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Clinical Pharm Exam 2 (Jaclyn) > Hyperlipidemia > Flashcards

Hyperlipidemia Flashcards

1
Q

How long should one undergo lipid therapy?

A

Indefinitely

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2
Q

Lipid levels return to pretreatment levels in how much time?

A

2-3 weeks

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3
Q

Lipid-lowering drugs in conjunction with ________ and _______ optimize prevention of heart disease

A

Diet changes & exercise

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4
Q

Drugs that lower LDL can prevent progression, slow progression, & cause regression of…..

A

Atherosclerotic disease

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5
Q

Most cholesterol in carried in

A

LDL (unless increased TGs)

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6
Q

____ TG levels and _____ HDL levels increase risk for heart disease

A

Increased; decreased*

*even if LDL is normal

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7
Q

If you decrease TGs, you will likely

A

Increase HDL

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8
Q

Shape of saturated FAs

A

Straight chained

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9
Q

Saturated FAs vary in

A

Chain length

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10
Q

Unsaturated FAs vary in

A

Number, position, & geometry of double bonds

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11
Q

Double bonds of naturally occurring oils & fats are in the ____ configuration

A

Cis

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12
Q

Double bonds of industrial products are in the ____ configuration. What are the implications of this?

A

Trans

Raises the melting point

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13
Q

2 components of prevention

A

Exercise & diet

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14
Q

What diet has the best data

A

Mediterranean

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15
Q

Screening recommendations (two steps)

A

Step 1: Assess for traditional RF (e.g. BP, DM, smoking) q4-6yr in pt. 20-79
Step 2: Based on lipid & RFs, calculate 10 yr ASCVD risk

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16
Q

Lipoprotein abnormalities are classified into 2 groups:

A
  1. High LDL

2. Combined dyslipidemia (low HDL, high TG, high non-HDL, normal LDL)

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17
Q

Why did the approach to guidelines change? (NCEP/ATPIII - 2004 -> ACC/AHA - 2013)

A

Aiming for LDL targets is NOT based on evidence

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18
Q

New ACC/AHA guidelines focus on these 3 things:

A
  1. Statins
  2. Less use of non-statins (e.g. fibrates, niacin, bile acid sequestrants etc.)
  3. Abandon LDL “goals”
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19
Q

What does the ACA/AHA CVD risk calculator determine?

A

Patient’s 10-year risk of AMI or CVA

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20
Q

How does the ACA/AHA CVD risk calculator determine?

A

Based on patient’s sex, age, race, total and HDL cholesterol, diabetes, systolic BP, HTN tx, & smoking status

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21
Q

ACA/AHA CVD risk calculator is used for

A

PRIMARY prevention

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22
Q

ACA/AHA CVD risk calculator is not valid if

A

The patient is being treated (use pre-statin values to assess risk)

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23
Q

Why does mot ASCVD events occurs in lower risk patients?

A

Because they make up most of the population

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24
Q

Who gets a high-intensity statin?

A
  • Pt. w/ clinical atherosclerotic CVD
  • Pt. w/ DM + age 40-75 + LDL 70-189 AND an ASCVD risk >7.5%
  • Pt. w/ LDL >190
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25
Q

Who gets a moderate-intensity statin?

A
  • Pt. w/ DM + age 40-75 + LDL 70-189 AND an ASCVD risk <7.5%
  • Pt. w/o DM + age 40-75 + LDL 70-189 AND an ASCVD risk >7.5%*
  • eligible for moderate-to-high-intensity statin therapy
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26
Q

Examples of high intensity statins

A

Atorvastatin

Rosuvastatin

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27
Q

Examples of moderate intensity statins

A 
Atorvastatin (lower dose c/t high) 
Rosuvastatin (lower dose c/t high) 
Simvastatin 
Pravastatin 
Lovastatin
Fluvastatin 
Pitvastatin
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28
Q

High intensity statins lower LDL how much

A

> 50%

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29
Q

Moderate intensity statins lower LDL how much

A

30-49%

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30
Q

NICE recommends using ________ toool to calculate % risk of developing CVD

A

QRISK2

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31
Q

What does QRISK2 take into accound

A

Age, smoking hx, cholesterol, BP, Afib, BMI, & FH of HD

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32
Q

R/o secondary causes of hyperlipidemia if LDL-C >_____ on initial evaluation

A

190mg/dL

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33
Q

What else must you do if pt. has LDL-C >190mg/dL on initial eval?

