Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CRT > E3Hyperlipidemia Drugs > Flashcards

E3Hyperlipidemia Drugs Flashcards

This deck covers the pharmacologic agents associated with hyperlipidemia management.

1
Q

Lipoproteins

A

Proteins used in the transportation of lipids through the extracellular fluid around the body.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Examples of Lipoportiens.

A

VLDL
IDL
LDL
HDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

LDL

A

Low Density Lipoprotein.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

LDL is predominantly _________.

A

Cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Apolipoprotein B is a precursor to _________

A

Low Density Lipoprotein (LDL)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

VLDL

A

Very Low Density Lipoprotein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

VLDL is mostly comprised of ___________.

A

Triglycerides.

Excess leads to plaque build up which leads to restricted blood flow.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

IDL

A

Intermediate Density lipoprotein

Formed when muscle and fat tissues take TGs from VLDL.

High Cholesterol Content

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

HDL

A

High Density Lipoprotein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Role of HDL

A

Take cholesterol back to the liver to be recycled.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

HDL is mostly ________

A

protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Apolipoprotein A is a precursor for ________

A

HDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Rank Lipoproteins by size relative to a chylomicron.

A

Chylomicron (largest)
VLDL
LDL
HDL (smallest)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Chylomicrons are predominantly ___________

A

Triglycerides.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

All adults should have a lipid panel screened when?

A

All adults greater than 20 years old should be screened every 5 years.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Lipid panels should be tested after a _________.

A

9-12 hour fast.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is measured on a lipid panel?

A
  1. Total Cholesterol (associated with CHD risk)
  2. LDL (reduction leads to decreased CHD risk)
  3. HDL (strong independent predictor of CHD)
  4. Triglycerides (Not consistently linked to CHD risk)
  5. Friedewald Equation (estimates LDL)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Friedewald Equation

A

Estimates LDL

LDL = TC - HDL - (TG/5)

This formula is only accurate with TG under 400 mg/dL. If it is greater than this we can just measure LDL directly.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

When is the Friedewald equation not reliable?

A

Triglycerides >400 mg/dL.

if it is higher than this we should simply measure LDL directly.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are lifestyle modifications to reduce ASCVD risk?

A
  1. Heart Healthy Diet
  2. Regular, Moderate Intensity Exercise
  3. Smoking Cessation
  4. Healthy Weight Managment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the major ASCVD risk factors? [7]

(6/7 needed for good)–> perfect 7 for perfect.

A
  1. Cigarette Smoking
  2. HTN
  3. Diabetes
  4. Advanced Age
  5. Lipid Panel Abnormalities
  6. CKD.
  7. Family ASCVD history
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are current recommendations for a heart healthy diet?

A

DASH DIET

-Vegetables, Fruits, Whole Grains
- Low Fat Dairy Products, Poultry, Fish, Legumes
- Limit Intake of sweets, sugary beverages, and red meats.
- Reduce intake of saturated fat (5-6 % of calories)
- Limit intake of trans fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the current exercise recommendations to reduce ASCVD risk?

A

Moderate to Vigorous physical activity 3-4 times a week lasting at least 40 minutes per session.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What guidelines were utilized in class to review non-statin cholesterol lowering therapies?

A

2022 ACC Expert Consensus Decision Pathway on the Role of Nonstatin Therapies for LDL-Cholesterol Lowering in the Management of Atherosclerotic Cardiovascular Disease Risk.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Who are non-statin therapies indicated in? (3 answers)

A

High Risk Patients who:
1. Have less than anticipated response to statins.

  1. Unable to tolerate recommended intensity of statin.
  2. Completely intolerant to statin therapy.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What patients should be referred to a lipid specialist and RDN?

A

Those who are at high risk, that either do not tolerate statin therapy or don’t receive optimal effect and have either:
1. LDL 250 mg/dL +
2. HoFH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Generic Name for Nexletol

A

Bempedoic Acid (Note this drug is brand name only currently)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Nexletol Dose

A

180 mg PO QD
With or without food.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Nexletol Mechanism of Action.

(slide 19 of Hyperlipidemia 1)

A

Adenosine Triphosphate-Citrate Lyase (ACL) Inhibitor.
ACL is an enzyme which is upstream in the cholesterol synthesis pathway.

Bempedoic acid and its active metabolite require CoA activation by a very long chain acyl-CoA synthetase 1 (ASCVL1).

