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Dyslipidemia Flashcards

0
Q

Which BAS does not increase TGs?

A

Colesevelam (Welchol)

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1
Q

Name 3 Bile Acid Sequestrants

A

Cholestyramine (Questran)
Colestipol (Colestid)
Colesevelem (Welchol)

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2
Q

What is an absolute contraindication (CI) to BAS therapy?

A

severe hypertriglyceridemia (super high TGs)

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3
Q

What are the common side effects of BAS?

A

Constipation

Bloating

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5
Q

What are the three formulations of nicotinic acid (niacin)?

A

IR *causes the most flushing but the least hepatotoxicity
ER (Niaspan)
SR (Slo-Niacin) *causes more hepatotoxicity

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5
Q

What formulation is the least likely to be hepatotoxic?

A

Immediate Release (IR)

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6
Q

What are the common side effects of nicotinic acid?

A 
FLUSHING
itching
hyperglycemia
gout 
hepatotoxicity
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7
Q

Name 2 fibric acid derivatives.

A

Gemfibrozil

Fenofibrate

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8
Q

What are absolute CIs to niacin therapy?

A 
people with liver insufficiency (LFTs > 2-3 x ULN) (niacin can cause hepatotoxicity)
persistent hyperglycemia
acute gout
unexplained abdominal of GI problems
new onset of wt loss or A. fib
(NOT sure about answer)
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9
Q

Which fibrate may be used most safely in combination with statins?

A

fenofibrate

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11
Q

Which fibrates MUST be taken with food?

A

fenofibrate formulations:
LoFibra
original TriCor
Lipofen

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12
Q

What is the mechanism of action of statins?

A

They inhibit HMG CoA reductase, which is the rate-limiting step in cholesterol synthesis. By inhibiting this enzyme, intracellular cholesterol decreases and the liver increases LDL-R & HMG CoA reductase expression resulting in more plasma cholesterol uptake into the cells (decreases plasma chol levels)

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13
Q

What is the MOA of Niacin?

A

niacin inhibits adenylyl cyclase (inhibits ATP –> cAMP) which in turn inhibits TGs in adipocytes from breaking down into free FAs. Less FFAs –> less TG synthesis in liver, decrease in VLDL synthesis & decrease in LDL in circulation

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14
Q

What is the MOA of fibrates?

A

Fibrates (+) PPAR-alpha –> decrease in plasma TGs

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14
Q

What are the common side effects of fibrates?

A

myalgia
GI problems (N/V)
gallstones

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15
Q

What is the MOA of ezetimibe?

A

ezetimibe blocks NCP1L1 which decreases cholesterol ABSORPTION and leads to CMs low in cholesterol

Liver response: upregulates LDL-R & HMG-CoA reductasej

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16
Q

What is a cholesterol absorption inhibitor (CAI)?

A

Zetia (ezetimibe)

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17
Q

Contraindications of fibrate therapy?

A

people with . . .
previous/ pre-existing gallbladder disease
renal failure
liver failure

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18
Q

What is the name of the combination product with a CAI in it?

A

Vytorin (Zetia + Simvastatin)

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19
Q

Name the 7 statins currently on the market.

A 
rosuvastatin (crestor)
pitavastatin (Livalo)
atorvastatin
lovastatin
fluvastatin
simvastatin
pravastatin 
"random pictures always look funny, silly & preposterous"
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20
Q

What are the common side effects of a CAI?

A

Ezetimibe can cause
joint pain, abdominal pain, diarrhea
(it is usually well tolerated)

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21
Q

What are the common side effects of statins?

A 
myopathy
liver failure (rare)
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22
Q

Which statins may be used most safely in combination with fibrates?

A

gemfibrozil: no statin
fenofibrate: all except Fluvastatin & Rosuvastatin (b/c they are metabolized by CYP2C9)

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23
Q

Contraindications to statin therapy?

A

pregnancy
previous muscle disorder
excess alcohol use

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24
Q

Which statin works best at lowering TGs?

A

Atorvastatin (can decrease TGs ~50%)

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25
Q

Which statin MUST be taken with food to be absorbed?

A

Fluvastatin

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26
Q

Which statins must be taken at night/bedtime to work best?

A

Fluvastatin (take with evening meal)
Simvastatin
Pravastatin
Lovastatin

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27
Q

Which statins should you avoid taking with large volumes of grapefruit juice?

A

Lovastatin
Simvastatin
perhaps Atorvastatin (only minorly metabolized by CYP3A4)

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28
Q

What % can cholestyramine and colestipol increase TGs?

