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Block 2.3
Day 3: Dr. Williams Hyperlipidemia
Question | Answer |
---|---|
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 |