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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
In which demographics can resins be useful?
pregnant patients and children
26
What are the side effects of resins?
GI- bloating, constipation and abdominal pain
27
Which resin is available as a capsule?
Colesevelam
28
How do Atorvastatin and Rosuvastatin reduce cholesterol and TGs?
Longer T1/2 allows higher increase in LDL receptors so there is also clearance of IDL (ApoE)
29
What is the MOA of the statins?
Inhibition of HMG-CoA Reductase --> inhibition of cholesterol synthesis
30
Where do statins work?
The liver
31
How do statins reduce cholesterol levels?
By increasing hepatic LDL receptors
32
How do polymorphisms in CYP2D6*4 and SCLO1B1 increase myalgia?
The increase t1/2 and hepatic uptake of Simvastatin leading to increased levels in the blood and increased muscle pain
33
What are the main side effects of statins?
1. Elevated plasma ALT/AST levels (liver damage) | 2. Increased CPK (myalgia)
34
What increases the risk of elevated ALT/AST levels with statins?
1. Prior renal/hepatic disease 2. High doses 3. Use of CYP 3A4 inhibitors (Gemfibrozil, Nicotinic Acid, Erythromycin or Ketoconazole)
35
Which statins have a lower incidence of myalgia?
Fluvastatin and Pravastatin
36
What are the contraindications to statins?
1. Pregnancy 2. Nursing Mothers 3. Acute Liver Disease
37
How long does it take for statins to have their maximum effect?
2 Weeks
38
Which statin can be used in kids?
Pravastatin
39
Which statins should be given at night?
Simvastatin, Fluvastatin and Lovastatin
40
Which statin should be taken with food?
Lovastatin
41
What is the main SE of PCSK9 Inhibitors?
Hypersensitivity
42
How do Atorvastatin and Rosuvastin reduce cholesterol and TGs?
Longer T1/2 allows higher increase in LDL receptors so there is also clearance of IDL (ApoE)
43
Describe the MOA of fibrates
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
Which statins are metabolized by CYP2C9?
Rosuvastatin and Fluvastatin
45
Which statins are metabolized by CYP2D6?
Simvastatin
46
How do polymorphisms in CYP2D6*4 and SCLO1B1 increase myalgia?
The increase t1/2 and hepatic uptake of Simvastatin leading to increased levels in the blood and increased muscle pain
47
What is the target of Exetimibe?
Inhibition of dietary cholesterol absorption
48
Describe the MOA of Exetimibe
Inhibits NPC1L1 transporter of enterocytes at the brush border of the SI to prevent absorption of dietary cholesterol
49
Exetimibe works well in combo with what drug?
Statins
50
What is the most common side effect of Exetimibe?
GI- Diarrhea
51
What is the contraindication and risk of Exetimibe?
Contraindication- Hepatic Dysfunction; risk- elevated liver enzymes
52
What are the contraindications to nicotinic acid use?
1. Bleeding Disorders 2. Active Liver Disease 3. Active peptic ulcer
53
Describe the MOA of PSCK9 Inhibitors
Block PCSK9 degradation of the LDL-R, so recycling and increased number of LDL Receptors
54
How are PCSK9 Inhibitors given?
SubQ, every 2-4 weeks
55
What is the main SE of PCSK9 Inhibitors?
Hypersensitivity
56
What are Gemfibrozil, Clofibrate, Benzafibrate and Fenofibrate?
Fibrates that lower TGs
57
Describe the MOA of fibrates
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
What is the fxn of ApoC-III?
To inhibit lipoprotein lipase and VLDL ligand clearance
59
How do fibrates increase HDL?
By increasing fxn of Apo-AI and Apo-AII
60
Which fibrate can cause gallstone formation?
Clofibrate
61
Which fibrates are worst at precipitating myopathy with statins? Which is best?
Worst- Gemfibrozil and Clofibrate | Best- Fenofibrate
62
What are the contraindications to fibrate use?
1. Liver Dysfunction 2. Renal Disease 3. Preexisting Gallbladder Disease
63
What is the use of nicotinic acid?
To lower TGs and Cholesterol
64
Describe the MOA of nicotinic acid
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
What are the SE of nicotinic acid?
1. Itching and flushing 2. Elevated liver enzymes 3. CPK levels with statins 4. Hyperuricemia and glucose intolerance
66
What are the contraindications to nicotinic acid use?
1. Bleeding Disorders 2. Active Liver Disease 3. Active peptic ulcer
67
Familial Hyperchylomicronemia results in elevated what?
Chylomicrons and TGs
68
What is defective in Familial Hyperchylomicronemia (Type I)?
Lipoprotein lipase
69
What is the treatment for familial hyperchylomicronemia?
Diat, Fibrates and nicotinic acid
70
What is elevated in familial hypercholesterolemia (IIa)?
Cholesterol and LDL | **Cardiovascular risk
71
What is the treatment for familial hypercholesterolemia (IIa)?
Statins, ezetimibe and resins
72
What is elevated in familial combined hyperlipoprotein (IIb) and what is the treatment?
TGs (VLDL) and Cholesterol (LDL) | Tx-Nicotinic Acid, Atorvastatin, Rosuvastatin or Lovastatin
73
What is elevated in familial dysbetalipoproteinemia (III) and what is the treatment?
Elevated TGs and Cholesterol (decreased VLDL catabolism causing accumulation of IDL and presence of abnormal ApoE2) Tx- fibrates
74
What is elevated in Familial Hypertriglyceridemia (IV) and what is the treatment?
Elevated TGs and VLDL (associated with glucose intolerance and hyperuricemia) Tx- Fibrates **DO NOT give Nicotinic Acid
75
What diseases cause increased cholesterol?
1. Biliary Disease 2. Renal Disease 3. Hypothyroidism 4. DM
76
What diseases cause elevated TGs?
1. Renal Disease 2. DM 3. Alcoholism
77
What drugs can increase lipid levels?
1. Thiazide Diuretics 2. Beta Blockers 3. Oral Contraceptives

D&T3 Cardiology (7 decks)

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