A

Cholestyramine 12-25%

colestipol 12-15%

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29
Q

BAS can decrease LDLs by _______ %?

A

Colestipol & Cholestyramine: 15-30 % decrease

Colesevelam: 8-15% decrease

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30
Q

What is the usual daily dose of Cholestyramine?

A

4-16g

max dose = 24 g

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31
Q

What is the usual daily dose of Colesevelam?

A

2.6-3.8 g

max = 4.4 g

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32
Q

What is the usual daily dose of Colestipol?

A

5-20 g

max = 30 g

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33
Q

Counseling for BAS?

A

Take BAS 4 hours before other medications
Mix powders with non-carbonated beverages. Add fluid to powder.
Stir and Drink immediately
Drink powders in divided doses BID before meals
Drink a large glass of water with tablets ( >7 oz)
Titrate dose to minimize side effects
BAS are infamous for drug-drug interactions

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34
Q

Which lipid lowering drug is almost always given in combination with a statin?

A

Ezetimibe (Zetia)

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35
Q

What are 3 drugs that interact with Zetia?

A

Gemfibrozil
Cyclosporin
Cholestyramine (BAS)

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36
Q

What is the usual dose for ezetimibe?

A

10 mg

max = 10 mg

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37
Q

How much can IR niacin decrease LDLs?

A

10-25%

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38
Q

How much can SR niacin (Slo-Niacin) decrease LDL’s?

A

15-26%

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39
Q

How much can ER niacin (Niaspan) decrease LDL’s?

A

20-40%

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40
Q

True or False. Tolerance to niacin will not improve overtime.

A

False. it will improve.

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41
Q

How can you minimize flushing in patients taking niacin?

A

Take an enteric-coated Aspirin 325 mg 30 min before taking Niacin

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42
Q

Do you take Niacin with food?

A

Yes

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43
Q

What do you tell a patient to do if they miss a dose?

A

SKIP IT. DO NOT DOUBLE DOSE!!

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44
Q

[SATA] In which of the following should you titrate the dose?
A. Nicotinic Acid
B. BAS
C. Statins

A

A & B

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45
Q

What is the effect of fibrates on….
LDL
HDL
TGs

A

LDL: either an increase or decrease of ~30% (severe hypertriglyceridemia pts usually have an increase in LDLs when on fibrates, while mild hypertriglyceridemia patients usually have no effect or a decrease in LDLs)
HDL: increase 10-30%
TG: decrease by 30-50%

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46
Q

What is the dose regimen for LoFibra?

A

67, 134, 200 mg

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47
Q

What is the dose regimen for original TriCor?

What about new Tricor?

A

original: 54, 160 mg
new: 48, 145 mg

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48
Q

What is the dose regimen for Lipofen?

A

50, 100, 150 mg

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49
Q

What is the dose regimen for Antara?

A

43, 130 mg

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50
Q

What is the dose regimen for Triglide?

A

50, 160 mg

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51
Q

What is the dose regimen for Trilipix?

A

45, 135 mg

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52
Q

Which formulation of fenofibrate should not be taken if the tablet is chipped or broken?

A

Triglide (50 mg or 160mg)

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53
Q

What is the brand name for omega 3 Fatty Acids?

A

LOVAZA

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55
Q

What is the dose of EPA + DHA needed to be effective in decreasing TGs?

A

2-4 g (can decrease TGs by 35%)

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56
Q

What can you do to minimize the fishy burping due to Lovaza?

A

refrigerate Lovaza

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56
Q

What does a Class I recommendation mean in the guidelines?

A

Benefit&raquo_space;» Risk

SHOULD BE DONE

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57
Q

What is the typical “sig” for Lovaza?

A

2 tab po TID

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58
Q

What does a Class II recommendation mean in the guidelines?

A

Benefit&raquo_space; Risk
REASONABLE TO DO
(should be done unless there is a reason not to)

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59
Q

What does a Class IIb recommendation mean in the guidelines?

A

Benefit ≥ Risk
SHOULD BE CONSIDERED
(there might be more reasons not to, but it should have more benefit than risk)

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60
Q

What does a Class III recommendation mean in the guidelines?

A

No benefit or harm
SHOULD NOT BE DONE
DON’T DO IT!!

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61
Q

What does a Level of Evidence “A” mean?

A

Data came from MULTIPLE POPULATIONS (from multiple randomized trials or meta-analyses)

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62
Q

What does a Level of Evidence “B” mean?

