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Pharmacology > Dyslipidemia > Flashcards

Dyslipidemia Flashcards

1
Q

Rate limiting step in cholesterol biosynthesis

A

HMG-CoA reductase

=critical enzyme in the biosynthesis of cholesterol

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2
Q

Where is the B-48 adoliportoeins formed?

A
  • Intestine

- Found in chylomicrons and their remnants

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3
Q

Where is the B-100 adoliportoeins synthesized? Where is it found?

A
  • Synthesized in liver

- Found in VLDL, LDL, Lp(a) lipoproteins

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4
Q

Risk Factors= “FLASH”

A 
F-Family hx of premature CHD
L- Low HDl, <40 mg/dL
A- Age: Men>45, Women> 55
S- Smoking: Cigarettes
H- HTN; CKD
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5
Q

Risk Equivalents to CHD

A
  1. DM
  2. CAD
  3. PAD
  4. AAA
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6
Q

What is the most common cause for low HDL?

A

Obesity

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7
Q

What enzyme converts VLDL to VLDL remnants via lipolysis?

A

Lipoprotein lipase

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8
Q

Fibrate MOA

A

unregulates lipoprotein lipase

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9
Q

Niacin MOA

A

Decreases both VLDL and LDL levels

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10
Q

Bile acid resins MOA

A

Bind bile acids–>increasing the excretion of cholesterol in the stool

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11
Q

Statins MOA (2)

A
  1. Inhibits HMG-CoA reductase: directly reduces cholesterol production
  2. LDL receptors unregulated in liver: Lowers LDL
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12
Q

Ezetimibe MOA

A

Blocks the absorption of cholesterol from the small intestine

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13
Q

Statins primary effect?

A

Lowers LDL

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14
Q

Statins effect on atherosclerosis?

A

Prevention of atherosclerosis:

  1. Stabilizes/regressionof plaques
  2. Prevents formation of thrombus
  3. Control inflammatory response
  4. Improves endothelial function
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15
Q

How much does high-intensity statins decrease LDL?

A

> or equal to 50%

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16
Q

How much does moderate-intensity statins decrease LDL?

A

30-50%

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17
Q

How much does low-intensity statins decrease LDL?

A

<30%

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18
Q

Low intensity statins and dosage

A

Pravastatin 10-20 mg

Lovastatin 20 mg

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19
Q

Which statin is the most potent?

A

Pitavastatin

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20
Q

Which drug has the greatest efficacy?

A

Rosuvastatin 40 mg

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21
Q

What are the benefits of both Atorvastatin and Rosuvastatin?

A

It doesn’t matter what time of the day you take them

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22
Q

What is Atorvastatin metabolized by?

A

Cytochrome 3A4= most common enzyme=more drug interactions compared to Rosuvastatin

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23
Q

What is Rosuvastatin metabolized by?

A

Cytochrome 2C9/2C19

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24
Q

What are the two main differences between Atorvastatin and Rosuvastatin?

A
  1. Different metabolism

2. Different distribution

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25
Q

Is Atorvastatin and Rosuvastatin lipophilic?

A

Atorvastatin

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26
Q

What is Pitavastatin metabolized by?

A

UGTIA3/UGT 2B7

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27
Q

Severe side effects of Statins

A
  1. Rhabdomylosis-Monitor creatine kinase levels

2. Hepatic failure-Monitor LFTs

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28
Q

Contraindications of Statins

A
  1. Acute liver dz

2. Pregnancy

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29
Q

What is the risk for developing type 2 DM on statins?

A

approx. 30%

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30
Q

What lab values do you want monitor with Statins?

A
  1. LFT’s @ baseline
  2. Creatine Kinase levels @ baseline if @ increased risk = renal insufficiency, family hx
    3.
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31
Q

What is the anion transporter is there a genetic variation that is associated with severe myopathy and rhabdo induced by statins?

A

OATP1B1

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32
Q

Atorvastatin drug interaction

A

3A4 inhibitor and inducer

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33
Q

What is red yeast rice associated with?

A

Lovastatin

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34
Q

What statin is affected by grapefruit juice? (increased)

A

Atorvastatin

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35
Q

Rosuvastatin drug interaction

A

2C9 induces and inhibitor

36
Q

If someone is on Warfarin, what Statin would you recommend? What would you avoid?

A

Recommend: Atorvastatin
Avoid: Rosuvastatin= Vitamin K antagonist

37
Q

What can increase the levels/effects of Rosuvastatin?

A

Fibric acid derivatives= Gemfibrozil (contraindicated)

38
Q

Cholesterol absorption inhibitor

A

Ezetimibe

39
Q

Ezetimibe MOA

A

Inhibits cholesterol absorption in the small intestine, both:

  • Dietary Cholesterol
  • Biliary Cholesterol
40
Q

What transport protein does Ezetimibe target?

A

NPC1L1

41
Q

How much does Ezetimibe reduce LDL by?

A

18%

42
Q

What statin would you consider combining Ezetimibe with?

A

Simvastatin

43
Q

Ezetimibe contraindications

A
  1. Active Hepatic Dz

2. Unexplained persistent elevations in LFTs

44
Q

Drug interactions

A

Increased levels with fibrates

45
Q

Ezetimibe monitoring

A

LFTs increased: greater combo with statins

46
Q

Ezetimibe severe side effects

A

Cholelithiasis: greater in combo with fibrates

47
Q

How is Ezetimibe excreted?

