Term
| the endothelium controls...? |
|
Definition
| transfer of molecules, platelet agregation, blood clotting, blood flow, immune and inflammatory reactions, and vascular resistance. |
|
|
Term
| what can cause endothelial dysfunction? |
|
Definition
| cytokines, inflammation, blood stressors, hypoxia, and atherosclerosis |
|
|
Term
| what do dysfuctional enthothelial cells produce? |
|
Definition
| they produce other cytokines, growth factors, forms of pro/anti coagulant |
|
|
Term
| what can be classified as lipids? |
|
Definition
| triglycerides, phospholipids, cholesterol. |
|
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Term
|
Definition
| used for energy metabolism. 3 fatty acids with a glycerol molecule. |
|
|
Term
| what is an important structure of the lipoproteins? |
|
Definition
|
|
Term
| phosphate can be found in? |
|
Definition
| the myelin sheath, cell membranes, blood clotting components, and lipoproteins |
|
|
Term
|
Definition
| elevated levels of blood cholesterol |
|
|
Term
| cholesterol and triglyceride are insoluble in plasma. what are they encapsulized in? |
|
Definition
| a stabilizing coat of water soluble phospholipids and proteins called apoproteins |
|
|
Term
|
Definition
| transport cholesterol and triglycerides to various tissues for energy, lipid depositation, steroid production, and bile acid formation. |
|
|
Term
|
Definition
| very low density lipoprotein. they carry large amounts of triglycerides that have a lower density than cholesterol. |
|
|
Term
| what is the lipoproteins hydrophic core composed of? |
|
Definition
| esters, triglycerides, cholesterol, and phospholipids |
|
|
Term
|
Definition
| control the interactions and ultimat fate of the lipoproteins. |
|
|
Term
| what do recent studies indicate that apoproteins can accelerate when they don't work? |
|
Definition
| athersclerosis and hyperlipidemia. |
|
|
Term
| what is the major apoprotein in LDL? |
|
Definition
|
|
Term
| what is the major apoprotein of HDL? |
|
Definition
|
|
Term
| where are lipoproteins synthesized? |
|
Definition
| the liver and the small intestine. |
|
|
Term
| where are cylomicrons synthesized? |
|
Definition
| the wall of the small intestine |
|
|
Term
|
Definition
| they transport dietary triglycerides and cholesterol from the GI tract. |
|
|
Term
| Where do the clylomicrons transport the triglycerides to? |
|
Definition
| to the cells of adipose and skeletal muscle tissue |
|
|
Term
| the liver realeases and synthesizes...? |
|
Definition
|
|
Term
|
Definition
| the bodies main source of energy during prolonged fasting |
|
|
Term
| what takes LDL out of the blood circulation? |
|
Definition
| LDL receptors or monocytes and macrophages. |
|
|
Term
| How are LDL's metabolized? |
|
Definition
| the liver will engulf them and put them into a vessicle to be killed. |
|
|
Term
|
Definition
| low in cholesterol and rich in surface phosopholipids. |
|
|
Term
|
Definition
| is reduced LDLS ability to oxidize. |
|
|
Term
| an increase in lipproteins will cause...? |
|
Definition
| an increase in serum cholesterol levels. |
|
|
Term
|
Definition
| 2 types. primary and secondary |
|
|
Term
| primary hypercholesterolemia |
|
Definition
| most have a genetic base which leads to a defective apoprotein synthesis. |
|
|
Term
| secondary hypercholesterolemia |
|
Definition
| obesity and high caloric diets and diabetes mellitus. |
|
|
Term
|
Definition
| 25 percent protein. 50 percent cholesterol |
|
|
Term
|
Definition
|
|
Term
| lesion progression of atherosclerosis |
|
Definition
| endothelial injury, fatty streaks, fibrotic plaques, and a complicated lesion |
|
|
Term
| endothelial injury causes |
|
Definition
| cytokine release, macrophages adhering and releasing enzymes that futhur injure. smooth muscle proliferation |
|
|
Term
| what are the major complications of atherosclerosis? |
|
Definition
| ischemic heart disease, stroke, and peripheral vascular disease |
|
|
Term
| what is the major risk factor of atheosclerosis? |
|
Definition
|
|
Term
|
Definition
| the components of smoking can be toxic and cause oxidative stress and damage |
|
|
Term
|
Definition
| a major risk factor marker. it indicates inflammation, elevated levels can mean vascular disease. |
|
|
Term
|
Definition
| inhibites the anticoagulation cascade. causes endothelial damage and speeds up atherosclerosis |
|
|
Term
|
Definition
| macrophages and smooth muscle cells that accumilate under the intima lining |
|
|
Term
|
Definition
| composed of macrophages and smooth muscle cells that are full of lipids. |
|
|
Term
| fibrous atheromatous plaque |
|
Definition
| the basic lesion of clinical atherosclerosis. formational of scar tissue and calcification. |
|
|
Term
|
Definition
| the most important complication of atherosclerosis. caused by slowing of blood |
|
|
Term
| what can a thrombus cause? |
|
Definition
| it can cause occlusion of the heart and the brain |
|
|
Term
| what is thought to be the first cause of atherosclerosis? |
|
Definition
|
|
Term
| once the macrophages have migrated and attached to the lumen what happens? |
|
Definition
| they release free radicals which causes damage and the platelets will begin to clot |
|
|
Term
| what do the free radicals cause? |
|
Definition
| it causes the LDL to oxidize. this is toxic. |
|
|
Term
|
Definition
| lipids that become the core to an unstable lesion that can break off. |
|
|
Term
|
Definition
| causes a rupture whcih causes furthur damage |
|
|
Term
|
Definition
| over 30 percent over your body weight |
|
|
Term
| t or f: dabetics have to worry about beign more suceptable to atherosclerosis? |
|
Definition
|
|
Term
|
Definition
|
|
Term
| endothelial cell injury involves? |
|
Definition
| damage to the endothelium and adhesions of monocytes and platelets. |
|
|
Term
| the migration of inflammatory cells involve? |
|
Definition
| the begining of atherosclerotic lesions. monocytes etc migrate through the endothelial cells and transform into macrophages. |
|
|
Term
| lipid accumilation and smooth muscle proliferation involves |
|
Definition
| the activated macrophages release toxic oxygen species that oxidize LDL. they then ingest the LDL and become foam cells. they release growth factors. |
|
|
Term
| plaque structures are full of? |
|
Definition
| SMC's, macrophages, ECM, leukocytes, intracellular lipids. |
|
|
Term
| what the fibrous cap composed of? |
|
Definition
| smooth muscle cells and dense ECM |
|
|
Term
| the shoulder of plaque is composed of? |
|
Definition
| macrophages, SMC's, and lymphocytes |
|
|
Term
| what is bellow the fibrous cap? |
|
Definition
| a central core of lipid laden foam cells and fatty debris. |
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