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Cardiovascular > 04.07 - Lipids (Elam) > Flashcards

04.07 - Lipids (Elam) Flashcards

1
Q

Defect in Primary Chylomicronemia

A

Defective removal of CM (apoCII, LPL defect)

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2
Q

(according to elam) what drug to give if hyper-tg-emic

A

Statins

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3
Q

(According to firecracker) To decrease TG’s, use:

A

Fibrates (and Niacin)

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4
Q

2 Fibrates

A

Gemfibrozil, Fenofibrate

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5
Q

3 AE’s of Statins

A

Teratogen, Muscle, GI distress, (and neuro)

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6
Q

3 drugs that lower TG and raise HDL

A

Fibrates, Niacin, Fish Oil

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7
Q

4 potent inhibitors of CYP3A4

A

Macrolides, CCBs, Azoles, HIV protease inhibitors

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8
Q

Advantage of Pravastatin

A

Not p450, so fewer interactions

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9
Q

Adverse Effects of Fibrates

A

GERD, Diarrhea; Fenofibrate increases creatinine, paradoxical HDL lower

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10
Q

AE’s of Niacin besides flushing

A

Liver, GI, Gout, Eye, Insulin Resistance

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11
Q

Best LDL-lowering class of drugs

A

Statins

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12
Q

Better tolerated formation of Niacin (nicotinic acid)

A

ER formulation

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13
Q

Common mechanism of Cholesterol Lowering Drugs

A

Increase LDL receptors

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14
Q

Contraindications of Bile Acids Seqs

A

Hyper-TG-emia; Complex regimens, Constipation

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15
Q

Defect in Familial Combined Hyperlipidemia

A

Overproduction of ApoB (VLDL)

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16
Q

Defect in Familial Dysbetalipoproteinemia

A

Defective Metabolism of VLDL, Chylomicrons, ApoE defects

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17
Q

Defect in Familial Hypercholesterolemia

A

LDL receptor, ApoB defect; Decreased receptor-mediated removal of LDL from plasma

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18
Q

Defect in Familial Hypertriglyceridemia

A

Defective metabolism of VLDL (LPL defect)

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19
Q

Defective metabolism of VLDL (LPL defect)

A

Defect in Familial Hypertriglyceridemia

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20
Q

Defective Metabolism of VLDL, Chylomicrons, ApoE defects

A

Defect in Familial Dysbetalipoproteinemia

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21
Q

Defective removal of CM (apoCII, LPL defect)

A

Defect in Primary Chylomicronemia

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22
Q

Desirable HDL for men

A

> 40

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23
Q

Desirable HDL for women

A

> 50

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24
Q

Drug interactions of Bile Acid Seqs

A

Prevents absorption of other drugs: Digoxin, BB’s, Thyroxine, Coumadin

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25
Q

Drugs that inhibit p-glycoprotein-mediated intestinal reabsorption

A

Cyclosporine, Grapefruite Juice

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26
Q

Effect of Colestipol on Pancreatitis

A

May make worse

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27
Q

Effect of Niacin on HDL, LDL, TG

A

HDL up, LDL down, TG down

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28
Q

Effects of Bile Acid Seqs on LDL, HDL, TG

A

Dec LDL, Modest HDL, No change or inc. TG!

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29
Q

Effects of N-3 Fatty Acids on TG, HDL, LDL

A

Reduce TG, Little-no effect on HDL, LDL

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30
Q

Elevated Cholesterol and TG; Plasma has creamy top layer with clear infranate

A

Primary Chylomicronemia

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31
Q

Gallstones

A

Fibrates

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32
Q

General MOA of Ezetimibe

A

Prevents absorption of dietary cholesterol

33
Q

General MOA of Niacin

A

Reduces VLDL synthesis

34
Q

HDL Cholesterol level ranges

A

High >60 (Desirable: >40 for men, >60 for women)

35
Q

High Potency Statins

A

Atorvastatin, Rosuvastatin

36
Q

How do Bile Acid Sequestrants work

A

Positively charged, so bind negatively charged bile acids in gut

37
Q

How do stains increase number of LDL receptors

A

Promote ER to Golgi transport and cleavage of SREBP-2

38
Q

How is Ezetimibe used?

