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CDM1 > Exam 2: HLD > Flashcards

Exam 2: HLD Flashcards

1
Q

Statins: MOA

A 
HMG CoA reductase inhibitors (decrease cholesterol synthesis) 
Decrease LDL (upregulation of LDL receptors)
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2
Q

PSCK9i: Examples

A

Evolocumab (Repatha)

Alirocumab (Praluent)

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3
Q

PSCK91: MOA

A

Activate SREBP which inhibits PCSK9 and increase LDL receptors

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4
Q

Fibrates: MOA

A

Activate PPAR-alpha receptor

  • increase lipoprotein lipolysis (increase HDL)
  • decrease TG
  • increase LDL size
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5
Q

Fibrates: examples

A

Gemfibrozil (Lopid)
Fenofibrate (Tricor)
Clofibrate (Atromid)
Fenofibric acid (Trilipix)

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6
Q

Niacin: MOA

A

Increase HDL and decrease hepatic synthesis/secretion VLDL

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7
Q

Bile acid sequestrants: Examples

A

Cholestryramine
Colestipol
Colesevelam

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8
Q

Bile acid sequestrants: MOA

A

Decrease LDL

Decrease intestinal reabsorption of bile (makes liver use cholesterol to make more bile)

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9
Q

Ezetimibe: MOA

A

Inhibit cholesterol absorption in small intestine

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10
Q

Ezetimibe dosing

A

5-10mg po daily

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11
Q

Counseling for statins and fibrates

A

Weakness/pain/fatigue

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12
Q

Counseling for niacin

A

Flushing (take ASA 325mg 30min before)

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13
Q

Counseling for bile acids

A

No drugs 2 hrs before and 4hrs after bile acids

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14
Q

Which medications do NOT require LFTs

A

Bile acids and ezetimibe

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15
Q

Which agent is most potent for increase HDL and decrease TG

A

Niacin

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16
Q

Which agent is mostly used for decrease LDL but not increase HDL and decrease TG?

A

Ezetimibe

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17
Q

What is the primary fxn of lipoproteins?

A

Transportation of TG and cholesterol from liver to tissues vice versa

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18
Q

Chlyomicron TG/Chol/Protein

A

90/5/5

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19
Q

VLDL TG/Chol/Protein

A

60/30/10

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20
Q

LDL TG/Chol/Protein

A

10/60/30

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21
Q

HDL TG/Chol/Protein

A

10/30/60

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22
Q

What is the fxn of HDL

A

Transport excess cholesterol from body to liver

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23
Q

What is the fxn of LDL

A

Transport cholesterol from liver to body

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24
Q

T/F: APO A1 is artherogenic

A

False – APO A1 is artheroprotective and APO B is artherogenic

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25
Q

LDL Size: Fluffy LDL is a/w ___ ASCVD risk

A

Less – fluffier the less ASCVD risk

fibrates increase LDL particle size!

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26
Q

For every 1mg/dL decrease of LDL, there is a ___ decrease in ASCVD risk

A

1%

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27
Q

For every 1mg/dL increase of HDL, there is a ___ decreased risk of ASCVD

A

2%

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28
Q

Def: Primary hyperlipidemia

A

Familial hyperlipidemia

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29
Q

For every 7lbs lost, there is 1mg/dL increase of ____

A

HDL, and 2% decrease of ASCVD

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30
Q

Secondary hyperlipidemia: Diet: What increases LDL

A

sat/trans fat, weight gain, anorexia

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31
Q

Secondary hyperlipidemia: Diet: What increases TG

A

Weight gain, very low-fat diets, intake of refined carbs, excessive alcohol

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32
Q

Secondary hyperlipidemia: Diseases: What increases LDL

A

Hepatic disease, biliary obstruction, nephrotic syndrome

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33
Q

Secondary hyperlipidemia: Diet: What increases TG

A

Nephrotic syndrome, chronic renal failure, lipodystrophies

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34
Q

Secondary hyperlipidemia: Disorders/altered states of metabolism: What increases LDL and TG

A

DM, HYPOthyroidism, obesity, pregnancy

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35
Q

Secondary hyperlipidemia: Drug induced: What what are the effect on lipids for alcohol

A

Increased TG

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36
Q

Secondary hyperlipidemia: Drug induced: What what are the effect on lipids for thiazide diuretics

A

Increased LDL and TC

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37
Q

Secondary hyperlipidemia: Drug induced: What what are the effect on lipids for BB

A

Increased TG, decrease HDL

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38
Q

Secondary hyperlipidemia: Drug induced: What what are the effect on lipids for glucocorticoids

A

Increased VLDL, LDL, and TC

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39
Q

Secondary hyperlipidemia: Drug induced: What what are the effect on lipids for olanzapine

A

Increase LDL and TC

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40
Q

Secondary hyperlipidemia: TLC: For every 1% every from saturated fat replaced with CHO, decrease of LDL/HDL is ___

A

1.2 and 0.4

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41
Q

Secondary hyperlipidemia: TLC: For every 1% every from saturated fat replaced with Monounsaturated FA, decrease of LDL/HDL is ___

A

1.3 and 1.2

42
Q

Secondary hyperlipidemia: TLC: For every 1% every from saturated fat replaced with polyunsaturated FA, decrease of LDL/HDL is ___

A

1.8 and 0.2

43
Q

Secondary hyperlipidemia: TLC: diet adherence decreases LDL and CHD by

A

LDL: 10-15%
CHD: up to 25%

44
Q

Low-fat diet ___ HDL in all pts

A

lower

45
Q

Alcohol ___ HDL in dose-dependent manner

A

increase

46
Q

Caloric restriction ___ HDL

A

acutely lowers HDL

47
Q

What is the effect of smoking cessation on HLD?

