liver physiology Flashcards

1
Q

functions of the liver

A
  • filtration/storage of blood
  • metabolism pf CHO/fats/hormones/foreign chemicals/ammonia
  • bile formation and disposal of lipid soluble things
  • storage of vitamins and Fe
  • formation pf blood proteins
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2
Q

hepatic circulation

A

uses venous blood to metabolise products of digestion that come from the portal vein
blood is mostly deoxygenated

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3
Q

how does the liver get oxygen

A

also has an arterial supply
most - 80% - is nutrient rich blood
other 20% Is oxygen rich arterial blood

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4
Q

where does the blood from the liver go

A

to the vena cava

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5
Q

liver blood resistance

A

needs to be low pressure to allow diffusion
los resistance
liver provides limited resistance to blood flow

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6
Q

mixing arterial and venous blood

A

very different pressures

lots of fluid is produced - lots of lymph

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7
Q

resident macrophages of the liver

A

kupffer cells
modified resident macrophages
removal of >99% of GIt bacteria
involved in iron metabolism 0 accumulation of ferritin

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8
Q

flow control in the liver

A
  • NA vasoconstriction contracts venous and hepatic artery - fight or flight response, diverts blood away from the liver
  • no known vasodilator fibres
  • when the metabolism is high, liver produces adenosine which binds to receptors and vasodilator to increase flow
  • sinusoids can be isolated
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9
Q

NA vasoconstriction in the liver

A

contracts venous and hepatic artery

fight or flight response

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10
Q

countercurrent flow

A

of bile

goes in the opposite direction to blood flow

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11
Q

lymph

A

removes volume without moving nutrient

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12
Q

when there is too much plasma glucose

A

liver absorbs some through glucose channels

stored as glycogen - glycogenesis

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13
Q

when there is not enough plasma glucose

A

liver liberates some and puts it into the blood stream

break down glycogen by glycogenolysis

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14
Q

glucose-6-phosphatase

A

enables glycogen to go back too glucose

only present in the liver

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15
Q

without glucose-6-phosphatase

A

muscles can break down glycogen but only to glucose-6-phosphatase, not all the way to glucose

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16
Q

glucose-6-phosphate

A

doesn’t go through glucose transporters, trapped inside the cell and must be used in situ

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17
Q

gluconeogenesis

A

when glucose is made from fat (glycerol), some amino acids, lactate - via pyruvate

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18
Q

formation/interconversion of CHO intermediates

A

liver can convert between different types of monosaccharides
can be converted to glucose because it is he principle monosaccharide used throughout the body

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19
Q

beta oxidation

A

breakdown of FAs to acetyl CoA

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20
Q

acetyl CoA used to synthesis

A

fats and cholesterol

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21
Q

breakdown of cholesterol

A

not possible in the human body

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22
Q

uses of cholesterol

A

made into bile salts and excreted directly into bile and steroid hormones

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23
Q

cholesterol stored as

A

cholesterol esters

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24
Q

protein metabolism

A

deaminated

remove carbon skeleton and use as fuel

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25
Q

transamination

A

conversion between non-essential amino acids

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26
Q

removal of ammonia

A

converted into urea which is dumped into plasma and excreted into the kidneys

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27
Q

use of amino acids

A

used to make new proteins

all plasma proteins are synthesised in the liver eg. transferrin, albumin, angiotensin

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28
Q

ammonia-urea metabolism

A

NH3 is neurotoxic and is very permeable and can pass the BBB

converted to urea - only occurs in the liver

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29
Q

sources of ammonia

A

liver, colon, kidney etc

mainly liver

30
Q

where is ammonia converted into urea

A

only in the liver

31
Q

what happens to urea

A

excreted into plasma
most of it is excreted in the kidneys
some of it enters the GI and diffuses across the plasma membrane where it is broken down by bugs or is reabsorbed

32
Q

kupffer cells

A

macrophages

kill bugs

33
Q

drug metabolism

A

gets rid of lipid soluble drugs

34
Q

liver metabolising blood borne hormones

A

Vit D and A when acting as hormones
all steroids
insulin and glucagon

35
Q

cytochrome P450

A

enzymes

metabolise steroids

36
Q

storage of vits and mins

A
stores vit A 5-10 months supply 
vit B12 - 1 year supply 
vitamins D - 2-4 months 
vitamin K 
stores iron
37
Q

iron is bound to _ in the liver

A

ferritin - globular protein

38
Q

ferroxidase

A

Fe2+ > Fe3+ (safe storage)

