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BMS 615 Cardiovascular > Test 1: Wk1: 2 Lipoproteins - Valentovic > Flashcards

Test 1: Wk1: 2 Lipoproteins - Valentovic Flashcards

1
Q

hyperlipidemia

A

high levels of cholesterol and or triglycerides

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2
Q

Dyslipidemia

A

abnormal levels of cholesterol and or triglycerides (usually too high) and HDL levels are too low

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3
Q

Elevated Cholesterol associated with

A

increased atherosclerotic CVD

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4
Q

Elevated triglycerides associated with

A

pancreatitis

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5
Q

how are cholesterol and triglycerides transported

A

they are hydrophobic so must be transported by lipoproteins

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6
Q

lipoproteins

A

Lipoproteins have a hydrophilic outside layer with proteins,
phospholipids and unesterified cholesterol surrounding the
hydrophobic/lipophilic core of triglycerides and cholesterol esters

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7
Q

Lipoproteins transport

A

Lipoproteins transport fat soluble vitamins, cholesterol and

triglycerides in plasma, lymph as well as liver and peripheral tissues

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8
Q

3 Functions of Lipoproteins

A
  1. Involved in absorption and transport of dietary lipids from small
    intestine
  2. Transport lipids from the liver to peripheral tissues
  3. Transport lipids from peripheral tissue to liver and small intestine
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9
Q

5 Major lipoproteins

A

Chylomicrons

VLDL very low density lipoprotein

IDL intermediate density

LDL low density

HDL high density

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10
Q

Triglyceride mostly carried by — and —

A

Triglyceride mostly carried by chylomicrons and VLDL

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11
Q

Cholesterol mostly carried in — and —- as cholesterol

—

A

Cholesterol mostly carried in LDL and HDL as cholesterol

esters

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12
Q

Chylomicron Major Lipids

A

Triglycerides,

Retinyl esters

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13
Q

Chylomicron Apoprotein

A

Apo B-48, Apo E, Apo CII
and C III, Apo AI and AII

ApoB-48 only in chylomicron

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14
Q

VLDL Major Lipids

A

Triglycerides,

vit E

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15
Q

VLDL Apoproteins

A

Apo B100, Apo E, Apo

CII and Apo CIII

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16
Q

IDL Major Lipids

A

Triglycerides

Vit E

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17
Q

IDL Apoproteins

A

ApoB-100
Apo-E
Apo-CII
Apo-CIII

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18
Q

LDL Major Lipids

A

Cholesterol

Vit E

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19
Q

LDL Apoprotein

A

Apo B-100

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20
Q

HDL Major Lipids

A

Cholesterol

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21
Q

HDL Apoprotein

A 
Apo B-100
Apo-E 
Apo CII 
Apo CIII
Apo-Al
Apo AII
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22
Q

Chylomicron formation

A

Dietary Cholesterol, retinol are esterified, long chain (12 carbon) fatty
acids are incorporated into triglycerides and packaged with Apo B 48,
phospholipids to form chylomicrons

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23
Q

Chylomicrons secreted into — — and enter — —

A

Chylomicrons secreted into intestinal lymph and enter systemic
circulation

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24
Q

— — on — — of capillaries cleave off FFAs into circulation

A

Lipoprotein Lipase on endothelial cells of capillaries cleave off FFAs into circulation

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25
Q

Apolipoproteins transferred to —

A

Apolipoproteins transferred to HDL

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26
Q

Chylomicron must have — to interact with hepatic LDL receptor

A

Chylomicron must have Apo E to interact with hepatic LDL receptor

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27
Q

— are generated in the liver and are triglyceride rich

A

VLDL are generated in the liver and are triglyceride rich

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28
Q

Function of VLDL

A

esterification of LCFAs

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29
Q

VLDL contain what 4 lipoproteins

A

Apo B-100
Apo-E
Apo-CII
Apo-CIII

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30
Q

VLDL composition

Triglycerides -, Cholesterol -, -Proteins, - Other Fats

A

Triglycerides 70%, Cholesterol 10%, 10% Proteins, 10% Other Fats

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31
Q

VLDL Metabolism

A

Lipoprotein lipase on endothelial cells of capillaries (adipose tissue, heart skeletal
muscle) cleave off free fatty acids into the circulation form remnants

