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26 Cards in this Set

  • Front
  • Back
what are the optimal LDL-C goals for primary prevention?
no previous CHD
higher risk- lower target LDL-C goal dictates more aggressive therapy needed
what are the optimal LDL-C goals for secondary prevention?
past CHD event, lower risk in general population, but it may be higher risk forthis population
the higher the risk the lower the target LDL-C goal
how does decrease in LDL-C decrease CHD risk?
-change plaques w/ large lipid, thin fibrous layer to smaller lipid w/ more connective tissues and smooth muscle (harder lesion)- dec. risk of rupture
-may dec. plaque size
-endothelial dysfunction may reverse (improve vasodilatory property, inc. blood flow to ischemic areas)
-inflammatory processes may be reduced (measure CRP)
What are the ATP III risk factors?
cigarette smoking
HTN (>140/90mmHg or on anti-HTN)
low HDL-C
family history of premature CHD (in male 1st degreee relative <55y, in femila <65y)
age (men>45, women >55y)
DM is equivalent to CHD risk
HDL>60mg/dl counts as negative risk factor
What are the LDL-C goals according to risk factors?
CHD or CHD risk equivalent- <100mg/dl
multiple (2+)risk factors- <130mg/dl
zero to one risk factor- <160mg/dl
what are therapeutic lifestyle changes?
diet low in saturated fat and XOL, incy. physical activity, weight reduction, smoking cessation
what are soem of the TLC diet recommendations?
low fat does not mean low calories, complex carbs good replacement for saturated fat, replace satruated fats w/ unsaturated fats (canola oil, fish oil, olive oil)
mediterranean diet
More diet recommendations?
lean meat, grill or broil, smaller portions
skim milk
margarine instead of butter
low fat sof cheese instead of hard cheese
non-fat frozen yogurt instead of ice cream
avoid cream sauce or soup
low fat or not fat products if possible
what are some other dietary interventions?
viscous fiber (psyllium, oat gum)- can dec. LDL by 5%
fibers (whole grains, fruits, veggies)- can dec. LDL by 5%
plant stanol and sterol (benecol, total control)- dec. absorption of XOL in intestine- can dec. LDL by 5-15%
what is the mechanism of action of Statins?
inhibits HMG-CoA synthase, dec. hepatic XOL, Inc. LDL-R, dec. LDL circulating, dec. VLDL syn. and dec. TG
what are the statin pearls?
most potents XOL lowering agents
LDL-C dec log linear dose dependent
efficacy higher if given in evening
why give statin at night?
night time upturn of endogenous C biosynthesis, rosu and ator have long half-life so do not have to be taken at night.
giving does bid does not significantly improve efficacy
What is the most potent statsin? Least?
what are some of the adverse effects of statins?
HA, GI upset, myalgias, increase LFTs, myopahty (most serious), rhabdomyolysis, muyoglobinuria, acute tubular necrosis
what are signs of myophaty?
muslce pain or weakness with inc. CPK, r/o trauma or inc. physical activity, more in combined with gemfibrozil, DDI that inc. statin level (erythromycin)
what cyps are involved in statin metabolism?
cyp3A4- lova, sim, ator (a little)
cyp2c9- flu, rosu (only 10% metbolized)
What are some contraindications and precations for statin use?
caution if add gemfibrozil (2-4 fold inc. in statin level)
elderly, small frame, dec. renal fxn, multiple meds (interacting)- use smaller does, monitor closely
lovastatin and rosu incre INR, caution with warfarin
avoid in patients with liver disease
What is the mechanism of action of bile acid resin?
bind bile acids in intestine, decrease XOL absorption, inc. liver synthesis of XOL, inc. LDL-R, dec. LDL-C in circulation
What are some adverse effects of BAR?
bloating, constipation, flatulence, eipigastric, dec. absorption of fat soluble vitamins
How can a patient possibly decrease risk of adverse effects?
mix powder in juice, minimize air ingestion by using a straw, take tablet not powder, take vitamins either 1 hour before or 4 hours after BAR to inc. absorption of vitamins
What drugs do BAR interact with?
older BAR interact with Digitoxin, warfarin, beta blockers, HCTZ, thryoxine, iron, nicotinic acid, loperimide, other ionic drugs, colesevelam appears to be ok
What is the mechanism of action of cholesterol absroption inhibitors?
work locally in intestine, block absorption of XOL from gut, inc. liver synthesis of XOL, inc. LDL-R on liver, dec. LDL-C and VLDL in circulation
What are some adverse effects of Ezetimibe?
minimal, diarrhea, cough, fatigue, arthralgias, no evidence of DDIs yet
waht are some adverse effects of fibric acid derivatives?
ususally well tolerated, Gemfirbrozil can cause mild GI upset, muscle SE esp with statin (do not use with statin), XOL gallstones
fenofibrate- rash 2-4%, XOL gallstones
Are fibartes safe?
Clofibrate- dec. non-fatal MI by 25% but inc. total mortality
Gemfribrozil- helsinki trial- dec fatal and nonfatal MI, no net dec in total mortality, inc. non-CHD mortality
Fenofibrate- no major clinical trial
What is the mechanism of action of fibric acid derivatives?
activates PPAR-alpha (peroxisome proliferator activated receptors) nuclear hormone receptor super family
inc. synthesis of HDL, dec. VLDL, dec. TG, does not dec. LDL that much only 10-25%