Dyslipidemia Flashcards
What is the non-pharmacologic therapy for dyslipidemia?
lifestyle modifications: healthy diet, weight loss, exercise, stop smoking
What are the pharmacologic options for dyslipidemia?
- statins
- fibric acids
- bile acid resins
- nicotinic acid
- 2-azetidione
What is another name for the statin drug class?
-HMG CoA Reductase Inhibitors
What it the statin MOA?
- inhibit HMG CoA reductase, which is an enzyme in cholesterol production
- statins reduce, but don’t completely block, cholesterol synthesis
- increase LDL catabolism
- also have anti-inflammatory activity (decrease CRP)
Adverse Effects of Statins
- hepatic toxicity
- myopathy (myalgia, myositis, rhabdomyolysis)
- neuropathy
- small increased risk of DM at high doses
- non-serious and reversible cognitive side effects (memory loss, confusion)
Statin CI
- pregnancy (cat X) and lactation
- active or chronic liver dz
- concomitant use of CSA (cyclosporin A), gemfibrozil, niacin
Drug Interactions of Statins
- reports of myopathy when administered with CSA, gemfibrozil, clofibrate, niacin, azole antifungals, erythromycin, nefazodone, protease inhibitors
- may potentiate oral anticoagulants
- increased effect/toxicity of levothyroxine (thyroid med)
What kind of dose-response relationship do statins have?
-non-linear: substantial reduction in LDL at starting doses; each doubling of dose reduces LDL 6% more
When is dosing of statins most effective?
evening dosing usually yields greater effects on LDLs
Which statins have the most drug interactions?
lovastatin and simvastatin
MOA of Bile Acid Resins
- increase LDL catabolism
- decrease cholesterol absorption
AEs of Bile Acid Resins
-GI SXS MOST COMMON
Bile Acid Resins CI
- monotherapy for TGs > 500 MG/DL
- familial dysbetalipoproteinemia
- hx of severe constipation
Bile Acid Resins Drug Interactions
- binds with many coadministered acidic drugs (eg warfarin, NSAIDs, beta blockers)
- take 1 hour before or 4 hours after
Fibric Acid MOA
- increase VLDL clearance
- decreased VLDL synthesis
Fibric Acid AE
- GI complaints most common
- can increase bile lithogenicity
Fibric Acid CI
- hepatic or severe renal dysfunction
- pre-existing gallbladder dz
Nicotinic Acid/Niacin MOA
-decrease LDL and VLDL synthesis
Nicotinic Acid/Niacin AE
- flushing most common
- may cause glucose intolerance and increase uric acid levels
- hepatotoxicity
Nicotinic Acid/Niacin CI
- liver disease
- type 2 DM
- hout
- hyperuricemia
Ezetimibe MOA
blocks cholesterol absorption
Ezetimibe AE
-may cause fatigue, abd pain, diarrhea, arthralgia, back pain
Ezetimibe CI
-combination with statins in active liver dz or pts with persistent LFT elevations
Which dyslipidemia class is best at reducing LDL?
statins
Which dyslipidemia class is best at reducing TG?
fibric acids and nicotinic acid/niacin
Which dyslipidemia class is best at increasing HDL?
niacin/nicotinic acid
Which dyslipidemia class actually causes an increase in TG?
bile acid resins
MOA of Plant Stenol Esters
-decrease cholesterol absorption, TC, and LDL
What labs must be monitored for statin therapy?
- baseline ALT
- ALT as clinically indicated thereafter
- CK prn myositis
What labs must be monitored for fibric acid therapy?
- baseline ALT and alk phos
- ALT and alk phos 6-12 wks x2, then q12 mo thereafter
- fasting lipid profile 6-12 wks after dose change, q12mo
- CK prn myositis
What labs must be monitored for bile acid resin therapy?
-fasting lipid profile 6-12 wks after stable dose then q12mo
What labs must be monitored for nicotinic acid therapy?
- baseline ALT and alk phos,
- ALT and alk phos 6-12 wks, q12mo
- after stable dose achieved x2 mos, fasting lipid profile, uric acid and glucose
- fasting lipid profile q12 mo thereafter
- CK prn myositis
ACC/AHA Statin Benefit Groups
- pts with clinical ASCVD
- pts with LDL >190
- pts 40-75 yo with DM and LDL 70-189 (but no clinical ASCVD)
- pts w/o clinical ASCVD or DM with LDL 70-189 with 10 year risk of ASCVD >7.5%
