Pharmacology and Pharmcotherapy of Lipid Drugs and Disorders 2 Flashcards Preview

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Flashcards in Pharmacology and Pharmcotherapy of Lipid Drugs and Disorders 2 Deck (35)
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1
Q

What is the most potent oral LDL- lowering agents

A

Statins

2
Q

What are the significant health benefits of using statins

A

significant reduction in coronary heart disease death, nonfatal MI, revascularization procedures, strokes and total mortality

3
Q

What is the MOA of HMG CoA reductase

A

Competitively inhibit HMG CoA reductase

4
Q

T/F: Statins can lower triglycerides due to causing a reduction in hepatocellular cholesterol prompting more LDL receptors on liver and reducing the secretion of VLDL while increasing clearance

A

True

5
Q

What are the two main enzymes of the liver that metabolize statins

A

3A4 and 2C9

6
Q

What statin would be used if patients can’t handle side effects, why

A

Pravastatin, has no CYP metabolism

7
Q

What are the low intensity statins

A

Pravastatin 10, 20 mg/ Lovastatin 20 mg

8
Q

What are the moderate intensity statins

A

Atorvastatin 10 mg/ Rouvastatin 10 mg/ Simvastatin 20 mg, 40 mg/ Pravastatin 40 mg/ Lovastatin 40 mg/ Fluvastatin 40 mg BID

9
Q

What are the high intensity statins

A

Atorvastin 40, 80 mg/ Rosuvastatin 20 mg

10
Q

T/F: Low intensity statins are mostly used to treat hyperlipidemia

A

False: Low-intensity statins reserved for those who cannot tolerate higher intensity statins

11
Q

Who would qualify for moderate-intensity doses when high intensity doses would predispose patients to side effects

A

Greater than 75 years, impaired renal or hepatic impairment, history

12
Q

T/F: Efficacy is greater when taken in the morning

A

False: Increased efficacy when taken in the evening to coincide with nighttime upturn in endogenous cholesterol biosynthesis

13
Q

What are the contraindications for statins

A

Pregnancy, Lactation, active liver disease

14
Q

What medications can simvastatin interact with at a maximum dose of 10 mg, 20 mg

A

Verapamil and Dilitiazem/ Amiodarone, Amlodipine, Ranolazine

15
Q

What is the most unique adverse effect to statins, what are the other adverse effects

A

Myalgia and Rhabdomyolysis, headache, fatigue, GI upset

16
Q

T/F: It is advised to check LFT levels at baseline but not routinely monitored. IF LFTs are high the statin should be decreased or held until normalized

A

True

17
Q

If a patient complains about severe muscle symptoms or fatigue possibly due to the statin what should be done

A

Discontinue Statin

18
Q

If a patient complains about mild to moderate muscle symptoms or fatigue possibly due to the statin what should be done

A

Evaluate other risk, discontinue the statin

19
Q

If the symptoms of mild to moderate muscle fatigue are resolved after a statin is discontinued what further options can be done

A

Re-initiate same or lower dose of same statin AND if the relationship is casual discontinue and start low dose of different statin till tolerated than gradually increase dose as tolerated

20
Q

T/F: ASCVD risk reduction benefit outweighs risk of diabetes and cognitive impairment in most patients

A

True

21
Q

When a statin is taken a lipid panel is done at baseline when would another one be done after initaition, when is the next after that

A

Within 4 to 12 weeks, every 3 to 12 months

22
Q

How much should LDLs reduce due to statin intensity use

A

Greater than 50% (high intensity), 30% to 50% (moderate intensity)

23
Q

If a patient is on a high intensity statin what would the LDL level need to be over time in order to consider adding on non-statin cholesterol-lowering medication

A

Greater than 70 mg/dl

24
Q

What is the first drug that would be added to a statin in order to lower cholesterol, what is the MOA

A

Ezetimibe, selectively inhibits absorption of dietary and biliary cholesterol at brush border of intestine

25
Q

What are the contraindications of ezetimibe

A

Acute liver disease, pregnancy, lactation

26
Q

What are the advere effects of using ezetimibe, drug interactions

A

Diarrhea and Abdominal pain/ Fibrates and Cholestyramine

27
Q

What do LDL- receptors on the hepatocyte do when LDL binds

A

Bind to free LDL circulating where they are brought into the cell metabolized to release the LDL-receptor then placed back on the surface

28
Q

T/F: PCSK9 proteins lead to lower chosterol

A

T/F: PCSK9 proteins lead to more circulating LDL since it doesn’t allow the LDL to be brought into the hepatocyte by the LDL-Receptors to be metabolized

29
Q

What type of medication is PCSK9 inhibitors, what is the MOA

A

Monoclonal antibody, indirectly decreases LDL levels by binding PCSK9 leading to more LDL receptors on hepatocytes

30
Q

What is a large adverse effect of PCSK9 inhibitors

A

Decrease in neurocognitive ability

31
Q

Why are PCSK9 not indicated to be used before ezetimibe

A

The cost does not outweigh the benefit

32
Q

What are the bile acid sequestrants

A

Cholestyramine, Colestipol, Colesevelam

33
Q

Though patients could add bile acid sequestrants they are not preferred over adding ezetimibe and PCSK9 inhibitors

A

True

34
Q

When would fibrates be first line medicationsm what are the fibrates

A

If the patient has triglycerides over 500 mg/dl/ gemfibrozil, fenofibrate, fenofibric acid

35
Q

T/F: Niacin can decrease TG and increase HDL but has not proven to reach clinical endpoints and therefore there is no scenario in which a patient would need to use Niacin

A

True