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GI > Liver > Flashcards

Liver Flashcards

1
Q

How much of the blood supply to the liver is from the hepatic portal vein?

A

75%

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2
Q

Why can the liver be described as a factory?

A

metabolism: CHO, proteins, lipids
synthesis: bile, proteins, nucleotides, cholesterol

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3
Q

what waste management does the liver carry out?

A

internal waste products e.g. bilirubin, ammonia, hormones (insulin, growth hormones, oestogen)
treats hazardous material e.g. food toxins, drugs

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4
Q

what 2 components are found in the space of disse?

A

collagen, stellate cells

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5
Q

what is the function of stellate cells

A

contractile

control connective tissue turnover and collagen synthesis

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6
Q

what percentage of liver cells do hepatocytes contribute to and what is their function?

A

60%

most metabolic functions

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7
Q

where are kupffer cells found and what do they do?

A

in sinusoidal lining

remove antigens, produce cytokines, immune ‘sieving’ system

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8
Q

what are pit cells?

A

liver associated lymphocytes

NKCs –> protect from viruses/ tumours

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9
Q

what is the immunological function of the liver?

A

degrades bacteria and antigens

kupffer cells –> immunoglobulins, TNF, collagenase, lysosomal hydrolases

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10
Q

what are the 3 internal waste products that the liver disposes of?

A

bilirubin, ammonia –> urea, hormones

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11
Q

What are xenobiotics?

A

potentially toxic compounds such as food toxins, drugs, food addictives

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12
Q

how many phases are involved in the metabolism of xenobiotics?

A

2

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13
Q

what occurs in the 1st stage of xenobiotic metabolism?

A

Cytochrome P450 enzyme
oxidation (oxygen donor), reduction (required NADH), hydrolysis, hydroxylation
–> MORE REACTIVE COMPOUND
in ER

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14
Q

what happens during the 2nd phase of xenobiotic metabolism?

A

conjugation - glucuronyl, acetyl, sulphate, glycyl, methyl groups added
occurs in liver, lungs, kidney
INACTIVE PRODUCTS MORE WATER SOLUBLE

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15
Q

how are xenobiotics eventually excreted from the body?

A

in urine or bile

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16
Q

how does the alcohol metabolism pathway change with chronic alcohol consumption?

A

induced CP450 production so more metabolised by this pathway

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17
Q

which enzyme is involved in the 1st stage of alcohol metabolism and where does this occur?

A

alcohol dehydrogenase in the cytosol of hepatocytes –> acetaldehyde

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18
Q

What happens to NAD during alcohol metabolism?

A

reduced to NADH

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19
Q

What happens during the 2nd stage of alcohol metabolism and where does this take place?

A

acetaldehyde dehydrogenase:

acetaldehyde –> acetate

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20
Q

what is the product of alcohol metabolism and what happens to it?

A

acetate –> acetyl coA –> krebs cycle –> ATP

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21
Q

Which cofactor is required for phase 1 xenobiotic metabolism?

A

NADPH

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22
Q

where do phase 2 xenobiotic metabolism reactions occur?

A

liver, kidney, lungs

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23
Q

Why is xenobiotic metabolism a problem with pharmacology?

A

ist pass metabolism –> inactives srug if taken orally –> poor bioavailability

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24
Q

where are RBCs disposed of?

A

spleen, liver, bone marrow by kupffer cells

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25
Q

where is haem degraded to bilirubin?

A

kupffer cells

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26
Q

how is haem degraded to bilirubin?

A

haem –> biliverdin –> bilirubin

NADPH required at each step

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27
Q

what colour is biliverdin?

A

green

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28
Q

what colour is bilirubin?

A

yellow

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29
Q

how is bilirubin transported to the liver hepatocytes?

A

attached to albumin

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30
Q

what happens to bilirubin in the liver hepatocytes?

A

conjugated mainly with glucuronic acid

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31
Q

is conjugated bilirubin secretion active or passive?

A

active

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32
Q

where is conjugated bilirubin secreted into?

A

bile canaliculi –> bile –> intestines

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33
Q

how is urobilinogen formed?

A

bacteria in the gut convert bilirubin to urobilinogen

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34
Q

why is urine yellow?

A

contains urobilin = derivative of bilirubin

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35
Q

why is faeces brown?

