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Cardio Exam 2 > Treatment of Dyslipidemia > Flashcards

Treatment of Dyslipidemia Flashcards

1
Q

Class I

A

Benefits&raquo_space;> Risk

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2
Q

Class IIa

A

Benefits&raquo_space; Risk

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3
Q

Class IIb

A

Benefits >/= Risk

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4
Q

Class III

A

No benefit or harm

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5
Q

Level A-B of Evidence

A 
A = most
C= least
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6
Q

Dietary advice for LDL lowering

A

Intake of veggies, fruits, whole grains, low-fat dairy, pultry, fish, legumes, non-tropical veg oil
Limit sweets, sodas, red meats
5-6% of total calories form saturate fats
Reduce calories from trans fat

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7
Q

Exercise fo Dyslipidemia

A 
Aerobic activity
Decrease LDL and Increase HDL
3-4 sessions, 40 minutes per session
Moderate to vigorous activity
Resistance training may decrease LDL, TG and non HDL
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8
Q

Optimal LDL

A

<100

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9
Q

HDL levels

A

> 41

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10
Q

Desirable TC

A

<200

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11
Q

Total Cholesterol =

A

HDL, LDL, and TGs

So just bc this is high doesn’t mean the bad stuff is high

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12
Q

CK Labs

A

Creatinine Kinase to see if there is muscle breakdown

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13
Q

Who should have CK labs taken?

A 
Personal history of statin intolerance
FH of statin intolerance or muscle disease
Concomitant therapy that make increase risk of interactions
Clinical presentation (not serial)
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14
Q

Secondary causes of elevated LDL

A

saturated or trans fat, weight gain, anorexia
Giuretics, cyclosporine, glucocorticoids, amiodarone
Bilary obstruction, nephrotic syndrome
Hypothyroidism, obesity, pregnancy

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15
Q

Secondary causes of elevated TGs

A

Weight gain, lower fat diet, high intake of refine carbs, alcohol
Oral estrogens, glucocorticoids, BAS, PI, anabolic steroids, BB, thiazides
Nephrotic syndrome, CRF, lipodystrophies
DM, hypothyroidism, obesity, pregnancy

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16
Q

Risk factors for ASCVD

A

Primary relative with LDL >160 or genetic hyperlipidemia
Premature ASCVD in primary relative (men less than 55, women less than65)
Elevated hs-CRP >2
Elevated CAC
Ankle-branchial index less than 0.9

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17
Q

Primary Therapy

A

Statin based

  • Decreases LDL
  • Increases HDL and decreased TGs
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18
Q

Primary prevention =

A

Have NOT had a CV event before

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19
Q

Secondary prevention =

A

Have had a CV event before

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20
Q

High intensity treatment =

A

Needing 50% or more decrease in LDL levels
</=75 yeras without contraindication
No drug-drug interaction
No history of intolerance
— someone who has already had a MI should be on high

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21
Q

Moderate intensity treatment =

A

Needing 30-49% decrease in LDL levels
>75 years
Not able to tolerate high intensity

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22
Q

TG > 500 =

A

Assess underlying causes and target first because it can lead to pancreatitis

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23
Q

Statin Benefit Groups - Clinical ASCVD

A 
ACS (heart attack)
History of MI
Stabel or unstable angina
Coronary or arterial revascularization (stent)
Stroke or TIA
PAD of atherosclerotic origin
High risk of havinga  future ASCVD
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24
Q

High intensity drugs

A

Atorvastatin (Lipitor) 40-80 mg

Rosuvastatin (Crestor) 20-40 mg

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25
Q

Other groups that benefit from statin therapy

A

Primary elevations in adults greater than 21 with greater than 190 mg/dL
Primary prevention Diabetes age 40-75 with LDL 70-189 mg/dL
Primary prevention with LDL 70-189 mg/dL

