Term
| Triglycerides synthethized and excreted by the liver travel on which lipoprotein? |
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Definition
|
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Term
| What B protein is associated with liver lipoproteins? |
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Definition
|
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Term
| What fat soluble compound is typically found in VLDL's? |
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Definition
| Cholesterol (as Cholesterol Esters) |
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Term
| What is the key difference between B48 and B100? |
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Definition
| B100 has low affinity binding for LDL receptor |
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Term
| What receptor recruits lipoprotein lipase? |
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Definition
|
|
Term
| What is the function of Apoprotein A2? |
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Definition
|
|
Term
| Where does the glycerol come from for adipocyte triglyceride synthesis? |
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Definition
|
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Term
| What receptor does the liver use for metabolizing VLDL's? |
|
Definition
| LDL/Apo E receptor and Hepatic Lipase |
|
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Term
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Definition
| As the triglyceride level lowers on a VLDL it begins to kick off Apo-proteins (except B100). Result in a cholesterol rich lipoprotein |
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|
Term
| What is the half life of LDL? |
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Definition
|
|
Term
| What is the half life of VLDL? |
|
Definition
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Term
|
Definition
| Intermediate density lipoprotein. Remember that the conversion from VLDL to LDL is a dynamic process |
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|
Term
| What is significant about Lp(a)? |
|
Definition
| Associated with higher mortality from coronary heart disease |
|
|
Term
| ACAT is activated by what? |
|
Definition
| High levels of Cholesterol |
|
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Term
|
Definition
| Adds a fatty acid (activated) to a cholesterol making a cholesterol ester for storage |
|
|
Term
| What supresses LDL receptor synthesis? |
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Definition
| Persistently high levels of cholesterol, further high levels will initiate LDL degradation |
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|
Term
| What is the Intima layer of blood vessels? |
|
Definition
| layer closest to the endothelium, place where cholesterol collects |
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Term
| How does Atherosclerosis form? |
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Definition
| As cholesterol collects in the intima monocytes will differentiate into macrophages and attempt to break the cholesterol down. Since cholesterol cannot be broken down the macrophages will pour out growth factors and eventually "wall" the cholesterol off with smooth muscle, forming a plaque. |
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Term
| What is the first recognizable manifestation of atherosclerosis? |
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Definition
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Term
| Why do macrophages fill up with cholesterol and not lose it, resulting in atherosclerosis? |
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Definition
| Macrophages have an extra scavenger mechanism of cholesterol that tips the scales towards retention |
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|
Term
| Can atherosclerotic plaques reverse? |
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Definition
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|
Term
| Do all plaques grow into the lumen of a blood vessel? |
|
Definition
| No, plaque can grow downwards as well |
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|
Term
| Do all plaques grow into the lumen of a blood vessel? |
|
Definition
| No, plaque can grow downwards as well |
|
|
Term
| What is the difference between stable and unstable plaque? |
|
Definition
| Stable plaque has a larger layer of smooth muscle, protecting the patient from a rupture |
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|
Term
| Why is astherosclerotic plaque named the silent killer? |
|
Definition
| Because typically the level of occlusion necessary to present with clinical symptoms (~75%) is much higher then the range at which a plaque occlusion is at high risk for rupture (~45%) |
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