A

80% through feces

48
Q

List PCSK9 inhibitors

A
  1. Alirocumab

2. Evolucmab

49
Q

PCSK9 inhibitors MOA

A

Monoclonal antibodies inhibit PCSK9= Reduce LDL up to 70%

50
Q

Where is PCSK9 found? It’s function?

A
  • Protease in Liver

- Degradation of hepatocyte LDL=increases LDL levels

51
Q

Who should we consider PCSK9 inhibitors for?

A
  1. Adults w/ heterozygous familial hypercholesterolemia
  2. Primary hyperlipidemia- (Homozygous familial hypercholesterolemia)
  3. ADD onto maximal tolerated statin dose and/or exetimibe
  4. Intolerance of statins
52
Q

PCSK9 inhibitors adverse reactions

A
  1. URI and flu-like sx’s
  2. Local runs @ injection site(frequently)
  3. Hypersensitivity (rare)
53
Q

How are PCSK9 inhibitors given?

A

SQ every 2 weeks

54
Q

Why do we want to monitor lipid panels every 4-8 weeks in PCSK9 inhibitors?

A

Patient adherence

55
Q

Define and list MTP inhibitor

A

MTP: Microsomal Triglyceride Transfer Protein inhibitor

= Lomitapide

56
Q

MTP inhibitor MOA

A
  1. Binds directly to and inhibits MTP
  2. Prevents assembly of apo-B containing lipoproteins
  3. Reduced production of chylomicrons and VLDL
  4. Reduced plasma LDL
57
Q

MTP inhibitor indication

A

Homozygous familial hypercholesterolemia

58
Q

Sever side effects

A

HEPATOTOXICITIY=BLACK BOX WARNING

59
Q

What program are MTP inhibitors through?

A

JUXTAPID REMS PROGRAM

60
Q

Other MTP inhibitor major side effect

A

GI upset: Diarrhea=79%

61
Q

PK of MTP inhibitor

A
  1. 99.8% protein bound
  2. Hepatic metabolism of CYP3A4-inducer and inhibitors are going to effect level of this drug
  3. Renal elimination
62
Q

What drug levels with MTP inhibitor increase?

A

Lovastatin

63
Q

MTP inhibitor contraindications

A
  1. Pregnancy

2. Active hepatic dz/impariement

64
Q

What is recommended with MTP inhibitor to avoid GI effects?

A

Low fat diet, <20%

65
Q

Mipomersen sodium (Kyanamro) MOA

A

Inhibitor of apoldprotein B-100 synthesis

66
Q

Mipomersen sodium (Kyanamro) major side effect

A

BLACK BOX WARNING=HEPATOTOXICITY

KYANMOS REMS

67
Q

Fibrates MOA

A

Upregulates lipoprotein lipase:

  1. Increase catabolism of VLDL
  2. Elimination of TG-rich particles
68
Q

What is the primary effect of Fibrates?

A

TG lowering=35-50%

69
Q

What may fibrates potentially increase?

A

LDLs in pt’s with elevated TGs

70
Q

Severe side effects of fibrates?

A
  1. Acute renal failure!!!

2. Cholelithiasis

71
Q

Fibrate contraindications

A
  1. Severe renal impairment CrCl <30
  2. Hepatic dysfunction
  3. Breastfeeding
72
Q

Fibrate drug interactions

A
  1. Statins!!!! Increases risk of myopathies–> rhabdo
  2. Warfarin
  3. Sulfonyluereas- may enhance hypoglycemic effects
73
Q

Nicotnic Acid MOA

A

Inhibits synthesis and secretion of VLDL–>and therefor LDL

74
Q

Niacin indication

A
  1. High LDL and low HDL

2. Isolated triglyceridemia

75
Q

Why has Niacin fallen out of favor?

A

Has not shown to decrease morbidity and mortality

76
Q

What is unique to Nicotinic Acid dosing?

A

Titration

77
Q

3 main side effects of Nicotinic Acid

A
  1. Flushing
  2. Hyperglycemia
  3. Hyperuricemia=Increaed risk for gout
78
Q

Nicotinic Acid drug interactions

A
  1. Anticoagulants- May increase bleeding time

2. Statins-Increase risk of myopathies

79
Q

Caution Nicotinic Acid use with?

A
  1. Diabetics

2. Renal impairment

80
Q

Bile Acid Sequestrants MOA

A
  • Cholesterol is a precursor to bile acids
  • Bind with bile acids in intestines–>eliminated via feces
  • Increased bile acid secretion increased cholesterol catabolism to form more bile acids
81
Q

BASs therapeutic effects

A

Decrease LDL 15-30%

Minimal effect on HDL and TG

82
Q

Severe side effects of BASs

A

Bleeding with chronic use

=affects Vitamin K absorption

83
Q

BASs drug interactions

A

All bind with other medications, absorbant!!!

84
Q

Omega-3 Acid Ethyl Esters (O3FAs)

A

Lovaza

85
Q

O3FAs drug interactions

A

Inhibit platelet aggregation and cause bleeding

Pharmacology (9 decks)

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