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GI > Flipped Classroom: Lipoproteins III > Flashcards

Flipped Classroom: Lipoproteins III Flashcards

1
Q

The second receptor-mediated fate for circulating LDL is via the

A

Scavenger receptor

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2
Q

Has a lower affinity but broader specificity than the LDL receptor

A

Scavenger receptor

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3
Q

The scavenger receptor can recognize both

A

Normal and damaged LDL

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4
Q

Macrophages and some endothelial cell types possess the

A

Macrophage scavenger receptor (SR-A)

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5
Q

Significant percentages of LDL uptake in organs such as the intestine and spleen are accounted for by the

A

Scavenger receptor

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6
Q

SR-A has a higher affinity for

A

Oxidized (damaged) LDL

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7
Q

Leads to foam cell formation

A

SR-A

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8
Q

Even after mRNA has been fully processed, it may undergo additional posttranscriptional modification in which a base in the mRNA is altered. This is known as

A

RNA editing

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9
Q

The apoB mRNA is made in the

A

Liver and small intestine

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10
Q

However, in the small intestine only, the C residure in the codon CAA for glutamine is deaminated to U, changing this to a

A

Stop codon

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11
Q

This results in translation of the shorter protein known as

A

ApoB-48

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12
Q

What makes

  1. ) ApoB-100
  2. ) ApoB-48
A
  1. ) Liver (incorporated into VLDL)

2. ) Intestines (Chylomicron)

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13
Q

A circulating, abnormal varient of LDL

A

Lipoprotein(a) aka Lp(a)

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14
Q

Forms when ApoA forms a disulfide bonded complex with the ApoB-100 component of LDL

A

Lp(a)

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15
Q

A modest independent risk factor for atherosclerotic cardiovascular disease events, especially an MI

A

Lp(a)

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16
Q

Certain SNPs of the LPA gene maybe be associated with higher population risks for

A

CVD

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17
Q

VLDLs travel in the circulatory system until they associate with LPL. This association is mediated via

A

ApoC-II

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18
Q

Serves to remove excess cholesterol from the peripheral tissues and return it to the liver

A

Reverse cholesterol pathway

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19
Q

This movement is accomplished by

A

HDL

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20
Q

Transport of cholesterol from the liver to peripheral tissues is called

A

Cholesterol transport

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21
Q

While the transport of cholesterol from the peripheral tissues to the liver and steroid producing tissues is called

A

Reverse cholesterol transport

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22
Q

Formed in the blood by the addition of ipid to ApoA-I

A

HDL

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23
Q

Accounts for about 70% of the apoproteins in HDL

A

ApoA-I

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24
Q

Serves as a circulating reservoir of ApoC-II and ApoE

A

HDL

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25
Q

The apolipoprotein that is transferred to VLDL and chylomicrons and is an activator of LPL

A

ApoC-II

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26
Q

The apolipoprotein required for the receptor-mediated endocytosis of IDLs and chylomicron remnants

A

ApoE

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27
Q

Nascent HDL particles are derived from both the

A

Liver and intestine

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28
Q

Unlike the chylomicron and VLDL, the nascent HDL is not spherical but rather

A

Disc-shaped

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29
Q

Are also derived from surface components of both chylomicrons and VLDLs

A

HDL particles

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30
Q

ApoA-I activates

A

LCAT

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31
Q

ApoA-II activates

A

HL

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32
Q

Protein that is secreted by the liver and circulates in plasma, bound mainly to HDL

A

Cholesterol Ester Transfer Protein (CETP)

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33
Q

Promotes the redistribution of cholesterol esters, triglycerides, and, to a lesser extent, phospholipids netween plasma lipoproteins

A

CETP

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34
Q

The overall net effect of CETP is a net mass transfer of cholesterol esters from HDL to triglyceride-rich lipoproteins and

A

LDL

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35
Q

Also has the net effect of moving triglycerides from triglyceride-rich lipoproteins to LDL and HDL