Inhibition of ACL leads to:
1. Lowered Cholesterol synthesis
2. Lower LDL by upregulating LDL receptors in the liver.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What enzyme is responsible for the activation of Nexletol? Where is this enzyme primarily expressed?

A

ASCVL1 (Very Long Chain Acyl-CoA Synthetase 1). This is primarily expressed in the liver.

Note: Nexletol is a PRO DRUG!!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the primary effect of Nexletol?

A

Lowers LDL.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What was the outcome of the CLEAR Harmony Trial?

A

Showed Nexletol increased LDL reduction by ~17-20 % in patients already taking max statin therapy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What did the Clear Wisdom trial determine?

A

Evaluated patients taking maximum tolerated statin vs non statin at all and the additional benefit of Nexletol.
Found that Nexletol had a ~17-19% reduction of LDL in patients on statin therapy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What did the CLEAR Tranquility Trial determine?

A

The clear tranquility trial evaluated the benefit of Nexletol for statin intolerant patients who were currently taking ezetimibe.

This found Nexletol to further reduce LDL levels by approximately 29%.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What did the CLEAR SERENITY trial determine.

A

This trial evaluated the use of Nexletol in statin intolerant patients to reduce LDL.

This trial found Nexletol to reduce LDL by 21%. However, there was also an increased incidence of adverse events compared to placebo.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Nexletol ADEs

A
  1. Gout with prior history or Hyperuricemia
  2. Tendon Rupture
  3. Myopathy w/ concomitant use of simvastatin or pravastatin. –> these statins have a max daily dose with nexletol. (Note myopathy was not reported to occur with Nexletol monotherapy.)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Which statins have a max daily dose with nexletol?

A

Simvastatin and Pravastatin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Brand Name for Ezetimibe

A

Zetia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Zetia Dose

A

10 mg PO QD
With or without food.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Zetia Mechanism

A

Inhibits absorption of cholesterol at the brush border of the small intestine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Zetia Beneficial Effects

A
  1. Decrease LDL (up to 25% additional reduction with statin therapy, 18% without.)
  2. Decreased TC
  3. Decreased TG
  4. Increased HDL.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Zetia ADEs

A
  1. URTI
  2. Diarrhea
  3. Arthralgias
  4. Sinusitis
  5. Pain in Extremities

Myopathy when used in conjunction with statins. (rare without concomitant statin use.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What was the outcome of the IMPROVE-IT trial?

A

The addition of ezetimibe to moderate-intensity statin in patients with recent ACS resulted in lower LDL-C and reduced the primary cardiovascular composite endpoint.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What was the outcome of the SHARP trial?

A

This trial evaluated simvastatin and ezetimibe dual therapy. It found it to reduce LDL-C and reduce the primary endpoint of first major ASCVD benefit.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

T or F: Zetia has CV benefit?

A

True!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

T or F: Nexletol has CV benefit?

A

False: At least not studied.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is the combinational therapy consisting of Bempedoic Acid and Ezetimibe?

A

Nexlecet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is the mechanism of action of a PCSK9 inhibitor?

A

PCSK9 inhibitors are monoclonal antibodies which bind to PCKS9 to increase the number of LDL receptors that are available to clear circulating LDL.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is the physiologic role of PCSK9 in the body?

See Slide 23/37 in Hyperlipidemia Part I notes

A

PCSK9 is an enzyme which binds to LDL receptors on the liver and degrades them. This leads to a decrease in hepatic clearance of LDL, causing an overall systemic increase in LDL.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What type of drug is Praluent

A

PCSK9 Inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Generic Name for Praluent

A

Alirocumab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Praluent Indication

A
  1. HeFG, HoFG
  2. Clinical ASCVD who need more LDL reduction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Praluent Dosing

A
  1. ASCVD of HeFG:
    75 mg SQ Q2W (may increase to 150)
    OR
    300 mg SQ QW
  2. HoFH
    150 mg SQ Q2W
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Praluent Efficacy

A

With statin it lowers LDL by an additional 45% (75 mg dose) and 58% (150 mg dose)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What type of drug is Repatha?

