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CV II Exam 2 > Anti-Hyperlipidemics > Flashcards

Anti-Hyperlipidemics Flashcards

1
Q

What should LDL level be lower than?

A

<100

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2
Q

What is a desirable total cholesterol level?

A

<200

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3
Q

What are the risk equivalents?

A
  • Symptomatic carotid artery disease
  • Peripheral arterial disease
  • Abdominal aortic aneurysm
  • Diabetes
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4
Q

What are the hyperlipidemia risk factors? (5)

A
  • Age
  • Family history of premature CHD
  • Cigarette smoking
  • Hypertension
  • Low HDL (< 40 mg/dL)
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5
Q

What should a patient with CHD try to maintain as far as their LDL goal?

A

Under 100

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6
Q

If a patient has two risk factors for hyperlipidemia than what should their LDL goal be?

A

under 130

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7
Q

What are the nonpharmacologic treatment options?

A
  • Therapeutic lifestyle change (TLC)
  • Diet
  • Exercise
  • Smoking cessation
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8
Q

What are the pharmacologic treatment options for hyperlipidemia?

A
  • HMG-CoA Reductase Inhibitors (Statins)
  • Nicotinic Acid, Vitamin B3 (Niacin)
  • Fibric Acid Derivatives (Fibrates)
  • Bile Acid Sequestrants (Resins)
  • Cholesterol Absorption Inhibitors
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9
Q

What are the benefits of therapeutic lifestyle changes?

A
  • May obviate need for drug therapy
  • Augment LDL lowering agents
  • Allow for lower doses
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10
Q

When should you not solely employ therapeutic lifestyle changes?

A
  • Severe hypercholesterolemia
  • Known CHD
  • CHD risk equivalents
  • PVD
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11
Q

What are the major Anti-hyperlipidemic groups?

A
  1. HMG-CoA Reductase Inhibitors (Statins)
  2. Niacin (Nicotinic Acid, Vitamin B3
  3. Fibric Acid Derivatives (Fibrates)
  4. Bile Acid Sequestrants (Resins)
  5. Cholesterol Absorption Inhibitors
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12
Q

What is the big drug combination that was listed in the drug list?

A

Simvastatin and Ezetimibe

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13
Q

What were the drugs that should be employed for homozygous familial hypercholesterolemia?

A
  • Lomitapide (Juxtapid)
  • Mipomersen (Kynamro)
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14
Q

What drug was presented as a good choice for those suffering from heterozygous familial hypercholesterolemia?

A

Alirocumab (Paluent)

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15
Q

Lipids are essential for what three things?

A
  1. Cell Membrane Formation
  2. Hormone Synthesis
  3. Source of free fatty acids (FFA’s)
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16
Q

What are the LDL levels associated with the following classifications?

Optimal

Near Optimal/Above optimal

Borderline High

High

Very High

A

Optimal: <100

Near Optimal/Above optimal: 100-129

Borderline High: 130 - 159

High: 160 - 189

Very High: over 190

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17
Q

What are the Total cholesterol levels associated with…

Desirable

Borderline High

High

A

Desirable: <200

Borderline High: 200-239

High: >240

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18
Q

What are the HDL levels associated with…

Low

High

A

Low: <40

High: >60

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19
Q

What are the HMG-CoA Reductase Inhibitors (Statins)?

(7)

A
  1. •Atorvastatin (Lipitor)
  2. •Fluvastatin (Lescol)
  3. •Lovastatin (Mevacor)
  4. •Pitavastatin (Livalo)
  5. •Pravastatin (Pravachol)
  6. •Rosuvastatin (Crestor)
  7. •Simvastatin (Zocor)
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20
Q

What are the fibric acid derivatives (fibrates)? 2

A
  • Fenofibrate (Tricor)
  • Gemfibrozil (Lopid)
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21
Q

What are the bile acid sequestrants we are responsible for?

A
  1. •Cholestyramine (Questran)
  2. •Colesevelam (Welchol)
  3. •Colestipol (Colestid)
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22
Q

What cholesterol absorption inhibitor do we need to know?

A

Ezemitibe (zetia)

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23
Q

In the presence of CYP inhibitors such as cyclosporine, ketoconazole and fibrates, what happens to Statin concentrations?