39
Q

ferroductase

A

Fe3+ > Fe2+ (soluble release)

40
Q

ferric iron

A

oxidised form
completely insoluble
storage form

41
Q

ferrous iron

A

reduced form

water soluble - useful for transport

42
Q

liver iron sensing

A

stores/releases iron is a controlled fashion
liver sense elevated plasma and releases hepcidin which switches off iron channels in the gut and in the liver (ferroportin)

43
Q

bile

A

for emulsification and absorption
emulsifies fats in chyme
increases access to lipase
facilitates uptake of digested fat products by intestinal epithelial cells

44
Q

excretion of waste products from blood

A

bilirubin - Hb breakdown product

excess hydrophobic stuff - cholesterol, drugs, xenobiotics, toxins

45
Q

HDL uptake by

A

SR-B1

46
Q

BSEP

A

exports bile salts

47
Q

once bile is exported

A

can be stores in the gallbladder or released

48
Q

production of bile salts

A

expensive too produce - mostly reabsorbed

49
Q

ASBT

A

apical sodium dependant bile salt transporter
in the ileum
scavenger - secondary active transport
puts bile salt into the blood stream where it goes to the liver via the portal vein

50
Q

haem disposal

A

Hb phagocytosed, split into global and haem
ferrous reused by being picked up with ferritin and sent to the liver
the rest of the Hb is toxic
enzymes converted it to bilirubin
haem-oxigenase and biliverdin reductase both located in the spleen

51
Q

haem-oxygenase

A

ring cleavage and Fe-release

52
Q

biliverdin reductase

A

reduces biliverdin to bilirubin

53
Q

bilirubin is bound to _ in the plasma

A

albumin

54
Q

once albumin-bound bilirubin enters the liver

A

transport proteins for the bilirubin - organic anion transport protein
bilirubin enters the cell
add glnucaronic acid to make bilirubin di-gluconeride and/or bilirubin gluconeride

55
Q

why cant you dump bilirubin into bile

A

is will be reabsorbed into plasma

56
Q

why conjugate the bilirubin

A

so it can’t cross plasma membranes and be reabsorbed into plasma

57
Q

how do you conjugate the bilirubin

A

by using glucuronyl transferase on smooth endoplasmic reticulum

58
Q

multidrug-resistance protein -2

A

pumps conjugated bilirubin into canaliculus in order to secrete into bile

59
Q

how is conjugated bilirubin secreted into bile

A

via multi-drug resistance-protein 2

60
Q

what do bacteria do to the conjugated bilirubin

A

deconjufate and and metabolise it to form urobilinogen which can be reabsorbed and sent back to the liver again

61
Q

bacteria turn conjugated bilirubin into

A

urobilinogen

62
Q

what happens to absorbed urobilinogen

A

sent back to the liver to attempt to remove again, some also lost via kidneys

63
Q

jaundice

A

yellow tinted issues from excess bilirubin which causes a yellow pigment which dissolves into fatty tissues and eyes and skin

64
Q

jaundice cause by either

A
  1. haemolytic - excessive RBC destruction/myolysis
  2. hepatic - impaired uptake, disturbed processes
    - disturbed secretion, obstruction, obstructive jaundice
65
Q

assay of plasma of someone with haemolytic jaundice

A

excess free bilirubin

66
Q

assay plasma of someone with hepatic jaundice caused by impaired uptake

A

excess free bilirubin

67
Q

assay of plasma of someone with hepatic jaundice caused by disturbed secretion, obstruction - Obstructive Jaundice

A

excess free conjugated bilirubin

68
Q

jaundice of the neonate

A

newborn infants have poorly developed bilirubin conjugation enzymes and jaundice is common - premature infants more affected

69
Q

infants more commonly affected by jaundice

A

premature infants

70
Q

problems with infants with jaundice

A

unconjugated bilirubin in the brain causes permanent damage

71
Q

what is it called when there is unconjugated bilirubin in the brain causing damage

A

kernicterus - eten fatal

72
Q

how to prevent brain damage in neonates

A

phototherapy

blue light converts the bilirubin to a photo isomer which is water soluble and can be excreted in the kidneys