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32
Q

IDL are

A

equal amounts cholesterol and triglycerides

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33
Q

IDL are endocytosed by

A

the liver

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34
Q

IDL - hepatic lipases hydrolyze TG and apoB-100 transferred to —

A

IDL - hepatic lipases hydrolyze TG and apoB-100 transferred to HDL

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35
Q

IDL forms

A

LDL

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36
Q

the majority of cholesterol in the blood stream is

A

LDL

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37
Q

LDL apoproteins

A

B100 and ApoE

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38
Q

LDL has a positive correlation with

A

atherosclerotic CVD

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39
Q

LDL composition
Cholesterol —, Triglycerides —, Proteins —, Other
fats —

A

Cholesterol 26%, Triglycerides 10%, Proteins 25%, Other

fats 10%

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40
Q

Chylomicrons are generated from

A

dietary lipids

41
Q

VLDL is synthesized in

A

liver

42
Q

— cleaves FFA from chylomicrons and —

A

LPL cleaves FFA from chylomicrons and VLDL

43
Q

VLDL cleaved by — to —

and —

A

VLDL cleaved by LPL to IDL

and LDL

44
Q

LDL receptors recognize

A

LDL receptors recognize

Apo B 100 and Apo E

45
Q

HDL is generated

A

in the SI and liver

46
Q

HDL composition
— Apoprotein, —
phospholipid and —
lipids

A

50% Apoprotein, 30%
phospholipid and 20%
lipids

47
Q

— has a negative risk for CVD

A

HDL has a negative risk for CVD

48
Q 
Cholesterol not
metabolized in
---,
must be transported
to the --- for
excretion in ---
A 
Cholesterol not
metabolized in
peripheral tissue,
must be transported
to the liver for
excretion in bile
49
Q 
--- and
other cells provide
free cholesterol that
is esterified by LCAT
Form mature
A 
Macrophages and
other cells provide
free cholesterol that
is esterified by LCAT
form mature HDL
50
Q

LCAT

A

•(lecithin cholesterol

acyltransferase)

51
Q

Reverse Cholesterol Transport
higher lipids in
predominantly

A

peripheral tissue

HDL

52
Q

— taken up by liver via SR BI

A

HDL taken up by liver via SR BI

53
Q

HDL Cholesterol ester can be transferred by — to VLDL and chylomicrons

A

HDL Cholesterol ester can be transferred by cholesteryl

ester transfer protein (CETP) to VLDL and chylomicrons

54
Q

Dyslipidemias

A

Excess levels of cholesterol and triglycerides due to

multiple causes

55
Q

Primary Dyslipidemias

A

dietary and genetic

56
Q

Secondary Dyslipidemias

A

Disease and Drugs

57
Q

High — decreases risk of cardiovascular disease

A

High HDL decreases risk of cardiovascular disease

58
Q

— positive correlation with Coronary Heart Disease

A

LDL C positive correlation with Coronary Heart Disease

59
Q

first line of therapy to reduce plasma cholesterol and triglycerides

A

diet

60
Q

High cholesterol therapy

A

Decrease total daily fat intake

Decrease Saturated fat and cholesterol

61
Q

High triglycerides therapy

A

May be due to high carbohydrate intake

Reduce carbohydrates and alcohol

62
Q

Increase exercise will help reduce cholesterol and triglycerides by increasing —

A

Increase exercise will help reduce cholesterol and triglycerides by increasing HDL

