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Flipped Classroom: Lipoproteins I Flashcards

1
Q

Lipoproteins are rich in

A

Cholesterol and triglycerides

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2
Q

Can vary over a greater range than glucose

A

Lipid levels

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3
Q

Hypercholesterolemia is usually a result of

A

High LDL/HDL ratios

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4
Q

Leads to narrowing of artery walls, decreased blood and oxygen supply to the heart, and possibly heart attack and death

A

Hypercholesterolemia

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5
Q

In population studies, there is a very strong correlation between plasma LDL cholesterol and the incidence of

A

Coronary Artery Disease (CAD)

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6
Q

What percentage of adult Americans have atherosclerotic narrowing of their coronary arteries?

A

70%

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7
Q

Contain cholesterol-laden foam cells, and their location depends on the cause of the dyslipidemia

A

Xanthomas

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8
Q

Patients with hypercholesterolemia but no hypertrygliceridemia have

A

Tendon xanthomas (achilles and hands/fingers)

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9
Q

Patients with combined hypercholesterolemia and hypertriglyceridemia have

-form over joints

A

Tuberous xanthomas

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10
Q

Yellowish cholesterol deposits under the skin of the eyelids are known as

A

Xanthelasmas

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11
Q

Xanthelasmas are most commonly seen in patients with high

A

LDL cholesterol

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12
Q

The type of LDL that leads to plaque formation

A

Oxidized LDL

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13
Q

The initiation of an atherosclerotic plaque involves which three stages of development?

A
  1. ) Fatty streak formation
  2. ) Conversion to fibrous plaque
  3. ) Alteration to complex lesion
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14
Q

Lined by a monolayer of endothelial cells that is in contact with blood overlying a basement membrane

A

Tunica intima

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15
Q

The initial steps of atherosclerosis includes the recruitment of monocyte-macrophages to the subendothelial space and the infiltration of

A

Oxidized plasma LDLs

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16
Q

These oxidized LDLs are taken up by macrophages, leading to the formation of

A

Foam cells

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17
Q

A these cholesterol laden foam cells accumulate, we see further recruitment of

A

Monocyte-macrophages

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18
Q

Release cytokines an growth factors that lead to smooth muscle cell proliferation and synthesis of extracellular matrix molecules such as collagen, elastin, and proteoglycan

A

Monocyte-macrophages

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19
Q

These changes form the earliest lesion of atherosclerosis, known as the

A

Fatty streak

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20
Q

Fatty streaks form in most people by the age of 20 in the

A

Aorta and coronary arteries

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21
Q

Plaque macrophages and smooth muscle cells can die in advancing lesions by

A

Necrosis and apoptosis

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22
Q

A mixture of lipid and subintimal smooth muscle that grows into the lumen

A

Atheroma

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23
Q

In a complicated lesion, the endothelial cell layer covering the lesion is lost. As a result, the surface of the lesion becomes

A

Thrombogenic (induces clot formation)

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24
Q

This results in an increase in cellular debris and the appearance of calcification and

A

Cholesterol crystals

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25
Q

Lastly, the complicated lesion emerges with calcification and further damage to the arterial wall and alterations in the structure of the

A

Fibrous cap

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26
Q

This leads to complete occlusion of the artery, called

A

Infarction

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27
Q

Also we can see disruption of the plaque and thrombosis, leading to

A

Stroke

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28
Q

A metabolic disorder caused by a mutation in the DHCR7 gene on chromosome 11

A

Smith-Lemli-Opitz Syndrome (SLOS)

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29
Q

This DHCR7 gene codes for an enzyme that is involved in the production of

A

Choleterol

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30
Q

Are unable to make enough cholesterol to support normal growth and development

A

SLOS patients

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31
Q

Shows the facial features of microcephaly, ptosis, broad nasal ridge, upturned nose, and micrognathia (small jaw)

A

SLOS

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32
Q

The most frequently reported clinical finding in the limbs of SLOS patients is

A

Syndactyly of the 2nd and 3rd toes

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33
Q

Cleft palate, short thumbs, and polydactyly are also signs of

A

SLOS

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34
Q

In a steady state individual, the normal levels of cholesterol can be twice the normal levels of

A

Glucose

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35
Q

Consists of four fused hydrocarbon rings (A-D) called the “steroid nucleus”

A

Cholesterol

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36
Q

Cholesterol has an 8 carbon branched hydrocarbon chain attached to

A

Carbon 17 of the D ring

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37
Q

Ring A of cholesterol has a hydroxyl group at

A

Carbon 3

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38
Q

Ring B of cholesterol has a double bond between carbons

A

5 and 6

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39
Q

Most plasma cholesterol is in an esterified form. I.e it has a

A

Fatty acid attached to carbon 3

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40
Q

A very hydrophobic compound

A

Cholesterol

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41
Q

Not found in membranes, and are normally only present in small amounts in most cells

A

Esterified cholesterol

42
Q

Because of their hydrophobicity, cholesterol and its esters must be transported in association with a protein component (lipoprotein) or be solubilized by

A

Phospholipids and bile salts

43
Q

The body’s supply of cholesterol, derived from the diet and de novo synthesis is always transported in the blood packaged into

A

Lipoprotein particles

44
Q

The lipoprotein particle derived form the intestine is the

A

Chylomicron

45
Q

The lipoprotein particle derived from the liver is the

46
Q

Part of the exogenous pathway of lipoprotein metabolism

A

Chylomicron

47
Q

Part of the endogenous pathway of lipoprotein metabolism

-seen before in the context of de novo synthesized TAGs

48
Q

Takes place in the cytosol of virtually all cell types

A

Cholesterol synthesis

49
Q

The two major organs that contribute de novo cholesterol to the body’s pool

A

Liver and intestine

50
Q

The source for all carbon atoms in cholesterol

A

Acetyl-CoA

51
Q

The major co-factor required for cholesterol synthesis is

52
Q

Also consumed during cholesterol synthesis

53
Q

The rate limiting step in cholesterol synthesis is catalyzed by

A

HMG CoA reductase (HMGR)