A

Increase

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24
Q

In the presence of cyp inducers such as pheytoin and ketoconazole, what happens to statin concentrations?

A

They decrease

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25
Q

What are the meds we use for niacin therapies?

A

Nicotinic acid and vitamin B3

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26
Q

What is the mechanism of action for statins?

A

Inhibit HMG-CoA reductase, which is the rate limiting step in cholesterol synthesis

Also, cause upregulation of cholesterol receptors

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27
Q

What is the oral absorption fraction for statins?

A

40-75%

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28
Q

To what extent are statins hit by first pass metabolism?

A

Extensively

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29
Q

The half lives for most statins are 1-3 hours, knowing this, and another key piece of information I am withholding to be a jerk… when should you instruct a patient to take this medication?

A

The other piece of info is that our peak cholesterol synthesis occurs not long after onset of sleep. Thus, patients should take the medication before bed.

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30
Q

Which statins have the 14 and 19 hour half lives?

A

14 hrs - atorvastatin

19 hrs - rosuvastatin

31
Q

Which statin drug is not metabolized by CYP’s?

A

Pravastatin

32
Q

Name four adverse drug reactions associated with statins.

A
  • LFT elevation
  • CK elevation
  • Rhabdomyolysis
  • Myopathy
33
Q

In what situation(s) are statin drugs contraindicated?

A

Pregnancy

34
Q

What is the mechanism of action of the Niacin agents?

A

Inhibit triglyceride lipolysis in adipose tissue, and reduces circulating FFA’s

35
Q

Name four ADR’s for Niacin drugs

A
  • Cutaneous flush (prostaglandin-mediated)
  • Pruritus
  • Acanthosis nigricans
  • Hepatotoxicity
36
Q

What are three CI’s (one is relative) associated with Niacin drugs?

A
  1. Hepatic Disease
  2. Active PUD
  3. Caution DM
37
Q

What is the MOA of gemfibrozil and fenofibrate?

A

Fibric acid derivatives

•PPARα agonists, regulates expression of proteins involved in lipoprotein structure and function, increased expression of LPL

38
Q

What is the most important ADR to know about Niacin drugs?

A

cutaneous flush - mediated by prostaglandins, will be aggravated by warmth, including showers, tea, coffee, etc. Often resolves after a couple of days

39
Q

Why are niacin’s to be used with caution in DM?

A

Increased insulin resistance

40
Q

What is a unique accolade of Niacin drugs?

A

They are the most potent upregulator of HDL synthesis

41
Q

Fibric acid drugs are well absorbed, but bind to something in plasma, what?

A

Protein, thus they can end up competing with other protein bound drugs if used in combination.

42
Q

What are the ADR’s associated with Fibric acid derivatives?

A
  • Gastrointestinal
  • Lithiasis
  • Myositis
  • Myopathy
43
Q

Fibric acid derivatives are contraindicated in what settings?

A
  1. Hepatic dysfunction
  2. renal dysfunction
  3. Pregnancy
44
Q

What DDI’s do we need to be aware of when considering Fibric acid derivative therapy?

2

A
  1. Potentiates action of warfarin
  2. Increased risk of rhabdomyolysis when combined with statin drugs.
45
Q

What is the mechanism of action of resins?

A

•bind bile acids increasing excretion 10x, enhanced conversion of cholesterol to BA’s, increased LDL clearance

46
Q

What are the ADR’s to know for Resins?

A
  • GI (constipation, nausea)
  • Impaired ADEK absorption (vitamins)
47
Q

What are the contraindications for Bile acid sequestrants (resins)?

A

Diverticulitis

Bowel Disease

Cholestasis

48
Q

What DDI is important to keep in mind for Bile acid sequestrants?

A

They impair drug absorption. Make sure to administer at seperate times.

49
Q

What is the MOA of ezetimibe?

A

•inhibits NPC1L1; inhibits absorption of cholesterol and plant sterols

50
Q

What ADR is associated with Cholesterol absorption inhibitos?

A

diarrhea

51
Q

What DDI’s are associated with Cholesterol absorption inhibitors?

A

Note to be administered with bile acid sequestrants

52
Q

Based on the attached image, what drug fits the effects shown?

