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DT 3 Test 1 > 4. Lipid drugs > Flashcards

4. Lipid drugs Flashcards

1
Q

What cholesterol lowering meds can be used in pregnancy?

A

resins

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2
Q

In what way do resins interfere with the action of other drugs?

A

interfering with absorption

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3
Q

What is the MOA of statins?

A

competitive HMG CoA reductase inhibitor

increases number of LDL receptors in liver

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4
Q

Which statins can be used to decrease triglycerides in addition to cholesterol?

How do they do this?

A

atorvastatin, rosuvastatin

larger half life, higher increase in LDL receptors, ability to clear IDLs

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5
Q

What are the adverse effects of statins?

Which statins are least likely to cause these?

A

increased AST/ALT, increased CPK (myalgias)

fluvastatin, pravistatin

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6
Q

Which drugs cannot be concurrently used with statins?

A

CYP3A4 inhibitors: gemfibrozil, ketoconazole, erythromycin, nicotinic acid

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7
Q

For which patient groups are statins contraindicated?

A

nursing and pregnant mothers

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8
Q

How long does the maximal effect of statins take?

A

2 weeks

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9
Q

Which statins need to be taken at night?

A

simvastatin, lovastatin, fluvastatin

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10
Q

Which drug has increased muscle pain due to SNPs?

A

simvastatin

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11
Q

What drug has a therapeutic advantage when combined with statins?

What risk does this combo carry?

A

ezetimibe

risk of increased transaminase levels

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12
Q

What is the MOA of ezetimibe?

A

inhibiting cholesterol uptake at brush border of enterocytes

by inhibiting NPC1L1 transporter protein

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13
Q

What drug cannot be combined with resins?

Why not?

A

ezetimibe

undergoes enterohepatic recirculation

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14
Q

Which drugs are PCSK9 inhibitors?

What is their net result?

A

alirocumab and evolocumab

increased LDL receptors

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15
Q

What is the MOA of fibrates?

A

activating PPAR alpha and increasing FA oxidation, reducing FFA

reducing ApoCIII,, increasing endothelial LPL

increasing ApoCII and CIII

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16
Q

Which fibrate increases gallstone risk?

A

clofibrate

17
Q

Which fibrate has the worst CPK risk when given with statins?

Why?

A

gemfibrozil

OATP2 inhibitor

18
Q

What is the difference between nicotinic acid and fibrates?

A

nicotinic acid: hormone sensitive lipase on fat cells, doesn’t inhibit PPAR alpha

fibrates: inhibits endothelial cell LPL, inhibits PPAR alpha

19
Q

What are the side effects of nicotinic acid?

A

itching and flushing

elevate AST/ALT levels (titrate and monitor CPK)

20
Q

What is he defect in familial hypercholesterolemia type I?

How is it treated?

A

ApoCII or LPL

gemfibrozil and nicotinic acid

21
Q

What is the worst familial hypercholesterolemia?

A

IIa (defective LDL clearance)

statins, ezetimibe, resins

22
Q

How is hyperlipoproteinemia IIb treated?

How does it manifest?

A

statins, nicotinic acid

elevated LDL and VLDL

23
Q

What is the defect in familial dysbetalipoproteinemia?

What drugs work the best?

A

ApoE2 results in faulty VLDL clearance, buildup of IDL

fibrates

24
Q

What is the MOA of resins?

A

removing feedback inhibition on 7 alpha hydroxylase

due to increased fecal excretion of bile acids

25
Q

What are the main side effects of resins?

A

bloating, constipation, abdominal pain

26
Q

Which statins are prodrugs?

A

lovastatin, simvastatin

27
Q

Which statins are metabolized by CYP3A4?

A

simvastatin, atorvastain, lovastatin

28
Q

Which statins are metabolized by CYP2C9?

A

fluvastatin and rosuvastatin

29
Q

Which statin is metabolized by CYP2D6?

A

simvastatin

30
Q

Which statins need to be taken at night?

A

fluvastatin, lovastatin, simvastatin

DT 3 Test 1 (8 decks)

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