A

Screen family members

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34
Q

Causes of secondary hyperlipidemia (must r/o)

A
  • Meds
  • Hypothyroidism
  • Obstructive biliary disease
  • Nephrotic disease
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35
Q

Universal lipid screening in pediatric patients occurs in those __-__yr and __-__yr

A

9-11; 17-21

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36
Q

Screen pediatric patients if they

A
  • Use tobacco

- Have HTN

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37
Q

What drug classes target LDL?

A
  • HMG-CoA reductase inhibitors (statins)
  • Cholesterol absorption inhibitors
  • Bile acid sequestrants
  • PCSK9 inhibitors
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38
Q

“Newer” statins

A 
Atorvastatin 
Rosuvastatin 
Simvastatin 
Pravastatin 
Pitvastatin
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39
Q

“Older” statins

A

Lovastatin

Fluvastatin

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40
Q

What formulation do all statins come in

A

Tablets

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41
Q

Which statin is the most potent, cheapest, has the best data & fewest CYP interactions

A

Atorvastatin

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42
Q

Which statins do we actually use?

A

Atorvastatin
Rosuvastatin
Simvastatin

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43
Q

Statin MOA

A

Inhibit de novo synthesis of cholesterol via inhibition of HMG-CoA reductase (decrease synthesis -> increased LDL-R expression -> more LDL cleared from the blood)

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44
Q

Lipid effects of statin

A

↓ LDL
↓TG
Modest ↑ in HDL

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45
Q

Other beneficial effects of statins

A
  • Improve endothelial fcn
  • Replace plasma viscosity
  • Plaque stabilization (↓ plt aggregation & thrombin formation)
  • Reduce inflammation
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46
Q

Primary indication for statins

A

Primary AND secondary prevention of CAD

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47
Q

Other indications for statins

A
  • DM (@ diagnosis)

- Post-AMI (upon d/c home)

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48
Q

When should simvastatin, lovastatin, fluvastatin be dosed and why?

A

qhs d/t short 1/2 life

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49
Q

When should atorvastatin, rosuvastatin, pravastatin, pitvastatin be dosed and why?

A

any time d/t long 1/2 life

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50
Q

Up to __% of pt. on a statin stop taking in within a year?

A

50

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51
Q

What do we monitor in pt. on statins?

A
  • LFTs
  • Fasting BS, HgBA1C
  • CPK
  • Fasting lipid profile (1-3mo after tx initiated, then q3-12mo -> monitor adherence & lifestyle)
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52
Q

What is a risk of scheduling a f/u appt for a fasting lipid panel?

A

Pt. non-adherence

Do it same day: nonfasting lipid profile > no lipid profile

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53
Q

Most cases (~60%) of statin-induce rhabdo are due to….

A

Drug interactions

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54
Q

Simvastatin and atorvastatin are CYP___ substrates

A

3A4 (major)

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55
Q

If simvastatin and atorvastatin are given with CYP3A4 inhibitors, there is an increased risk of

A

Myopathy (x5)

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56
Q

Some statins are P-gp substrates (sim > ator > prava). If given with P-gp inhibitors such as ______, ______, _____, _______ may increase risk of myopathy

A

Clarithro, non-DHP CCBs, amiodarone, carvedilol

57
Q

Niacin + statin =

A

Additive myopathy

58
Q

Fibrates + statin =

A

Additive hepatotoxicity or myopathy (AVOID!)