A

Increase HDL 15-20% within 30-60 days after smoking cessation

48
Q

What is the difference between Omega 6 and 3?

A

Omega 6: corn, safflower, sunflower – BAD (more thrombotic/inflammatory)
Omega 3: flaxseed, canola, soybean, oily fish, fish oil caps, PUFA – GOOD (less thrombotic/inflammatory)

49
Q

Cholestin is basically a low dose of which statin?

A

Lovastatin

50
Q

Cholestin effect on HLD

A

Decrease LDL and TG

51
Q

Does soy have an effect on HLD

A

Slightly – 50g/day

52
Q

What are risk enhancers of ASCVD?

A

FHx of premature ASCVD (males <55, females <65)
Primary hypercholesterolemia (LDL 160-189 or non-HDL 190-219)
CKD (eGFR 15-59)

53
Q

Lipid panel labs: What is assessed and do you need to fast?

A

TC, TG, and HDL

At least 12 hr fast

54
Q

Lipid panel labs: What happens if pt does NOT fast?

A

TG levels may be increased

TC and HDL not significantly affected by food

55
Q

Lipid panel labs: When do you need to have a 2nd lipid panel done?

A

When TC >200

56
Q

Non-HDL goal

A

30mg/dL above LDL goal (25mg/dL above LDL goal if extreme risk)

57
Q

LDL Goal in general

A

lower LDL by ≥50% and/or LDL ≤100mg/dL

58
Q

HLD: ASCVD Primary Prevention: LDL ≥190 – recommendation and F/U

A

High intensity statin

F/U if LDL ≥70 add ezetimibe (and then add PCSK-9i if needed)

59
Q

HLD: ASCVD Primary Prevention: Age 40-75, LDL ≥70 AND DM– recommendation and F/U

A

Mod intensity statin and/or 10yr risk

F/U modify via 10yr risk

60
Q

HLD: ASCVD Primary Prevention: Age 40-75, LDL ≥70 AND DM AND uncontrolled RF– recommendation and F/U

A

high intensity statin and/or 10yr risk

F/U modify via 10 yr risk

61
Q

HLD: ASCVD Primary Prevention: Age 40-75, LDL 70-189– recommendation and F/U

A

Check 10 yr risk

F/U modify via 10 yr risk

62
Q

HLD: ASCVD Primary Prevention: 10yr risk – <5%

A

Emphasize LTC to reduce risk factors

63
Q

HLD: ASCVD Primary Prevention: 10yr risk – 5-7.5%

A

If risk enhances present –> mod intensity statin

64
Q

HLD: ASCVD Primary Prevention: 10yr risk – <7.5-20%

A

If risk estimate + risk enhancers favor statin –> moderate-intensity statin to reduce LDL 30-49%

65
Q

HLD: ASCVD Primary Prevention: 10yr risk – ≥20%

A

initiate statin to reduce LDL ≥50%

66
Q

HLD: ASCVD Secondary Prevention: Very high risk

A

High intensity statin or maximal dose statin

F/U if LDL ≥70 add ezetimibe (and then add PCSK-9i if needed)

67
Q

HLD: ASCVD Secondary Prevention: Not very high risk and ≤75 yo

A

High intensity statin

F/U if LDL ≥70 add ezetimibe (and then add PCSK-9i if needed)

68
Q

HLD: ASCVD Secondary Prevention: Not very high risk and > 75yo

A

Mod-high intensity statin

F/U if LDL ≥70 add ezetimibe (and then add PCSK-9i if needed)

69
Q

Def: Peripheral arterial Disease (PAD)

A

progressive narrowing of the arteries due to atherosclerosis in the peripheries (most common form of peripheral vascular disease)
Associated with elevated risk of morbidity/mortality from CVD even without a PMH of acute MI/stroke

70
Q

Def: Intermittent claudation

A

Fatigue, discomfort, cramping, pain, or numbness in affected extremities during exercise and resolves within minutes with rest

**primary indicator of PAD

71
Q

Def: Critical limb ischemia

A

Chronic ischemic, at-rest pain, ulcers, or gangrene in one or both legs (amputation ranges from 10-40%)