A

CETP

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36
Q

Subsequently, the TAGs are removed from HDL by

A

HL

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37
Q

One consequence of these CETP-mediated transfers of cholesterol esters from HDL is a reduction in the cholesterol content and size of

A

HDL

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38
Q

The overall effect of CETP is a net mass transfer of cholesterol esters from HDL to

A

VLDL

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39
Q

The overall effect of CETP is also a net mass transfer of triglycerides from VLDL to

A

HDL

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40
Q

Nascent HDL form chiefly in the liver and intestine by loading phosphatidylcholine, cholesterol, and cholesterol esters onto

A

ApoA-I

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41
Q

Used by the liver to enrich discoidal HDL w/ phosphatidylcholine and cholesterol

A

ABCA1 transporter

42
Q

When colesterol is taken up by HDL, it is immediately esterified by the plasma enzyme

A

LCAT

43
Q

LCAT is synthesized and secreted by the

A

Liver

44
Q

LCAT binds to nascent HDL and is activated by

A

ApoA-I

45
Q

Transfers the fatty acid from carbon 2 of phosphatidylcholine to cholesterol, producing a hydrophobic cholesterol ester

A

LCAT

46
Q

Whic HDL is more cholesterol ester rich, HDL3 or HDL2?

A

HDL2

47
Q

CETP moves some of the cholesterol esters from HDL to VLDL in exchange for TAG, relieving product inhibition of

A

LCAT

48
Q

Because VLDLs are catabolized to LDL, the cholesterol esters transferred by CETP are ultimately taken up by the

A

Liver

49
Q

The uptake of cholesterol esters by thge liver is mediated by a cell-surface receptor

-Binds HDL

A

SR-B1

50
Q

The HDL particle itself is not taken up. Rather, there is selective uptake of the cholesterol ester from the

A

HDL particle

51
Q

With it’s ability to degrade both TAG and phospholipids, participates in the conversion of HDL2 to HDL3

A

HL

52
Q

Elevation of plasma cholesterol, triglycerides (TGs), or both, or a low HDL level that contributes to atherosclerosis

A

Dyslipidemia

53
Q

Can result from a single inherited gene defect, or more commonly, are caused by a combination of genetic and environmental factors

A

Primary hyperlipidemias

54
Q

The result of a metabolic disorder such as DM, obesity, hypothyroidism, or primary biliary cirrhosis

A

Secondary hyperlipidemias

55
Q

How do we calculate LDL cholesterol?

-the Friedewald equation (mg/dL)

A

LDL cholesterol = Total cholesterol - HDL - VLDL

56
Q

The Friedewald equation is inaccurate when the concentration of triglycerides is high (greater than 400) or when there is an appreciable number of

A

Chylomicrons

57
Q

How do we calculate VLDL cholesterol?

A

Total triglycerides/5

58
Q

Patients who have hypertriglyceridemia mayhave normal or elevated

A

LDL cholesterol

59
Q

Hypertriglyceridemia is defined as total plasma triglycerides in the fasting state in excess of

A

150 mg/dL

60
Q

The hyertriglyceridemia is due to an abnormally high quantity of

A

Chylomicrons, VLDL, or both

61
Q

The major risk of very severe hypertriglyceridemia is

A

Pancreatitis

62
Q

Patients who hace very severe hypertriglyceridemia may also have

A

Eruptive and tuberous xanthomas

63
Q

Characterized by the pathologic presence of chylomicrons after a 12-14 hour period of fasting

A

Familial chylomicronemia

64
Q

In familial chylomicronemia, samples of lipemic plasma that are refridgerated overnight develop a

A

Creamy supernatant

65
Q

When the plasma is tested, fasting triglyceride measurements are typically above

A

1000 mg/dL

66
Q

Lowering of plasma triglycerides to below 500 mg/dL virtually eliminates a person’s risk of a repeat episode of hypertriglyceridemia-induced

