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Cardiovascular Block > Lipid Disorders Treatment > Flashcards

Lipid Disorders Treatment Flashcards

1
Q

Primary chylomicronemia

A

Defect: defective removal of CM (ApoCII, LPL Defect)

Manifestation: chylomicrons, elevated VLDL, pancreatitis

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2
Q

Familial hypertrigkyceridemia

A

Defect: defective metabolism of VLDL (LPL defect)

Manifestation: elevated VLDL, hypertriglyceridemia, pancreatitis

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3
Q

Familial Dysbetalipoproteinemia

A

Defect: defective metabolism of VLDL, Chylomicrons, ApoE defect (E2/E2 alleles)

Manifestation: VLDL and CM remnants (IDL) elevated, cholesterol and TG elevated 1:1, atherosclerosis

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4
Q

Familial Combined Hyperlipidemia (FCH)

A

Defect: overproduction of ApoB (VLDL)

Manifestation: variable phenotype, elevated VLDL, LDL, or both; premature atherosclerosis

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5
Q

Familial Hypercholesterolemia (FH)

A

Defect: LDL receptor, ApoB defect, decreased receptor mediated removal of LDL from plasma

Manifestation: LDL increased, premature atherosclerosis

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6
Q

Desirable cholesterol levels

A

total cholesterol < 200
LDL cholesterol < 130
HDL cholesterol > 40

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7
Q

Statin MOA

A

HMG-CoA Reductase Inhibitors; inhibits the rate limiting step of cholesterol biosynthesis; lowers LDL by 35-60%

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8
Q

Bile Acid Resins MOA

A

Bind to bile acids, preventing reabsorption and re-use of bile acid cholesterol; lowers LDL by up to 20%

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9
Q

Ezetimibe MOA

A

prevents absorption of dietary cholesterol; lowers LDL by up to 20%

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10
Q

Niacin MOA

A

Reduces VLDL synthesis; lowers LDL by up to 20%

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11
Q

Common mechanisms of cholesterol lowering drugs

A

increase LDL receptor; promote uptake of LDL

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12
Q

Lovastatin, Simvastatin

A

Inactive lactone prodrugs, lipid soluble, metabolized by CYP3A4, intermediate potency and efficacy

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13
Q

Pravastatin

A

Water soluble, active open lactone ring, low potency/efficacy

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14
Q

Atorvastatin, Rousuvastatin

A

Flourine containing congeners, active as given, long plasma half life, high potency/efficacy

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15
Q

SREBP-2 role in statin therapy and cholesterol metabolism

A

protein that binds to SRE-1 which is a transcription factor that promotes up regulation of LDL receptors; promoted by statins by promoting ER to Golgi and cleavage of SREBP to increase number of LDL receptors

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16
Q

Statins to use in patients with atherosclerotic vascular disease

A

High efficacy statins - Atorvastatin and Rosuvastatin

17
Q

Statins metabolized by CYP3A4

A

Simvastatin and Atorvastatin (also oxidization)

18
Q

Statins metabolized by sulfation

A

Pravastatin

19
Q

Statins metabolized by CYP2C9

A

Fluvastatin and Rosuvastatin

20
Q

Statins metabolized by UGT1A1

A

all statins undergo glucaronidation by UGT1A1

21
Q

Bile acid sequestrants

A

Colestipol (powder and tablet), Cholestyramine (powder), Colesevelam (tablet)

22
Q

Bile sequestrants drug interactions

A

prevents absorption of digoxin, beta blockers, thyroxine, coumadin

23
Q

Bile sequestrates contraindications

A

hypertriglyceridemia, complex drug regimens and critical medications, history of constipation (elderly)

24
Q

Ezetimibe

A

inhibits absorption of cholesterol by small intestine; no effect on fat soluble vitamins (ADEK); localizes to brush border of small intestinal epithelium; reduces delivery of cholesterol to liver; reduced hepatic cholesterol up regulates LDL receptors, increases clearance of LDL from plasma; distinct and complementary effect of statins

25
Q

Drugs that lower TGs and raise HDL-cholesterol

A

Fibric Acid Derivatives (Fibrates), Nicotinic Acid (niacin), omega 3 polyunsaturated fatty acids (fish oil)

26
Q

Fibric Acid Derivatives

A

Gemfibrozil and Fenofibrate

MOA: ligand for activation fo PPARalpha nuclear receptor

Reduces VLDL, increases HDL, TGs reduced, LDL unchanged

SE: GERD, diarrhea, increased liver enzymes, increased creatinine, gallstones, Teratogenic

27
Q

Gemfibrozil

A

metabolized by liver (UGT1A1), reduces VLDL, TGs; increased HDL; can be used in pts with renal disease

28
Q

Fenofibrate

A

hepatic metabolsim, renal excretion so avoid in renal insufficiency

29
Q

Niacor

A

Immediate release nitrate which requires slow up-titration to minimize flushing

30
Q

Niaspan

A

Extended release - less flushing, better tolerated

31
Q

MOA of Nicotinic Acid

A

Niacin inhibits mobilization of FFA from adipocytes, reduced TG synthesis, ApoB, VLDL; increased HDL; promotes conversion of VLDL to LDL via enhanced Lipoprotein Lipase

Reduction Lp(a) by 30% - unique feature

32
Q

Nicotinic Acid SE

A

cutaneous flushing (treat with aspirin), elevated transaminase, hepatitis, hepatic failure, GI irritation, hyperuricemia/gout, insulin resistance, pregnancy risk C

33
Q

Effects of Omega3s

A

reduce TGs and CV risk, also have anti platelet, anti arrhythmic, and BP lowering effect

Cardiovascular Block (11 decks)

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