Medical Pharmacology: Drugs Used in Treating Hyperlipidemia

Physiology and Pharmacology of Antilipidemic Drugs: Table of Contents
Introduction Definitions Hyperlipidemias--Clinical consequences Athersclerosis Acute pancreatitis Lipoprotein Classification Plasma proteins in atherogenesis Athersclerotic Plaques Components Factors promoting Development Properties High-density lipoproteins (HDL) and atherogenesis Cigarette smoking and CHD Hyperlipoproteinemia Pathophysiology Lipoprotein Metabolism: Normal Catabolism and Synthesis Chylomicrons VLDL LDL Lp(a) Lipoprotein HDL Lipoprotein disorders Overview Primary Hypertriglyceridemia Triglyceride elevation: mechanism Associated conditions Familial hypertriglyceridemia (severe) Familial hypertriglyceridemia (moderate) Familial combined hyperlipoproteinemia Familial lipoprotein lipase deficiency clinical presentation Familial Apoprotein CII Deficiency Familial dysbetalipoproteinemia Clinical presentation Treatment Primary Hypercholesterolemia Familial hypercholesterolemia Clinical manifestations (heterzygous) Clinical manifestations (homozygous) Mechanism Clinical management Familial Ligand-Defective Apolipoprotein B Mechanism Clinical consequence Treatment Familial Combined Hyperlipoproteinemia Lp(a) Hyperlipoproteinemia HDL Deficiency Genetic Factors Familial hypoalphalipoproteinemia Secondary Hyperlipoproteinemia Hypertriglyceridemia Hypercholesterolemia	Dietary Treatment For patients with elevated serum LDL For patients with elevated triglycerides Pharmacological Management of Hyperlipidemia Overview Niacin Overview Chemistry/Pharmacokinetics Mechanism of Action Clinical Use Toxicity Gemfibrozil Overview Pharmacokinetics Mechanism of Action Clinical Use Toxicity Bile acid Binding Resins Overview Chemistry/Pharmacokinetics Mechanism of Action Clinical Uses Toxicity HMG-CoA reductase Inhibitors Overview Chemistry/Pharmacokinetics Mechanism of Action Clinical Use Toxicity Drug Combinations Overview Gemfibrozil and Bile Acid-Binding Resin Reductase inhibitor and Binding Acid-Binding Resin Niacin and Bile Acid-Binding Resin Niacin and Reductase Inhibitor Combination of Resin, Niacin, and Reductase Inhibitor

**Atherosclerotic Plaques**

"The two morphologic components are: The fibrous cap which is sub-endothelial and contains lipid laden macrophages (foam cells), lymphocytes, and smooth muscle cells. The underlying atheroma "soft center", consisting of masses of lipid, cell debris and foam cells." Ó 1999 KUMC Pathology and the University of Kansas, used with permission; courtesy of Dr. James Fishback, Department of Pathology, University of Kansas Medical Center.

Atherosclerotic Plaques

"The two morphologic components are:
- The fibrous cap which is sub-endothelial and contains lipid laden macrophages (foam cells), lymphocytes, and smooth muscle cells.
- The underlying atheroma "soft center", consisting of masses of lipid, cell debris and foam cells."
- Ó 1999 KUMC Pathology and the University of Kansas, used with permission; courtesy of Dr. James Fishback, Department of Pathology, University of Kansas Medical Center.

**Red-brown thrombus is seen occluding the coronary artery**

"The red-brown thrombus is seen occluding the coronary artery. Thrombosis occurs with injury to the endothelium, for example, when an atherosclerotic plaque ruptures. This can occur at any time, even before the plaque has significantly occluded the coronary. Thrombosis, of course, will cause 100% occlusion, and can occur within a matter of seconds. Thrombosis is definitely linked to the onset of angina, as is often demonstrated in the cardiac catheterization lab." Ó 1999 KUMC Pathology and the University of Kansas, used with permission; courtesy of Dr. James Fishback, Department of Pathology, University of Kansas Medical Center.

Red-brown thrombus is seen occluding the coronary artery

"The red-brown thrombus is seen occluding the coronary artery.
Thrombosis occurs with injury to the endothelium, for example, when an atherosclerotic plaque ruptures.
This can occur at any time, even before the plaque has significantly occluded the coronary.
Thrombosis, of course, will cause 100% occlusion, and can occur within a matter of seconds.
Thrombosis is definitely linked to the onset of angina, as is often demonstrated in the cardiac catheterization lab."
- Ó 1999 KUMC Pathology and the University of Kansas, used with permission; courtesy of Dr. James Fishback, Department of Pathology, University of Kansas Medical Center.

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