Hepatic Flashcards
functional subunit of liver
liver->lobe-> lobule
lobule made up of cords of hepatocytes, portal triads, central vein and is hexagonal shaped
metabolic zonation
cells closest to hepatic artery have greatest aerobic property (zone 1)
-zone 2 and 3 less aerobically capable but can still do things
genomic equivalence
all cells have same blueprint/ genetic code
-local factors influence/ act as promoters
promoter
binds to receptor to activate transcription or translation
bile composition
bile acid
bile pigments
H2CO3-
H2O
Electrolytes
chalangiocytes
cells that line the bile ducts
bile acids
cholesterol derivatives (steroid hormones)
amphipathic
primary bile salt
made by liver
secondary bile salt
produced by bacteria in the gut
emulsification
prevent small lipids from colisting into larger lipids
GI tract cannot digest large fat molecules
steatorrhea
oily feces caused by:
pancreatic/ hepatic disease
hyper/hypo secretion
failure to synthesize apoprotein B
icterus/ jaundice
yellowing of mucous membranes
lethargic
sign of liver malfunction
negative energy balance
body takes stored fat for energy
bile pigments
heme being exposed from heme-oxygenase (commited step)
Bilirubin needs albumin to chaperone
causes of hyperbilirubinemia
excessive hemolysis
hepatic/ bile obstruction
ineffective erthropoiesis
hepatic overproduction of bilirubin
hepatic defects
cholestasis
stopping bile flow
ketones
derived from LCFA
ex: acetone and acetoacetate
3-ketoacid transferase
can use ketones and reduce for energy if present
liver cannot use ketones
venous admixture
place where there is confluence of flows
venous blood flow from portal vein (low O2) mixes with hepatic artery blood (high O2)
triglyceride
3 fatty acids with glyceride
lipoprotein lipase
in liver, frees fat from chlyomicrons
hormone sensitive lipase
enzyme in adipose tissue that frees lipase
reduction of ketones
acetoacetone can be reduced for energy
-3 hydroxybuterate reduced to acetoacetate
both can be reduced to LCFA
oxidation of ketones
occurs in peripheral tissues
- 3 ketoacid CoA transferase
liver phase I
redox reactions
liver phase 2 reactions
conjugation
break bond, kick off carboxyl, attach sugar
clearance
removes ? from bloodstream by using metabolism, excretion, and biotransfermation
therapeutic dose
less than ingested dose
-dose required to achieve intended dose, needs time to get to steady state
1st order kinetics
ability of liver to do biotransformation
substrate availability doesnt exceed enzyme
gallbladder
helps deal with lipids
CCK and PZK enzymes influence
rate limiting step in bilirubin formation
Heme oxygenase, Heme ring gets cracked open, then can’t go back
urobilinogens
end up in urine
sterocobilinogens
end up in stool
translocase
brings LCFA into the cell
thiolase
turns acetyl CoA into acetoaceytl CoA
committed to ketogenesis at this step
HMG-synthase
turns Acetoacetyl CoA into hydroxymethylglutaryl-CoA
HMG-lyase
turns hydroxymethylglutaryl-CoA into acetoacetate (1st ketone)
D-3 hydroxybutate dehydrogenase
turns acetoacetate into 3-hydroxybutyrate (2nd ketone)
acetyl CoA carboxylase
turns LCFA CoA into triglycerides
ONLY HAPPENS IN EXCESS
LCFA CoA
gets translocated into mitochondrial membrane to go to CAT 1 and CAT 2, then beta oxidized to get Acetyl CoA
xenobiotics
compounds from outside coming inside
