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Block 2.3

Day 3: Dr. Williams Hyperlipidemia

QuestionAnswer
Where does cholesterol come from? The body produces about 75% of cholesterol de novo from various precursors. ~20% made in liver ~80% made by other cells
T/F Ingested/recycled cholesterol in the guy makes up the other 25% T
Where can ingested cholesterol be found? How much of it is esterified? animal sources, >50%
T/F Only free unesterified cholesterol can be absorbed through the gut T
What is Apolipoprotein A-I (apoA-I)? Found where? Forms lipoproteins with higher densities, it is found on HDL.
What is Apolipoprotein B (apoB)? Found where? Forms lipoproteins with lower densities, it is found on LDL. There is only one apoB molecule per LDL particle.
What is Lp(a)? A subset of LDL, where apoB protein attaches to another protein called apo(a). Highly associated with CV risk
What drugs causes elevated LDL and TG? Thiazide, steroids, immunosuppressants (cyclosporine, tacrolimus, sirolimus), isotretinoin, beta blockers, protease inhibitors, efavirenz, atypical antipsychotics, mirtazapine
What drugs causes elevated TG only? IV lipid, propofol, bile acid sequestrants, alcohol, interferons, azole antifungals.
What is the desirable LDL value? When is it too high? <100, >190 respectively.
What is the desirable HDL value for men and women? >40, >50 respectively.
What is the desirable TG value? When is it too high? <150, >500 respectively.
What is the desirable Non-HDL value? <130
T/F Can not use LDL=TC-HDL(TG/5) if TG > 400mg/dL T
What is primary prevention? Patient does not have clinical atherosclerotic cardiovascular disease (ASCVD), then all efforts to delay the treatment of ASCVD
What is secondary prevention? Patients does have ASCVD, and all treatments given are in an effort to prevent a subsequent manifestation of ASCVD
T/F Evidence for secondary prevention is substantially better than the evidence for primary prevention T
Who has ASCVD? A patient who has had: acute coronary syndrome (ACS), history of MI, stable or unstable angina, coronary or other arterial revascularization, stroke, TIA, peripheral arterial disease (PAD), including aortic aneurysm
What strength(s) of statins will cause high intensity (>50%)? Atorvastatin 40mg, 80mg and Rosuvastatin 20mg,40mg
What strength(s) of statins will cause low intensity (<30%)? Simvastatin 10mg, Pravastatin 10-20mg, Lovastatin 20mg, Fluvastatin 20-40mg
What are the four key statin benefit groups? 1. ASCVD = high intensity statin 2. Pts with severe hypercholesterolemia (LDL >190 mg/dL)= high intensity statins 3. Pts with diabetes (moderate to high intensity) 4. Primary prevention (statins?....maybe)
T/F If a pt age 40-76 yeas with LDL 70-189 ml/dL has >20% ASCVD risk should be treated with high intensity T
T/F If a pt age 40-76 yeas with LDL 70-189 ml/dL has <5% ASCVD risk should be treated no statin T
T/F If pt has ASCVD not at high risk, age <75 YO, high intensity statin should be started T
T/F If pt has ASCVD not at high risk, age <75 YO, high intensity statin should be started, and if it is not tolerated, use moderate intensity T
T/F If pt has ASCVD not at high risk, age <75 YO, high intensity statin should be started and LDL >70 mg/dL, add ezetimibe T
T/F if pas has ASCVD not at high risk, age > 75 YO, initiation of moderate or high intensity is reasonable. T
T/F Patients <75YO started with high intensity and <50% reduction in LDL was achieved or LDL >100mg/dL, add ezetimibe T
T/F If <50% reduction in LDL achieved on max tolerated statin and ezetimibe and TG <300 mg/dL, consider bile acid sequestrant T
T/F If pt <75YO has FH and LDL >100mg/dL on max statin and ezetimibe, use PSK-9 inhibitor T
T/F If patient is high risk ASCVD, start max statin T
T/F If patient is high risk ADCVD, start max statin and LDL >70mg/dL, add ezetimibe T
T/F If patient is high risk ADCVD, start max statin and PCSK9-I is considered, add ezetimibe FIRST T
T/F If pt 40-75 YO with DM, start moderate intensity T
T/F if pt 50-75 YO with DM and multiple ASCVD, consider high intensity T
T/F If pt 20-39 YO with DM and additional risk factor, consider moderate intensity T
T/F If pt >70 YO with DM and already on statin, continue it T
T/F Age 40-75 YO, LDL >70 to <190mg/dL, without DM, for primary prevention, <5% low risk ASCVD risk score, emphasize to reduce risk factors T
T/F Age 40-75 YO, LDL >70 to <190mg/dL, without DM, for primary prevention, >20% low risk ASCVD risk score, initiate statin T
What pleotropic effects do statins have? plaque stabilization and improvements in endothelial function, anti-inflammatory/oxidant properties, anti-thrombotic, increase nitric oxide bioavailability, potentially other effects
T/F Statins lower LDL levels (18-63%) but NOT Lp(a) levels, increase HDL, and decrease TG levels. T