72
Q

T/F: Pathophysiology for PAD and hyperlipidemia is the same

A

True – arthersclerosis is the underlying cause for both

73
Q

PAD risk factors

A 
Age >40
Smoking
Diabetes
HTN
HLD
74
Q

PAD: Factors that increase risk of limb loss in pts with CLI

A

DM, severe renal failure, severely decreased CO (severe HF/shock), smoking

75
Q

PAD s/sx

A

Most are asymptomatic

Atypical leg pain, classical (typical claudation), CLI

76
Q

Claudation s/sx

A

Aching/burning in leg muscles
Reliably reproduced at a set distance of walking
Relieved within minutes on rest (never present at rest)
Not exacerbated by position

77
Q

CLI s/sx

A

1 or more: Ulceration, gangrene, rest pain in foot for more than 2 weeks
May be resistant to opiate analgesia
Difficult to distinguish from neuropathy

Typically occurs later in the disease when the blood supply is not adequate to perfuse the extremity
Often felt at night in feet while lying in bed (pts frequently hang their leg out of bed to try to relieve their pain)

78
Q

Acute limb-threatening ischemia (ALI)

A

Rare
Sudden onset symptoms : pain at rest, pallor, pulseness, paraesthesia, paralysis, “perishingly” cold
Indicated by sudden deterioration of claudation

79
Q

Def: ABI

A

Ankle brachial index = highest ankle SBP/highest brachial SBP

80
Q

Interpretation of ABI: ABI > 1.3

A

likely to be PAD – if ankle branchial artery too calcified to be compressible

Need toe brachial index (TBI)

81
Q

Interpretation of ABI: ABI 1-1.3

A

Not PAD

82
Q

Interpretation of ABI: ABI 0.91-0.99

A

Maybe PAD

83
Q

Interpretation of ABI: ABI ≤0.9

A

Yes PAD

84
Q

Interpretation of ABI: Resting ABI normal but post exercise ABI ≤0.9 or decrease of more than 20% in ABI after exercise

A

Yes PAD
Mild: Resting and post exercise ≤0.9
Mod: Resting ≤0.7, post exercise ≤0.5
Severe: Resting ≤0.5, post exercise ≤0.15

85
Q

Treatment for PAD: Goals

A

Limb outcome – improve ability to walk by increasing peak walking distance, pain free walking distance, and improve QOL

CVD morbidity/mortality – control of RF (HTN, HLD, DM), decrease morbidity/mortality of MI or stroke

86
Q

Treatment for PAD: Confirmed PAD but no significant functional disability

A

No treatment required

F/U annually

87
Q

Treatment for PAD: Confirmed PAD with lifestyle limiting symptoms

A

Supervised exercise program + drug therapy (antiplatelet + cilostazol (if claudation)

F/U annually

If still significant disability –> endovascular therapy or surgical bypass per anatomy

88
Q

Treatment for PAD: Confirmed PAD with lifestyle limiting symptoms WITH evidence of inflow disease

A

Further anatomic def by more extensive noninvasive or angiographic diagnostic techniques

F/U if bad – endovascular therapy or surgical bypass per anatomy

89
Q

Treatment for PAD: Supervised exercise therapy: How often and for how long?

A

35-45min sessions, x3-5/week for at least 3 months

Type of exercise: treadmill or track walking to near-maximal claudication pain

90
Q

Treatment for PAD: Nonpharmacological: Diet types

A

NCEP ATP III
DASH
TLS

91
Q

Treatment for PAD: Revascularization Therapy: Endovascular options

A

Percutaneous transluminal angioplasty (PTA)

Stents (controversial, not recommended in femoral, popliteal, or tibial arteries)

92
Q

Treatment for PAD: Revascularization Therapy: Surgical options

A 
Aortoiliac/artofemoral reconstruction
Femoropopliteal bypass (above knee and below)
Femorotibial bypass
93
Q

Treatment for PAD: Antiplatelet therapy

A

ASA, aggrenox, clopidogrel

First line is ASA or clopidogrel (if ASA allergy)

94
Q

Treatment for PAD: Cilostazol (Pletal): Dosing

A

50-100mg po BID

95
Q

Treatment for PAD: Cilostazol (Pletal): Class

A

PDE III inhibitor

96
Q

Treatment for PAD: Cilostazol (Pletal): Pharmacologic properties

A 
Platelet aggregation inhibitor
Vasodilation
Increased HDL 10%
Decrease TG 15%
Inhibit sm muscle cell proliferation in vitro
97
Q

Treatment for PAD: Cilostazol (Pletal): Efficacy

A

increase max walking distance and pain-free walking distance

98
Q

Treatment for PAD: Cilostazol (Pletal): Safety

A

SE: headaches, dizziness, diarrhea
CI: HF, active bleeding

DONT GIVE CILOSTAZOL TO PT WITH HF

99
Q

Treatment for PAD: Amputation: Evaluate if

A

significant necrosis of weight-bearing portions of foot
Paresis (slight paralysis) of extremity
Refactory ischemic rest pain
Sepsis
Limited life expectancy due to comorbid conditions

100
Q

Treatment for PAD: _____ ok if life expectancy <2 yrs or can’t do bypass

A

angioplasty

CDM1 (19 decks)

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