A

PCSK9 Inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Repatha Generic Name

A

Evolocumab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Repatha Indication

A
  1. HeFH
  2. HoFH
  3. Clinical ASCVD who need more LDL reduction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Repatha Dosing

A
  1. ASCVD or HeFH
    140 mg SQ Q2W or 420 mg SQ Q month
  2. HoFH
    420 mg SQ Q month

420 mg dose needs to be given as 3 injections (140 mg each) consecutively within 30 minutes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Repatha Efficacy

A

With a statin, Repatha lowers LDL by an additional 64 % (140 mg Q2W) and 58% (420 mg Q month)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

PCSK9i ADEs

A
  1. Nasopharyngitis
  2. Injection Site Reactions
  3. Influenza
  4. URTI
  5. Back Pain

Evolucumab (Repatha) Only—-> Self-Reported Cognitive ADEs

61
Q

PCSK9i drug interactions

A

None, ha made you look.

62
Q

What did the ODYSSEY OUTCOMES trial investigate and what were the outcomes.

A

Showed use of Alirocumab (Praluent) reduced ischemic events (including all-cause mortality, MI) compared with placebo among patients with an ACS event within the preceding 1-12 months in combination with statin therapy.

63
Q

What did the FOURIER trial investigate and what did it conclude.

A

Showed Evolocumab (Repatha) demonstrated reduced primary end point of CV death, MI, Stroke, Revascularization or hospiutalization for UA in patients with PRIOR MI, storke, or PAD on atorvastatin greater than or equal to 20 mg or equivalent.

64
Q

What is the mechanism of action of bile acid sequestrants?

A

Binds with bile acids in the small intestine to form an insoluble complex that is eliminated in the feces to prevent reabsorption.

Normally bile acids undergo hepatic recirculation. Therefore, when they are bound by resins, this interferes with this process stimulating HMG-CoA reductase activity. However, in this case this does not promote LDL production b/c cholesterol is shunted into the bile acid pathway.
The hepatocyte responds by increasing uptake of LDL, which drops plasma cholesterol concentrations.

65
Q

What type of drug are Cholestyramine and Colestipol?

A

Bile Acid Sequestrant Powders

66
Q

What kind of drug is Colesevelam?

A

Bile Acid Sequestrant (powder or tablet)

67
Q

What is dose of colesevelam? (Welchol)

A
  1. 6 tablets by mouth once daily. (can split to 3 tablets twice daily)
68
Q

What other disease state is Colesevelam indicated for?

A

TIIDM

69
Q

What is the therapeutic effect of bile acid sequestrants?

A
  1. Reduce LDL
  2. Increases VLDL (do not use in patients with hypertriglyceridemia)
  1. Colesevelam Monotherapy (reduces LDL 15%–> 10-16% with statin therapy)
  2. Colestipol Monotherapy (reduces LDL 16 to 27%)
  3. Cholestyramine Monotherapy (reduces LDL 10.4%)
70
Q

Who should Bile Acid Sequestrants not be used in and why?

A

Bile Acid Sequestrants should not be used in individuals with high triglycerides (>300 mg/dL).

This is because BAS can increase VLDL which are primarily composed of triglycerides–> worsening pre-existing hypertriglyceridemia.

71
Q

Bile Acid Sequestrant ADE

A
  1. Constipation
  2. Dyspepsia
  3. Nausea
  4. Bowel Obstruction
  5. Dysphagia
  6. Hypertriglyceridemia
  7. Pancreatitis
  8. Increased Transaminases
72
Q

Bile Acid Sequestrant Drug Interactions

A
  1. Phenytoin (decrease concentration—> increased seizure activity.)
  2. Warfarin (decreased INR–> increased clot risk)
  3. Levothyroxine/THR–> Increase TSH levels
73
Q

How long should you separate bile acid sequestrants from other medications?

A

At least 4 hours.

74
Q

What was the result of the CV outcomes trials involving bile acid sequestrants?

A

19% reduction in CHD death or nonfatal MI in patients who took cholestyramine for an average of 7.4 years

However, it should be noted this data is not particularly strong and is falling out of favor. These are still occasionally sued for those who are ezetimibe intolerant and have high triglycerides.

75
Q

Niacin is Vitamin ___________

A

B3 or Nicotinic Acid

76
Q

Niacin Mechanism of Action

A
  1. Reduces Hepatic Synthesis of VLDL —> Lowers LDL
  2. ## Inhibits Diacyl-glycerol acetyl transferase -2 and inhibits hepatic catabolism of HDL. (This leads to increased HDL.)*It also acts on the peripheral circulation causing vasodilation which increases BF to the face, chest, neck. This is what causes “niacin flushing” —> This does not happen with Nicotinamide.
77
Q

Which drug in this section causes flushing?