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26
Q

Primary elevations in adults >21 with > 190 mg/dL

A

At high risk bc of genetic causes (FH)
Should receive high intensity and should intensify until at least greater than 50% LDL reduction
After max on statin, can add other drugs to help
Need to screen family members

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27
Q

Primary Prevention Diabetes age 40-75 with LDL 70-189 mg/dL

A

At least moderate therapy
If 10 year risk is greater than 7.5% consider high
If less than 40 or greater than 75 weigh risks and benefits

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28
Q

Primary prevention with LDL 70-189 mg/dL

A

Pool Cohort Equation: Estimate 10 year and lifetime risk
Greater than 7.5 moderate to high
5-75 moderate

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29
Q

Statin Cholesterol Effects

A

Decrease LDL 18-63%
Decrease TG 7-30%
Increase HDL 5-15%

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30
Q

Moderate Intensity Drugs

A 
Atorvastatin 10 mg
Rosuvastatin 10 mg
Simvastatin 20-40 mg
Pravastatin 40 mg
Lovastatin 40 mg
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31
Q

Low Intensity Drugs

A

Pravastatin 10-20 mg

Lovastatin 20 mg

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32
Q

QPM Drugs

A

Lovastatin
Pravastatin
Simvastatin

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33
Q

Statin AE

A

Increased LFTs (baseline –> 6-12 wks later –> annually)
Myotoxicity (myalgia, myopathy)
Rhabdomyolysis
Increased risk with Fibric acid derivatives
Pain, tenderness, stiffness, cramping, weakness, or fatigue
New onset diabetes

34
Q

Define myalgia

A

Muscle aches, soreness or weakness with minimal or no elevation in CK

35
Q

Define myopathy

A

Muscle symptoms associated with elevation in CK >10X ULN

36
Q

Define Rhabdomyolysis

A

A CK > 10,000 IU/L or 10X ULN with an elevation in serum creatinine or requiring IV hydration therapy
- Dark brown pee (dehydrated)

37
Q

Treatment of Muscle pain

A

D/C until it goes away, restart with a low dose of same statin
If it comes back d/c and let resolve and start a low dose different statin
If not the statins fault, restart statin at original dose

38
Q

Statin contrindications

A

Liver disease
Unexplained LFTs
Pregnancy

39
Q

Statin Drug interactions

A

Warfarin
3A4 Inhibitors
Grapfruit juice
Anything with an increase risk of myopathy

40
Q

Statin Monitoring

A

Recheck FLP in 4-12 weeks
Assess every 3-12 months after
Reinforce adherence at each visit

41
Q

Fibric Acid Derivatives

A

Primarily for hyperTGs

42
Q

Fibric Acid Derivatives Cholesterol effects

A

Decreased TGs 20-50%
Increased HDL 10-20%
Decrease LDL 5-20% (may increase with gemifibrozil)

43
Q

Gemfibrozil Outcomes

A

Primary prevention of CHD and secondary prevention of cardiac events in men with low HDL
600 mg BID

44
Q

Fenofibrate Outcomes

A

Prevent CHD in T2DM
Fenofibrate + simvastatin in T2DM pts
40-200 mg QD

45
Q

Fibric Acid Derivatives AE and Monitoring

A

GI, rash, hepatoxicity, myalgias
Drug interactions: warfarin, concurrent use with statins
Renal function at baseline, 3 months then Q 6 months

46
Q

Fibric Acid Derivatives Clinical Pearls

A

First line for hyperTG
Fenofibrate preffered with statins
Monitor renal esp with feno

47
Q

Bile Acid Sequestrants

A

Primarily LDL lower

48
Q

Bile Acid Sequestrants Cholesterol Effects

A

Decrease LDL 15-30%
Increase HDL 3-5%
TG +/- or Increased

49
Q

Bile Acid Sequestrants Outcomes

A

Primary prevent in men

Secondary prevention in men

50
Q

Cholestyramine resin

A

4 g 1-2 times/day up to 16-34 g/day
Mixed with water
Taken with meals

51
Q

Micronized Colestipol

A

2-16 g/day in 2-4 doses

52
Q

Colesevelam

A

2 tablets or 1.875 g packet BID

53
Q

Bile Acid Sequestrants AE and Monitoring

A

GI
Contraindicated in complete bowel obstruction
Not absorbed
Some contain phenylalanine
Avoid if TG >300 and caution if 250-299
Check FLP baseline, 3 months and 6-12 months