54
Q

The rate limiting step of cholesterol synthesis, catalyzed by HMG CoA reductase produces

A

Mevalonic acid (releases free CoA)

55
Q

The rate limiting step of cholesterol synthesis, catalyzed by HMG CoA reductase uses up

56
Q

The formation of mevalonic acid is the step of cholesterol synthesis that is

57
Q

Mevalonic acid gives rise to isoprene squaline, which ‘folds up’ and through a series of intramolecular reactions gives rise to

A

Lanosterol

58
Q

Mevalonic acid gives rise not only to cholesterol, but also to

A

Terpenes (isoprenoids/isoprenes)

59
Q

Farnesyl pyrophosphate, dolichol, ubiquinones, and geranyl pyrophosphate are the terpenes we get from

A

Mevalonic acid

60
Q

Can be conjugated with proteins and then serve as lipid anchors

A

Farnesyl pyrophasphate and geranyl pyrophosphate

61
Q

Can be reduced to ubiquinols which can donate their electrons to the electron transport chain

A

Ubiquionones

62
Q

Excess cholesterol activates

-makes cholesterol esters

63
Q

Stimulates the proteolysis of HMG CoA reductase and influences RNA polymerase II’s rate of HMG-CoA reductase mRNA synthesis

A

Cholesterol

64
Q

Stimulates the activity of HMG-CoA reductase

65
Q

Inhibits the activity of HMG-CoA reductase

A

Glucagon and cholesterol

66
Q

Inhibits the uptake of cholesterol into liver cells

A

Excess cholesterol

67
Q

Reduces the levels of HMG-CoA reductase through stimulation of its degredation

A

Cholesterol

68
Q

Makes the cholesterol ore hydrophobic, enabling it to be packaged and stored and transported more easily

A

Esterification

69
Q

In epithelial cells of the intestine, some cholesterol is converted to cholesterol ester by

70
Q

Hepatocytes and steroid producing cells store cholesterol as cholesterol esters inside lipid droplets in the

71
Q

Uses a fatty acid from the phospholipid lecithin (phosphatidylcholine) on a peripheral cell to esterify cholesterol to cholesterol esters

A

Lecithin cholesterol acyltransferase (LCAT)

72
Q

In the blood, LCAT is bound to

73
Q

Regulation of HMGR through covalent modification occurs as a result of

A

Phosphorylation and dephosphorylation

74
Q

HMGR is most active in the

A

Unphosphorylated form

75
Q

Phorphorylated by AMP-activated protein kinase (AMPK) which decreases its activity

76
Q

Negatively affect cholesterol biosynthesis by increasing the activity of the inhibitor of phosphoprotein phasphatase inhibitor-1 (PPI-1)

A

Glucagon and epinephrine

77
Q

Stimulates the removal of phasphates and thereby activates HMGR

78
Q

Cholesterol synthesis is trancriptionally controlled by

79
Q

A cholesterol sensor that is the main regulator of HMGR activity

A

Sterol Regulatory Element Binding Protein (SREBP2)

80
Q

An integral membrane protein of the ER that senses the concentration of cholesterol in the ER membrane

81
Q

When the concentration of cholesterol in the ER is abnormally low, SREBP-containing visicles form and move to the

A

Golgi apparatus

82
Q

There, proteases cleave

83
Q

The N-terminal segment of SREBP2 then moves into the nucleus and enhances transcription of several genes, including the genes for

A

HMGR and also LDL receptors

84
Q

When cholesterol levels are high, there is no stimulation of

85
Q

HMGR is the target of a very widely used class of drugs called

86
Q

Structural homologues of HMGR and compete for HMG-CoA binding on the reductase, reducing its ability to promote cholesterol synthesis

87
Q

An exampleof a statin is

A

Lovastatin

88
Q

Lower blood cholesterol levels while also restoring the liver cholesterol pool

89
Q

The liver accomplishes this by upregulating the quantity of

A

LDL receptor molecules on hepatocytes

90
Q

In a small subset of the population, statins can result in profound

91
Q

Prescribed both as a preventative and in respone to CAD and MI

92
Q

Most lipids are transported in the blood as part of soluble complexes called

A

Lipoproteins (LPs)

93
Q

Plasma LPs are spherical particles composed of a hydrophobic lipid core surrounded by a

A

Hydrophilic layer

94
Q

The lipid core contains primarily

A

Triglycerides (TG) and Cholesterol Esters (CE)

95
Q

Composed of amphipathic lipids such as phospholipids, unesterified cholesterol, and special proteins called apolipoproteins or apoproteins

A

External layer of lipoproteins

96
Q

These proteins facilitate lipid solubilization and help to maintain the structural integrity of

97
Q

Serve as ligands for LP receptors and regulate the activity of LP metabolic enzymes

A

Apolipoproteins and apoproteins

98
Q

What are the 4 major categories of lipoproteins?

A
  1. ) Lipoproteins
  2. ) VLDL
  3. ) LDL
  4. ) HDL
99
Q

The largest lipoproteins but the least dense due to the large amount of triacylglycerides in these molecules

A

Chylomicrons

100
Q

The smallest lipoproteins but the most dense due to low lipid and high apoprotein content

GI (59 decks)

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