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Cardiovascular 2 > Drugs for Lipid Disorders - Kruse > Flashcards

Drugs for Lipid Disorders - Kruse Flashcards

1
Q

Dietary measures are the first mechanism of treatment for hyperlipoproteinemia UNLESS… (3)

A
  • Coronary or peripheral vascular disease
  • Familial hypercholesterolemia
  • Familial combined hyperlipidemia
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2
Q

Things that increased LDL

Things that increase TGs

A
  • Cholesterol, fats

- Fats, alcohol, excess calories

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3
Q

MOA of Statins

A
  • Direct inhibitors of HMG-CoA reductase, inhibiting de-novo cholesterol synthesis
  • Depleted intracellular cholesterol –> increased membrane LDL receptors –> REDUCED CIRCULATING LDL
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4
Q

Absorption, location of action, and excretion of statins

A
  • Absorbed and FIRST-PASS in liver
  • Acts in liver
  • Excreted mostly in bile
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5
Q

Statins w/ long half lives (most potent)

A

Atorvastatin, Rosuvastatin

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6
Q

Statin absorption is enhanced how?

A

With FOOD (take w/ meal)

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7
Q

Statin not metabolized by CYP450 system

A

Pravastatin

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8
Q

Statin highly absorbed even w/o food

A

Fluvastatin

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9
Q

Statins are used for what?

A

Lowering plasma cholesterol in ALL hyperlipidemias

  • Atherosclerotic vascular disease
  • Acute coronary syndromes
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10
Q

Definite contraindications of statins

A
  • Pregnancy, lactating, likely to be pregnant
  • Liver disease
  • Skeletal muscle myopathy
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11
Q

Statins and children

A

ONLY in homozygous familial hypercholesterolemia

- maybe heterozygous too

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12
Q

Drug interactions w/ statins

A

CYP 3A4 or 2C9 inhibitors, competitors, or inducers

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13
Q

Most effective agent for INCREASING HDL

A

Niacin (vitamin B3)

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14
Q

MOA of niacin

A
  • Inhibits lipolysis of TGs (ApoA1) in adipose tissue

- Less free FAs –> liver makes less VLDL –> LDL LEVEL DECREASES

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15
Q

Additional benefit of niacin

A
  • Reduced fibrinogen + increased tPA –> decreased thrombosis via hypercholesterolemia and atherosclerosis
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16
Q

Excretion of niacin

A

URINE

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17
Q

Uses of niacin

A
  • Heterozygous familial hypercholesterolemia (+ RESIN or STATIN)
  • Mixed lipemia - not fully responsive to diet
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18
Q

Adverse effect of niacin

A

Intense cutaneous flush and feeling of warmth

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19
Q

How to combat niacin adverse effect

A

Take w/ aspirin or ibuprofen (PG decrease)

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20
Q

Contraindications of niacin (2)

A

Hepatic disease, active peptic ulcer

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21
Q

CAUTION when using niacin

A

Diabetes mellitus (niacin-induced insulin resistance)

22
Q

Fibric acid derivatives - drug names (2)

A
  • Gemfibrozil

- Fenofibrate

23
Q

Administration of fibric acid derivatives

A

WITH FOOD

24
Q

Gemfibrozil vs. Fenofibrate

A

Fenofibrate = MUCH longer half-life

25
Q

MOA: fibric acid derivatives

A
  • Agonists for PPAR-alpha nuclear txn factor

- INCREASED expression of LIPOPROTEIN LIPASE –> lipoplysis of TGs –> DECREASED plasma TG’s and VLDL secretion

26
Q

3 uses of fibric acid derivatives

A
  • VLDL hypertriglyceridemias
  • Dysbetalipoproteinemia
  • Hypertriglyceridemia via HIV viral protease inhibitors (-navir)
27
Q

Adverse effects of fibric acid derivatives (4)

A
  • Mild GI disturbances
  • Gall stones (increased GB cholesterol excretion)
  • Myositis (evaluate for muscle weakness/tenderness)
  • Rhabdo (when taking statins + fibrates)
28
Q

Drug interaction of fibrates

A

Potentiated action of anticoagulants (coumarin, indanedione)

29
Q

CAUTIONS when using fibrates

A
  • Biliary tract disease

- Those at risk of above (women, obese, native american)

30
Q

Resins - drug names (3)

A
  • Colestipol
  • Cholestyramine
  • Colesevelam
31
Q

Other name for resins

A

Bile acid sequestrants

32
Q

MOA of Resins

A
  • (+) polymers that bind (-) bile acids in gut
  • Increased excretion of bile acids (FECES)
  • Enhanced conversion of cholesterol –> bile acids (via 7-alpha hydroxylation)
  • Decreased hepatic cholesterol –> increased hepatic LDL receptor –> DECREASED circulating LDL level
33
Q

