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35 Cards in this Set
- Front
- Back
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Dyslipidaemia pathological levels of ________ that predispose to ____________. |
lipoproteins cardiovascular disease |
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Lipoproteins (complexes of lipid and protein) transport ? |
lipids and cholesterol in the blood stream |
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Lipoproteins are classified according to their density on _________. |
ultracentrifugation |
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The classifications of lipoproteins are |
HDL LDL VLDL Chylomicrons |
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Increased risk of cardiovascular disease linked to increased levels of ___ and decreased levels of ____ (anti-atherogenic) |
LDL HDL |
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Cholesterol transport and sites of action of lipid lowering drugs Statins decrease sythesis of C |
Statins |
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Cholesterol transport and sites of action of lipid lowering drugs _____,_____,_____ increase uptake |
Statins, resins, fibrates |
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Cholesterol transport and sites of action of lipid lowering drugs _________ decrease secretion |
Fibrates |
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Cholesterol transport and sites of action of lipid lowering drugs _______ bind to bile acids to eliminate faecally |
Resins |
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Cholesterol transport and sites of action of lipid lowering drugs _________ enhance lipoprotein lipase |
Fibrates |
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Endothelial cells bind LDL and if injured, release ________, which oxidise LDL to form __________ that destroy the receptors needed for ______________. |
free radicals lipid peroxides receptor-mediated clearance of LDL |
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modified LDL is taken up by ________ which migrate under the endothelium and form fatty streaks which are the beginnings of _________. |
macrophages atherosclerosis |
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Platelets, macrophages and endothelial cells release _______ and __________, which result in proliferation of __________,___________ and _________. |
cytokines growth factors smooth muscle cells, connective tissue and inflammatory changes |
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Atherosclerotic plaque if ruptured can form a ___________. |
thrombosis |
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LDL-cholesterol has a relationship with _________. |
atherosclerosis |
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_____ help to sequester cholesterol and preventits deposition in tissues |
HDL |
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Chylomicrons drug treatment |
none |
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LDL drug treatment |
HMG-CoA reductase +/- resins |
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LDL + VLDL treatment |
Fibrates, HMG-CoA reductase inhibitor, nicotinic acid |
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BVLDL treatment |
Fibrates |
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VLDL treatment |
Fibrates |
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Chylomicrons + VLDL treatment |
none |
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Lipid lowering drugs include |
Bile acid sequestrants Fibric acid derivatives Statins |
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Bile acid sequestrants include |
Cholestyramine Colestipol |
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Bile acid sequestrants mechanism? |
Promote bile acid excretionand increase LDL receptors in liver |
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Nicotinic acid mechanism |
Decreases VLDL and LDL synthesis |
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Fibric acid derivatives include |
Gemfibrozil |
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Fibric acid derivative mechanism? |
Stimulate lipoprotein lipase Reduce secretion of VLDLs Increase LDL receptors in liver |
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Statins include |
Atorvastatin Pravastatin Simvastatin |
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Statin mechanism ? |
HMG-CoA reductase inhibitors Reduce cholesterol Synthesis Upregulate LDL receptors in liver |
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Statins target ____________________? |
HMG-CoA reductase |
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Statins inhibit the conversion of ______ to _________, a rate-limiting step in the synthesis of cholesterol in the _______ and _______ (the two main sites for production of cholesterol in the body). |
HMG-CoA (3-hydroxy-3-methylglutaryl) mevalonic acid liver and intestines |
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Statins are __________, _____________ inhibitors of ____________. |
reversible competitive HMG-CoA reductase |
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Statins lower blood cholesterol levels by ? |
inhibiting liver cholesterogenesis |
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Statins increase ???? and, hence, increase clearance of LDL |
expression / synthesis of LDL receptors |