54
Q

Bile Acid Sequestrants Drug Interactions

A

Decrease absorption of other medications
Take other meds 1 hour before or 4 hours after
Supplement with vitamin ADEK, folic acid and Fe

55
Q

Bile Acid Sequestrants Clinical pearls

A

Limited use due to tolerability and outcome data

Option for patients with contraindications due to liver impairment or another

56
Q

Niacin Cholesterol effects

A

Decreased LDL 5-25%
Decreased TG 20-50%
Increased HDL 15-35%

57
Q

Niacin Outcome

A

Inconsistent demonstrating benefits

58
Q

Laropiprant

A

Decreased niacin induced flushing

59
Q

Niacin IR

A

Usual dose 2 g/day doses up to 6 g/day

60
Q

Niacin SR

A

1000 mg BID max of 2 g

61
Q

Niacin ER

A

500 mg QHS x 4 weeks, increase to 100 mg QHS

Max 2 g

62
Q

Niacin AE and monitoring

A

Flushing and itching secondary to PG-mediated vasodilation
325 mg aspirin 30 minutes before dose may decrease reaction
Avoid spicy foods, alcohol, hot beverages, hot baths, to avoid flushing
May increase uric acid and blood glc
Hepatotoxicity
GI

63
Q

Niacin Labs

A

ALT, glc, hgb, A1c, uric acid

During titration and 6 months after stable

64
Q

Do not use Niacin if:

A

ALTs >2-3 x ULN
Persistent cutaneous symptoms
Persistent hyperglycemia, acute gout or unexplained ab pain or GI symptoms

65
Q

Niacin Drug interactions

A

Statins (myopathy)

Cholestyramine (Decrease absorption)

66
Q

Niacin Clinical Pearls

A

Most potent to increase HDL
Limited use due to lack of data and tolerability
Do not use “no flush niacin” - inostilhexalicainate or nicotinamide (increased risk of hepatotoxicity)

67
Q

Ezetimibe cholesterol effects

A

Decreased LDL 19%
Decreased TG 8%
HDL +/-

68
Q

Ezetimibe AE and Monitoring

A

Generally well tolerated

With adn w/o statin: increase myopathy and LFTS

69
Q

Ezetimibe Drug Interactions

A

Increased warfarin
Decreased BAS
Increase conc with cyclosporine

70
Q

Ezetimibe Clinical Pearls

A

Do see modest reduction

Expensive

71
Q

FA Cholesterol effects for Lovaza

A

Decreased TG 44%
Increased HDL 9%
Increased LDL 45%

72
Q

FA Cholesterol effects for Vascepa

A

Decreased TG 27%
Decreased HDL 4%
Decreased LDL 5%

73
Q

FA Outcome data

A

Lacking

Secondary prevention

74
Q

FA Adverse reaction

A

GI

Taste perversion

75
Q

Lovaza dosing

76
Q

Icosapent dosing

77
Q

FA Clinical Pearls

A

May consider in patient with high TG
Decreased risk for hepatotoxicity and CYP450 interactions
Icospanent (V) dose not decrease LDL
Icospanent is NOT as effect at lower TGs

78
Q

Statin + BAS

A

Improved LDL reduction

79
Q

Statin + Ezetimibe

A

Improved LDL reduction

80
Q

Statin + Fibric acid derivative

A

Decreased TGs and likely LDL

81
Q

Statin + niacin

A

Improved LDL and TGs

82
Q

Naicin + BAS

A

Improved LDL

Cardio Exam 2 (10 decks)

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