liver structure and function Flashcards
hepatic vein
removes deoxygenated blood
sinusoids
allow rapid exchange of solutes
hepatocytes
perform metabolic functions
kupffer cells
perform defence functions
portal vein
provides nutrient rich blood supply into the liver
toxic break down from blood cells
bilirubin
build up of bilirubin leads to
jaundice
key precursor for cholesterol
acetly CoA
enzyme key in the production of cholesterol
HMG CoA
proper hepatic artery
takes oxygenated blood into the liver
hepatic vein take what? to where?
deoxygenated blood to vena cava
portal vein carries blood returning from
GI tract
liver acts as what type of system?
filtation system for the nutrients, toxins etc before the blood goes back to the heart
lobules are
collection of cells
structure of hepatic lobule
hexagonal structure
portal triad contains
bile duct
portal vein
hepatic artery
structure of sinusoids
one cell thick
have gaps to allow macromolecules to pass through
what are sinusoids?
small blood vessels between radiation rows of hepatocytes
function of hepatocytes and kupffer cells
hepatocytes- perform most metabolic function
kupffer cells- perform a lot of defence functions
kupffer cells are a
type of tissue macrophage
billary system
bile secreted by hepatocytes - canalinculi- ductules- hepatic ducts- common bile duct
canaliculi
series pf channels between cells
sinusoids function (being one cell thick)
allows for exchange of large solutes
bile is secreted by
hepatocytes
bile composition
water, electrolytes, bilirubin, cholesterol and bile salts
bilirubin formation
breakdown of haemoglobin
colour of bilirubin
yellow pigment
where is bilirubin secreted
into the duodenum
where is bile stored?
in the gallbladder
bile function
-fat digestion and absorption
-eliminition of waste products especially bilirubin and cholesterol
Cholecystokinin (CCK)
hormone that causes contraction of the gallbladder leading to ejection of bile into the duodenum
what gets released when there is a detection of lipid rich food
Cholecystokinin to release bile to break it down and absorb into out bloodstream
blood clotting factors
Fibrinogen
Prothrombin
other factors - V, VI, IX, X, XII
Vitamin K is stored
in the liver
importance of vitamin K
for the formation of clotting factors
warfarin acts as a anticoagulant?
blocks the activity of epoxide reductase which means that vitamin Kstays in its oxidised form so cannot get reduced form of Vit K produced = fewer clotting factors
chylomicron remnants
fat molecules that get left over from digestion process
Chylomicron remnants transported where? via?
liver via portal vein
cholesterol sources
chylomicron remnants
synthesis in liver
HDL
end result of glucose metabolism in liver produced by?
Acetyl-CoA precursor by mitochondria
what enzymes acts on acetyl- CoA ? what does it do?
HMG- CoA
converts it into cholesterol
VLDL
very low density lipoprotein
VLDL breaks down into?
IDL and LDL
When liver is empty what does HDL do?
picks up excess cholesterol and brings it back to the liver
why is high levels HDL good?
efficient at picking up excess cholesterol and bringing it back to the liver = not a lot of cholesterol floating in the bloodstream
liver metabolises drugs and hormones in 2 phases
phase 1 and phase 2
phase 1 is primarily
primarily oxidation/ reduction
-form more chemically reactive products
phase 2 is
conjugation - to make it more water soluble
results in inactive and polar products
where is cytochrome p450 found?
endoplasmic reticulum
cytochrome p450
made up of 50 different enzymes, they are haem proteins and related to mitochondrial enzymes
paracetamol aka
acetaminophen
what type of therapeutic index does paracetamol have?
narrow
paracetamol is metabolised through 3 routes
45-55 %Glutathione conjugation (phase2)
20-30%Sulfation (phase2)
15%N-Hydroxylation by cytochrome p450
(phase 1)
NAPQI
toxic metabolite formed as intermediary by cytochrome p450 metabolism
toxic metabolite formed as intermediary by cytochrome p450 metabolism
NAPQI
effect of alcohol on NAPQI
p450 enzymes induced , so become much more active, more paracetamol process- accumulation of toxic metabolite
how does accumulation of toxic metabolite from phase 1 affect phase 2 from alcohol?
phase 2 becomes saturated (body unable to convert toxic metabolite into phase 2 compound which is damaging to the body
saturation kinetics
the kinetics of a reaction when the velocity of the reaction increases to a maximal value as the concentration of the reactant is increased
saturation kinetics results in
acetaldehyde build up
disulfiram is given to
people with alcohol dependency issues
function of disulfiram
inhibits the acetaldehyde dehydrogenase
what does acetaldehyde cause?
increased HR, nuasea, vomiting
acetaldhyde dehydrogenase function
converts acetaldehyde to acetate
metabolism of ethanol shows what and what does this mean?
saturation kinetics so plasma concentration falls linearly rather than exponentially
stages of alcohol-induced liver damage
fatty liver, liver fibrosis, cirrhosis
jaundice
excessive quantities of bilirubin accumulation in extracellular fluid (ECF
)
normal plasma bilirubin conc
<17uM
Jaundice at pre-hepatic stage (haemolytic)
excessive breakdown of RBC
Jaundice at hepatic stage
hepatocyte damage
e.g. cirrhosis, hepatitis A,B,C,E: gilberts syndrome
jaundice at post-hepatic (obstructive)
obstruction to passage into duodenum
enters circulation and into urine
e.g. gallstones, carcinoma of pancreas/bile ducts
pre-hepatic jaundice is easily cured in babies how?
blue light- breaks down bilirubin
hepatitis
inflammatory condition of liver
cause of hepatitis
viral infection, alcohol toxins, autoimmune
3 stages of alcohol liver damage
1: fatty liver
2: alcohol hepatitis (cells die resulting in inflammation)
3: cirrhosis includes fibrosis, scarring and cell death
as the cirrhotic liver cant function properly what will accumulate? results in?
ammonia, neurotoxicity, coma & death
as the cirrhotic liver cant function properly what will accumulate? results in?
ammonia, neurotoxicity, coma & death