A

data came from LIMITED POPULATIONS (single RCT or non-RCT study)

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63
Q

What does a Level of Evidence “C” mean?

A

data came from VERY LIMITED POPULATIONS

consensus opinion, expert, case studies or standard of care

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64
Q

What does “consensus opinion” mean?

A

everyone sitting at the table thought it was a good idea

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65
Q

What estimates the 10 year hard ASCVD risk of 1st event?

A

Pooled Cohort Equation

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66
Q 
The Pooled Cohort Equation is BEST used in. . . 
A. Non-hispanic Caucasians & Asians
B. African Americans & Native Americans
C. Non-hispanic Caucasians & AAs
D. Asians & Native Americans
A

C

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67
Q 
What age range (in years) does the Pooled Cohort Equation work best in?
A. 45-75 
B. 35-79 
C. 40-79 
D. 40-70
A

C. 40-79

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68
Q

What LDL levels does a patient need for the Pooled Cohort Equation to work best?

A

70-189

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69
Q

In what races does the Pooled Cohort Equation overestimate risk?

A

Hispanics & Asians

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70
Q

In what races does the Pooled Cohort Equation underestimate risk?

A

Native Americans (American Indians)

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71
Q

What are the Novel Risk Markers for Dyslipidemia?

A
  • Premature CVD in FH: 1st ˚ relative (male < 55 yo or female < 65 yo)
  • hsCRP > or equal to 2 mg/L
  • CAC score > or equal to 300 Agaston units or > or equal to 75th percentile for age, sex or ethnicity
  • ABI < 0.9
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72
Q

ABI

A

Ankle Brachial Index

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73
Q

What novel risk marker is the most useful for decision making?

A

CAC score

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74
Q

What are the Traditional Risk Factors for Dyslipidemia?

A 
Age: men ≥45 & women ≥55
Premature FH of ASCVD: men ≤55 or female ≤65
Current Smoker
Diabetes
Elevated systolic BP 
    use of anti-HTN medications
Sex (male > female)
TC > 200
HDL < 40
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75
Q

If a patient is between 20 & 79 WITHOUT ASCVD, how do you screen or manage the risk of dyslipidemia?

A

assess traditional risk factors q 4-6 years

counsel on controlling those and staying healthy

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76
Q

If a patient is between 40 & 79 WITHOUT ASCVD, how do you screen or manage the risk of dyslipidemia?

A

do the pooled cohort equation q 4-6 years
risk ≥ 7.5% –> counsel via cholesterol guidelines
risk < 7.5% –> counsel via lifestyle guidelines

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77
Q

Patient M.K. has an ASCVD risk score of 8.2%, has no HTN, has a (+) FH for CVD, is positive for DM and has a TC level of 242 and an HDL level of 75. What is your first step towards treatment?

A

Cholesterol Guidelines

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78
Q

TC

A

total cholesterol

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79
Q

ASCVD

A

Atherosclerotic Cardiovascular Disease

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80
Q 
Patient A.S. has an 
ASCVD risk score of 6.5%
(-) for smoking
(+) HTN
(-) FH of CVD
(-) DM
TC = 206 
HDL = 42
What is your first step toward treatment?
A

Counsel on lifestyle management

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81
Q

What is critical component of healthy living before and along with cholesterol lowering drug therapies?

A

Lifestyle modification

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82
Q

What does Lifestyle modifications (∆) include?

A

Heart healthy diet
regular exercise
smoking cessation and tobacco use
weight maintenance

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83
Q

If you start a patient in a statin when should You follow up?

A

1-3 months

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84
Q

After you patient is steady on a statin, when should you follow up?

A

3-12 months

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85
Q

Which guideline was a secondary prevention trial?
A. Asteroid
B. Meteor
C. AIM-HIGH

A

A

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86
Q

SATA: Which trial used rosuvastatin 40 mg in studying its effect?
A. Asteroid
B. Meteor
C. AIM-HIGH

A

A, B

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87
Q

Which trial showed that Crestor slowed progression but had no regression in carotid intima-media thickness (CIMT)?

A

Meteor

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88
Q

C-RP

A

C-reactive protein

89
Q

TIA

A

Transient ischemic accident

Mini stroke

90
Q

CVA

A

Cardiovascular accident

Stroke

91
Q

What are the 4 benefit groups that will benefit from statin therapy?

