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BBC pharm
CH 37: hyperlipidemia drugs
| Question | Answer |
|---|---|
| any disorder marked by excess erum lipids | hyperlipidemia |
| two types of hyperlipidemias | hypertriglyceridemia and hypercholesterolemia |
| typically defined as serum triglycerid elevel in excess of 150 mg/dL general trmt geared toward diet modification. meds used only if unsuccessful. fibric acid agnets are the drugs of choice | hypertriglyceridemia |
| the CV risk factors for cholesterol management? | smoking, hypertension, fam history of CAD, age, high LDL, low HDL, smoking, hypertension, fam history |
| persons at high risk? | those patients with heart disease or any of its equivalents. this includes all patients with a history of stable angina, unstable angina, MI, mesenteric ischemia, AAA, peripheral vascular disaease, atherosclerosis mediated cerebrovascular accident, DM. |
| also known as nicotinici acid. it decreaess hepatic uptake of released free atty acids. inhibits lipolysis in fat cells, and, therefore, decreases free fatty acid levels. ultimate effects include increasing HDL and decreasing LDL. | niacin |
| this is a type of fibric acid agent, is not used often du eto its significant side effects. works to increase lipoprotein lipase activity, thus decreasing chylomicron and VLDL levels by increasing tissue uptake of hte triglycerides. | clofibrate |
| this is a bile acid sequestrant, binds cholesterol in the gut. therefore, there is increaed hepatic cholesterol synthesis. this increases hepatic serum LDL uptake. overall, plasma LDL is decreased bu 30%, VLDLs are increased by 20%,. | cholestyramine. colestipol and colesevelam fall into this class. |
| this is a representative HMG CoA reductase inhibitor (statin). others include simvastatin, rosuvastatin | lovastatin |
| AE of all HMG CoA reductase inhibitors? | hepatotoxic. |
| MOA of HMC CoA reductase inhibitors? | decrease the initial rate limiting step of cholesterol synthesis, especially in hepatocytes. therefore, this decreases the pool of intracellular cholesterol, increasing the need for exogenous cholesterol. |
| this upregulates ACE production. staatins, through their inhibition of HMGCoA reductase and its pathways, cause a reduction in mevalonate levels | mevalonate |
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aferdo01
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