A

contains stercobilin

bilirubin –> stercobilinogen –> oxidised to stercobilin

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36
Q

why does jaundice occur?

A

problem with haem degredation

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37
Q

why might pre-hepatic jaundice occur?

A

overload of haem

haemolytic anaemia breaking down RBCs

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38
Q

why might intra-hepatic jaundice occur?

A

liver damage

Gilbert’s syndrome

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39
Q

which forms of jaundice result in raised unconjugated bilirubin levels?

A

pre-hepatic and intra-hepatic

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40
Q

why might extra-hepatic jaundice occur?

A

obstruction to bile duct e.g. blockage from gallstones, pancreatic carcinoma

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41
Q

what is globin degraded to?

A

amino acids

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42
Q

What are the 2 things that dietary amino acids can be use for?

A

synthesis of new compounds

breakdown for energy

43
Q

Name 6 types of N containing metabolites

A

haem, NTs (dopamine, noradrenaline, adrenaline)

serotonin, histamine, creatinine, purine bases

44
Q

which amino acid forms histamine?

A

histidine

45
Q

which 3 AAs form purine bases?

A

glycine, aspartate, glutamine

46
Q

why must the amino group be removed from AAs before they are used for energy?

A

ammonia is very toxic so blood levels must be kept very low

47
Q

what are the symptoms of hyperammonia?

A

tremor vomiting cerebral oedema death

48
Q

why might hyperammonia arise?

A

genetic defect - urea cycle enzyme deficiencies

liver disease

49
Q

what is kwashiorkor?

A

protein deficiency disease

50
Q

what are the symptoms of kwashiorkor?

A

abdominal bloating, lower leg oedema, poor nutrient absorption, poor skin condition, hair/skin colour changes, susceptible to infection

51
Q

why does kwashiorkor result in hair and skin colour changes?

A

melanin = nitrogen containing (from amino acids)

52
Q

which 3 ways can the carbon skeleton of AAs be used?

A

ketogenic pathways –> fatty acids and ketone bodies
glucogenic pathways –> glucose precursors, gluconeogenesis –> glucose
krebs cycle –> ATP (All AAs)

53
Q

which 2 amino acids cannot be used in gluconeogenesis and why?

A

leucine, lycine because they only form acteyl coA –> carbon atoms released as CO2

54
Q

when are AAs used for fatty acid synthesis?

A

storage

55
Q

when are ketone bodies formed from AAs?

A

fasting

56
Q

When are AAs used for gluconeogenesis?

A

fasting, exercise

57
Q

where does gluconeogenesis occur?

A

liver and kidney mainly in cytosol

58
Q

what 3 compounds can be used in gluconeogenesis to produce glucose?

A

anaerobic respiration –> lactate
AAs –> keto acids
triacylglycerol –> glycerol

59
Q

which AA in particular can be used in gluconeogenesis?

A

alanine

60
Q

what is the Cori cycle?

A

helps to maintain muscle metabolism by removing lactate from anaerobic respiration –> used in liver to produce glucose

61
Q

what are the 3 stages of amino group removal?

A

transamination, deamination, urea cycle

62
Q

where does transamination occur and what happens?

A

peripheral tissues
amino group from AAs attached to a-ketoglutarate to form glutamate
extra amino group –> glutamine

63
Q

which enzyme is involved in transamination?

A

transaminase

64
Q

which cofactor is required for transamination?

A

Pyroxidal phosphate (active form of vit. B6)

65
Q

what symptoms arise from a lack of B6 (pyroxidal phosphate)

A

poor growth, skin lesions, poor immune response (synthesis of AAs)
neurological symptoms (required for energy metabolism and NT synthesis)
anaemia (required for haem synthesis)

66
Q

where does deammination occur?

A

liver hepatocytes

67
Q

which enzyme is required for deamination?

A

glutamate dehydrogenase

68
Q

why must transamination occur?

A

to transport toxic ammonia in the blood to the liver

69
Q

where does the urea cycle occur?

A

in mitochondria and cytosol of liver hepatocytes

70
Q

which 2 compounds enter the urea cycle?

A

CO2 and NH3

71
Q

what is the control step of the urea cycle?

A

formation of carbamoyl phosphate

72
Q

which enzyme is responsible for carbamoyl phosphate synthesis?

A

carbamoyl phosphate synthetase 1

73
Q

what role does N-acetyl glutamate play in the control step of the urea cycle?