A
  1. Clinical ASCVD
  2. LDL ≥ 190 mg/dL (age ≥21)
  3. Diabetes (age 40-75 & LDL b/w 70-189 mg/dl)
  4. ASCVD Risk Score ≥7.5% (age 40-75 & LDL b/w 60-189 mg/dL)
92
Q

How would you counsel a patient on a heart healthy diet?

A

DASH diet
emphasize veggies, fruits & whole grains
eat LOW-fat dairy, poultry, fish, legumes, non-tropical oils & nuts
limit sweets, sugar-sweetened beverages & red meat
keep saturated fats around 5-6% and lower trans fat
lower SODIUM intake (1500mg-2400mg/d)

93
Q

How would you counsel a patient on exercising?

A

GOAL = 40 min of aerobic exercise 3-4 x a week

if patient needs to they can start with10 min increments and build up to 40 minutes

94
Q

If your patient has Clinical ASCVD and is less than 75 yo, what do drug therapy do you start them on?

A

HIGH-INTENSITY STATIN
rosuvastatin 20 or 40 mg
atorvastatin 40 or 80 mg

95
Q

If your patient has Clinical ASCVD and is older than 75 yo, what do drug therapy do you start them on?

A 
Moderate intensity statin
atorvastatin 10 or 20 mg
rosuvastatin 5 or 10 mg
simvastatin 20 or 40 mg
pravastatin 40 or 80 mg
lovastatin 40 mg
fluvastatin XL 90 mg
fluvastatin 40 mg BID
Pitavastatin 2 or 4 mg
96
Q

If your patient is older than 21 yo and has LDL ≥190, what drug therapy should you start them on?

A

High Intensity Statin
Atorvastatin 40 or 80 mg
Crestor (rosuvastatin) 20 or 40 mg

97
Q

M.P is 46 yo, has Diabetes with an LDL level of 110 and and has an ASCVD risk score of 9.5%. What drug therapy do you recommend?

A

High intensity statin

98
Q

L.D. is 46 yo, has Diabetes with an LDL level of 90 and and has an ASCVD risk score of 5.5%. What drug therapy do you recommend?

A 
Moderate intensity statin
atorvastatin 10 or 20 mg
rosuvastatin 5 or 10 mg
simvastatin 20 or 40 mg
pravastatin 40 or 80 mg
lovastatin 40 mg
fluvastatin XL 90 mg
fluvastatin 40 mg BID
Pitavastatin 2 or 4 mg
99
Q 
[SATA] Which statin trials studied the effects of PravastatiN 40 mg?
A. ALLHAT-LLT
B. ASCOT-LLA
C. 4S
D. LIPID
E. CARE
F. PROVE IT
G. PROSPER
H. JUPITER
A

A, D, E, F, G

100
Q 
[SATA] Which statin trials studied the effects of Atorvastatin?
A. ALLHAT-LLT
B. ASCOT-LLA
C. SPARCL
D. TNT
E. CARDS
F. PROVE IT
G. PROSPER
H. JUPITER
A

B, C, D, E, F

101
Q

A moderate intensity statin can decrease the ASCVD risk % by ______ %?

A

30%

102
Q

What does NCP1L1 do?

A

pumps dietary & biliary cholesterol into intestinal cells

103
Q

What happens when PPAR-alpha is activated?

A

Fibrates activate PPAR-alpha which:
increase apa AI & AII syn in hepatocytes (increases plasma HDL)
increase scavenger receptor ß-1 (SRß1) expression (promotes reverse cholesterol transport)
DECREASE apo CIII syn in hepatocytes (increases FA uptake by muscle cells & increase FA oxidation in muscle cells –> decrease in plasma TGS)
increase FA oxidation in hepatocyts (decreases TG syn & VLDL, IDL and LDL –> decrease in plasma TGs)

104
Q

Which trial showed that the LDL levels decreased more than 50% and the lipid layer (atheroma) in the area that need it most, shrunk the most (regression) with rosuvastatin 40 mg daily for 2 years?

A

ASTEROID

2ndary prevention trial (pts had to have ≥1 obstructions with >20% stenosis in any major coronary artery)

105
Q

Which trial slowed progression of the atheroma, but showed no signs of regression in patients taking rosuvastatin 40 mg daily.

A

METEOR
primary prevention trial
pts only coronary risk factor was age or had a 10-yr FRS of <10% and had modest CIMT thickening with elevated LDL (avg. of 154 mg/dL)

106
Q

CIMT

A

Carotid Intima-Media thickness

107
Q

How does a pt fit into the category of Clinical ASCVD?

