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CVPR > CVPR Week 4: Introduction to lipids > Flashcards

CVPR Week 4: Introduction to lipids Flashcards

1
Q

Objectives

A
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2
Q

Epidemiology

A
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3
Q

Leading cause of death worldwide

A
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4
Q

Approaches to CVD prevention

4 listed

A
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5
Q

Lipoprotein management

A
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6
Q

CVD Risk

A
  • Abnormal lipid metabolism
  • ↑ LDL
  • ↑ ApoB
  • ↓ HDL
  • ↑ Triglycerides
  • Age, gender, race, FHx
  • Inflammation, hypercoagualation
  • HTN
  • Smoking, physical inactivity
  • Unhealthy eating
  • Insulin resitance
  • Obesity/overweight
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7
Q

Heart deaths during the last century

A
  • in 1900 CVD very low
  • decrease in mid-80s because the first statin was released in 1984 and HTN drugs
    *
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8
Q

Features of a ruptured atherosclerotic plaque

A

eccentric

lipid-rich

prior luminal obstruction

visible rupture and thrombus

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9
Q

Identify

A
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10
Q

What are these?

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11
Q

What is this?

A
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12
Q

What do statins inhibit?

A

HMG-CoA Reductase

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13
Q

What do biphosphonates inhibit?

A

Farnesyl-PP synthase

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14
Q

Synthesis of cholesterol biochemistry

A
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15
Q

Ubiquinone AKA

A

Co-enzyme Q10

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16
Q

Muscle aches and pains from statin therapy

A

(Co-Q10) Ubiquinone supplement to decrease myalgias on statins (Co-Q10)

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17
Q

The process of fat digestion

8 steps listed

A
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18
Q

APO-lipoprotein B48

A

on chylomicron

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19
Q

Apoprotein C-II

A

increases efficiency of lipoprotein lipase on the intestinal wall

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20
Q

Lipoprotein lipase

A

breaks down triglycerides into Free-fatty acids

feeds muscle tissue and adipocytes and cells that can use FFAs

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21
Q

Identify

A
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22
Q

Lipoprotein subclasses

A
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23
Q

Lpa is. . .

A

thrombogenic

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24
Q

Apo B can cause

A

CVD

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25
Q

ApoAI is

A

good cholesterol kind of

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26
Q

Lipoprotein metabolism

A

Fats into intestine LPL lipoprotein lipase breaks down into FAs and make chylomicron remnant to the liver and forms VLDL

CII improves LPL, CIII is antagonistic to CII

VLDL with LPL forms IDL

IDL with Hepatic lipase forms LDL

LDL donates cholesterol to the liver but sometimes it gets into the interluminalmedial space and gets oxidized

oxidized LDL gets phagocytosed by macrophages

ABCA1 (ATP binding Cassette A1) on macrophage allows free cholesterol to get into a Free nascent HDL particle that has APO-AI and some has APO-AII

HDL has a scavenger receptor B1 to donate cholesterol to the liver or other tissues and take excess cholesterol back to the liver and the liver can make bile and can be excreted or recycled