A

Adjunct to Statin, not by itself; or in statin-intolerant patients

39
Q

If existing heart disease, what type of stains do you want to use

A

high-intensity: Atorvastatin over Pravastatin, (Rosuvastatin too)

40
Q

Increased creatinine, paradoxical HDL lowering

A

Fenofibrate

41
Q

LDL Cholesterol level ranges

A

Desirable less than 130, high greater 160

42
Q

LDL for use of high intensity statin for >21 yo patients

A

> 190

43
Q

LDL receptor, ApoB defect; Decreased receptor-mediated removal of LDL from plasma

A

Defect in Familial Hypercholesterolemia

44
Q

Lipoprotein effects of Fibrates

A

VLDL down, HDL up, TG down, LDL unchanged

45
Q

Main beneficial effects of N-3 Fatty Acids

A

Reduced plasma TG

46
Q

Metabolism of Fibrates

A

Gemfibrozil and Fenofibrate by liver

47
Q

MOA of Fibrates

A

Ligand-activation of PPARalpha nulcear receptor

48
Q

MOA’s of Niacin

A

Inhibits moblization of FFA from adipocytes; Reduces hepatic TG synthesis and ApoB (VLDL) synthesis

49
Q

Most common muscle syndrome on statins

A

Myalgia (10%), no rise in CPK

50
Q

Overproduction of ApoB (VLDL)

A

Defect in Familial Combined Hyperlipidemia

51
Q

PRIMARY tx to reduce risk of recurrent Coronary Disease Events?

A

Rosuvastatin

52
Q

Principal dietary components that increase LDL-C

A

Cholesterol, Saturated and Trans-saturated fats

53
Q

Promote ER to Golgi transport and cleavage of SREBP-2

A

How do stains increase number of LDL receptors

54
Q

Pros of Bile Acid Seqs

A

Liver Disease OK, Powder and Pill, non-systemic

55
Q

Statin metabolized by sulfation

A

Pravastatin

56
Q

Statins metabolised by CYP3A4

A

Atorvastatin, Lovastatin, Simvastatin

57
Q

Statins metabolized by CYP2C9

A

Fluvastatin, Rosuvastatin

58
Q

T/F: Adverse effect of Ezetemibe is inhibiting absorption of fat soluble vitamins

A

FALSE

59
Q

T/F: Statins are cleared almost completely first-pass?

A

TRUE

60
Q

T/F: There are proven CV benefits of adding TG lowering drugs to statins

A

False, uncertain

61
Q

TG level ranges

A

Desirable less than 120, High greater than 200

62
Q

To Decrease LDL, use

A

Statins, can add Ezetimibe

63
Q

To Increase HDL, use

A

Niacin

64
Q

Total Cholesterol level ranges

A

Desirable less than 200, high greater 240

65
Q

Type of fats that are recommended

A

Cis-mono unsaturated fats

66
Q

Unique feature of Niacin

A

Reduces Lipoprotein(a)

67
Q

What can limit use of Bile Acid Seqs

A

GI side effects (bloating, constipation)

68
Q

What causes GI irritation in Niacin use

A

Release of Histamine in gut –> Increase gastric acid –> irritation

69
Q

What does SREBP bind

A

sterol-regulatory-element 1

70
Q

What drug causes insulin resistance

A

Niacin

71
Q

What is side effect of immediate release niacin

A

flushing

72
Q

What is SREBP-2

A

Binds to sequence in LDL promoter that is sterol-responsive –> transcribe LDL receptor

73
Q

What should not be used with hx of Peptic Ulcer Disease

A

Niacin

74
Q

What type of statin do you use in high risk ASCVD patients

A

High intensity if under 75, moderate if over

75
Q

Which class is teratogenic

A

Statins

76
Q

Which Fibrate can be given with renal disease

A

Gemfibrozil

77
Q

Which Fibrate cannot be given with renal disease

A

Fenofibrate (renal excretion)

78
Q

Which fibrate cannot be given with statins and why

A

Gemfibrozil is metabolized in liver by UGT1A1, same as statins

79
Q

Which fibrate is excreted by Kidney

A

Fenofibrate

Cardiovascular (18 decks)

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