A 
They must have:
•ACS
•MI 
•UA or CSA
•PTCA, CABG (coronary or other vascularization)
•CVA or TIA
•PAD, PVD of atherosclerotic origin
108
Q

ACS

A

acute coronary syndrome

109
Q

MI, AMI

A

myocardial infarction,

acute myocardial infarction

110
Q

CSA

A

stable angina

111
Q

UA

A

unstable angina

112
Q

CVA

A

STROKE

113
Q

TIA

A

transient ischemic attack

114
Q

PTCA

A

percutaneous transluminal coronary angioplasty (procedure that opens a blocked coronary artery)

115
Q

CABG

A

coronary artery bypass surgery

116
Q

How do we treat patients who have clinical ASCVD?

A

≤75 yo: high intensity statin

you can give a moderate intensity statin to patients with predisposing issues with statins, if the moderate is tolerated better, or if CI’s exist with high intensity statin

117
Q

What are predisposing factors that can make a pt with clinical ASCVD need a moderate intensity statin instead of High intensity?

A

multiple or serious comorbidities (renal/hepatic impairment)
history of previous statin intolerance or muscle disorder
unexplained elevation of ALT > 3x ULN
pt characteristics or concomitant use of drugs affecting statin metabolism
>75 yo
asian ancestry
histor of hemorrhagic stroke (SPARCL)

118
Q

Why can Asians not take high intensity statins?

A

CYP2C19 metabolism is different in asians

119
Q

ULN

A

upper limit of normal

120
Q

What is the age limit for high intensity statins?

A

cannot give to someone older than 75

121
Q

T/F. All statins are metabolized by the liver and flushed through the kidney.

A

True

122
Q

CI’s to high intensity statins?

A

pregnancy
breast-feeding (precaution–>statins are secreted in breast milk)
excessive alcohol use (b/c this elevates liver enzymes)
active liver disease (ALT >3x ULN)

123
Q

True/False? You can start a patient on a high intensity statins immediately without titrating or giving a lower dose first.

A

True

124
Q

What is the benefit of giving a moderate intensity statin to a patient with Clinical ASCVD that is OLDER than 75?

risks?

A

Benefit: ASCVD risk reduction
Risks: adverse effects, drug interactions

125
Q

How do we treat patients with LDL ≥190?

A

*evaluate for secondary cause of LDL increase
older than 21: start on high intensity statin if possible
older than 75: start on moderate intensity statins

126
Q

Hypothyroidism, obesity, and pregnancy can increase _________.

A

LDL’s

127
Q

Hypothyroidism, obesity, pregnancy, and poorly controlled DM can increase _________.

A

TGs

128
Q

How do we treat patients with LDL ≥190 once they are already on therapy and we are monitoring them?

A

intensify statin therapy to achieve at least a 50% reduction in LDLs

after max intensity statin is reached and the LDLs still aren’t reduced enough, you can add a non-statin therapy.

129
Q

If your patient is diabetic and between 40-75 yo and have an LDL of 70-189, what type of statin do you give them?

A

Moderate intensity statin

130
Q

How do we treat patients between 40-75 yo, with LDL between 70-189 and with an ASCVD risk score ≥ 7.5%?

A

moderate to high intensity statin
Clinically, if risk is greater than 20%–>HIGH
if risk is between 5% and 20% –>MODERATE

131
Q

What do you do if your patient doesn’t fit into any statin benefit groups?

A

Look at additional factors to see if they may benefit from statin therapy.

132
Q

What additional factors should you look into for patients that do not fit into a Statin Benefit Group?

A

At baseline. . .
LDL ≥160 mg/dl or other evidence of genetic hyperlipidemia
FH: premature ASCVD
hs-CRP > 2mg/L
CAC score ≥ 300 Agatston units or ≥ 75th percentile for age, sex & ethnicity
ABI < 0.9
lifetime risk of ASCVD

133
Q

What does the CAC score measure?

A

how much calcium shows up in your heart

134
Q

hs-CRP

A

high sensitivity C reactive protein

135
Q

When do you follow up with a patient after you initiate statin therapy?

A

1-3 months

then follow up every 3-12 months

136
Q

When your patient has returned for monitoring following statin therapy, he has reached your anticipated response. Now what?

A

Reinforce (good job! keep taking this medicine consistently) & follow up q 3-12 months

137
Q

When your patient has returned for monitoring following statin therapy, he has NOT reached your anticipated response. Now what?

A

treatment optimization
make sure they are taking the med
lifestyle change (have they changed their diet? are they exercising? stopped smoking?)
evaluate for secondary dyslipidemia

138
Q

What is the goal LDL decrease when on a high-intensity statin?