Co-administration w/ Resins

A

RESIN + STATIN = decreased compensatory HMG-CoA reductase upregulation (cholesterol synthesis) due to decreased levels

34
Q

Uses of Resins (3)

A
  • Primary hypercholesterolemia (reduces LDL)
  • Digitalis toxicity
  • Relief of pruritis due to bile salt accumulation (biliary obstruction)
35
Q

Adverse effects of resins

A
  • Constipation, nausea, flattulance
  • Impaired absorption of fat-soluble vitamins (ADEK)
  • Impaired absorption of many drugs
36
Q

How to administer other drugs w/ resins

A

1 hour before OR 2 hours after (avoid absorption decrease via resin)

37
Q

Contraindications to Resins (3)

A
  • Diverticulitis
  • Bowel disease
  • Cholestasis (obstructed bile flow)
38
Q

Cholesterol absorption inhibitor - drug name

A

Ezetimibe

39
Q

MOA of Ezetimibe

A
  • Inhibits intestinal absorption of cholesterol (via NPC1L1) in brush border
  • Inhibits reabsorption of cholesterol excreted in bile
  • Reduced incorporation of cholesterol in chylomicrons
  • Reduced delivery of cholesterol to liver
40
Q

Uses of Ezetimibe (w/ what else?) (3)

A
  • Primary hypercholesterolemia (alone or w/ statin)
  • Homozygous familial hypercholesterolemia (w/ statin)
  • Mixed hyperlipidemia (w/ fenofibrate)
41
Q

What NOT to give w/ Ezetimibe

A

Bile acid sequestrant (resin) - would inhibit Ezetimibe absorption

42
Q

Where does ezetimibe act?

A

W/in enterohepatic circulation

43
Q

Which drug class is best at lowering LDL?

Which drug class is best at raising HDL?

WHich drug class is best at lowering TGs?

A
  • Statins
  • Niacin
  • Fibrates
44
Q

4 acceptable drug combinations

A
  • Niacin + resin
  • Niacin + statin
  • Statin + fibrate
  • Statin + ezetimibe
45
Q

Lomitapide MOA

A

Direct inbibitor of MTP w/in ER –> prevents assembly of apo-B containing lipoproteins –> reduced chylomicrons and VLDL –> reduced LDL-C concentration

46
Q

Benefits of omega-3 PUFAs

A
  • Inhibit thrombus formation
  • Decrease inflammation
  • Lower plasma TGs
  • Altered myocardium electrical activity
47
Q

Type 1 Familial Hyperchylomicronemia:

  • What is it?
  • Cause?
  • Associated w/ heart disease?
  • Treatment?
A
  • Massive hyper-chylomicrons during fasting –> high TGs
  • Deficiency of lipoprotein lipase
  • NO
  • Tx = low fat diet, NO DRUGS
48
Q

Type 2A Familial Hypercholesterolemia:

  • What is it?
  • Cause?
  • Associated w/ ?
  • Treatment?
A
  • High LDL, normal VLDL, normal TGs - via blocked LDL degradation
  • LDL receptor synthesis defect
  • ISCHEMIC HEART DISEASE = VERY accelerated
  • Diet + statin, or diet + resin + niacin
49
Q

Type 2B Familial Mixed Hyperlipidemia:

  • What is it?
  • Cause?
  • Associated w/ ?
  • Treatment?
A
  • High LDL, VLDL, and TGs
  • Overproduction of VLDL by liver
  • Common heart disease
  • See type 2 A treatment
50
Q

Type 3 Familial Dysbetalipoproteinemia:

  • What is it?
  • Cause?
  • Associated w/ ?
  • Treatment?
A
  • Increased IDL, increased TGs, increased cholesterol
  • Mutant ApoE –> Overproduction or underuse of IDL
  • Xanthomas and accelerated vascular disease
  • Tx = diet + statin, or diet + niacin + fibrate
51
Q

Type 4 Familial Hypertriglyceridemia:

  • What is it?
  • Cause?
  • Associated w/ ?
  • Treatment?
A
  • Increased VLDL and TGs, normal LDL and cholesterol
  • Overproduction or decreased removal of VLDL TGs
  • W/ accelerated ischemic heart disease (frequently obese, diabetic, and hyperuricemic)
  • Tx = Diet + niacin +/or fibrate
52
Q

Type 5 Familial Mixed Hypertriglyceridemia:

  • What is it?
  • Cause?
  • Associated w/ ?
  • Treatment?
A
  • High VLDL, chylomicrons, cholesterol, TGs…normal LDL
  • Increased production or decreased clearance of VLDL/chylomicrons (genetic defect)
  • W/ Obesity or diabetes
  • Tx = Diet + niacin and/or fenofibrate, or statin

Cardiovascular 2 (20 decks)

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