Lipoprotein Drugs Flashcards Preview

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Flashcards in Lipoprotein Drugs Deck (22):

Cholestyramine; side effects

Dose-dependent Most common - constipation, bloating Effects absorption of other drugs - statins, thiazide, digitalis


Cholestyramine; uses

hypercholesterolemia w/out hyperTAGs - second agent after statins; 11-20 year olds


Statin; side effects

Major - myopathy, rhabdomyolysis Hepatotoxic - increased enzymes Minor - GI


Statins; lipid profile

Decrease TAGs - the higher the baseline level, the stronger the lowering effect Decrease LDL Increase HDL


Niacin; lipid profile

TAG/LDL/Lp(a) = decrease HDL = increase


Statin; pharmacokinetics

Life-long treatment 1st pass effect - necessary for accumulation in liver High plasma protein binding Metabolism - CYP3A4


Niacin; CI

Peptic ulcer Gout Liver disease Diabetes


Hypertriglyceridemia treatment

Fibrates - first-line Niacin


Niacin; uses

Hypercholesterolemia and hypertriglyceridemia


Cholestyramine; mechanism

Dose-dependent Quaternary amine; Anion-exchange w/ bile acid; positively charged resin binds w/ negatively charged bile Increased bile excretion = increased bile synthesis = decreased hepatic cholesterol = increased LDL-R expression = decreased LDL levels


Myopathy/rhabdomyolysis; risk factors

Genetic - SCLO1B1 polymorphisms Dose - direct relationship CYP3A4 inhibition Gemfibrozil - blocks OATP1B1 - increased statin in circulation Female sex, old age Renal sufficiency Hypothyroidism


Niacin; pharmacokinetics

o Oral – doses much higher than those used as vitamins o Three types  Immediate release – 2-3 times a day  Long-acting release  Extended release – once a day


Statins; CI

Hypersensitivity - lovastatin, simvastatin Liver disease Pregnancy/breast feeding


Only drug that can lower Lp(a) levels

Niacin/nicotinic acid


Bile acid binding resins



Niacin; mechanism

o In adipose – inhibits FFA mobilization; niacin receptor 1 in adipose tissue; Activates niacin receptor 1 = decreased cAMP = no PKA activation = no perilipin/HSL phosphorylation = no TAG is broken down = decreased FFA release o In liver – decreased synthesis of VLDL-TAGs  Inhibits DGAT2 – catalyzes final reaction in TG synthesis  Increased ApoB degradation o Inhibits uptake of HDL-apoAI  Increase in HDL-apoA1 levels = good thing


List statins

Atrovastatin - Lipitor; active, highest half-life Lovastatin - Mevacor; prodrug; hypersensitivity Simvastatin - Zocor; prodrug; hypersensitivity


Statin mechanism

HMG-CoA analogs Competitive, reversible inhibitors of HMG-CA reductase = bind w/ higher affinity Decrease de novo cholesterol synthesis = increase in LDL-R expression (SREBP/Scap) = decreased LDL levels


Myopathy/rhabdomyolysis; symptoms

Major SE of statins Signs - myalgia, fatigue, elevated CK levels Myopathy - pain w/out increased CK Rhabdomyolysis - pain w/ increased CK


Niacin; side effects

o Major – intense cutaneous flush/pruritus  Soon after taking drug – poor compliance  Mediated by vasodilatory PGs – PGD2  Tolerance over time  Treat w/ NSAIDs o Severe  GI effects – avoid in patients with peptic ulcer  Elevated liver enzymes – MAJOR CONCERN WHEN COMBINED W/ STATINS • Increased risk of myopathy  Hyperurecemia – avoid w/ gout  Increased fasting glucose/insulin resistance – avoid w/ diabetes


Hypercholesterolemia treatment

Statins - first line; life-long; >12 years of age Cholestyramine - second agent after statins; 11-20 years of age Niacin - not first line PCSK9 - future Statins + niacin = hepatotoxicity risk


Cholestyramine; lipid profile

TAGs - transient increase; return to baseline >250mg/dl = signficant increase