liver structure and function Flashcards by Rosemary Ndara

hepatic vein

removes deoxygenated blood

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sinusoids

allow rapid exchange of solutes

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hepatocytes

perform metabolic functions

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kupffer cells

perform defence functions

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portal vein

provides nutrient rich blood supply into the liver

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toxic break down from blood cells

bilirubin

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build up of bilirubin leads to

jaundice

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key precursor for cholesterol

acetly CoA

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enzyme key in the production of cholesterol

HMG CoA

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proper hepatic artery

takes oxygenated blood into the liver

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hepatic vein take what? to where?

deoxygenated blood to vena cava

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portal vein carries blood returning from

GI tract

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liver acts as what type of system?

filtation system for the nutrients, toxins etc before the blood goes back to the heart

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lobules are

collection of cells

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structure of hepatic lobule

hexagonal structure

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portal triad contains

bile duct
portal vein
hepatic artery

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structure of sinusoids

one cell thick
have gaps to allow macromolecules to pass through

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what are sinusoids?

small blood vessels between radiation rows of hepatocytes

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function of hepatocytes and kupffer cells

hepatocytes- perform most metabolic function
kupffer cells- perform a lot of defence functions

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kupffer cells are a

type of tissue macrophage

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billary system

bile secreted by hepatocytes - canalinculi- ductules- hepatic ducts- common bile duct

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canaliculi

series pf channels between cells

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sinusoids function (being one cell thick)

allows for exchange of large solutes

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bile is secreted by

hepatocytes

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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

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