Management of Hyperlipidemia Flashcards Preview

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Flashcards in Management of Hyperlipidemia Deck (28):

What are hereditary causes of hyperlipidemia?

familial hypercholesterolemia: Mutation in LDL receptor results in unregulated synthesis of LDL. Familial combined hyperlipidemia: increased secretions of VLDLs. Dysbetalipoproteinemia: defective form of apoE involved in catabolism of VLDL


What is recommended as initial therapy in patients with acute coronary syndrome?

intensive statin therapy or if unable to tolerate statins than treated with another lipid lowering agent


In what patient population is the target LDL below 70?

patients at very high risk for CHD events


Which patients are at very high risk for CHD events?

established coronary heart disease plus: DM, smoking, metabolic syndrome, or acute coronary syndrome


When should lipid panels be checked?

Beginning at age 20: obtain a fasting serum lipid profile of total cholesterol, LDL, HDL and triglycerides. Repeat testing every 5 years for acceptable values


What are ranges for HDL?

< 40 low, > 60 high


What are ranges for serum triglycerides?

< 150 normal, 150-199 boderline, 200-499 high, > 500 very high


What are ranges for total cholesterol?

< 200 desirable, 200-239 borderline, > 240 high


Name the 7 main statins

rosuvastatin (Crestor), Atorvastatin (Lipitor), Simvastatin (Zocar), Lovastatin (Mevacor), Pravastatin (Pravachol), Fluvastatin (Lescol), Simvastatin/Ezetimibe (Vytorin)


How do statins work?

HMG-CoA reductase inhibitors. Lower LDL and decrease morbidity/mortality. Well tolerated.


What are contraindications to statins?

pregnancy, active liver disease, unexplained elevated aminotransferase levels (ALTs), alcoholics


What are SE of statins?

GI upset, HA, elevated LFTs, muscle pain/weakness, protenuria and renal failure.


What drugs increase the SE of myopathy associated with statins?

erythromycin, niacin, gemfibrozil, cyclosporine


Why should statins be taken in the evening or at bedtime?

Significant amount of cholesterol production seems to occur during sleep. Lovastatin (Mevacor) and Atorvastatin (Lipitor) are exceptions


How do bile resins reduce hyperlipidemia?

Decrease cholesterol absorption through exogenous pathway. Are NOT absorbed through the GI tract. bind bile acids in the intestines, forming a complex that is excreted in the feces.


How can niacin be used to reduce hyperlipidemia?

improve cholesterol levels when used at doses 100-300 times the recommended daily allowance. decreases VLDL synthesis in liver and increase lipoprotein lipase activity


Name the bile acid resins

cholestryamine (Questran) and Colestipol (Colstid)


What are CI to niacin?

hepatic dsyfxn, hypotension, peptic ulcer, gout, can worsen glucose control


What are SE of niacin?

pruritis and flushing of face and neck, hepatotoxicity, uric acid and glucose increases


How does Ezetimibe (Zetia) a cholesterol absorption inhibitor work to reduce hyperlipidemia?

Inhibits the absorption of cholesterol and causes a reduction of hepatic cholesterol store. complementary to that of the STATINS


What are CI of ezetimibe (Zetia)?

if used with a statin hepatic disease or elevated ALTs


What are SE of ezetimibe (Zetia)?

HA, diarrhea, abdominal pain


What are the fibric acid derivatives?

Gemfibrozil (Lopid) and fenofibrate (Tricor)


How are fibric acid derivatives used?

Good for lowering triglycerides from the stimulation of lipoprotein lipase, which enhances the breakdown of VLDL to LDL, but have minimal effect on LDL


What are CI of fibric acid derivatives?

h/o gallstones, hepatic or renal dysfunction


What are adverse effects of fibric acid derivatives?

GI, myopathy if taken with statins, jaundice, increased effects of warfarin


What is xanthomas?

Soft, yellow skin plaques or nodules that contain deposits of lipoproteins inside histiocytes. found on skin of patients with hyperlipidemia


What are the steps of the framingham risk scoring?

age, total cholesterol, HDL-cholesterol, systolic BP, smoking status (add all together)