A

Niacin

78
Q

What are the therapeutic effects of niacin?

A
  1. Reduces LDL 5-25%
  2. Increase HDL 15-35%
  3. Decreases TG 20-50%
79
Q

Niacin ADEs

A
  1. Cutaneous Flushing (prostaglandin mediated)-> occurs in 88% of patients.
  2. headache, diarrhea, dyspepsia, abdominal pain
  3. Increase blood glucose (due to increase in fatty acids)
80
Q

How can we pretreat to avoid niacin flushing?

A
  • take with food
    -titrate dose slowly
  • give aspirin 325 mg 30 minutes prior to administration.
81
Q

What were the results of the CV outcomes trials for niacin?

A

Trick question! There were none. Made you look!

82
Q

What is the mechanism of action for Omega-3-Fatty Acids

A
  1. Hepatic Inhibition of Triglyceride Synthesis (lowered triglycerides)
  2. Decreased LDL-C Secretion (increased LDL)
  3. Increased VLDL-C metabolism (decreased VLDL)
83
Q

What are the therapeutic effects of Omega-3 Fatty Acids?

A
  1. Triglycerides: decreased 25-45%
  2. HDL–> increase <10%
  3. May increase LDL (due to DHA component)
84
Q

How can we avoid LDL increase with Omega-3-Fatty Acids?

A

Avoid those with DHA.

Remember Vascepa is EPA purified (no DHA component.)

85
Q

what type of drug is Lovaza

A

Omega-3-Fatty Acid

86
Q

what type of drug is Vascepa

A

EPA Purified Omega-3-Fatty-Acid

87
Q

what type of drug is Epanova

A

Omega-3-Fatty Acid

88
Q

what type of drug is Omtryg

A

Omega-3-Fatty Acid

89
Q

What is the typical dose of Omega-3-Fatty Acids?

A

1-3 grams of EPA + DHA daily in divided doses.

90
Q

What are the ADEs of Omega-3-Fatty Acids?

A
  1. GI upset
  2. Aftertaste/Belching
  3. Bleeding Risk–> only when used with other drugs which promote bleeding.
91
Q

What was the conclusion of the REDUCE-IT trial?

A

Found Patients with the following:
CVD or DM
Fasting TG: 135-499 mg/dL
LDL: 41-100 mg/dL
-> Had significant risk reduction (25%) with Vascepa and statin dual therapy in primary endpoint of first occurrence of a major adverse cardiovascular event.
—————————————
In other words, there was a relative risk reduction in the incidence of a first major cardiovascular event even in those with healthy triglycerides in those with CVD or diabetes.

92
Q

Fenofibrate Drug Class

A

Fibric Acid Derivative

93
Q

Gemfibrozil Drug Class

A

Fibric Acid Derivative

94
Q

Gemfibrozil Typical Dose

A

600 mg PO BID

95
Q

Fibric Acid Derivative Mechanism of Action

A

This receptor:
1. Increase Fatty Acid oxidation of free fatty acids.
2. Increases Metabolism of TG rich lipoproteins (VLDL, Chylomicrons)
3. Increase affinity of LDL for LDL receptor (decreases LDL C mildly)
4. Increases hepatocyte production of Apo A —> leads to HDL-R formation.

96
Q

What are the therapeutic effects of fibric acid derivatives.

A
  1. LDL: decrease 5-20%
  2. TGL Decrease 20-50%
  3. HDL: Increase 10-20%
97
Q

What is the most significant benefit to fibric acid derivatives?

A

Decreases TG by 20-50%

98
Q

What is the indication of fibric acid derivatives?

A

Primarily for patients with triglycerides above 500 mg/dL.

99
Q

What drug is contraindicated with gemfibrozil, and should be used with caution with fenofibrate?

A

Statins–> increased risk of myagia.

100
Q

Do Fibric Acid derivatives have CV outcomes data?

A

Not enough to support use with statins.

101
Q

Fibric Acid Derivative ADEs

A
  1. Abdominal Pain
  2. Diarrhea
  3. Arthralgia
  4. Myalgia
  5. Myopathy
102
Q

What did the AIM HIGH and ACCORD trials determine?

