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Cardiovascular > Atherosclerosis Treatment > Flashcards

Atherosclerosis Treatment Flashcards

1
Q

reasons for using statins over other cholesterol lowering therapies

A

Proven effective based on large number (21) of randomized clinical trials (RCTS)

More intensive statin therapy reduces rates of CHD, stroke and death more than less intensive therapy (5 RCTs)

Inexpensive (5 of 7 generic)

Safe when given as directed

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2
Q

statin benefit groups

A

clinical ASCVD

LDL-C >/= 190 mg/dL without secondar ycause

primary prevention/diabetes - ages 40-75, LDL-C 70-189 mg/dL

primary prevention/no diabetes - ages 40-75, LDL-C 70-189 mg/dL, ASCVD risk >/= 7.5%

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3
Q

When do results of stain treatment become the most prominent?

A

years 4-5

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4
Q

mechanism of action of statins

A

structurally similar to HMG-CoA and act as a competitive inhibitor of HMG-CoA reductase, thereby reducing synthesis of cholesterol

leads to increased LDL receptors

small elevations in HDL-c is also seen

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5
Q

drugs that lower LDL-C

A

statins

bile acid sequestrants

niacin

fibrates

omega-3’s

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6
Q

What happens to mean % change from baseline LDL-C every time the dose of statin is doubled?

A

there will be an extra 6% decrease

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7
Q

non-LDL effects of statins

A

endothelial function

reduction of inflammatory response

plaque stability

thrombus formation

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8
Q

statins with long half lives

A

rosuvastatin (19-20 hrs) and atorvastatin (15-30 hrs)

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9
Q

statins with short half lives

A

fluvastatin, lovastatin, pravastatin, simvastatin

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10
Q

toxicity of statins

A

liver enzyme rises (transaminases)

muscle myositis

interacts with cyclosporine, gemfibrozil (glucuronidation affected), grapefruit juice (P450), erythromycin

decrease in ischemic stroke but slight increase in hemorrhagic stroke

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11
Q

statins and diabetes

A

may raise blood sugar, 1 to 2 excess cases per year per 1000 patients

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12
Q

metabolism of statins

A

CYP3A4 for lovastatin, simvastatin, and atorvastatin

CYP2C9 for fluvastatin and rosuvastatin

pravastatin has no CYP activty

all statins undergo glucuronidation

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13
Q

lovastatin

A

fungal derivative

used for over a decade

moderate potency

has similar properties as red yeast rice, which has mevilonin

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14
Q

simvastatin

A

fungal derivative

at high doses, best at raising HDL-c and Apo A1

very inexpensive

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15
Q

pravastatin

A

fungal derivative

not metabolized by P450 system, sulfated

inexpensive

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16
Q

fluvastatin

A

synthetic

not as potent

17
Q

atorvastatin

A

synthetic

potent, long half life of 14 hours

18
Q

cerivastatin

A

synthetic

removed from market due to myositis risk with high dosages and with gemfibrozil

19
Q

rosuvastatin

A

synthetic

most potent due to low lipophilicity and high hepatocyte selectivity because of large polar side chain

19 hour half life

20
Q

pitavastatin

A

synthetic

can be used for those who don’t tolerate other statins

21
Q

GI active drugs

A

bile acid sequestrants

stanols, sterols

Eztimibe (cholesterol absorbtion inhibitor)

22
Q

bile acid sequestrants

A

cholestyramine and colestipol - resins

colesevelam - gel

binds bile acids in the gut and causes depletion of hepatic cholesterol pools

increased production of more LDL receptors

non-systemic, not absorbed

23
Q

Ezetimibe

A

cholesterol absorption inhibitor

hepatic glucuronidation and then intestinal villi

decreased absorption of biliary and dietary cholesterol

acts at brush borders of small intestins

helpful in sitosterolemia

only one year of SHARP trial data for safety and additive effect with statins

24
Q

plant/sterol esters

A

inhibit micellar cholesterol absorption

not additive to Ezetimibe therapy

25
Q

efficacy of GI active drugs

A

sequestrants and Ezetimibe lowers LDL-C about 20%

stanol ester about 10-14%

26
Q

combinint statin and GI active drugs

A

same result as 3 doublings of dosage of statins alone

27
Q

niacin (vitamin B3) mode of action

A

a. Potent inhibitor of adipose tissue lipolysis (G-coupled receptor) - Suppression of lipolysis in adipocytes by niacin activating its receptor GPR109A
b. Decreases flux of FFA used by liver for VLDL production
c. Inhibits VLDL synthesis; see decrease in large TG rich VLDL
d. Decrease in assembly of apo B containing lipoproteins
e. See decreased small dense LDL
f. See increased HDL Apo A-1 (prolongs half-life) - Inhibits hepatic removal, best drug for raising HDL-C
g. Reduces Lp(a) (only lipid drug to do this)

28
Q

clinical usage of niacin

A

Patients with high cholesterol and high triglyceride and low HDL-c

Raises HDL at low dose; less potent in lowering LDL c at low dose than statins

29
Q

niacin toxicity

A

1) Cutaneous vasodilation and flushing due to effects of receptors in the dermis
2) Hepatotoxicity; more prominent with Niacin than it is with statins.
3) Niacin raises blood sugar; increases hepatic glucose output-use carefully in diabetics
4) Elevates uric acid–can lead to gouty arthritis
5) Exacerbates peptic ulcer disease

30
Q

forms of niacin

A

sustained release (more GI side effects, hepatic toxicity)

intermediate release (bed time only, linear kinetics, best balance between flushing and liver concerns)

immediate release (cheapest, most flushing)

31
Q

fibrates - Gemfibrozil and Fenofibrate mechanism of action

A

Triglyceride rich lipoproteins – major effect on lowering TG levels, done through PPAR alpha effects on ApoCII (decrease) and LPL (increase)

LDL: Differing effects depending on LDL and TG levels - best LDL lowering if high LDL alone, paradoxical increases in LDL-C if LDL is not elevated

fenifibrate lowers LDL-C more thatn Gemfibrozil

HDL: increase if baseline levels are low, increase in ApoAI and AII

Fenofibrate lowers uric acid and raises homocystein

32
Q

efficacy of fibrates

A

reduce progression of coronary lesions

reduce major coronary events in primary and secondary prevention trials, bu tnot in trials of diabetics

33
Q

toxicity of fibrates

A

cholelithiasis

mild GI symptoms

myositis when combined with HMG CoA reductase inhibitors

34
Q

omega 3 fatty acids mode of action

A

Lower TG in a dose –related fashion (lipid reason to use omega 3 fatty acids)

Don’t use to lower LDL-c

Can see slight increase in HDL-c

Reduced CHD death in survivors of MI

35
Q

efficacy of omega 3 fatty acids

A

In those with very high TG; can lower TG up to 50%

In those with mild-moderate TG, can lower TG about 25%

36
Q

side effects of omega 3 fatty acids

A

well tolerated

can raise LDL-C if combined with hyperlipidemia

see increasing bruising

can be used in combined hyperlipidemia with statins

37
Q

therapies to increase HDL-C

A

apo A1 milano like IV preparations

CETP inhibitors –Torcetrapib caused increase in CHD and total mortality

Cardiovascular (46 decks)

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