tissue
list liver functions
what are the two blood sources of liver?
hepatic artery from aorta - O2
hepatic portal vein from GI - transfer nutrient
how does blood leave liver?
hepatic vein
most of the liver blood is ___ blood
venous
what are the liver functional units?
lobules
kupffer cells function
destroy old RBC and bacteria
exposed to large volume blood
stellate cells store what?
vitamin A as retinol
aka hepatocytes
what is space of disse?
between hepatocytes and sinusoids
fills with collagen = fibrosis
what’s the portal triad?
what are the three zones of oxygen supply?
zone 1 - periportal hepatocytes
zone 2 - centrilobular
zone 3 - hepatocytes
zone 1 oxygen supply has ___ oxygen tension, and ___ mitochondria
high
lots of mito
what’s zone 1 concerned with?
oxidative metabolism
bile acid secretion
glycogen and nutrient store
what is zone 2?
transition
zone 3 is ___ oxygen, ___ metabolism
low oxygen
anaerobic
which zone is most sensitive to damage, why?
zone 3
ischemia
list zone 1 hepatocyte functions
list zone 3 hepatocytes functions
which two capillary beds does blood run through before reaching heart?
mesenteric and portal
what 3 things drives blood through portal capillary bed?
- P in portal vein is higher than hepatic sinusoids -> precapillary R is low
- low R due to large central vein
- venous outflow of liver goes to vena cava
which area is affected by R side heart failure?
increases vena cava P -> reduces blood flow from intestine -> ascites
what situations cause zone 1 necrosis?
phosphorus poisoning (rat, fertilizer, firework) or eclampsia
what situations cause zone 3 necrosis?
ischemic injury, toxin, carbon tetrachloride exposure, chloroform ingestion
liver enzymes are released with ___ cell membrane permeability or cell death
increased
list the elevated plasma liver enzymes most commonly seen?
what’s indicated by elevated liver enzymes?
inflammation or damage to cells in liver
describe the decreased synthetic capacity in necrosis of hepatocytes (changes in lipid and protein)
why does hepatocyte necrosis cause decreased uptake and conversion of ammonium to urea?
HIGH ammonia in urine
since urine concentrating ability in kidney depends on medullary interstitial tonicity made by urea and NaCl
bile function
excretory route for solutes not secreted by kidney
lipid digestion/absorption
composition of bile
50% bile salt
40% phospholipid
bilirubin, electrolyte, water
bile is ___ secreted by hepatocytes into ____.
continuously
into canaliculi
what do bile canaliculi secrete into?
bile ducts at periphery of lobule
what are the two primary bile salts?
what are the two secondary bile acids?
bile salts are derivatives of ___ and are actively secreted into ___
cholesterol
into bile
what happens to bile salts after participating in fat digest/absorb?
reabsorbed into blood via active transport in distal ileum
returns to liver by hepatic vein
***enterohepatic circulation
CCK stim ___ contraction and relaxation of ___ for enterohepatic circulation
gallbladder contract
relax duodeal sphincter
bile salts ___ lipids
emulsify
what cotransport is in ileum for bile salt recycle?
Na-bile cotransport
describe the bile acid test, and what it tests
- does liver have enough healthy cells to function
- good blood supply
- bile moving freely in/out of liver
what is hepatocellular dysfunction?
inability of hepatocyte to produce/extract bile acids from portal circulation
what is abnormal portal blood flow?
portosystemic shunt or microvascular dysplasia that causes portal blood to bypass liver
unable to have efficient extraction of bile acids that would normally be available
what is cholestasis?
interference with transporters that deliver bile from hepatocytes to biliary canalicular system
increased bile acid concentration
ammonia levels increased due to either inability to produce urea or if the hepatocytes become overwhelmed and so ammonia crosses the blood brain barrier and is converted to glutamate which contributes to the fluid inside the brain and that causes an increase in intracranial pressure because of the accumulation of fluid which leads to neurological signs
what is bilirubin?
constituent of bile
NOT part of digestion
where does bilirubin come from?
degradation of heme part of Hb in RBC
carried in blood bound to albumin
extracted by hepatocytes to conjugate with glucouronic acid
what form is bilirubin excreted to bile as?
bilirubin glucouronide
how is bilirubin modified back to bilirubin and urobilinogen in intestinal lumen?
bilirubin glucouronide -> bilirubin -> urobilinogen
done via bacteria
what is done with urobilinogen?
- recirculate back to liver
- excrete in urine
- oxidized to urobilin and stercobilin (fecal color)
what are causes of increased bilirubin aka hyperbilirubinemia?
excessive production (increase RBC breakdown)
insufficient removal (blocked ducts, liver problem)
what’s the importance of conjugating bilirubin?
make it water soluble
so it can transport in GI
what occurs with increased unconjugated bilirubin?
NO liver passage or exceeding pace of liver conjugation
what occurs with increased conjugated bilirubin?
prevents secretion of bilirubin into bile (hepatitis, obstruction)
bilirubin is backing up into blood
how could bilirubin lead to jaundice?
when production exceeds excretion
accumulates in body
pt appears yellowish
what is pre-hepatic/hemolytic jaundice?
RBC breakdown
liver gets more bilirubin than it can excrete
what is hepatic jaundice?
liver diseased and unable to deal with normal bilirubin load
what is post-hepatic/obstructive jaundice?
bile duct blocked so bilirubin not excreted
what is cholelithiasis?
stones in bile duct or in gallbladder
how does cholelithiasis lead to lighter grey fecal color?
reduced secretion of urobilin and stercobilin
what are signs and treatment for cholelithiasis?
what type of hyperbilirubinemia is cholelithiasis? why?
conjugated
since it’s post-hepatic issue
what is neonatal isoerythrolysis aka jaundice foal?
foal gets RBC from mare in colostrum
can develop hemolytic anemia
since Ab from mare colostrum destroys foal RBC
what type of hyperbilirubinemia is neonatal isoerythrolysis? why?
unconjugated
since it’s pre-hepatic and exceeding amount liver can handle
what’s treatment for neonatal isoerythrolysis?
withhold milk from foal until JFA is negative or gut closes
foal needs to be muzzled and fed colostrum from NI negative mare
what is JFA aka jaundice foal agglutination test?
foal blood and mare milk -> does milk cause RBC agglutination