A

50% decrease from baseline

139
Q

What is the goal LDL decrease when on a moderate-intensity statin?

A

30-50% from baseline

140
Q

What if your patient is at higher ASCVD risk and is on the max statin intensity they can handle and their response is not enough?

A

add non-statin therapy (careful this increases risk of myalgia)

141
Q

What patients are considered to be “Higher ASCVD Risk Individuals”?

A

Clinical ASCVD and older than 75
baseline LDL ≥190 mg/dL
DM and between 40 and 75 yo

142
Q

What ezetimibe trial compared simvastatin alone to Vytorin (simvastatin + ezetimibe) for change in CIMT?

A

ENHANCE (2008)

143
Q

What were the results of the ENHANCE trial?

A

simvastatin + zetia (Vytorin) is NO MORE EFFECTIVE than simvastatin alone

144
Q

What trial compared simvastatin + zetia (Vytorin) to a placebo in patients with mild to moderate asymptomatic aortic stenosis or a composite of major CV events?

A

SEAS (2008)

145
Q

What were the results of the trial SEAS?

A

NO DIFFERENCE between vytorin and placebo

146
Q

What trial compared statin + zetia to statin + niacin in pts with CHD or CHD equivalent?

A

ARBITER 6-HALTS

147
Q

What was the outcome of the trial ARBITER 6-HALTS?

A

statin + niacin showed a significant reduction in mean CIMT while statin + ezetimibe did NOT have a reduction in mean CIMT

148
Q

What trial compared simvastatin vs. simvastatin + ER niacin in patients with T2DM and established CVD with maintained LDL but low HDL or high TGs?

A

AIM-HIGH

149
Q

What was the result of the AIM-HIGH trial?

A

simvastatin + niacin ER did not help prevent CV outcomes

150
Q

What trial compared ER niacin vs. placebo (all pts were also on simvastatin or vytorin & had CHD, CVA or other circulatory disease)?

A

HPS2-Thrive (2014)

151
Q

What was the result of HPS2-Thrive?

A

niacin did not do better at preventing death than the placebo

152
Q

What are things to monitor when your patient is on a statin?

A 
muscle pain
LFTs
blood glucose
memory
drug interactions 
LDL<40
153
Q

What are some reasons CK can be elevated in the body?

A

muscle cramps, injury, exercise

baseline levels can be higher than 10 x ULN

154
Q

What is the normal range for CK in men?

A

men: 25-90 IU/L

155
Q

What is the normal CK level in women?

A

women: 10-70 IU/L

156
Q

What can statins cause due to elevated CK?

A

rhabdomyolysis

157
Q

Should you routinely check patient’s CK while they are on a statin?

A

NO, just take their baseline CK in patients with high risk of muscle problems

158
Q

Who are at risk for adverse muscle events (muscle problems)?

A

Personal or FH of statin intolerance
Muscle disease
Clinical presentation
concomitant drug therapy

159
Q

If a patient is on a statin an says they have muscle ____________, then measure their CK,

A 
pain
tenderness
stiffness
cramping
weakness
generalized fatigue
160
Q

What are ABSOLUTE CIs to statin therapy?

A

active or chronic liver disease

pregnancy

161
Q

What are RELATIVE contraindications to statin therapy?

A

excess alcohol abuse (like binge drinking)

162
Q

What are adverse reactions of statins?

A

myopathy
increase liver transaminases

hepatotoxicity (rare)
rhabdomyolysis (rare)

163
Q

What are other conditions that can cause muscle pain that we should consider when patients are on statins?

A 
hypothyroidism
reduced renal or hepatic function
rheumatologic disorders 
vitamin D deficiency
primary muscle disorders
164
Q

When a patient is on a statin what should you do about LFTs?

A 
take baseline LFTs before starting a statin
Measure LFTs if symptoms arise such as 
   unusual fatigue or weakness
   loss of appetite
   abdominal pain
   dark colored urine
   yellowing of skin or sclera
165
Q

Can statins increase blood glucose levels?

A

yes
JUPITER (0.6%)
HPS (0.8%)

166
Q

What are risk factors for DM?

A 
high risk ethnic groups include: AA, hispanic, native american, asian, pacific islander
FH
Gestational DM
Baby > 9 lbs
PCOS
HDL 250
167
Q

PCOS

A

Polycystic ovarian syndrome

168
Q

True or false? It is strongly recommended to evaluate patients on statins for new onset of DM.

