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Spring Pharm Block 3 > Hyperlipidemia > Flashcards

Hyperlipidemia Flashcards

1
Q

List and describe two lipids derived from dietary sources or synthesized by the body.

A

Cholesterol: primarily synthesized by the liver
Triglycerides: dietary triglycerides account for 75% of the total

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2
Q

How are lipids transported to sites of use or storage in the body?

A

Via lipoproteins: chylomicrons, VLDL, IDL, LDL, and HDL

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3
Q

What is the clinical significance of LDL?

A

Accumulate in the subendothelial space of arteries and form plaques and/or initiate an inflammatory response.

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4
Q

Describe the basic pathophysiology of a plaque becoming unstable.

A

When a stable plaque ruptures, a thrombus forms at the site of the plaque and partially or completely occludes the vessel

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5
Q

What drug class is the most effective at lowering LDL?

A

Statin drugs

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6
Q

Describe the mechanism of action of statin drugs.

A

They are HMG Co-A Reductase inhibitors. HMG Co-A Reductase is an enzyme essential in the production of cholesterol.

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7
Q

What effect do statin drugs have on LDL, HDL, and triglycerides?

A

LDL: decrease
HDL: slight increase
Triglycerides: decrease

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8
Q

What is the benefit of increasing HDL?

A

HDL is responsible for transporting other cholesterols back to the liver to be recycled

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9
Q

How does dosing effect the action of statin drugs?

A

LDL reduction is dose dependent –> higher doses = more reduction in LDL
Effects on HDL are not dose dependent

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10
Q

Why is it theorized that statin drugs may reduce inflammation?

A

Statins cause a reduction in CRP. CRP is a marker of inflammation.

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11
Q

Differentiate older statins from newer statins in terms of how they are administered?

A

Older: should be taken at night because they have a short half-life and cholesterol is mostly made during sleep
Newer: can be taken at any time because they have a longer half life

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12
Q

T/F: Most statin drugs have a lot of drug interactions.

A

True: most statins go through CP 450 in the liver

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13
Q

Describe the AEs of statin drugs

A

Few AEs –> they are generally well tolerated
Statins can cause myalgias and cause rhabdomyolysis –> less common than most people believe
GI complaints: dyspepsia, heartburn, abdominal pain –> most frequent AE
AST and ALT can rise depending on dose

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14
Q

What is the major contraindication of statin drugs and why is this the case?

A

Contraindicated in pregnancy because the developing fetus is almost all fat. Statins interfere with fetal development.

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15
Q

State some drugs we’ve talked about in class that induce or inhibit CP 450 and thus, will interact with statin drugs.

A

Inhibitors: cobicistat, rintonavir
Inducer: rifampin

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16
Q

List the statin drugs that are classified as older statin drugs.

A

Fluvastatin, Lovastatin, Pravastatin, Simvastatin

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17
Q

List the statin drugs that are classified as newer statin drugs.

A

Atorvastatin, Pitavastatin, Rosuvastatin

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18
Q

What are the only two statins that do not undergo CP 450 metabolism?

A

Pravastatin and Pitavastatin –> both renally eliminated

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19
Q

What is the most potent statin based on its LDL lowering ability?

A

Rosuvastatin –> closely followed by atorvastatin

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20
Q

What is the least potent statin based on its LDL lowering ability?

A

Fluvastatin –> closely followed by lovastatin and the other “older statins”

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21
Q

What is the mechanism of action of Bile Acid Sequestering Agents?

A

They bind to and sequester bile acids in the colon so they are not absorbed. The subsequent decrease in bile acids causes the liver to attempt to make more bile acids. In this process, the liver consumes more cholesterol and LDL decreases.

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22
Q

How are bile acid sequestering agents administered?

A

In large chewable tablets or in a powder that is mixed with water then ingested

23
Q

What AEs are associated with bile acid sequestering agents?

A

GI –> dyspepsia, abdominal pain, bloating, flatulence

24
Q

In what way do bile acid sequestering agents negatively impact lipids?

A

They increase triglycerides –> Triglycerides cannot be processed without bile acids.

25
Q

What two drugs do bile acid sequestering agents interact with and how is this managed?

A
  • Warfarin and Levothyroxine –> they stick to the bile acid sequestering agents and are not absorbed.
  • Space administration of bile acid sequestering agents from drugs they interact with.
26
Q

Name three bile acid sequestering agents.

A

Colesevelam, Colestipol, Cholestyramine

27
Q

Other than high triglycerides, what is another contraindication for bile acid sequestering agents?

A

Ileus –> drug must be able to pass through the colon

28
Q

What is the mechanism of action of niacin?

A

It is a B vitamin that increases HDL by a mechanism that isn’t fully understood.

29
Q

How is niacin used?

A

As an adjunct with another lipid lowering agent to raise HDL.

30
Q

What formulation of niacin is favored?

A

Extended Release because it causes fewer AEs

31
Q

What side effects might patients complain of after taking niacin and why and how might this be mitigated?

A

Facial flushing and headaches because niacin causes release of prostaglandins.
Take an NSAID with niacin to lessen release of prostaglandins

32
Q

What three conditions can be exacerbated by taking niacin?

A

Hepatotoxicity, Hyperglycemia, Peptic Ulcer Disease

33
Q

What is the mechanism of action of fibrate medications?

A

Lower triglycerides by increasing catabolism of triglyceride-rich remnant proteins

34
Q

What are the primary AEs of fibrates?

A

Typically well tolerated –> mostly GI effects

35
Q

What is the interaction of fibrates and statins?

A

Synergistic increase in risk of myalgias and rhabdomyolysis

36
Q

What are the two fibrates and how are they administered?

A

Gemfibrozil: BID
Fenofibrate: QD

37
Q

How are the fibrates eliminated from the body?

A

Renally

38
Q

Which fibrate carries a higher risk of myalgias and rhabdomyolysis?

A

Gemfibrozil

39
Q

Describe the use of cholesterol absorption inhibitors?

A

Always used as an adjunct with another lipid agent to decrease LDL

40
Q

What are the AEs of cholesterol absorption inhibitors?

A

Not well tolerated –> GI distress, abdominal pain, diarrhea, steatorrhea

41
Q

Name the only cholesterol absorption inhibitor available.

A

Ezetimibe

42
Q

What is the dietary way to increase intake of omega-3 fatty acids?

A

Eat more fish

43
Q

What is the physiologic benefit of omega-3 fatty acids

A

Decrease triglycerides and have some anticoagulant properties

44
Q

T/F: Omega-3 fatty acids are only available by prescription.

A

False: some are prescription and some are non-prescription

45
Q

What are the AEs of omega-3 fatty acids?

A

Taste perversion, belching, loose stools, fishy body odor

46
Q

In summary, what is the major effect of each class of the hyperlipidemia medications?

A

Statins: decrease LDL
Bile Acid Sequestering Agents: decrease LDL
Niacin: increases HDL with some decrease in triglycerides
Fibrates: decrease triglycerides
Omega-3 Fatty Acids: decrease triglycerides
Cholesterol Absorption Inhibitors: as an adjunct only to help decrease LDL

47
Q

Describe the mechanism of action of PSK9 inhibitors.

A

PSK9 is an enzyme that metabolizes LDL receptors in the liver. By inhibiting the enzyme, LDL receptors in the liver increase and more LDL is pulled into the liver for recycling and elimination.

48
Q

T/F: PSK9 inhibitors are monoclonal antibodies.

A

True: they end in “ab”

49
Q

Name the two PSK9 inhibitors and state how they are dosed.

A

Alirocumab: q 2 weeks
Evolocumab: q month

50
Q

What are the disadvantages of PSK9 inhibitors?

A

They are expensive and must be injected sub-Q

51
Q

What is the mechanism of action of benpedoic acid?

A

Inhibits ACL –> ACL is another enzyme that is essential in the synthesis of cholesterol

52
Q

How is benpedoic acid used?

A

Adjunct to diet and/or you have maximized the patient’s statin dose.

53
Q

What are the AEs associated with benpedoic acid?

A

Hyperuricemia, tendon rupture, URIs

54
Q

What other drugs discussed previously in class carry a risk of tendon rupture?

A

Fluoroquinolones

Spring Pharm Block 3 (7 decks)

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