A

Adding Niacin and Fenofibrate to statin therapy did not increase ASCVD risk reduction.

Therefore, the risk of using these drugs together exceeds the benefit.

103
Q

Leqvio Generic Name

A

Inclisiran

104
Q

What is the mechanism of action of Inclisiran?

A

DS small interfering RNA. Prevents translation of PCSK9 in the liver. (synthesis is dependent on RNA).

This leads to an overall increase in LDL-R expression, causing a decrease in LDL as more can be hepatically cleared.

105
Q

How is Inclisiran Dosed?

A
  1. Initial Dose
  2. 2nd Dose 3 months Later
  3. Continuous dosing every 6 months.
106
Q

What were the conclusions of the ORION-9 Trial?

A

Showed Inclisiran reduced LDL cholesterol levels by almost 50% with twice yearly administration in:

  • patients with HeFH who had been receiving maximally tolerated statin therapy.
107
Q

What were the conclusions of the ORION-10 and ORION-11 Trials?

A
  1. A regimen of Inclisiran every 6 months was feasible and significantly reduced LDL cholesterol levels by approximately 50%.
  2. More injection site ADE ocurred with Inclisiran than placebo.
108
Q

What is the mechanism of statins?

A

  1. Decrease cholesterol synthesis (decrease LDL, TC, TG)
  2. Increase LDL-R expression (decrease LDL)
  3. Decrease C-Reactive protein (Anti-Inflammatory Effect)
  4. Pleotropic Effects
109
Q

What are the pleiotropic effects of statin therapy.

A
  1. Improve endothelial function
  2. Atherosclerotic plaque stabilization.
  3. Decrease oxidative stress and inflammation.
  4. ## Inhibition of thrombogenic response.

These effects are the reason we continue statin therapy even if cholesterol levels return to normal.

110
Q

HMG-CoA Reductase

A

Enzyme which catalyzes the rate limiting step of cholesterol synthesis. Converting HMG-CoA to Mevalonate.

111
Q

High Intensity Statins decrease LDL by _____________

A

50%+

112
Q

Moderate intensity statins decrease LDL by ____________

A

30-49%

113
Q

Low Intensity Statins decrease LDL by _______

A

<30%
These are really only used for those who can not tolerate statin.

114
Q

How do we decide statin strength to use?

A

Based on our goal for LDL reduction.

115
Q

High Intensity Statins

A
  1. Atorvastatin 40-80 mg
  2. Rosuvastatin 20-40 mg
116
Q

Moderate Intensity Statins

A
  1. Atorvastatin 10-20 mg
  2. Rosuvastatin 5-10 mg
  3. Simvastatin 20-40 mg
  4. Pitavstatin 40-80 mg
  5. Lovastatin 40 mg
  6. Fluvastatin 80 mg
  7. Pitavastatin 2-4 mg
117
Q

Low Intensity Statins

A
  1. Simvastatin 10 mg
  2. Pravastatin 10-20 mg
  3. Lovastatin 20 mg
  4. Fluvastatin 20-40 mg
  5. Pitavastatin 1 mg
118
Q

Rosuvastatin 20-40 mg Intensity

A

High Intensity Statin

119
Q

Atorvastatin 40-80 mg Intensity

A

High Intensity

120
Q

Atorvastatin 10-20 mg Intensity

A

Moderate Intensity Statin

121
Q

Rosuvastatin 5-10 mg Intensity

A

Moderate Intensity

122
Q

Simvastatin 20-40 mg Intensity

A

Moderate intensity

123
Q

Pravastatin 40-80 mg Intensity

A

Moderate intensity

124
Q

Lovastatin 40 mg Intensity

A

Moderate Intensity

125
Q

Fluvastatin 80 mg Intensity

A

Moderate Intensity

126
Q

Pitavastatin 2-4 mg Intensity

A

Moderate intensity

127
Q

Simvastatin 10 mg intensity

A

Low Intensity

128
Q

Pravastatin 10-20 mg intensity

A

Low Intensity

129
Q

Lovastatin 20 mg intensity

A

Low Intensity

130
Q

Fluvastatin 20-40 mg intensity

A

Low Intensity

131
Q

Pitavastatin 1 mg intensity

A

Low intensity

132
Q

The amount of ASCVD risk reduction with a statin is directly related to __________

A

This is associated with statin “intensity”

133
Q

Which Statins are metabolized by CYP3A4?

