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CPR II Exam #1 > Drugs for Lipid Disorders > Flashcards

Drugs for Lipid Disorders Flashcards

1
Q

4 things known to increase VLDL

A

Total fat
Sucrose
Fructose
EtOH (via increased hepatic secretion of VLDL)

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2
Q

How long does it take to determine if dietary changes are sufficient to manage one’s lipid profile?

A

Approx. 1 mo.

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3
Q

Dietary recommendations to lower cholesterol (3)

What sort of reduction in serum cholesterol is seen?

A
  1. Limit cals from fat to 20-25% of daily intake.
  2. Keep saturated fats to less than 8% of daily intake.
  3. Limit cholesterol to less than 200 mg/day

Ranges from 10-20% adhering to these recs.

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4
Q

Which statins are not metabolized by CYP450s?

A

Pravastatin

Pitavastatin

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5
Q

Most of the absorbed doses of statins are excreted in what substance?

A

Bile

Approx. 5-20% in urine

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6
Q

2 most potent statins

Least potent statin

A

Atorvastatin = Rosuvastatin

Fluvastatin

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7
Q

Adverse effects of statins at the liver

A

Elevates serum AST, but levels decrease upon cessation of therapy.

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8
Q

Adverse effects of statins in muscle

A

CK activity increases.

Rhabdomyolysis can occur rarely ad cause renal injury.

Myopathy.

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9
Q

Effect of statins and Warfarin levels

A

Increases Warfarin levels

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10
Q

Who are statins contraindicated in? (3)

A

Women who are pregnant, lactating or want to become pregnant.

Pts. w/ liver DZ

Pts. w/ skeletal muscle myopathy

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11
Q

In what disease should statins be given to children?

A

Homozygous familial hypercholesterolemia and some w/ heterozygous familial hypercholesterolemia

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12
Q

PKs of Fibric acid derivatives (Fibrates):

Half-life of Gemfibrozil and Fenofibrate

A

Well-absorbed when taken w/ a meal, less otherwise.

Gemfibrozil: 1.5 hrs.
Fenofibrate: 20 hrs.

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13
Q

Fibrates are best used in the management of hypertriglyceridemias where what lipoprotein predominates?

Pts. on which type of ABX-caused hypertriglyceridemia would also benefit?

A

VLDL

Hypertriglyceridemia from Tx w/ viral protease inhibitors

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14
Q

Adverse effects (2) and contraindications (2) of Fibrates

A

GI effects, biliary problems (gallstones)

Increased AST

Muscular problems: myositis, myopathy, rhabdomyolysis

If pt. is taking anti-coagulation -> fibrates potentiate anti-coags.

Avoid in pts. w/ hepatic or renal dysfunction.

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15
Q

PKs of bile acid sequestrants

A

Not absorbed at all - excreted in feces.

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16
Q

Which 2 drug classes should not be used in tandem when treating lipid disorders?

A

HMG-CoA reductases (statins) and bile acid sequestrants

17
Q

Which pts. would best benefit from therapy w/ bile acid sequestrants?

What can it be combined w/ to treat type IIa and type IIb hyperlipidemias?

What else can it relieve?

A

Pts. w/ primary hypercholesterolemia

Combined w/ Niacin.

Pruritis in pts. w/ bile salt accumulation.

18
Q

Adverse effects of bile salt sequestrants

A

GI problems are most common.

High doses may impair fat-sol. vitamin absorption.

19
Q

Pts. w/ which pre-existing conditions should not be given bile salt sequestrants?

A

Diverticulitis
Bowel DZ
Cholestasis

20
Q

Lomitapide MOA

A

Inhibits MTP (microsomal transfer protein) in lumen of ER. The MTP inhibition prevents the assembly of Apo-B -> reduced chylomicrons, VLDL and LDL.

21
Q

What is the problem with prescribing Lomitapide and Mipomersen?

A

It is over $250K/$176K and only available to people w/ Familial hypercholesterolemia

22
Q

Mipomersen MOA

A

Inhibits Apo-B synthesis in liver -> decreased VLDL and LDL.

23
Q

PCSK9 inhibitor MOA

What is it used for?

A

Abs bind to PCSK9 and inhibits LDL receptor metabolism.

Familial hypercholesterolemia

24
Q

Complex MOA of Statins

A
  1. Inhibit HMG-CoA reductase -> decreased cholesterol.
  2. Low IC [cholesterol] -> increased LDL R synthesis.
  3. Increased LDL reuptake from blood.
  4. Decreased IC [cholesterol] -> decreased secretion of VLDL.
25
Q

Complex MOA of Niacin

A

Inhibit HSL -> decrease [FFA] -> decreased VLDL synthesis.

Decrease Apo A1 clearance -> increased HDL.

26
Q

Complex MOA of Fibrates

A

Activate PPAR-a

  1. Activate expression of Apo A1 and A2 -> increase HDL.
  2. Activate lipoprotein lipase -> increased clearance of TGs at endothelium and FFA oxidation at liver.
27
Q

Major side-effects of niacin

A

Flushing

Hyperuricemia - gout, etc.

28
Q

Ezetimibe is a…

A

Cholesterol absorption inhibitor

29
Q

Bile salt sequestrant drugs

A

Colestipol

Cholestyramine

Colesevelam

CPR II Exam #1 (30 decks)

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