59
Q

How do fibrates (esp. gemfibrozil) cause hepatotoxicity

A

Inhibit hepatic glucuronidation of statin -> interferes statin elimination

60
Q

Simvastatin + dabigatran =

A

↑ hemorrhage risk

61
Q

Statins + daptomycin =

A

↑ myopathy risk

62
Q

Which statin is most associated with rhabdomyolysis

A

Simvastatin

63
Q

How can we further evaluate a patient who complains of myalgia

A

Vitamin D deficiency, thyroid disorder, polymyalgia rheumatic (PMR)

64
Q

What lab should we get initially and recheck with complaints of myalgia

A

CPK

65
Q

At what CPK levels should we consider stopping or stop statin?

A

Consider if <3-10x ULN

Stop for severe sx or >10x ULN

66
Q

What must we do before blaming the statin for causing myalgia, weakness, or rhabdo in a patient?

A

r/o other causes (e.g. vitamin D deficiency)

67
Q

Adding exercise to statin therapy improves

A

Survival (better than either alone)

68
Q

Should we encourage pt. on statins to increase duration or intensity of exercise first?

A

Duration

69
Q

What should we do if a pt. on a statin has ↑ LFTs (>3x ULN)?

A

Consider switching to another statin or low the dose of the same one

70
Q

Statins are ok in patients with elevated LFTs d/t

A

Chronic stable liver disease (esp. NASH)

- Statin may even ↓ LFTs AND ↓ inflammation

71
Q

Statins proven to ↑ _______ & _______

A

HbA1C & blood glucose (mostly in pt. with DM RF)

72
Q

What statin is more likely to cause ↑ HbA1C & blood glucose

A

It’s a class effect (& it’s dose-dependent)

73
Q

Adding what drug can mitigate the↑ HbA1C & blood glucose caused by statins?

A

Metformin (the lectures are TALKING)

74
Q

What must your consider prior to choosing a statin

A
  • Degree of hyperlipidemia
  • Pk properties
  • Presence of renal impairment
  • Presence of chronic liver disease
  • Cost & data
75
Q

Which statins are good for pt. with renal impairment as they do not require a dose adjustment

A

Atorvastatin, fluvastatin

76
Q

Which statins are probably safest for pt. with chronic liver disease?

A

Low dose pravastatin or rosuvastatin

77
Q

What drug is a cholesterol absorption inhibitor?

A

Ezetimibe

78
Q

Ezetimibe MOA

A

Inhibit intestinal absorption of both dietary & biliary cholesterol by blocking transport at SI brush border -> ↓ LDL (20-25%)

79
Q

Ezetimibe may ↑ the effect of what drug

A

Warfarin

80
Q

What should we monitor in pt. on ezetimibe

A

FLP

81
Q

Bile acid sequestrants

A

Cholestyramine
Colestipol
Colesevelam

82
Q

Bile acid sequestrant MOA

A

Enhance excretion of bile salts by binding to them -> liver must use cholesterol to make new salts -> promotes synthesis of LDL receptors -> LDL receptors bind plasma LDL

83
Q

Lipid effects of bile acid sequestrant

A

↓ LDL (up to 20%)

May raise TG in pt. with hypertriglyceridemia

84
Q

Do NOT use bile acid sequestrants if TGs >____

A

300

85
Q

Which bile acid sequestrant is more tolerable?

A

Colesevelam

86
Q

What should we monitor in pt. on bile acid sequestrants?

A

FLP

87
Q

Drug interactions of bile acid sequestrants

A
  • No systemic interactions (not absorbed systemically)

- May bind & impair absorption of other drugs (e.g. digoxin, warfarin, fat soluble vitamins, other anti-lipid meds)

88
Q

How do we mitigate drug interactions w/ bile acid sequestrants?

