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D&T3 Cardiology > Dyslipidemia Drugs > Flashcards

Dyslipidemia Drugs Flashcards

1
Q

What is an ideal level of Cholesterol?

A
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2
Q

What is an ideal level of Cholesterol?

A
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3
Q

What is an ideal level of LDL-C?

A
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4
Q

What is an ideal level of Tgs?

A
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5
Q

What is the first line tx to lower cholesterol and Tgs?

A

Diet

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6
Q

What type of drug are Cholestyramine, Colesevelam and Colestipol?

A

Resins

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7
Q

Describe the absorption of Resins

A

No GI absorption; 0 bioavailability

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8
Q

Describe the MOA of Resins

A
  1. Bind bile acids in the SI and increase fecal excretion –> reduction in enterohepatic recirculation
  2. Increase conversion of hepatic cholesterol into bile acids
  3. Result in compensatory increase in hepatic LDL receptors
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9
Q

How do resins increase conversion of hepatic cholesterol into bile acids?

A

Bile acids have a negative feedback effect on 7a-Hydroxylase; resins decrease the amount of BAs, so they remove the negative feedback and allow 7a-hydroxylase to convert cholesterol into bile

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10
Q

What is the clinical use of resins?

A

To control hypercholesterolemia

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11
Q

How long until the maximum effect of resins?

A

4 weeks

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12
Q

In which demographics can resins be useful?

A

pregnant patients and children

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13
Q

What are the side effects of resins?

A

GI- bloating, constipation and abdominal pain

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14
Q

What effect can resins have on other substances absorption?

A

Resins can interfere with absorption of fat soluble vitamins and drugs

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15
Q

What effect can resins have on other substances absorption?

A

Resins can interfere with absorption of fat soluble vitamins and drugs

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16
Q

What is an ideal level of LDL-C?

A
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17
Q

What is an ideal level of Tgs?

A
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18
Q

What is the first line tx to lower cholesterol and Tgs?

A

Diet

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19
Q

What type of drug are Cholestyramine, Colesevelam and Colestipol?

A

Resins

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20
Q

Describe the absorption of Resins

A

No GI absorption; 0 bioavailability

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21
Q

Describe the MOA of Resins

A
  1. Bind bile acids in the SI and increase fecal excretion –> reduction in enterohepatic recirculation
  2. Increase conversion of hepatic cholesterol into bile acids
  3. Result in compensatory increase in hepatic LDL receptors
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22
Q

How do resins increase conversion of hepatic cholesterol into bile acids?

A

Bile acids have a negative feedback effect on 7a-Hydroxylase; resins decrease the amount of BAs, so they remove the negative feedback and allow 7a-hydroxylase to convert cholesterol into bile

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23
Q

What is the clinical use of resins?

A

To control hypercholesterolemia

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24
Q

How long until the maximum effect of resins?

A

4 weeks

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25
Q

In which demographics can resins be useful?

A

pregnant patients and children

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26
Q

What are the side effects of resins?

A

GI- bloating, constipation and abdominal pain

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27
Q

Which resin is available as a capsule?

A

Colesevelam

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28
Q

How do Atorvastatin and Rosuvastatin reduce cholesterol and TGs?

A

Longer T1/2 allows higher increase in LDL receptors so there is also clearance of IDL (ApoE)

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29
Q

What is the MOA of the statins?

A

Inhibition of HMG-CoA Reductase –> inhibition of cholesterol synthesis

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30
Q

Where do statins work?

A

The liver

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31
Q

How do statins reduce cholesterol levels?

A

By increasing hepatic LDL receptors

32
Q

How do polymorphisms in CYP2D6*4 and SCLO1B1 increase myalgia?

A

The increase t1/2 and hepatic uptake of Simvastatin leading to increased levels in the blood and increased muscle pain

33
Q

What are the main side effects of statins?

A
  1. Elevated plasma ALT/AST levels (liver damage)

2. Increased CPK (myalgia)

34
Q

What increases the risk of elevated ALT/AST levels with statins?

A
  1. Prior renal/hepatic disease
  2. High doses
  3. Use of CYP 3A4 inhibitors (Gemfibrozil, Nicotinic Acid, Erythromycin or Ketoconazole)
35
Q

Which statins have a lower incidence of myalgia?

A

Fluvastatin and Pravastatin

36
Q

What are the contraindications to statins?

A
  1. Pregnancy
  2. Nursing Mothers
  3. Acute Liver Disease
37
Q

How long does it take for statins to have their maximum effect?

A

2 Weeks

38
Q

Which statin can be used in kids?

A

Pravastatin

39
Q

Which statins should be given at night?

A

Simvastatin, Fluvastatin and Lovastatin

40
Q

Which statin should be taken with food?

A

Lovastatin

41
Q

What is the main SE of PCSK9 Inhibitors?

A

Hypersensitivity

42
Q

How do Atorvastatin and Rosuvastin reduce cholesterol and TGs?

A

Longer T1/2 allows higher increase in LDL receptors so there is also clearance of IDL (ApoE)

43
Q

Describe the MOA of fibrates

A

Bind to PPARa to stimulate FA oxidation, reduce ApoCIII (which increases lipoprotein lipase activity), decrease hepatic production of VLDL, and increasing HDL (increased ApoAI and AII)

44
Q

Which statins are metabolized by CYP2C9?

