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30 Cards in this Set
- Front
- Back
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Lipoproteins
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Have a central core of lipids (triglycerides and cholesterol esters)
Outer case of phospholipids, free cholesterol and proteins (apoproteins) |
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Classes of Lipoproteins
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Chylomicrons, VLDL, IDL, LDL, HDL
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Chylomicrons
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Large diameter
Contain mostly triglycerides from dietary lipids |
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VLDLs
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smaller diameter
Rich in endogenous triglycerides |
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IDLs
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have cholesterol and triglycerides
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LDLs
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carry most of plasma cholesterol
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HDLs
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very small in size
very little cholesterol Rich in apoproteins |
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Hyperlipidemia
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&uarr plasma lipids in general
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Hypercholesterolemia
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&uarr plsma cholesterol, indicated by &uarr in LDL
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Hypertriglyceridemia (Hyperlipemia)
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&uarr triglycerides, indicated by &uarr VLDL
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Mixed Hyperlipidemia
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&uarr cholesterol and &uarr triglycerides (LDL and VLDL)
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&uarr Risk Coronary Artery Disease
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High LDL cholesterol
Low HDL cholesterol Hypertriglyceridemia (&uarr VLDL) |
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Desirable Plasma Cholesterol Levels
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Total = <200
LDL = <130 |
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Borderline-High Plasma Cholesterol level
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Total = 200-239
LDL = 130-159 |
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High Plasma Cholesterol levels
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Total = > 240
LDL = >160 |
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HDL (High Density Lipoproteins)
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HDL contain protiens and a little cholesterol
HDL is secreted into plasma by various tissues In plasma, HDL acquire cholesterol Cholesterol removal from arterial cells may be responsible for antiatherogenic effect of HDL |
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Lipid Lowering Drugs
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1. HMG-CoA reductase inhibitors (Statins)
2. Niacin (Nicotinic Acid) 3. Fibric acid derivatives 4. Bile acid binding agents 5. Inhibitors of intestinal sterol absorption |
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HMG-CoA Inhibitors (Statins)
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Lovastatin
Atrovastin Pravastatin Fluvastatin Simvastatin Rosuvastatin |
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Where is cholesterol synthesized?
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In the Liver
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HMG-CoA Reductase Inhibitors
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Reduce cholesterol synthesis by inhibition of HMG-CoA reductase
First-pass hepatic extraction Most effective in reducing LDL |
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HMG-CoA Reductase Inhibitors
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&uarr LDL receptors = &uarr extraction of LDL by the liver and &darr LDL in plasma
&darr triglycerides (VLDL) &uarr HDL |
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Use for HMG-CoA Reductase Inhibitors
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Hypercholesterolemia (&uarr LDL)
Mixed Hyperlipidemia (&uarr LDL and &uarr VLDL) First line of txt post MI |
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HMG-CoA Reductase Inhibitors: Adverse Effects
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Hepatitis (&uarr hepatic enzymes such as serum amino transferase)
Myalgia (Myositis) To be discontinued if serum levels of creatine phophokinase are elevated or if myopathy (rhabdomyolysis and myoglobinuria) occurs |
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Niacin (Nicotinic Acid)
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&darr VLDL secretion from liver = &darr production of LDL
Inhibits lipolysis in adipose tissue = &darr FFA supply to liver and VLDL synthesis &darr catabolism of HDL &uarr plasma HDL Useful in Mixed Hyperlipidemia (favorable effects on LDL, VLDL, HDL) |
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Niacin: Adverse Effects
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Useful only in large doses, which produce vasodilation and cause skin flushing, pruritis
These effects can be reduced by pre-txt with Aspirin Tachyphylaxis to skin flushing usually occurs within a few days of txt with Niacin &uarr serum transaminase level, gastric distress, glucose intolerance, hyperuricemia |
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Fibric Acid Derivatives
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Gemfibrozil
Fenofibrate Clofibrate |
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Fibrica Acid Derivatives: Pharmacology
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&darr triglycerides (VLDL) by stimulation of LPL (hydrolysis of VLDL), promote delivery of FFA to adipose tissues
May &darr VLDL synthesis in liver Variable effects on LDL, may &uarr HDL |
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Fibric Acid Derivatives: Use
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Hypertriglyceridemia (&uarr VLDL)
May be used in Mixed Hyperlipidemia Best drug to &darr triglycerides |
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Fibric Acid Derivatives: Adverse Effects
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Allergic rxn, myalgia, blood cell deficiencies, hypokalemia, &uarr serum aminotransferase
Risk of myopathy increases when used with HMG-CoA Reductase Inhibitor Contraindicated in hepatic or renal dysfunction &uarr effects of warfarin (binding to plasma proteins) |
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Bile Acid Binding Agents
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Colestipol
Cholestyramine Colesevelam Moderately effective for &darr cholesterol |
