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PMCOL 344 > Plasma Lipids > Flashcards

Plasma Lipids Flashcards

1
Q

what are some good things that happens if you lower plasma lipids (like cholesterol)

A

reduces incidence of CV disease and associated risks

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2
Q

what are 5 beneficial things about lipids

A
  • stored fuel
  • cell membrane
  • bile acid synthesis
  • steroid hormone synthesis
  • signalling molecules
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3
Q

what is the main precursor for bile acids

A

cholesterol

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4
Q

what are 2 examples of lipid signalling molecules

A

leukotrienes, prostaglandins

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5
Q

what are 4 adverse effects of lipids

A
  • dyslipidemias
  • atherosclresis
  • pancreatitis
  • fatty liver disease
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6
Q

what are the 2 major lipids

A

cholesterol and triglycerides

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7
Q

what kind of structure is cholesterol

A

a sterol

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8
Q

how much of cholesterol is from liver

A

80% is synthesized in the liver

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9
Q

how much of cholesterol is from diet

A

usually 20%

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10
Q

what are triglycerides (structure)

A

ester of glycerol and 3 fatty acids

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11
Q

what is the major dietary fat

A

triglycerides

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12
Q

how are triglycerides synthesized in the body

A

in the liver from free fatty acids or excess carbs in the diet

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13
Q

how is triglycerides stored

A

in adipose tissues

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14
Q

what is dyslipedemia

A

alterations in levels of lipids in the blood

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15
Q

what is hypercholesterolemia

A

high cholesterol levels in the blood

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16
Q

what is hypertriglyceridemia

A

high TG levels in the blood

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17
Q

what is hyperlipoproteinemia

A

high LDL or VLDL

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18
Q

what are 4 types of dyslipidemia

A

hypercholesterolemia, hypertriglyceridemia, hyperlipoproteinemia, low HDL

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19
Q

what do LDL and VLDL do (generally)

A

transport mechanisms in the blood stream, bind to parts of body and release cholesterol and TG where needed

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20
Q

how are plasma lipids transported

A

transported in large molecules (lipoproteins), aids solubility in aqueous plasma

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21
Q

what is the structure of plasma lipids like

A

central core of hydrophobic lipid (cholesteryl esters)

hydrophilic coat of free cholesterol, phospholipids and apoproteins

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22
Q

what are apoproteins

A

stabilize particles, function as ligands for lipoprotein uptake - regulate lipoprotein metabolism

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23
Q

where are plasma lipids assembled

A

in the liver

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24
Q

what are chylomicrons + what do they do

A

plasma lipoprotein that transports dietary TGs and cholesterol absorbed from GI tract to tissues

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25
Q

what is the largest plasma lipoproteins

A

chylomicrons

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26
Q

when are chylomicrons present

A

3-6 hours after meals

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27
Q

what does lipoprotein lipase do

A

releases free fatty acids and glycerol from TGs to leave CM remnant

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28
Q

what are CM remnants +where do they go

A

largely cholesterol, taken up by liver

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29
Q

how are CM remnants taken up by liver

A

via a receptor recognizing apoE

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30
Q

what happens once chylomicrons goes to a cell

A

lipoprotein lipase releases free fatty acids and glycerol from TGs to leave CM remnant

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31
Q

what doe VLDL stand for

A

very low density lipoproteins

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32
Q

where are VLDL

A

made in liver

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33
Q

what is the half life of VLDL

A

less than 30 mins

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34
Q

what do VLDL do

A

transport TGs and cholesterol to tissues

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35
Q

what happens once VLDL gets to cells

A

TGs are hydrolyzed by lipoprotein lipase to release free fatty acids and glycerol, leaves LDL and IDL (intermediate)

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36
Q

what does LDL do

A

deliver cholesterol to the body

37
Q

what is the half life of LDL

A

1-2 days

38
Q

what is LDL made up of

A

largely cholesterols (2/3 of plasma cholesterol)

39
Q

how is LDL taken up by tissues and liver

A

via apoB-100 receptors (LDL receptor)

40
Q

what is the most effective way to reduce plasma cholesterol

A

increasing hepatic LDL receptor expression

41
Q

why is increasing hepatic LDL receptor expression the most effective way to reduce plasma cholesterol (example)

A

by reducing dietary cholesterol, inhibiting hepatic cholesterol synthesis

42
Q

what regulates LDL receptor expression

A

sterol regulatory element binding proteins

43
Q

what does LDL receptor mutations cause

A

hypercholesterolemia

44
Q

what do sterol regulatory element binding proteins (SREBPs) do

A

regulates LDL receptor expression

45
Q

what is lipoproteina (Lp(a))

