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Cholesterol lowering agents

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morauch630's version from 2017-12-11 06:09

Mechanism of action

Question Answer
Mechanism of action: statin (hmg-coA reductase inhibitor)inhibition of cholesterol synthesis by blocking enzyme hmg-coA reductase. Reversible and competitive for this enzyme
Mechanism of action: fibric acid derivativeincreased lipoprotein lipase activity, increased catabolism of VLDL
Mechanism of action: bile acid sequestrantsbind to bile acids and increase excretion -> leading to diversion of cholesterol into bile acid synthesis. liver increases catabolism of LDL to cholesterol to make up for loss bile acids
Mechanism of action: nicotinic acid (niacin)Acts as an hormone sensitive lipase -> inhibition of free fatty acid release from adipose tissue -> reduced free fatty acid transport to the liver and decreased synthesis of VLDL -> decreased LDL
Mechanism of Mechanism of action: selective cholesterol absorption inhibitorWorks on the brush border of intestinal epithelial cells to selectively inhibit cholesterol from being absorbed from bile & diet sources
Mechanism of action: omega-3 acid ethyl ester (lovaza)decreased hepatic triglyceride synthesis
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Section 1

Question Answer
Effects of statins(decrease + LDL + triglycerides + CRP lvls), improve endothelial function at site of coronary plaque, inhibition of platelet aggregation
Effects of fibric acid derivativesuppress lipolysis in adipose tissue, decrease free fatty acid flux, lower rate triglyceride synthesis
Effects of bile acid sequestrantsdecreased LDL, increased triglycerides, no change in HDL
Effects of nicotinic aciddecreased triglycerides, increased HDL. (Similar to bile acid sequesterants in lowing LDL)
Effects of selective cholesterol absorption inhibitordecreased LDL, decreased triglycerides, increased HDL
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Section 2

Question Answer
Adverse effects of atorvastatin, lovastatin, fluvastatin, simvastatin, rosuvastatinfatigue, rash, cough, chest pain, abd pain, anemia, progression cataracts, gynecomastia, sun sensitivity, rhabdomyolysis, increased LFTs
Adverse effects of gemfibrozil, fenofibrate, lofibrahepatotoxicity, cholelithiasis, fatigue, rash, a fib, abd pain, rhabdomyolysis, increased glucose, N/V
Adverse effects of cholestyramine, colestipol, colesevelamfatigue, weight gain/loss, chest pain, HA, hematuria, constipation, abd pain, malabsorption medications/nutrients
Adverse effects of niacinhyperglycemia, hyperuricemia, arrythymias, GI upset, N/V, rhabdomyolysis, HA, hepatotoxicity, vision disturbances
Adverse effects of ezetimibe (zetia), vytorinfatigue, cough, abd pain, diarrhea, dizziness
Adverse effects of lovazaflu- like symptoms, dyspepsia, rash
What can happen when especially first taking NiacinFlushing. Can be blunted by aspirin
How to improve flushing when prescribing NiacinUse slow escalation in dose over 3 to 4 week. Tolerance usually develops
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Section 4

Question Answer
Cautions with bile acid sequestrantscontraindicated in biliary obstruction, interferes with absorption of fat soluble vitamins
Cautions with niacingout, diabetes, liver disease, gallbladder disease
Cautions with selective cholesterol absorption inhibitorsnot recommended with hepatic insufficiency (pro-drug)
Cautions with lovazafish allergy
Which drug should patients with phenylketonuira avoidQuestran light, which contains aspartame
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Kinetics

Question Answer
Statin metabolismCYP 450
Statin excretionMostly excreted in feces
Statin onset of activity 2 weeks
Statin Maximal effect achieved in4 to 6 weeks
Bile Acid Sequestrants absorptionNot absorbed orally
Bile Acid Sequestrants metabolismNo metabolism
Bile Acid Sequestrants excretionCompletely excreted in feces
Bile Acid Sequestrants Maximal effect seen in ___1 month
Niacin absorptionWell absorbed
Niacin metabolismHepatically metabolized
Niacin excretionRenally cleared
Selective Cholesterol Absorption Inhibitors absorptionLittle oral absorption
Selective Cholesterol Absorption Inhibitors metabolismEnterohepatic recirculation. Metabolized in liver and small intestine to active drug
Selective Cholesterol Absorption Inhibitors eliminationEliminated in feces
omega-3 acid ethyl ester (lovaza) metabolismliver. CYP450 inhibition
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MISC

Question Answer
What does the enzyme HMG-COa do?HMG-CoA reductase catalyzes the conversion of HMG-CoA to mevalonate in the liver
What is Mevalonate?a cholesterol precursor
Which drugs are chosen first to decrease lipid lvlsstatin (hmg-coA reductase inhibitor)
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Monitoring

Question Answer
Monitoring statinsLFTs and Fasting lipid profile
When to check for LFTs in statinsBaseline, 6 week after initiation, 12 weeks after initiation, q3months for a year then annually
When to decrease dose or discontinue in statinsIf AST or ALT become three times upper limit or greater,
Monitoring Fibric Acid DerivativesSimilar to statins. Lipid profile Gemfibrozil. CBC q3months for 12 monthsLFTs at baseline, 6 weeks, 12 weeks, and twice yearly thereafter
Monitoring NiacinLipid lvls. LFTs baseline, 6 weeks, 12 weeks, and twice yearly thereafter
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Drug Interactions

Question Answer
Drug Interactions Fibric Acid DerivativesStatins (Increased risk of rhabdomyolysis), Warfarin (Increased anticoagulation response)
Drug Interactions Bile Acid SequestrantsDecreased absorption of most medications. Take other medications 1 hr before or 4 hr after sequestrants
Drug interactions NiacinHMG-CoA reductase inhibitors, gemfibrozil. Increased risk of rhabdomyolysis
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