click below
click below
Normal Size Small Size show me how
Lecture 13
Lipids/Lipoproteins
Question | Answer |
---|---|
Cholesterol travels in circualtion in shperical particles containing both lipids and proteins. These particles are called? | lipoproteins |
what are the three main classes of lipoproteins measured in the serum | VLDL, LDL, HDL |
VLDL are composed mostly of? | triglycerides |
what is the main atherogenic class of lipoproteins | LDL |
How does HDL affect ones risk for development of atherosclerosis | inversely |
how often should a fasting lipoprotein profile be obtained | in adults over 20 it should be obtained every 5 years |
In a patient that is non-fasting what parts of the fasting lipoprotein profile will be usable | the Total and HDL will be usable (get follow-up if total is >200 or HDL is <40) |
what is the optimal level for LDL | <100 |
what level of LDL is high | >160 |
what level of Total cholesterol is desirable | <200 |
what level of total cholesterol is high | >240 |
what level of HDL is desireable | >40 |
what are the 5 modifiable CHD risk factors | 1) Smoking 2)Hypertension 3) Low HDL 4) Family Hx 5) Age |
what is the LDL goal if you have CHD or CHD risk equivalents | <100 |
what is the LDL goal if you have 2+ risk factors | <130 |
what is the LDL goal if you have 0-1 risk factors | <160 |
oxidation of LDL has been shown to increase atherogenesis how can that be inhibited | anti-oxidants |
what is the only gentically determined component of lipoproteins | apolipoproteins |
what is the major protein component of HDL particles | Apolipoprotein A1 |
what is the major protein component of LDl | Apolipoprotein B100 |
how does Lp(a) affect thrombosis | Lp(a) can compete for the binding of plasminogen to its cell membrane receptor on the endothelial surface |
how does homocysteine enhance the atherosclerotic process | Generation of superoxide and hydrogen peroxide, enhanced coagulation, inhibiting dilation of small arteries, promoting smooth muscle proliferation |
what happens when Homocystein and LDL interact | they form LDL-homocysteine thiolactone aggregates which are taken up by macrophages and subsequently incorporated into foam cells in early atherosclerotic plaques |
how can you lower serum concentrations of homocysteine | treatment with daily supplements of folic acid, vitamins B6 and B12 |
what is a better predictor of cardiovascular events fasting or non-fasting triglycerides | non-fasting triglycerides |
how are foam cells formed from LDL | Ox-LDL is taken up in macrophage scavenger receptors, promoting cholesterol ester accumulation and foam cell formation |