A

subset of LDL which in addition to apoB-100 also has apo(a)

46
Q

how is apo(a) attached to apoB-100 in lipoproteina

A

disulfide bond

47
Q

where is lipoproteina often found

A

localized in plaques

48
Q

what is the structure of apo(a) like (what does this cause)

A

related to plasminogen, interferes with fibrinolysis on plaque surface (pro thrombotic)

49
Q

what might lipoproteina make a link between

A

cholesterol and thrombosis

50
Q

is lipoproteina pro or anti atherogenic

A

pro

51
Q

is apo(a) pro or anti thrombotic

A

pro

52
Q

what happens to plaque breakdown if Apo(a) is on the surface

A

prevent breakdown of plaques

53
Q

what might provide the link between cholesterol and thrombosis

A

lipoproteina

54
Q

what is apoB-100 receptor

A

LDL receptor

55
Q

what is apoE

A

part of chylomicron remnants, a receptor in the liver recognizes it and takes it up

56
Q

What is the main role of HDL

A

remove cholesterol from tissues (reverse cholesterol transport)

57
Q

where is HDL made

A

in the liver

58
Q

what is HLD made of

A

mostly phospholipids and apo A1

59
Q

what does HLD to with VLDL and LDL

A

they can transfer cholesterols to vlDZL and LDL

60
Q

how is free cholesterol from cells transported to HDL

A

via ABCA1 membrane transporters

61
Q

what is ABCA1

A

membrane transporter that facilitates transport of free cholesterol from cells to HDL

62
Q

what happens if you have an ABCA1 mutation

A

low plasma HDL and cholesterol accumulation in tissues

63
Q

what is lecithin cholesterol acyltransferase (LCAT)

A

it esterifies free cholesterol and moves it to the core of HDL

64
Q

what is cholesteryl ester transfer protein (CETP)

A

it transfers cholesterol from HDL to VLDL and LDL

65
Q

where is Apo A1 found

A

in high levels in HDL

66
Q

where does apo a1 bind

A

with phospholipids on non HDL particles

67
Q

how is cholesterol esterified before moving into the core of HDL

A

lecithin cholesterol acyltransferase (LCAT)

68
Q

what transfers cholesterol from HDL to VLDL and LDL

A

cholesteryl ester transfer protein (CETP)

69
Q

how is HDL taken up by the liver

A

with an HDL receptor that recognized apo A1

70
Q

how does the liver recognize HDL so it can take it up

A

it recognizes apo A1

71
Q

what happens if you have Apo A1 mutations

A

reduced HDL uptake, accelerated atherosclerosis

72
Q

which lipid particle is associated with apo A1

A

HDL

73
Q

which lipid particle is associated with apo(a) and apoB-100

A

Lipoprotein a (subset of LDL)

74
Q

which lipid particle is associated with apoB-100

A

LDL

75
Q

which lipid particle is associated with apoE

A

chylomicron remnants

76
Q

how is plasma HDL level and risk for coronary heart disease

A

inversely

77
Q

what may be the strongest predictor of coronary heart disease related events

A

low levels of HDL

78
Q

what a re 4 benefits of HDL other than lipid stuff

A

anti: inflammatory, coaguland, oxidant and aggregatory

79
Q

what is the role of liver cholesterol levels

A

it acts as feedback mechanism to regulate further synthesis and uptake

80
Q

what does high liver cholesterol levels cause

A

decreased synthesis and inhibit LDL receptor expression

81
Q

what happens if the liver reduces LDL receptor expression (like when you have high liver cholesterol levels)

A

it means that you will reduce uptake, which then causes elevated circulating LDL

82
Q

what is the mechanism to get rid of cholesterol in liver

A

bile production

83
Q

how many mechanisms are there to get rid of cholesterol in liver

A

1- bile production

84
Q

how is bile produced

A

cholesterol is oxidized to bile acids or excreted in bile

85
Q

what is a critical gateway for regulation of plasma cholesterol levels

A

the liver

86
Q

how much % of bile acids is reabsorbed further down the GI tract

A

more than 95%

87
Q

what happens if you interrupt bile acid reabsorption

A

it is effective in increasing hepatic bile synthesis

88
Q

how does increasing hepatic bile synthesis help you? + 1 bad thing

A

it depletes hepatic cholesterol, then increases LDL receptor expression, so more LDL uptake
but then it may also increase hepatic cholesterol synthesis

PMCOL 344 (27 decks)

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