What is the biggest ADR of statins? Myopathy, Co-Q10 not recommended, order CK level if severe symptoms/objective weakness, or lower lipophilicity results in less muscle pain
T/F starting dose of rosuvastatin is 5mg in Asian patients T
T/F If you are looking for a medication that has no drug interactions, go for Pravastatin T
T/F If you are looking for a medication that has minimal drug interactions, but more potent, go for Rosuvastatin T
What is the max dose of Simvastatin may be given with diltiazem, dronedrone, and verapamil based on FDA recommendations? 10mg
What is the max dose of Simvastatin may be given with amiodarone, amlodipine, and ranolazine based on FDA recommendations? 20mg
What is Zetia? MOA? Effect on lipids? C/I? Available in combination with? Inhibits intestinal absorption of cholesterol. Consistent reduction of 20% of LDL, increase HDL, and insignificant reduction TG, C/I in severe hepatic impairment. Available in combination with simvastatin (Vytorin) and atorvastatin (Liptruzet)
What are PCSK-9 Inhibitors? MOA? Effects on lipids? ADRs? Dosing? Cost consideration? Increases the amount of LDL receptors, therefore clear LDL. Dec LDL, Inc HDL, and dec TG. Alirocumab (Praluent) 75-150mg SC q2wks or 300mg SC q4wks Evolocumab (Repatha) 140mg SC q2wks or 420mg SC q month EXPENSIVE
What are Omega 3 FA? Effects on lipids? ADRs? C/I? DDIs? EPA and DHA. LDL is increased. Vascepa only EPA, less LDL increases seen (~3% increase in REDUCE-IT). ADRs: fishy burps, diarrhea, gas. C/I: allergy to fish/shellfish. DDIs: increase bleeding risk in patients on anticoagulant or antiplatelets.
What are Bile Acid sequestrants? MOA? Effects on lipids? ADRs? C/I? DDIs? Questran (cholestyramine), Welchol (colesevelam), Colestid (colestipol). MOA: binds to bile acids to prevent reabsorption. Can Increase TG. ADRs: GI upset. C/I: TG > 300mg/dL. DDIs: binds to meds/vitamins. Take 1 hour before or 4 hours after other meds
What are Fibrates? MOA? ADRs? C/I? DDIs? Activates PPARalpha, causes lipolysis. Gemfibrozil, Antara, Tricor, Trilipix, Fibricor, Triglide, Lipofen, Fenoglide. ADRs: myopathy, elevated LFTs, gallstones, C/I: gemfibrozil and statins, renal/hep impair, avoid statins and CYP3A4 substrate
What is Niacin? ADRs? C/I? Vit B3-nicotinic acid. Rx (Niaspan); target 2-3g/day. ADRs: flusing, hepatoxicity, hyperglycemia, hyperuricemia. C/I: active liver disease, peptic ulcer disease, and arterial bleeding.
T/F Kynamro is injectable. T
T/F When it comes to lifestyle modifications, you should exercise 3-4 times per week for 40 minutes T
What are the clinical components of ASCVD? MI, stroke, TIA, stable and unstable angina, stent replacement, PAD, arterial revascularization.
What medications to treat cholesterol increase LDL? What medications increase TG? What is the C/I of Bile Acid Sequestrants? Omega 3 FA to lower TG. Bile Acid Sequestrants. if TG >300
If you're taking simvastatin, what is your max dose if you're also taking amlodipine, amiodarone, or ranolazine? 20mg
If you're taking simvastatin, what is your max dose if you're also taking diltiazem, dronedarone, or verapamil? 10mg
T/F Statins are C/I in pregnant patients per package insert. If patient has active liver disease, LFT's greater than 3x the normal, is it contraindicated? T, yes it is C/I
What drugs cause increase of TG ONLY? IV lipid, propofol, bile acid sequestrants, alcohol, azole antifungs, and interferons
What are some lifestyle modifications for dyslipidemia? weight management: recommend to lower weight, if normal weight maintain it. Exercise 3-4 times a wk for 40 minutes. Eat vegetables, grains, fruits, low fat dairy, etc.
What is Apo-A1, associated with what lipid particle? HDL
What is Apo-B, associated with what lipid particle? LDL
Lp(a) is what lipid particle? LDL
How to create Lp(a)? Apo(a) + Apo-B
What lipid-lowering agents are injectable? PCSK-9 inhibitors (Repatha & Praluent) and Kynamro.
What class can be dose once a month? PCSK-9 inhibitors
When do I order a CK level? Severe pain or signs of muscle weakness
Do you recommend Co-Q10? NO
When do I recommend switching from a high lipophilic to a lower lipophilic statin? muscle pain or weakness caused by the drug
Would you stop giving a statin to switch to something that doesn't have the same life saving evidence? No unless they are allergic or can not tolerate
If you have CKD, what intensity statin do you give? high intensity
What percentage will be dropped giving a high intensity statin? >50%
When should you consider giving ezetimibe? if on statin, and LDL is >70
What statins are high intensity? atorvastatin 40,80. rosuvastatin 20,40.
What statins are low intensity? simvastatin 10, pravastatin 10-20, lovastatin 20, fluvastatin 20
Created by: SPangKee
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