A

Rosuvastatin and Fluvastatin

45
Q

Which statins are metabolized by CYP2D6?

A

Simvastatin

46
Q

How do polymorphisms in CYP2D6*4 and SCLO1B1 increase myalgia?

A

The increase t1/2 and hepatic uptake of Simvastatin leading to increased levels in the blood and increased muscle pain

47
Q

What is the target of Exetimibe?

A

Inhibition of dietary cholesterol absorption

48
Q

Describe the MOA of Exetimibe

A

Inhibits NPC1L1 transporter of enterocytes at the brush border of the SI to prevent absorption of dietary cholesterol

49
Q

Exetimibe works well in combo with what drug?

A

Statins

50
Q

What is the most common side effect of Exetimibe?

A

GI- Diarrhea

51
Q

What is the contraindication and risk of Exetimibe?

A

Contraindication- Hepatic Dysfunction; risk- elevated liver enzymes

52
Q

What are the contraindications to nicotinic acid use?

A
  1. Bleeding Disorders
  2. Active Liver Disease
  3. Active peptic ulcer
53
Q

Describe the MOA of PSCK9 Inhibitors

A

Block PCSK9 degradation of the LDL-R, so recycling and increased number of LDL Receptors

54
Q

How are PCSK9 Inhibitors given?

A

SubQ, every 2-4 weeks

55
Q

What is the main SE of PCSK9 Inhibitors?

A

Hypersensitivity

56
Q

What are Gemfibrozil, Clofibrate, Benzafibrate and Fenofibrate?

A

Fibrates that lower TGs

57
Q

Describe the MOA of fibrates

A

Bind to PPARa to stimulate FA oxidation, reduce ApoCIII (which increases lipoprotein lipase activity), decrease hepatic production of VLDL, and increasing HDL (increased ApoAI and AII)

58
Q

What is the fxn of ApoC-III?

A

To inhibit lipoprotein lipase and VLDL ligand clearance

59
Q

How do fibrates increase HDL?

A

By increasing fxn of Apo-AI and Apo-AII

60
Q

Which fibrate can cause gallstone formation?

A

Clofibrate

61
Q

Which fibrates are worst at precipitating myopathy with statins? Which is best?

A

Worst- Gemfibrozil and Clofibrate

Best- Fenofibrate

62
Q

What are the contraindications to fibrate use?

A
  1. Liver Dysfunction
  2. Renal Disease
  3. Preexisting Gallbladder Disease
63
Q

What is the use of nicotinic acid?

A

To lower TGs and Cholesterol

64
Q

Describe the MOA of nicotinic acid

A
  1. Decrease production of hepatic VLDL by inhibiting lipolysis and fat cell’s hormone sensitive lipases to decrease the FFA available
  2. Increase lipoprotein lipase activity to increase VLDL clearance
65
Q

What are the SE of nicotinic acid?

A
  1. Itching and flushing
  2. Elevated liver enzymes
  3. CPK levels with statins
  4. Hyperuricemia and glucose intolerance
66
Q

What are the contraindications to nicotinic acid use?

A
  1. Bleeding Disorders
  2. Active Liver Disease
  3. Active peptic ulcer
67
Q

Familial Hyperchylomicronemia results in elevated what?

A

Chylomicrons and TGs

68
Q

What is defective in Familial Hyperchylomicronemia (Type I)?

A

Lipoprotein lipase

69
Q

What is the treatment for familial hyperchylomicronemia?

A

Diat, Fibrates and nicotinic acid

70
Q

What is elevated in familial hypercholesterolemia (IIa)?

A

Cholesterol and LDL

**Cardiovascular risk

71
Q

What is the treatment for familial hypercholesterolemia (IIa)?

A

Statins, ezetimibe and resins

72
Q

What is elevated in familial combined hyperlipoprotein (IIb) and what is the treatment?

A

TGs (VLDL) and Cholesterol (LDL)

Tx-Nicotinic Acid, Atorvastatin, Rosuvastatin or Lovastatin

73
Q

What is elevated in familial dysbetalipoproteinemia (III) and what is the treatment?

A

Elevated TGs and Cholesterol (decreased VLDL catabolism causing accumulation of IDL and presence of abnormal ApoE2)
Tx- fibrates

74
Q

What is elevated in Familial Hypertriglyceridemia (IV) and what is the treatment?

A

Elevated TGs and VLDL (associated with glucose intolerance and hyperuricemia)

Tx- Fibrates
**DO NOT give Nicotinic Acid

75
Q

What diseases cause increased cholesterol?

A
  1. Biliary Disease
  2. Renal Disease
  3. Hypothyroidism
  4. DM
76
Q

What diseases cause elevated TGs?

A
  1. Renal Disease
  2. DM
  3. Alcoholism
77
Q

What drugs can increase lipid levels?

A
  1. Thiazide Diuretics
  2. Beta Blockers
  3. Oral Contraceptives

D&T3 Cardiology (7 decks)

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