A

Pancreatitis

67
Q

Due to deficiency of LPL and ApoC-II activity

A

Familial chylomicronemia

68
Q

Has secondary factors and a greater elevation of total cholesterol relative to that in familial chylomicronemia

A

Primary mixed hyperlipidemia

69
Q

Characterized by the accumulation of remnants of chylomicrons and of VLDLs

A

Dysbetalipoproteinaemia

70
Q

This is because Dysbetalipoproteinaemia develops due to a deficiency of

A

ApoE

71
Q

Has a population prevalence of 1-2 in 20,000

A

Familial dysbetalipoproteinaemia

72
Q

Plasma levels of LDL levels are decreased and plasma levels of IDL are increased because of interrupted processing of VLDL in

A

Dysbetalipoproteinaemia

73
Q

An increased VLDL:triglyceride ratio and an ApoE homozygosity are therefore diagnostic for

A

Familial Dysbetalipoproteinaemia

74
Q

The onset of Familial Dysbetalipoproteinaemia occurs after

A

Childhood

75
Q

In women, onset of Familial Dysbetalipoproteinaemia is typically delayed until

A

Menopause

76
Q

Clinical manifestations may very from no physical signs to severe cutaneous and tendinous xanthomata, atherosclerosis of coronary and peripheral arteries, and pancreatitis when severe hypertriglyceridemia is present

A

Familial Dysbetalipoproteinaemia

77
Q

The cornerstone of treatment for hypertriglyceridemia

A

Lifestyle modification

78
Q

Reduces VLDL production in a high dose

A

Statin

79
Q

Increases LPL activity

A

Sipplement of fish oil rich in omega-3 FA

80
Q

Activate PPARa transcription factors that lead to both increased lipoprotein lipase activity and an increased rate of fatty acid B-oxidation

A

Fibrate drugs

81
Q

Works in part by activating niacin receptor 1 that inhibits lipolysis

A

Nicotinic acid (Vitamin B3)

82
Q

People with hypercholesterolemia have a high risk of developing

A

Coronary artery disease

83
Q

People that have two alleles for a defective LDL receptor have

A

Homozygous familial hypercholesterolemia

84
Q

Have an LDL concentration that is 10x the normal concentration

A

Patients with Homozygous familial hypercholesterolemia

85
Q

In less frequent circumstances, a patient can have Homozygous familial hypercholesterolemia due to two loss-of-function mutations in

A

ApoB-100

86
Q

About 5% of heterozygous familial hypercholesterolemia pateints have a mutant

A

ApoB-100

87
Q

About 2% of heterozygous familial hypercholesterolemia pateints have overactive

A

PCSK9 enzyme

88
Q

Most patients who have heterozygous familial hypercholesterolemia have a mutant allele for the

A

LDL receptor

89
Q

Patients with heterozygous familial hypercholesterolemia typically have how much more LDL than usual?

A

2x

90
Q

Patients with heterozygous familial hypercholesterolemia that is untreated typically have heart attacks before their

A

Late 50’s

91
Q

Patients with Homozygous familial hypercholesterolemia typically have heart attacks in their

A

Teens and twenties

92
Q

The most common lipoprotein abnormality among pateints with CAD

A

Low HDL (less than 40 mg/dL)

93
Q

Low HDL is also a component trait of the

A

Metabolic syndrome

94
Q

The most common genetic disorder of HDL is

A

Familial hypoalphalipoproteinemia (FHA)

95
Q

Common finding in patients with premature CAD

A

FHA

96
Q

Results in a profound decrease in HDL (less than 5 mg/dL)

A

Complete loss of ApoA-1

97
Q

ApoA-1 deficient patients can be distinguished from other causes of HDL deficiency by the complete absence of

A

ApoA-1

98
Q

Patients with ApoA-1 deficiency also have normal levels of

A

LDL and TAGs

99
Q

Patients with HDL deficiency due to ApoA-1 deficiency may also exhibit mild to moderate

A

Corneal opacification or corneal clouding

100
Q

Another cause of low HDL is

A

LCAT deficiency

GI (59 decks)

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