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GIGU Midterm > Liver Biochemistry > Flashcards

Liver Biochemistry Flashcards

1
Q

What is the makeup of the blood supply to the liver?

A

75% of the blood supply to the liver comes from the portal vein; 25% of the blood supply to the liver comes from the hepatic artery

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2
Q

what is the biliary component made of?

A

bile ducts and the gallbladder

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3
Q

what is the one way blood gets out of the liver?

A

blood flows out of the liver through 3 hepatic veins into a big vein called the inferior vena cava

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4
Q

what is the main cell type found in the liver?

A

hepatocytes

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5
Q

what is the main function of the hepatocytes?

A

they carry out most of the metabolic functions of the liver

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6
Q

where are the endothelial cells of the liver found?

A

in the lining of the sinusoids

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7
Q

how can the endothelial cells of the liver be characterized?

A

they present loosely, they have pores and fenestrations in the plasma membrane to allow exchange of material from the liver to the blood

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8
Q

where are Kupffer cells found?

A

they are present in the lining of the sinusoids

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9
Q

what are kupffer cells?

A

they are macrophages that protect the liver from gut-derived microbes, removed damageed/dead RBCs, and orchestrate an immune response by secreting cytokines

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10
Q

what do the kupffer cells have?

A

a well-developed endocytic and phagocytic function and lots of lysosomes

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11
Q

What are the hepatic stellate cells?

A

they are lipid-filled cells and they serve as the primary storage site for vitamin A

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12
Q

what do the hepatic stellate cells control?

A

the turnover of hepatic connective tissue and extracellular matrix and regulate the contractility of the sinusoids

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13
Q

what are pit cells?

A

liver associated lymphocytes or natural killer cells

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14
Q

what is the function of pit cells?

A

they serve as a defense mechanism against the invasion of the liver by potentially toxic agents

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15
Q

what are cholangiocytes and where are they found?

A

they line the bile ducts and they control bile flow rate and bile pH

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16
Q

what blood proteins does the liver synthesize?

A

albumin, IgGs (antibodies), apoproteins, fibrinogen, prothrombin, blood clotting proteins and acute phase response proteins

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17
Q

what are acute phase response proteins?

A

acute phase response encompasses all systemic changes in response to infection or inflammation

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18
Q

what are two examples of acute phase response proteins?

A

C-reactive protein and protease inhibitors (alpha-1 Antitrypsin and alpha-1 antichymotrypsin)

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19
Q

where does the arterial and venous blood mix in the liver?

A

in the sinusoids

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20
Q

what features of the liver allow for greater access and increased contact between liver and blood?

A

lack of basement membrane and absence of tight junctions between hepatocytes and endothelial cells and fenestrations (pores) in the endothelial cell membrane

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21
Q

what is bile made of?

A

bile acids, bile salts, and cholesterol

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22
Q

what is the main function of bile acids and bile salts?

A

they emulsify fats so that they can be broken down and absorbed

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23
Q

what are bile acids and salts known to be?

A

strong detergents; amphipathic- with polar and non-polar regions

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24
Q

what are bile acids and salts synthesized from?

A

hepatic cholesterol

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25
Q

where is bile made?

A

in hepatocytes

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26
Q

where is bile released?

A

into bile canaliculi

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27
Q

when is bile released into the duodenum?

A

in response to food

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28
Q

what form is a bile acid in?

A

the protonated form (COOH)

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29
Q

what form is bile salt in?

A

the de-protonated form (COO-)

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30
Q

what surface of the bile salt molecule associates with the TAG?

A

the hydrophobic surface

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31
Q

what surface of the bile salts faces outward, allowing the micelle to associate with pancreatic lipase/colipase?

A

the hydrophilic surface

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32
Q

what is the rate limiting enzyme of the synthesis of bile acids?

A

7 alpha- hydroxylase

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33
Q

what does 7 alpha-hydroxylase transform cholesterol into?

A

7 alpha-hydroxycholesterol (adds a hydroxyl group on the 7th position- so now there are 2 hydroxyl groups)

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34
Q

where is the hydroxyl group positioned on cholesterol?

A

3rd position

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35
Q

what happens when 7 alpha-hydroxycholesterol gets 1 COOH group added?

A

it becomes chenodeoxycholic acid

36
Q

what happens when 7 alpha hydroxycholesterol gets 1 COOH group and another OH group added?

A

it becomes cholic acid

37
Q

why do we need to conjugate?

A

by conjugating, you have increased the efficiency of the bile acid to emulsify

38
Q

what is pKa’s association to efficiency of the bile acid to emulsify?

A

the lower the pKa, the more ionized the molecule, the better the detergent effect

39
Q

what happens to bile acids before secretion?

A

they are conjugated

40
Q

what are the primary bile acids?

A

cholic acid and chenodeoxycholic acid

41
Q

how many primary conjugated bile acids are there?

A

4

42
Q

how do you get the primary conjugated bile acid Glycocholic acid?

A

you add glycine to cholic acid

43
Q

how do you get the primary conjugated bile acid taurocholic acid?