63
Q

Familial hyperchylomicronemia Fredrickson Type

A

I

64
Q

Familial hyperchylomicronemia

A

Fasting plasma turbid, creamy top layer due to

chylomicrons

65
Q

Familial hyperchylomicronemia deficiencies

A

LPL or Apo C II deficiency

66
Q

Familial hyperchylomicronemia TG

A

TG >1000 mg/dl

67
Q

Familial hyperchylomicronemia Tx

A

dietary fat restriction

68
Q

Lipoprotein lipase, GPIHBP1 and Apo

CII deficiency elevated

A

chylomicrons and VLDL

69
Q

Lipoprotein lipase needed to hydrolyze — to —

A

Lipoprotein lipase needed to hydrolyze TG to Free fatty

acids

70
Q

GPIHBP1 transports —- to the apical surface

of the endothelial cells

A

GPIHBP1 transports lipoprotein lipase to the apical surface

of the endothelial cells

71
Q

Apo CII activates lipoprotein lipase on —

A

Apo CII activates lipoprotein lipase on capillaries

72
Q

Familial

dysbetalipoproteinemia (Apo E2) Fredrickson Type

A

III

73
Q

Familial

dysbetalipoproteinemia (Apo E2) high — and —

A

cholesterol and TG

74
Q

Familial

dysbetalipoproteinemia (Apo E2) inability to clear

A

VLDL and LDL

75
Q

Familial
dysbetalipoproteinemia (Apo E2)
Abnormal apo E called Apo E2 does not bind as efficiently
to — receptor

A

LDL

76
Q 
Familial hypercholesterolemia (LDL receptor)
Fredrickson Type
A

II

77
Q

Familial hypercholesterolemia (LDL receptor) LOF mutation for

A

LDL receptor resulting in diminished LDL activity

78
Q

Familial hypercholesterolemia (LDL receptor) Excess — and —

A

Excess LDL, cholesterol

79
Q

Familial hypercholesterolemia (LDL receptor) high risk for

A

CHD

80
Q

Familial hypercholesterolemia (LDL receptor) other sx

A

corneal arcus and tendon xanthomas

81
Q

Familial hypercholesterolemia (LDL receptor) autosomal —

A

dominant

82
Q

Familial Hypercholesterolemia incidernce

A

1/250

83
Q

Familial Hypercholesterolemia high

A

cholesterol

84
Q

Familial Hypercholesterolemia variants in —, —, —

A

LDL receptor
ApoB100
PCSK9

85
Q

Familial Hypercholesterolemia defective ApoB 100 results in

A

defects in receptor binding domain needed to interact with LDL receptor

86
Q

Autosomal dominant hypercholesterolemia

A

Autosomal dominant hypercholesterolemia type 3 PCSK9

Gain of function mutation in PCSK9

87
Q

PCSK9 synthesized in ER of —,

  • –, — and other
  • –
A

PCSK9 synthesized in ER of liver,
kidney, small intestine and other
tissues

88
Q

PCSK9 in blood binds to –
receptor and is endocytosed
with —

A

PCSK9 in blood binds to LDL
receptor and is endocytosed
with LDL

89
Q

PCSK9 present LDL receptor not
—, less efficient clearance
of —

A

PCSK9 present LDL receptor not
recycled, less efficient clearance
of LDL C

90
Q

Familial combined

hyperlipidema type of disorder

A

polygenic

91
Q

Familial combined

hyperlipidema high —, and —; high —, and —

A

VLDL and LDL

TGs and Cholesterol

92
Q

Familial combined
hyperlipidema
high levels of — relative to plasma —

A

high levels of apo B-100 relative to plasma LDL-C

93
Q

Familial combined

hyperlipidema small dense particles of

A

LDL

94
Q

4 results of Excessive VLDL secretion

A

High VLDL, high TG

Low HDL

Elevated Apo B 100

LDL C may be increased

95
Q

5 Secondary Causes of Excess VLDL

A

Alcohol abuse

High Carbohydrate diet

Insulin resistance

Obesity

Renal impairment

96
Q

LIPIDS ELEVATED SECONDARY TO

DISEASE Cholesterol

A 
Biliary disease
Renal disease
Hypothyroidism
Diabetes mellitus
Cushing’s syndrome
97
Q

LIPIDS ELEVATED SECONDARY TO

DISEASE Triglycerides

A 
Alcoholism
Renal disease
Diabetes mellitus
Obesity
Cushing’s syndrome (high VLDL
98
Q

exogenous pathway

A

transports dietary lipids to the periphery and the liver

99
Q

endogenous pathway

A

transports hepatic lipids to the periphery

BMS 615 Cardiovascular (49 decks)

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