Hyperlipidemia Drugss Flashcards

1
Q

High intensity: Atorvastatin

A

(Lipitor): 40-80 mg

High Intensity Statin therapy: Lower LDL ~50%

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2
Q

High intensity: Rosuvastatin

A

(Crestor): 20-40 mg

High Intensity Statin therapy: Lower LDL ~50%

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3
Q

Moderate Intensity: Atorvastatin

A

Lipitor: 10-20 mg

Moderate intensity drug therapy: Lower LDL 30-50%

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4
Q

Moderate Intensity: Rosuvastatin

A

Crestor: 5-10mg

Moderate intensity drug therapy: Lower LDL 30-50%

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5
Q

Moderate Intensity: Simvastatin

A

(Zocor): 20-40 mg

Moderate intensity drug therapy: Lower LDL 30-50%

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6
Q

Moderate intensity: Pravastatin

A

Pravachol: 40-80 mg

Moderate intensity drug therapy: Lower LDL 30-50%

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7
Q

Moderate intensity: Lovastatin

A

Mevacor: 40 mg

Moderate intensity drug therapy: Lower LDL 30-50%

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8
Q

Low intensity: Simvastatin

A

Zocor: 10 mg

Low-intensity statin therapy: Lower LDL < 30%

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9
Q

Low intensity: Pravastatin

A

(Pravachol): 10-20 mg

Low-intensity statin therapy: Lower LDL < 30%

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10
Q

Low intensity: Lovastatin

A

(Mevacor): 20 mg

Low-intensity statin therapy: Lower LDL < 30%

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11
Q

Ezetimbe

A

(Zetia)- 10 mg
MOA: inhibits CHOL transporters at the intestinal border and thereby inhibiting intestinal absorption of dietary and biliary CHOL

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12
Q

Cholestyramine

A

(prevalite)
Bile-acid Binding Resins
MOA: forms a non-absorbable complex w/ bile acids, which increases fecal loss of bile salt bound LDL CHOL and increases LDL receptor for LDL uptake

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13
Q

Colesevelam

A

(Welchol)
Bile-acid Binding Resins
MOA: forms a non-absorbable complex w/ bile acids, which increases fecal loss of bile salt bound LDL CHOL and increases LDL receptor for LDL uptake

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14
Q

Colestipol

A

(Colestid)
Bile-acid Binding Resins
MOA: forms a non-absorbable complex w/ bile acids, which increases fecal loss of bile salt bound LDL CHOL and increases LDL receptor for LDL uptake

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15
Q

Niacin

A

(Vitamin B3)
MOA: inhibits release of FFA from adipose tissue and increases lipoprotein lipases, to increase chylomicron tg removal from the plasma

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16
Q

Alirocumab

A

(praluent)
Proprotein Convertase Subtilisin/Kexin Type 9 Inhibitors: Aka PCSK9 inhibitors
MOA: Binds to LDL-R on hepatocyte surface, leading to decreased LDL-R and increased plasma CHOL levels

17
Q

Evolocumab

A

(Repatha)
Proprotein Convertase Subtilisin/Kexin Type 9 Inhibitors: Aka PCSK9 inhibitors
MOA: Binds to LDL-R on hepatocyte surface, leading to decreased LDL-R and increased plasma CHOL levels

18
Q

Gemfibrozil

A

(Lopid)
Fibric Acid Derivatives
MOA: perioxisome proliferative-activated receptor-apha agonists that increase VLDL catabolism, FA oxidation, and elimination of TG rich particles

19
Q

Fenofibrate

A

(Fenoglide, fibricor, Lofibra)
Fibric Acid Derivatives
MOA: perioxisome proliferative-activated receptor-apha agonists that increase VLDL catabolism, FA oxidation, and elimination of TG rich particles

20
Q

Statins MOA:

A
  • inhibit hydroxylmethylglutaryl coA (rate-limiting enzyme in CHOL synthesis)
  • increased LDL receptors for removal