Chapter 20
ď ˝
Advances in the diagnosis of lipid disorders have helped to identify clients at greatest risk for CV disease and those most likely to benefit from pharmacologic intervention.
Hyperlipidemia –general term referring to high levels of lipids in the blood Is a major risk factor for CV disease Hypercholesterolemia— elevated blood cholesterol—ingestion of saturated fats
Triglycerids (neutral fats) ◦ Most common ◦ 3 fatty acids attached to glycerol ◦ Energy source
Phospholipds
◦ Phosphorous group replaces one of the fatty acids ◦ Essential to building plasma membrane ◦ Lecithins (found in egg yolk & soybeans)
Steroids ◦ Sterol nucleus or ring ◦ Natural vital component of plasma membrane ◦ Necessary for production of Vitamin D Bile acids Cortisol, estrogen, testosterone
◦ Body makes enough cholesterol ◦ Not necessary in diet
Lipids are carried through the blood as lipoproteins Lipid molecules do not mix with water Lipoproteins—protein carrier and mixture of cholesterol, triglycerides and phospholipids
Three most common lipoproteins:
Based on weight or density
1. High-density lipoproteins (HDL) ◦ 50% protein ◦ AKA good cholesterol
2. Low density lipoproteins (LDL) ◦ Highest amount of cholesterol ◦ AKA bad cholesterol
3. Very low density lipoproteins (VLDL) ◦ Triglyceride carrier
LDL transport cholesterol from liver to tissues and organs ◦ Created in liver ◦ Build plasma membranes and produce steroids ◦ Stored in tissues ◦ Contribute to plaque deposits and CAD
VLDL
◦ Changed to LDL in blood
HDL
◦ Packaged in tissues and other organs ◦ Cholesterol portion carried to liver
◦ Becomes part of bile and excreted in feces.
The ratio of LDL to
HDL is an important factor in predicting CV disease
Goal to maximize HDL and minimize LDL
Same as with CV disease plus Periodic blood cholesterol test
Reduce dietary saturated fats and cholesterol
Increase soluble fiber in diet.
Statins are drugs of first choice in reducing blood lipid levels—Table 20.2 pg. 355.
Inhibit HMG CoA reductase
Liver produces less cholesterol
More LDL receptors on liver cells
More LDL removed from blood
Blood levels of LDL and cholesterol reduced.
Remain on statins rest of life—effect not permanent DP Lipitor pg. 354
Binding bile acids and accelerating their excretion can reduce cholesterol and LDL Levels —Table 20.2 pg. 355. Bile acid resins bind cholesterol in the intestines so it can’t be reabsorbed Cholesterol eliminated in feces More frequent side effects than statins DP—Questran pg. 355
Nicotinic acid can reduce LDL levels but side effect limit its usefullness AKA niacin—water soluble B-complex vitamin High dosages needed to produce antilipidemic effects
Decrease VLDL levels and triglycerides
Increase HDL levels
More side effects than statins
Used in combination with a statin or bile binding agent.
Fibric acid agents lower triglyceride levels but have little effect on LDL levels
Replaced by the statins
Used in combination with statins
Reduce VLDL levels and increase HDL level
DP Lopid pg. 357