A

N-actyl glutamate allosterically activates carbamoyl phosphate synthetase 1, which is required for the synthesis of carbamoyl phosphate
high levels of glutamate forms N-acetyl glutamate
high levels of AAs activate the urea cycle

74
Q

what is uric acid?

A

formed from purine nucleotides

75
Q

what are the symptoms of hyperuricaemia?

A 
kidney stones (sodium urate crystals in kidneys)
gout (sodium urate crystals in joints)
76
Q

why might hyperuricaemia occur?

A

too much high purine foods (red meat seafood)
poor excretion from kidneys
over-production of urate

77
Q

which protein is not synthesised in the liver?

A

gamma globulins

78
Q

what are the 3 control steps in glycolysis?

A

glucose –> glucose -6-phosphate
fructose-6-phosphate –> fructose 1,6-bisphosphate
phosphoenolpyruvate –> pyruvate

79
Q

which enzyme converts glucose to glucose-6-phosphate?

A

hexokinase/ glucokinase

80
Q

which enzyme converts fructose 6 phosphate to fructose 1,6 bisphosphate?

A

phosphofructokinase

81
Q

which enzyme converts phosphoenolpyruvate to pyruvate?

A

pyruvate kinase

82
Q

which enzyme is the main control point for glycolysis?

A

phosphofructokinase

83
Q

where does glycolysis take place?

A

in the cytoplasm

84
Q

what are the 3 main factors that activate phospho-fructokinase?

A

high AMP (allosteric activation), insulin (alters transcription to increase gene expression), F2,6-bisP

85
Q

what effect does glucagon have on glycolysis and where does it affect the pathway?

A

inhibits production of F2,6-bisP therefore inhibits phosphofructokinase
glucagon dephosphorylates an enzyme which inhibits F2,6 bisP

86
Q

what are high levels of AMP indicative of and why?

A

low energy levels because 2 ADP join together to form ATP and AMP (enzyme = adenylate kinase)
AMP-activated protein kinases activate key enzymes

87
Q

how many pyruvate molecules are formed from one molecule of glucose?

A

2

88
Q

how many NAD coenzymes are required in glycolysis?

A

2 (to produce 2 pyruvate)

89
Q

how many ATP are directly made from glycolysis?

A

2

90
Q

overall including oxidative phosphorylation how many ATP can be make from aerobic glycolysis?

A

5-7 (2 directly and a further 3-5 from oxidative phosphorylation of 2 NADH)

91
Q

how does glucagon inhibit glycolysis?

A

phosphorylates an enzyme that inactivate F2,6BisP

92
Q

what inhibits hexokinase/glucokinase and what is this an example of?

A

product inhibition from glucose 6 phosphate

93
Q

which 2 enzymes are key to guconeogenesis?`

A

fructose 1,6 bisphophatase

glucose 6 phosphatase

94
Q

where do alanine and lactate enter gluconeogenesis?

A

converted into pyruvate

95
Q

does ATP inhibit gluconeogenesis or glycolysis?

A

glycolysis (because signals high energy state)

inhibits phosphofructokinase and pyruvate kinase

96
Q

what 4 factors regulate the activity of fructose1,6 bisphosphatase in gluconeogenesis?

A

AMP, insulin –> inhibit

citrate, glucagon –> activate

97
Q

which enzyme is involved in breaking down glucagon into glucose 1 phosphate?

A

glycogen phosphorylase

98
Q

in which organs can glycolysis produce glucose?

A

liver and kidneys

99
Q

why can’t glucose be released from muscle tissue?

A

glucose 1 phosphate can’t be broken down into glucose as lacking the enzyme for conversion (glucose 6 phosphatase)

100
Q

how many ATP/ GTP are required for gluconeogenesis to take place?

A

6

101
Q

why does alcohol inhibit gluconeogenesis and make you feel hungry?

A

alcohol metabolism produces NADH which favours the conversion of alanine to pyruvate then to lactate not lactate to pyruvate. glyceraldehyde is also converted back to glycerol. Gluconeogenesis is therefore inhibited

102
Q

what are the 2 phases of glycolysis?

A

preparative phase

generating phase

103
Q

what is produced in the preparative phase?

A

fructose 1,6-bisphosphate

104
Q

why is ATP needed for the first step of glycolysis?

A

to activate glucose by phosphorylating it

GI (10 decks)

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