A

Give other meds 1 hr before or 4-6 hours after bile acid sequestrants

89
Q

In what patient population should we avoid the use of bile acid sequestrant

A

Pt. w/ bowel disease

90
Q

ADR of bile acid sequestrants

A

GI intolerance (constipation)

91
Q

PCSK9 inhibitors

A

Alirocumab

Evolocumab

92
Q

PCSK9 inhibitor MOA

A

Monoclonal Abs target & prevents PCSK9 binding (normal physiology: PCSK9 binds to LDL receptors on hepatocytes -> promotes receptor degradation -> prevents LDL-C clearance from blood & ↑ serum LDL)

93
Q

PCSK9: rate of cholesterol clearance __ rate of synthesis

A

>

94
Q

Clinical indication for PCSK9

A
  • Adjunct to diet + maximally tolerated statin therapy for adults w/ hetero or homozygous familial hypercholesterolemia
  • Approved for pt. w/ ASCVD who require additional LDL lowering
95
Q

Route of PCSK9

A

Injection

96
Q

Lipid effects of PCSK9

A

↓ LDL-C ~60% (additional reduction when combined with statin)

97
Q

PCSK9 pearls

A

$$$

May need to store in fridge & warm before use

98
Q

What drug classes target HDL & TGs?

A
  • Niacin
99
Q

What B vitamin is niacin?

A

3

100
Q

Niacin MOA

A

Inhibits mobilization of FFA from adipose tissue to liver -> ↓ synthesis & secretion of VLDL & ↓ conversion of VLDL to LDL
Can also ↑ HDL (via reduction of lipid transfer of cholesterol from HDL to VLDL & delayed clearance of HDL)

101
Q

Lipid effect of niacin

A

↑ HDL 15-35%
↓TG 10-50%
↓ LDL 5-25%

102
Q

When do we dose niacin

A

qhs (start @ 500mg x1mo, then titrate to max dose SLOWLY)

103
Q

Recent studies showed that adding niacin to a statin……

A

Does NOT improve outcomes more than statin alone

104
Q

Niacin has been found to be associated with

A

A small increased risk of ischemic CVA (AIM-HIGH trail = death of niacin)

105
Q

What do we have to monitor in pt. on niacin?

A
  • CPK
  • FLP
  • LFTs (baseline, then q6-12wks, then 6mo)
  • Uric acid & glucose (baseline fasting, at 3mo, then annually or as clinically indicated)
  • glucose bump is substantial
106
Q

Careful with coadministration of niacin w/ these two drug classes

A

Statins & fibrates

107
Q

Niacin ADRs

A
  • FLUSHING (mostly IR)
  • Hepatotoxicity (mostly sustained release)
  • May aggravate glucose & gout (avoid in these pt.)
  • ER has the least flushing & hepatotoxicity
108
Q

How are we approaching lowering TGs that is different than in the past?

A
  • No longer relying on fibrates
  • More use of fish oil and lifestyle changes (modest wt. loss, ↓ added sugars, eliminating trans fat, ↑ fiber & unsaturated fats, limiting alcohol can ↓ TGs)
109
Q

What drug classes target TGs?

A
  • Fibric acid derivatives

- Fish oils

110
Q

Examples of fibric acid derivatives

A

Gemfibrozil
Fenofibrate (micronized, non-micronized)
Fenofibric acid

111
Q

Fibric acid derivatives MOA

A

PPAR-alpha agonist

112
Q

Lipid effects of fibric acid derivatives

A

↓ LDL (minimal effect w/ gemfibrozil, ↓20% with fenofibrate
↓TG 25-50%
May ↑ HDL

113
Q

Other clinical uses of fibric acid derivatives

A
  • Persistent hypertriglyceridemia severe enough to be at rik for pancreatitis (>800mg/dL)
  • Fenofibrate has uricosuric activity & is used for gout prevention
114
Q

Fibric acid derivatives contraindication in patients with

A

Liver or gallbladder disease

115
Q

What do we have to monitor in pt. on fibric acid derivatives?

A
  • CPK (if concurrent statins or niacin)
  • FLP
  • LFTs (baseline, then q6-12wks, then 6mo)
116
Q

Gemfibrozil is a strong inhibitor of CYP___ & CYP___

A

2C9 & 2C19

117
Q

What might happen if a pt. is taking fibric acid derivatives and a TZD for DM?