A

true

169
Q

What are some drug interactions with fluvastatin?

A

CYP2C9
cholestyramine (BAS)
gemfibrozil

170
Q

What are some drug interactions with Pravastatin?

A

cyclosporine
gemfibrozil

no CYP3A4 interactions because it is metabolized by glucoronidation

171
Q

What are some drug interactions with Atorvastatin?

A 
CYP3A4-macrolide ABx
azole antifungals
amiodarone
cyclosporine
gemfibrozil
lots of grapefruit juice
172
Q

What are some drug interactions with rosuvastatin?

A

limited CYP2C9
cyclosporine
WARFARIN
gemfibrozil

173
Q

What are some drug interactions with pitavastatin?

A

limited CYP2C9 & 2C8 (gemfibrozil & fenofibrate)
cyclosporine
erythromycin

174
Q

What drugs are contraindicated with SIMVASTATIN?

A

Azole antifungals (itraconazole, ketoconazole, posaconazole)
Erythromycin, Clarithromycin, Telithromycin
HIV protease inhibitors (PIs)
Nefazodone
Gemfibrozil
Cyclosporine
Danazole

175
Q

Do not exceed Simvastatin 10 mg daily with:

A

non-DHP CCBs (verapamil & diltiazem)

176
Q

What drugs are CI with Simcor?

A

non-DHP CCBs (b/c Simcor is only available as Simvastatin 20 and 40)

177
Q

What drugs can you not take with any Simvastatin dose higher than 20mg?

A

Amlodipine
Amiodarone
Ranolazine

178
Q

What should you avoid while on simvastatin and lovastatin?

A

large amounts of grapefruit juice (more than a quart a day)

because it inhibits CYP3A4 which is the primary metabolizer of simvastatin & lovastatin

179
Q

What drugs are CI with LOVASTATIN?

A

Azole antifungals (itraconazole, ketoconazole, posaconazole)
Erythromycin, Clarithromycin, Telithromycin
HIV protease inhibitors (PIs)
Nefazodone
BOCEPREVIR
TELEPREVIR

180
Q

What drugs should you avoid with lovastatin?

A

Gemfibrozil

Cyclosporine

181
Q

Do not exceed lovastatin 20 mg if you are taking which drugs?

A

danazol

diltiazem & verapamil (non-DHP CCBs)

182
Q

Do not exceed lovastatin 40 mg if you are taking which drugs?

A

Amiodarone

183
Q

If your patient is on tipranavir + ritonavir or telaprevir, can you give them atorvastatin?

A

NO, it is contraindicated (CI)

184
Q

If your patient is on lopinavir + ritonavir, can you give them atorvastatin?

A

use with CAUTION and use with the lowest atorvastatin dose necessary

185
Q 
If your patient is on:
daranavir + ritonavir
fosamprenavir
fosamprenavir + ritonavir
saquinavir +ritonavir
can you give them atorvastatin?
A

Do not exceed atorvastatin 20 mg daily

186
Q

If your patient is on nelfinavir, can you give them atorvastatin?

A

do not exceed atorvastatin 40 mg

187
Q

True or false? If your patient is already on Simvastatin 80 mg and doing fine, they can stay on it, but NO other patient should ever be put on Simvastatin 80mg.

A

True

188
Q

What are 4 reasons we should use caution in patients on ANY dose of a statin?

A
  1. > 75 yo
  2. taking concomitant meds that alter metabolism
  3. taking multiple meds
  4. on complex medication regimens (transplant, HIV)
189
Q

What do you do if your patient has had 2 consecutive LDL levels lower than 40 mg/dL?

A

decrease statin dose

190
Q

Before initiating NIACIN therapy, what tests should you take?

A

baseline LFTs
fasting blood glucose or A1c
uric acid

191
Q

When your patient is on NIACIN, when should you do the following tests?
baseline LFTs
fasting blood glucose or A1c
uric acid

A

before initiation
during up-titration
every 6 months after that

192
Q

Nitrates should not be used if LFTs _________ ULN, or if patient has persistent . . .

A 
>2-3 x ULN
severe cutaneous symptoms
hyperglycemia 
acute gout
unexplained abdominal pain/GI symptoms
new onset of A fib or wt loss
193
Q

How can you reduce cutaneous symptoms with niacin?

A

start at a low dose and titrate over a period of weeks
•for ER: titrate to a max of 2000 mg, max 500 mg per week
•for IR: titrate to a max of 3000 mg, start at 100 mg TID
take with food and pre-medicate with 325 mg of aspirin 30 min before EACH dose

194
Q

When titrating for niacin, what is the max dose for ER niacin? What is the max dose weekly?