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27
Q

Size of Lipoproteins

A
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28
Q

Types of hypercholesterolemia

6 listed

A
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29
Q

Fill in the table

Type I

A
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30
Q

Fill in the table

Type IIA

A
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31
Q

Fill in the table

Type IIB

A
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32
Q

Features of Type I Hypercholesterolemia

A
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33
Q

Features of Type IIA Hypercholesterolemia

A
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34
Q

Features of Type IIB Hypercholesterolemia

A
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35
Q

Features of Type III Hypercholesterolemia

A
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36
Q

Features of Type IV Hypercholesterolemia

A
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37
Q

Features of Type V Hypercholesterolemia

A
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38
Q

Cause of Type I Hypercholesterolemia

A
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39
Q

Cause of Type IIA Hypercholesterolemia

A
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40
Q

Cause of Type IIB Hypercholesterolemia

A
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41
Q

Cause of Type III Hypercholesterolemia

A
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42
Q

Cause of Type IV Hypercholesterolemia

A
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43
Q

Cause of Type V Hypercholesterolemia

A
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44
Q

Other features of Type I Hypercholesterolemia

A
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45
Q

Other features of Type IIA Hypercholesterolemia

A
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46
Q

Other features of Type IIB Hypercholesterolemia

A
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47
Q

Other features of Type III Hypercholesterolemia

A
48
Q

Other features of Type IV Hypercholesterolemia

A
49
Q

Other features of Type V Hypercholesterolemia

A
50
Q

Type I Hypercholesterolemia AKA

A

Familial hyperchylomicronemia

51
Q

Familial hyperchylomicronemia AKA

A

Type I Hypercholesterolemia

52
Q

Type IIA Hypercholesterolemia AKA

A

Familial hypercholesterolemia

53
Q

Familial hypercholesterolemia AKA

A

Type IIA Hypercholesterolemia

54
Q

Type IIB Hypercholesterolemia AKA

A

Familial combined (mixed) hyperlipidemia

55
Q

Familial combined (mixed) hyperlipidemia AKA

A

Type IIB Hypercholesterolemia

56
Q

Type III Hypercholesterolemia AKA

A

Familial dysbetalipoproteinemia

57
Q

Familial dysbetalipoproteinemia AKA

A

Type III Hypercholesterolemia

58
Q

Type IV Hypercholesterolemia AKA

A

Familial hypertriglyceridemia

59
Q

Familial hypertriglyceridemia AKA

A

Type IV Hypercholesterolemia

60
Q

Type V Hypercholesterolemia AKA

A

Familial mixed hypertriglyceridemia

61
Q

Familial mixed hypertriglyceridemia AKA

A

Type V hypercholesterolemia

62
Q

Type I hypercholesterolemia drug treatment

A

no effective drug treatment

63
Q

Type IIA hypercholesterolemia drug treatment

A

limits usefulness of some drugs, especially statins

64
Q

The initial steps in atherosclerosis

A

fatty streak is the first sign of atherosclerotic disease

65
Q

The fatty streak

A
66
Q

Question 1

A

C. Less than 50% stenosis

67
Q

Most myocardial infarctions are caused by what grade of stenosis

A

Low-grade stenosis because the thought is that a low-grade stenosis the fibrous cap is weaker when there is a small stenosis and haven’t had time to form a stable stronger fibrous cap

68
Q

Lab Cholesterol levels

A

< 200 is normal

69
Q

Lab LDL Cholesterol levels

A
70
Q

Lab HDL Cholesterol levels

A
71
Q

Lab Triglyceride levels

A
72
Q

High triglyceride and low HDL ratio clinical pearl greater than?

A

greater than 3.8

higher than normal risk for insulin resistance and heart disease

73
Q

Guiding principles for treating hyperlipidemia

A
74
Q

Mediterranean diet

A
75
Q

Diet recommendations for hyperlipidemia

A
76
Q

If you can eat more than 30g of fiber per day

A

you can decrease the chance of CVD by 30%

77
Q

Recommendations for hyperlipidemia

4 listed

A
78
Q

HMG Co-A Reductase inhibitors AKA

A

Statins

79
Q

Statins Effect on LDL

A

↓↓↓ LDL

80
Q

Statins effect on HDL

A

↑ HDL

81
Q

Statins effect on TG

A

↓

82
Q

Statins MOA

A

Inhibits the rate-limiting step of cholesterol precursor formation HMG Co-A Reductase

83
Q

Statins Side effects

A
  • Hepatotoxicity
  • Rhabdomyolysis (especially in combo with fibrates & niacin)
84
Q

Statins contraindicated in?

A

Active liver disease and pregnancy

85
Q

Statins caveats

A
86
Q

Statins pathway & effects

A
  • lower intracellular concentrations of cholesterol
  • when this happens it increases the number of receptors on the cell surface for cholesterol and thereby increases clearance
87
Q

Pleiotropic effects of statins

6 listed

A
88
Q
A
89
Q

Statin effect on thrombus formation

A

Reduce thrombus formation by

↓ PAI-1

↓ tF

90
Q

Statin effect on platelet aggregability

A

Reduce platelet aggregability

91
Q

Statin effect on plaque inflammation

A

reduced inflammation within plaque by

↓ CRP

↓ monocyte adhesion

92
Q

Statin effect on endothelial function & vasomotion

A

improve endothelial function & vasomotion by

↑ NO bioavailability

↑ circ. endothelial progenitor cells

93
Q
A
94
Q

Statin effect on matrix degradation

A

Decrease matrix degradation by

↓ macrophage metalloproteinase

↑ collagen content

95
Q

Statin effect on plaque remodeling

A

Promote plaque remodeling by

↑ HDL - Cholesterol

↓ LDL - Cholesterol

↓ TGL

96
Q

Comparison of statin dose response

A
97
Q

if you double a dose of a statin

A

6% lowering of LDL

double again another 6% dose

RULE OF 6

6% reduction for doubling the dose

98
Q

Risk-enhancing factors that favor the initiation of statin therapy

9 listed

A
99
Q

Summary of drugs to treat hyperlipidemia

A

KNOW THIS!

100
Q

the only drug in this group that lowers LP a

A

Niacin

101
Q

Omega 3 FAs effects

A
102
Q

CCT of hyperlipidemia

A

22% reduction by 1mmol/L

103
Q

HMG CoA reductase primary prevention

A
104
Q

HMG CoA reductase secondary prevention

A
105
Q

Proprotein convertase Substilisin / Kexin-9

A

PCSK-9 is made by the liver, it binds to LDL receptor and everything gets metabolized

when you dont have this you get degradation of LDL

so we now have antibodies to PCSK-9

which can decrease LDL by 60% on top of statins

want to get below 20 mg/dl of LDL and decrease events

if you get LDL below 50 and 40 can regress already built up plaque

lower the LDL the healthier the patient

106
Q

PCSK-9 AKA

A

Proprotein convertase Substilisin / Kexin-9

107
Q

Summary of cholesterol metabolism and synthesis and drug therapy

A
108
Q

Fibric acid derivatives AKA

A

Fibrates

109
Q

Homozygous hyperlipidemia drugs

A

1 in 1,000,000

have first coronary event between 10 and 20 years old

mipomersen APOb levels go down

Lomitapide inhibits microsomal transfer protein (MTP) Decreasing TG loading into VLDL

110
Q

New risk calculator

A
111
Q

Secondary prevention

A

means they’ve already had an event

under 75 need a minimum of 50% reduction and get under 70 mg/dl

112
Q

Primary prevention

A
113
Q

if unsure if they need treatment

A

CAC (coronary artery Ca2+) score will help make a decision

114
Q

LDL conc. vs particle number

A
115
Q

Apo and lipid measures relationship

A
116
Q

LDL and LDL

A
117
Q

CHD

A

CVPR (93 decks)

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