A

They are both PPAR agonists -> may potentiate them (increase effects)

118
Q

We should use fibric acid derivatives with what other lipid-lowering drug class?

A

Statins (overlapping toxicities)

119
Q

ADRs of fibric acid derivatives

A

Overall well tolerated

  • N/V, dyspepsia M/C
  • Reversible hepatotoxicity
  • Myositis & rhabdo (mostly gemfibrozil, check CPK w/ muscle complaints)
120
Q

Two types of fish oils

A

Both are long-chain unsaturated omega-3 fatty acids

  • Lovaza* contains EPA & DHA -> DHA may raise LDL in some pt.
  • Vascepa* contains only EPA -> less effective at ↓ TGs
  • brand names
121
Q

Fish oil MOA

A

Reduce hepatic TG production & ↑ TG clearance

122
Q

Lipid effects of fish oils

A

↓ TGs 20-50%
Long-term use may ↑ HDL
*no current evidence that fish oils prevent CVD

123
Q

Fish oil pearls

A
  • OTC products cost LESS than brand name drugs but require 3x daily dose for same effect
  • Do NOT interact with statins
  • Supplements are mercury-free
  • Seafood allergy to fish protein not oil, but advise pt. to be cautious with use
124
Q

What do we monitor with fish oils?

A

FLP

125
Q

High doses of fish oils have what effect? (potential drug interaction)

A

Anti-plt effect (caution w/ other drugs that effect coag)

126
Q

ADRs of fish oils

A

Generally well-tolerated

- Eructation (burping), dyspepsia, unpleasant aftertaste M/C

127
Q

Approach to lipid management (two steps)

A

Step 1: decide if therapy is indicated (shared decision-making + risk calculator)
Step 2: start mod to high intensity statin

128
Q

When do we consider a non-statin?

A

Statin intolerant pt.!

  • Non-statins as ADD ON: Add for pt w/ CVD who can’t tolerate a high-intensity statin or don’t get expected LDL-lowering effect
  • Non-statins as MONOTHERAPY: reserve for pt. at high CV risk who cannot take a statin
129
Q

What non-statin do we choose as ADD ON therapy in statin-intolerant pt.?

A

Ezetimibe

- Improves CV outcomes when added to statin (use in pt. post-ACS)

130
Q

What non-statin do we choose as MONOTHERAPY therapy in statin-intolerant pt.?

A
  • Bile acid sequestrants -> may improve outcomes when used alone
  • Ezetimibe - no evidence that it has CV benefit alone
  • PCSK9 inhibitors - for VERY HIGH RISK PT
131
Q

Good therapy regimen for pt. w/ high LDL

A

Statin +/- ezetimibe pr PCSK9 inhibitors

132
Q

Good therapy regimen for pt. w/ TG >500-1000

A

Fish oils > fenofibrate

133
Q

Good therapy regimen for pt. w/ low HDL

A

↓ fructose & increase fiber to ↓ TGs

Add exercise, wine, & EVOO

134
Q

ABCDE approach to pt. with metabolic syndrome

A 
A: assess CV risk &amp; ASA therapy
B: BP control
C: cholesterol/lipid mgmt
D: DM prevention &amp; diet therapy
E: exercise therapy
135
Q

What lipid-lowering drugs are category X

A

Statins

136
Q

What lipid-lowering drugs are category C

A
  • Fibric acid derivatives
  • Bile acid sequestrants
  • Ezetimibe
  • Niacin (can be A depending on dose)
  • Omega 3 FAs
137
Q

Take home message for lipid-lowering drugs in pregnancy

A

Generally do NOT treat lipids in pregnant women

138
Q

What is homozygous familiar hypercholesterolemia (HoFH)?

A

Rare inherited condition that is commonly caused by defects in the LDL receptor gene
- Causes VERY HIGH LDL levels & premature CVD & death w/o tx

139
Q

Two FDA approved drugs for HoFH

A

Mipomersen

Lomitapide

Clinical Pharm Exam 2 (Jaclyn) (2 decks)

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