A

2000 mg

weekly: 500 mg

195
Q

When titrating for niacin, what is the max dose for IR niacin? What is the starting dose?

A

3000 mg

start at 100 mg TID

196
Q 
If a patient has baseline TGs ≥ 300 mg/dL or type II hyperlipoprotienemia what drug should you not use?
A. Niacin
B. fibrates
C. statin
D. BAS
A

D. BAS

197
Q

if a patient is about to start a BAS, what tests should you run?

A

fasting lipid panel should be run at:
initiation
3 months
q 6-12 months after that

198
Q

If your patient has TGs between 250-299, should you start a BAS?

A

use with caution!
evaluate lipid panel in 4-6 weeks
D’C if TGs go over 400 mg/dL

199
Q

what tests should you run before starting ezetimibe?

A

baseline hepatic transaminases

monitor LFTs and D’C is ALT > 3 x ULN

200
Q

When would you use fenofibrate + statin?

A

fenofibrate + low/moderate intensity statin
ONLY if ASCVD benefit or
TGs > 500 mg/dL & outweigh risks of ADR

201
Q

Should you give Fenofibrate with a high-intensity statin?

A

NO, to high of a risk for myalgia

202
Q

What tests should you run before initiating fibrates?

A

renal status
SCr
eGFR
then take again within 3 months and q 6 months after that

203
Q

True/False? Fenofibrate can be used if eGFR <30 mL/min.

A

false, D’C fenofibrate if eGFR persistently decreases to ≤ 30 mL/min

204
Q

What dose of fenofibrate can you give to patients with eGFR b/w 30-59 mL/min?

A

no higher than 54 mg/day

205
Q

What are side effects of EPA and DHA (omega-3 FAs)?

A 
main complaint: fishy-tasting burping
RARE: 
GI disturbances
Skin changes
bleeding
206
Q

What is the OPTIMAL level for TGs?

A

<100

207
Q

What are the NORMAL levels for TGs?

A

<150

208
Q

What are BORDERLINE levels for TGs?

A

150-199

209
Q

What are HIGH levels for TGs?

A

200-499

210
Q

What are VERY HIGH levels for TGs?

A

≥500

211
Q

What are some lifestyle changes that can decrease TGs?

A 
reduce ethanol intake
reduce carb consumption
weight loss
heart healthy diet
increase marine-derived EPH/DHA (eat more fish!!)
physical activity--aerobic exercise
212
Q

How much can losing 5-10% of body weight decrease TGs?

A

20% decrease in TGs

213
Q

Eating a Mediterranean diet can decrease TGs by ______%.

A

10-15%

214
Q

What do we recommend for borderline hypertriglyceridemia?

A

weight loss (up to 5% bw)
eat LOTs of fish with EPH/DHA (0.5-1 g)
decrease fat and carbs in diet and increase protein intake
no drug therapy

215
Q

What do we recommend to patients with HIGH hypertriglyceridemia?

A

weight loss (5-10% bw)
eat even more fish with EPH/DHA (1-2 g)
decrease fat and carbs more in diet and increase protein intake more
no drug therapy

216
Q

What do we recommend to patients with VERY HIGH hypertriglyceridemia?

A

weight loss (5-10% bw)
eat even MORE fish with EPH/DHA (>2g)
decrease fat and carbs more in diet and increase protein intake more
*drug therapy

217
Q

What was the outcome of the FIELD (2004) trial?

A

there was NO DIFFERENCE between fenofibrate vs. placebo in type 2 DM

218
Q

What was the outcome of the ACCORD: Lipid (2010) trial?

A

fenofibrate + simvastatin vs. simvastatin alone
•men did better on fenofibrate than women
•in pts with TGs > 204 or HDL <34 fenofibrate worked even better

219
Q

What was the outcome in the Alpha Omega (2010), SU.FOI.OM3 (2008), and ORIGIN (2012) trials?

A

NO DIFFERENCE in all of them
Alpha Omega: EPA/DHA vs. placebo
SU.FOI.OM3 (2008): EPA/DHA to prevent major CV event
ORIGIN (2012): Lovaza to prevent death from CV causes in high risk CV pts

220
Q

When does the friedwald equation NOT work?

A

when TGs ≥ 400

221
Q

What is the friedwald equation?

A

TC = LDL + HDL + VLDL

ptx (7 decks)

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