A
  1. Atorvastatin
  2. Lovastatin
  3. Simvastatin
134
Q

Which Statins are Hydrophillic?

A
  1. Rosuvastatin
  2. Pravastatin
135
Q

Which statins have a prolonged half-life allowing for morning dosing if needed for adherence purposes?

A
  1. Atorvastatin
  2. Pitavastatin
  3. ## RosuvastatinThe other statins should ideally be taken at bedtime.
136
Q

Which statins are less likely to cause myalgia?

A

Hydrophilic statins (rosuvastatin and pravastatin)

137
Q

Statin ADEs

A

> 10%
Diarrhea| Arthralgia| Nasopharyngitis
———————————–
2-10%
Insomnia| New Onset Diabetes| Nausea| Dyspepsia|UTI|Myalgia| musculoskeletal pains
———————————–

138
Q

What are the severe ADE of statin therapy? (rare too)

A
  1. Hepatotoxicity
  2. Cognitive Dysfunction/Confusion (reversible)
  3. Drug Induced Skin reactions (SJS/TEN)
139
Q

Can statins be used in pregnancy?

A

No–> they are teratogenic.

140
Q

What are the absolute contraindications to statin therapy?[4]

A
  1. Active Liver Disease (elevated liver enzymes)
  2. Unexplained elevated transaminases. (3x ULN)
  3. Pregnant or nursing women.
  4. Major drug-drug interactions.
141
Q

What are the precautions/warnings of statin therapy?

A
  1. Substantial Alcohol consumption.
  2. Liver Disease Hx
  3. Significant drug-drug interactions.
142
Q

How does myalgia with statin therapy typically present? When?

A
  1. Typically it involves large, proximal muscle groups in a symmetrical manner.
  2. Typically occurs within 4 to 6 weeks after initiation. (NOT ALWAYS)
143
Q

Differentiate:
-Myalgia
-Myopathy
-Rhabdomyolysis

A
  1. Myalgia| Pain ( no creatine kinase elevation)
  2. Myopathy| objective muscle weakness/loss of function.
  3. Rhabdomyolysis| Emergent–> muscle breakdown–> requires immediate intervention.
144
Q

How should a patient who experiences mild to moderate muscle pain with statin therapy be managed?

A
  1. Hold statin for 2 to 4 weeks to evaluate for other causes.

If muscle pain resolves–> rechallenge with the same statin at the same or lower dose.

If muscle pain re-merges–> discontinue original statin. Once muscle symptoms resolve, use a low dose of a different statin.

When selecting a different statin a hydrophilic one is preferred. (rosuvastatin or pravastatin.)

If muscle pain persists without statin therapy:
Evaluate other causes, resume statin therapy at original dose.

145
Q

How should a patient with unexplained, severe muscle symptoms while on a statin be managed?

A
  1. Discontinue the statin and evaluate for rhabdomyolysis or other causes of myopathy.

once resolved. DO NOT REINITIATE statin therapy unless discussed by a specialist.

146
Q

Define statin intolerance.

A

Muscle related symptoms which:
1. Resolve upon statin discontinuation
2. Occur with re-challenge
3. Occur with at least 2-3 statins, preferably ones that use different metabolic pathways and lipophilicity profiles. At least 1 statin should have been prescribed at the lowest approved dose.

147
Q

How should statin intolerance be managed?

A
  1. Lower Dose
  2. Different statin
  3. Alternative dosing strategy (TIW for statins with long half-lives–> however this has not been studied in RCTs yet.)–> However, remember some statin is better than no statin at all.
148
Q

How should patients on statin therapy be monitoried?

A
  1. Fasting Lipid Panel:
    -4-12 weeks after initiation or therapy change.
    -3-12 months as clinically indicated after.
  2. Transaminases (ALT, AST)
    -may measure in patients with symptoms of hepatotoxicity.
  3. Monitor for obesity onset.
    -note: statins due not cause diabetes.
149
Q

Per the 2013 AACE guidelines, at what LDL should decreasing statin therapy be considered upon reviewing the fasting lipid panel?

A

2 consecutive LDL values below 40 mg/dL.

Note: these are old guidelines.

Now we typically, continue statin therapy for the pleiotropic effects mentioned earlier.

CRT (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions