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FPP MSS > Atherosclerosis Drugs > Flashcards

Atherosclerosis Drugs Flashcards

1
Q

What is the mechanism of Atorvastatin/Lovastatin/Simvastatin?

A

Competitive inhibitors for active site of HMG Co-A reductase (structural analog of HMG CoA intermediate)

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2
Q

Pharmacokinetics of Atorvastatin/Lovastatin/Simvastatin?

A
  • Extensive first pass metabolism by liver (limits systemic bioavailability)
  • High plasma protein binding
  • Variable half life
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3
Q

How is the statins metabolized?

A

CYB3A4

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4
Q

How are Lovastatin and Simvastatin metabolized?

A

Administered as inactive lactones that must be transformed in liver. Prodrugs.

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5
Q

What are the adverse effects of Statin drugs?

A
  • Usually well tolerated
  • Myopathy (symmetrical,proximal)
  • Rhabdomyolysis (breakdown of muscle fibers)
  • GI/liver
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6
Q

When are statins contraindicated?

A 
Pregnant
Lactating 
Likely to be pregnant
Active liver disease
Hypersensitivity
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7
Q

What are the clinical uses of statins?

A

First line therapy in Hypercholesterolemia when at risk for MI

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8
Q

What is the lipoprotein profile or statins?

A

TG - decrease 20-55%
LDL - decrease 20-55%
HDL - increase 5-10%

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9
Q

What is the bile acid binding drug?

A

Cholestyramine

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10
Q

What is the mechanism of Cholestyramine?

A

Highly positively charged that binds bile acids –> depletes bile acid pool and hepatic bile acid synthesis increases –> hepatic cholesterol declines and stimulates production of LDL receptors

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11
Q

What are the pharmacokinetics of Cholestyramine?

A
  • Not absorbed! (no systemic S/E)

- Administered as chloride salt/insoluble in water

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12
Q

What are adverse effects of Cholestyramine?

A

Constipation/bloating
Interferes with absorption of other drugs
Modest increase in TG/with time returns to baseline

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13
Q

What are C/I of Cholestyramine?

A

Hypercholesterolemia

Increased TG

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14
Q

What are clinical uses of Cholestyramine?

A

Hypercholesterolemia
Second line if statin does not lower LDL-C levels
Recommended for patients 11-20 years

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15
Q

What is lipoprotein profile of Cholestyramine?

A

TG - significant increase when levels increased to begin with
LDL - decrease by 12-25%
HDL - increase by 4-5%

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16
Q

What is the mechanism of Niacin?

A

Inhibits FFA mobilization in adipose tissue
Decreases synthesis of VLDL, TG in liver
Inhibits uptake of HDL

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17
Q

What are the pharmacokinetics of Niacin?

A

Oral administration
3 different formulations
Much greater dose needed for lowering TG than those used as vitamin

18
Q

What are adverse effects of Niacin?

A

Intense cutaneous flush (treat with NSAIDs)
GI effects
Elevated liver enzymes
Hyperurecemia
Increases glucose levels/insulin resistance

19
Q

What are C/I of Niacin?

A

Peptic ulcer
Hepatic disease (MAJOR)
Gout
Diabetes

20
Q

What are clinical uses of Niacin?

A

Hypercholesterolemia
Hypertriglyceridemia
Reduces Lp(a)

21
Q

What is lipoprotein profile of Niacin?

A

TG - decreased 35-50%
LDL - decreased 25%
HDL - increased 15-30%
Lp(a) - reduced 40%

22
Q

What is the mechanism of action of Ezetimibe?

A

It inhibits protein transporter Niemann Pick C10 like protein to cause decreased rate of cholesteryl ester incorporation into chylomicrons –> causes increased expression of hepatic LDL receptor

23
Q

What are the pharmacokinetics of Ezetimibe?

A

Oral administration
Metabolized to active metabolite
22 hour half life

24
Q

What are the adverse effects of Ezetimibe?

A

Normally well tolerated

S/E increase if combined with other drugs

25
Q

What are the clinical uses of Ezetimibe?

A

Hypercholesterolemia

Combined with statins - unsure if helpful

26
Q

What is the lipoprotein profile of Ezetimibe?

A

Modest decreases in TG, LDL and increases in HDL

27
Q

What are the drugs of choice for Hypercholesterolemia?

A

Statins - HMG CoA Reductase inhibitors
Bile acid resins - younger patient age range, add on to statins
Ezetimibe - safe as mono therapy
Niacin - patient compliance problems,

28
Q

What are the drugs of choice for Hypertriglyceridemia?

A

Gemfibrozil/Fenofibrate
Niacin
Omega 3 FA

29
Q

What are two examples of Fibric Acid?

A

Gemfibrozil and Fenofibrate

30
Q

What is the mechanism of action of Gemfibrozil and Fenofibrate?

A

They are ligands for a nuclear transcription regulator called Peroxisome proliferator activated receptor that regulates gene expression and causes decreased TG, decreased inflammation, increased HDL synthesis and Increased Lipoprotein Lipase

31
Q

What are the pharmacokinetics of Gemfibrozil and Fenofibrate?

A

Oral administration, plasma protein binding, half life varies, Fenofibrate is a prodrug

32
Q

What are the adverse effects of Gemfibrozil and Fenofibrate?

A

Well tolerated
GI symptoms
Hematological
Increased CK/renal failure when combined with statin

33
Q

When are Fenofibrate and Gemfibrozil C/I?

A

Renal impairment (esp Fenofibrate)

34
Q

What are the clinical uses of Fenofibrate and Gemfibrozil?

A

Patients with high TGs and low HDL (associated with metabolic syndrome and DM2)

35
Q

What are the effects of Omega 3 FA?

A

Lipid lowering effects; inhibits lipogenesis, stimulates B oxidation, phospholipid synthesis and apolipoprotein B degradation

36
Q

What is the clinical use for Omega 3 FA?

A

Adjunct to diet therapy in treatment of hypertriglyceridemia

37
Q

What does the protein PCSK9 do?

A

It degrades the LDL receptor

38
Q

What does the MTP protein do?

A

Transfers lipids between membrane vesicles; chaperone for biosynthesis of apoB containing TG rich lipoproteins (VLDL, chylomicrons)

39
Q

What would be the clinical use for a MTP inhibitor?

A

Homozygous Familiar Hypercholesterolemia

40
Q

What is the protein apo B 100?

A

It is an apolipoprotein essential for LDL-C and VLDL. IT helps LDL bind to it’s receptor on hepatocytes

41
Q

What would be the clinical use for an apoB inhibitor?

A

Homozygous Familial Hypercholesterolemia

FPP MSS (6 decks)

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