A

Statins

53
Q

What drugs fits the profile shown here?

A

Fibrates

54
Q

What drug matches the effects shown here?

A

Niacin

55
Q

What drug matches the effects shown here?

A

Bile acid sequestrants

56
Q

What drug matches the effects shown?

A

Cholesterol absorption inhibitor

57
Q

Ok, what are the effects of the following on LDL, HDL and TG’s?

  1. Statins
  2. Fibrates
  3. Niacin
  4. Bile Acid Sequestrants
  5. Cholesterol Absorption Inhibitors
A
58
Q

What are five things to be associated with atherosclerotic cardiovascular disease (ASCVD)?

A
  • History of MI
  • Stable or unstable angina
  • Coronary or other revascularization
  • Stroke or TIA
  • Peripheral vascular disease
59
Q

Doing what reduces ASCVD events?

A

Maximizing statin intensity

60
Q

What are the four statin benefit groups?

A
  • Clinical ASCVD
  • Primary elevation of LDL-C ≥ 190 mg/dL
  • Age 40-75 years with diabetes and LDL-C 70-189 mg/dL
  • No clinical ASCVD or diabetes who are 40-75 years and LDL-C 70-189 mg/dL with ASCVD risk of ≥ 7.5%
61
Q

Adults over 21 y/o who are candidates for statin therapy with clinical ASCVD should recieve what level statin therapy if they are…

  1. Aged more than 75 years
  2. aged under 75
A
  1. over 75 y/o or if not a candidate for the high intensity statins should recieve moderate intensity statins.
  2. Age less than 75 years gets High-intensity statin therapy (barring some good reason to shift to moderate intensity)
62
Q

DM I or II age 40-70 years should get moderate intensity statins, unless…

A

Estimated 10yr ASCVD risk is greater than 7.5%, in which case use High intensity statin therapy

63
Q

What are the high intensity statins?

MUST KNOW

A

Atorvastatin 40-80 mg

Rosuvastatin 20-40 mg

64
Q

What is the average LDL-C reduction from high intensity statins?

A

more than 50%

65
Q

Moderate intensity statins have an average LDL-C reduction of 30-49%. What are the ones we learned?

A

Atorvastatin 10 mg

rosuvastatin 10 mg

Simvastatin 20-40 mg

Pravastatin 40 mg

Lovastatin 40 mg

66
Q

Low intensity statins have an average LDL-C reduction of up to 30%. What are the examples we were given?

A

Simvastatin 10 mg

Pravastatin 10-20 mg

Lovastatin 20 mg

67
Q

What are the two drugs we should use for homozygous familial hypercholesterolemia?

A

Mipomersen (Kynamro)

Lomitapide (Juxtapid)

68
Q

Mipomersen (kynamro) is administered as a once weekly injection as adjunct to diet and other lipid therapy. What is its MOA?

A

Inhibits apo B-100 synthesis by binding to the mRNA of apoB reducing formation

69
Q

What ADRs are we to know for mipomersen?

A

Injection site reactions

  • erythema
  • pain

Flu-like symptoms

headache

elevation of liver transaminases

70
Q

What are the contraindications of mipomersen?

A

Moderate or severe hepatic impairment

Active liver disease

71
Q

Lomitapide (Juxtapid) is a once daily oral dose adjunct to diet and other lipid therapies, meant for tx of homozygoua familial hypercholesterolemia. What is the mechanism of action for this drug?

A

•binds and inhibits microsomal triglyceride transfer protein (located in lumen of endoplasmic reticulum); prevents assembly of apoB)

72
Q

What are the ADRs we should be aware of with regard to Lomitapide (Juxtapid)?

A

GI

  • diarrhea
  • nausea

Increased liver transaminases

Hepatic fat accumulation

73
Q

What is the contraindication of lomitapide?

A

pregnancy, is category X

74
Q

Alirocumab (praluent) is used in the tx of heterozygous familial hypercholesterolemia, once every two weeks by subcutaneous injection as adjuct to diet and maximally tolerated statin therapy.

What is its mechanism of action?

A

Human monoclonal antibody against PCSK9, which normally degrades LDL receptors on hepatocyte surfaces.

CV II Exam 2 (8 decks)

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