What are the cholesterol levels standards after an overnight fast?
What are risk factors for coronary heart disease? At what point should you start treating someone aggressively for CHD?
You treat aggressively when your patient has two or more of these factors or just one of the red factors.
An elevated level of what apolipoprotein is associated with decreased risk of coronary heart disease?
Apo A1. It is on HDL which pulls cholesterol out of plaques.
List 4 primary hypercholesterolemias.
Familial hypercholesterolemia, familial ligand-defective apolipoprotein B, familial combined hyperlipoproteinemia, Lp(a) hyperlipoproteinemia.
List 4 primary hypertriglyceridemias.
Primary chylomicronemia, familial hypertriglyceridemia, familial combined hyperlipoproteinemia and familial dysbetalipoproteinemia.
What are some secondary causes of hyperlipidemia?
How can you decrease cholesterol levels by 10-20% by just changing your diet?
Reduce intake of fats and cholesterol. Eat oat and rice (reduces LDL). Reduce sugar intake (sugar increases VLDL synthesis). Eat nuts (reduces LDL). Omega-3 oil in fish (increases HDL and reduces LDL).
What drugs can you prescribe to a patient with high cholesterol that are bile-acid sequestrates (resins)? What is the mechanism by which these drugs work?
Cholestyramine, colestipol and colesevelam (best one). They bind bile acids and inhibit reabsorption of bile acid. This increases channeling of cholesterol to bile acid production and decreases intra-hepatic cholesterol levels. As these levels decrease, the liver upregulates LDL (apoB and E) receptors and increases clearance of LDL, IDL and VLDL.
How effective are resins at decreasing CHD events (fatal and nonfatal)? Who are these drugs particularly good for?
They decrease them by 19%, decreasing LDL cholesterol levels by 15-30% and increasing HDL levels by 3-5%. These drugs are safe for pregnant women as statins are not. They are used in conjunction with statins in heterozygous familial hypercholesterolemia and combined hyperlipidemia.
What are adverse effects and interactions you need to keep in mind with bile-acid sequestrates?
What are the main statins you will use and how do they work?
Simvastatin, atorvastatin and rosuvastatin. The look like mevalonate, bind to HMG-CoA reductase, inhibit it and thus reduce cholesterol synthesis. Decreasing synthesis, results in up regulation of LDL receptors and incidentally more LDLs are taken up by the liver.
How effective are statins?
Rosuvastatin might be slightly better because it increases HDL more than atorvastatin.
What are contraindications to consider with statins?
Myopathy (they can cause it and possibly lead to rhabdomyolysis). Asians (don't metabolize them as well). Mild hepatotoxicity. Pregnant women (teratogenic). Memory loss. Increased blood sugar levels.
What are drug interactions you need to consider when prescribing lovastatin, simvastatin and atorvastatin? Why is rosuvastatin not considered?
Drugs that interact with CYP3A4. Rosuvastatin is not metabolized by CYP3A4.
Why are statins so good for patients that just survived an MI?
Induce endothelial production of NO and vasodilate. Stabilize plaques. Reduce CRP (reducing inflammation). Reduces thrombotic events.
What other chronic conditions aside from heart disease can benefit from statin therapy?
Multiple sclerosis (anti-inflammatory effect). Alzheimer's. Rheumatoid arthritis.
What groups of people should receive moderate to high intensity statin therapy?
What apolipoprotein was found in people in Italy that significantly decreased their incidence of CHD events?
Why is estrogen-replacement therapy a controversial topic in cholesterol management?
What drug prevents cholesterol absorption in your GI tract? What happens when you combine it with a statin?
Ezetimibe. It actually increases plaque formation when combined with statins.
What happens when your triglycerides (VLDL) get too high? What drug do you use treat this that causes the largest increase in HDL levels?
Pancreatitis and xanthomas. Niacin increases lipoprotein lipase activity (decreasing VLDL) and raises HDL.
What drugs are used to lower triglyceride (VLDL) levels in patients with familial hypertriglyceridemia and familial dysbetalipoproteinemia?
Fenofibrate (fibrin acid derivative). This drug binds to PPAR-alpha receptors, increasing LPL activity, increasing HDL and decreasing VLDL synthesis and excretion by the liver.
Why should you not use fenofibrate in patients with renal failure?
It is excreted by the kidneys
Why should you be wary prescribing gemfibrozil when a patient is on a statin?
What drug is used in combination with niacin to treat Lp(a) hyperlipoproteinemia?
Neomycin. It is an antimicrobial that actually inhibits resorption of cholesterol and bile salts.