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10 Cards in this Set
- Front
- Back
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Cholesterol vs Chol ester? |
-Cholesterol is polar and has a hydroxyl group (-OH) -Chol ester has a fatty acid connected to the hydroxyl group and losses polarity and cannot go through membranes |
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1) You eat chol and chol esters 2) The panc releases panc esterase which cleaves fatty acids from chol esters 3) In the intetines, the enzyme ACAT remakes CE. 4) Cholesterol esters combine with TG's, phospholipids, and Apo-B48 to make chylomicron 5) Abetalipoproteinemia - no Apo-B48, decreased serum TG and Chol |
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Chordoma -Cords and lobules of physaliferous (having bubbles or vacuoles) cells separated by fibrous septa with extensive myxoid stroma -Cells may be very large, with vacuolated cytoplasm, prominent vesicular nucleus -Small tumor cells with small nucleus -Rare mitotic figures |
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Why does HDL convert cholesterol to CE's in the blood? |
-Cholesterol is polar. All cells bump into one another the cholesterol can stick to other cells. -Chol determines membrane fluidity so if a cell is too fluid it would break -Via Apo-A on HDL, LCAT is activated converting Chol to CE. -CE are nonpolar and becomes trapped in lipoproteins |
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-Lipoproteins are a physical combo of prots and fat -Apoproteins are on the surface and have functions -Polar things are on the outer surface (such as the hydoxyl group on chol) |
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1) The food you eat becomes a CM (which has mostly TG's) 2) HDL gives CM Apo E & C. 3) Apo C activates Lipoprotein Lipase with takes fatty acids from CM and brings it to adipose. Since it lost a bunch of stuff, it's now called a CM remnant 4) HDL takes back Apo C, CMR enters liver via Apo-B48 |
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1) Liver releases VLDL which is mostly TG's and expresses Apo B100. 2) HDL gives VLDL Apo E & C 3) Insulin tells apidoctyes to express gene for lipoprotein lipase....Apo C activates it and takes FA's from VLDL. 4) HDL takes back Apo C. It can also take chol from IDL and convert to CE. 5) VLDL is now called IDL which has 2 fates: A) Go back to liver via Apo B100 B) Lose Apo E and become LDL |
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How do cells regulate cholesterol? |
3 ways 1) Stop expressing LDL receptors (the would bind to LDL's Apo B100 2) Use the enzyme ACAT to turn it's chol to CE's... this counts as a storage form 3) Stop making chol by decreasing HMG-Coa |
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What exactly makes LDL 'bad' ? |
1) Free radicals in the blood can take the free electrons from the Apo B-100 on LDL and now this is called oxided LDL 2) Now the entire Apo B-100 is defective so LDL can't enter cells anymore and also it is viewed as foreign to macro's 3) Macro's eat it via scavenger receptor SR-A. 4) Macro becomes and foam cell and dies and leads to calcification. And so LDL isn't bad....it's just the more of it you have the higher chance of it becoming oxidized. |
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What exactly makes HDL 'good' ? |
It picks up free/precipitated cholesterol and esterifies it. It then takes the cholesterol ester and either 1) gives it to IDL which will then become LDL or 2) give it back to the liver via 'reverse transport' by scavenger receptor B1. So it keeps chol moving and not sitting in a single place (where it can get calcified) |