A

you add taurine to cholic acid

44
Q

how do you get the primary conjugated bile acid Taurochenodeoxycholic acid?

A

you add taurine to chenodeoxycholic acid

45
Q

how do you get the primary conjugated bile acid glycochenodeoxycholic acid?

A

you add glycine to chenodeoxycholic acid

46
Q

how do you get secondary bile acids?

A

bacteria in the gut deconjugate and dehydroxylate primary bile salts

47
Q

what are the secondary bile acids?

A

deoxycholic acids and lithocholic acid

48
Q

what is an example of a medication used to treat hypercholesterolemia?

A

bile acid-binding resins

49
Q

what is an example of a bile acid-binding resin?

A

cholestyramine

50
Q

what effect does cholestyramine have?

A

they cause a large increase in secretion of bile acids, which in turn causes the rate of bile acid synthesis to be increased

51
Q

once the bile salts have done their jobs, what happens to them?

A

they are recycled back to the liver

52
Q

what happens when the rate of bile acid synthesis is increased?

A

there is depletion of the liver cholesterol pool, so there will be an increase in hepatic uptake of LDL from circulation–> lower plasma cholesterol levels

53
Q

what are gallstones?

A

crystals made up of bile supersaturated with cholesterol

54
Q

what is cholelithiasis?

A

insufficient secretion of bile salts into the gallbladder or excess cholesterol secretion into bile

55
Q

what does chronic disturbance in bile salt metabolism lead to?

A

malabsorption syndrome (steatorrhea) and deficiency in fat soluble vitamins

56
Q

the liver is the primary site for conversion and or degradation of what two things?

A

xenobiotics and/or metabolites

57
Q

what are xenobiotics?

A

compounds ingested from outside with no nutritional value/ potentially toxic

58
Q

what are metabolites?

A

compounds that are made in the body (intermediates and/or end products of metabolism)

59
Q

There are two phases to waste management. What do they entail?

A

first phase- polarity is increased. second phase- functional groups are conjugated to further increase polarity

60
Q

when the polarity of a compound is increased what happens?

A

it is easier to get rid of it (makes it more soluble)

61
Q

what are the phase I reactions catalyzed by?

A

cytochrome P450 (CYP) enzymes

62
Q

what happens in the phase one reactions and what do you get after them?

A

an oxygen is added to a xenobiotic or a waste metabolite- you get R-OH

63
Q

where are most drugs metabolized?

A

in the liver

64
Q

what does hepatic metabolism increase?

A

increases the hydrophilicity and hence their ability to be excreted

65
Q

hepatic metabolizing enzymes deal with infinite range of molecules that can be administered. How is this achieved?

A

by the responsible enzymes having low substrate specificity

66
Q

what is a characteristic of CYP?

A

they are a heme-containing protein present in the ER

67
Q

what do CYPs work with?

A

cytochrome P450 reductase (CYPR)

68
Q

Which CYP enzyme accounts for 30-40% of the CYP450 enzymes?

A

the CYP3A4 isoform

69
Q

how do CYPs operate?

A

via an electron transfer system

70
Q

the CYP protein is a heme containing protein that has iron in what form?

A

the ferric form

71
Q

what does the cytochrome P450 reductase provide as a releasing power?

A

NADPH

72
Q

Are CYPs present in high amounts in the liver?

A

no but they are induced by their substrates

73
Q

Agents that inhibit CYP will cause what?

A

increase in drug levels in the plasma

74
Q

agents that stimulate CYP will cause what?

A

decrease in drug levels in the plasma

75
Q

what is an example of a CYP inhibitor?

A

citrus juice

76
Q

what happens if a patient regularly takes their statins with a glass of grapefruit juice?

A

there will be an increase in statin levels in the plasma

77
Q

what is an example of a CYP inducer?

A

St. John’s Wort

78
Q

what happens if a patient takes a statin and St. John’s Wort?

A

there will be a decrease in statin levels in the plasma

79
Q

how is tylenol/acetaminophen eliminated?

A

it occurs via conjugation with glucuronic acid or sulfate

80
Q

what happens in acetaminophen overdose?

A

the capacity for normal conjugation is overwhelmed and it is oxidized by the liver CYP3A4 to NABQ1

81
Q

what is the NABQ1 detoxified by?

A

glutathione, but in acetaminophen overdose, the glutathione stores become depleted and the liver cells become damaged

82
Q

what can be given as an antidote to acetaminophen poisoning?

A

a sulphydryl compound called N-acetyl cysteine- it replenishes the glutathione

83
Q

what is the major change in all of the diseases of the liver?

A

the normally leaky basement membrane between endothelial cells and hepatocytes is replaced by high-density membrane containing fibrillar collagen

84
Q

what does increased stiffness of hepatic vascular channels offer?

A

resistance to free flow of blood through the liver, elevated intra-sinusoidal fluid pressure; portal hypertension

85
Q

what is the primary effect of all diseases of the liver?

A

impairment of free exchange of material between hepatocytes and blood

GIGU Midterm (19 decks)

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