Download Antilipemics

Antilipemics
I. Link of cholesterol and CAD-coronary artery disease-Atherosclerotic plaque
II. Desired Levels
Cholesterol
Desired Levels Cholesterol is needed for steroid hormones, cell
membranes, bile acids
Total Cholesterol <160
Limit fat intake to < 30% of total calories
Limit cholesterol to < 300 mg/day
Good HDL level
F>45 M>55
Can be increased with exercise
Bad LDL level
CAD <100
No risks <160; 2 risk factors of CHD <130
Triglycerides
</=148
Used as fuel by liver to produce cholesterol
Form of fat and excess carbohydrates
Increases with DM, pancreatitis
III. HMG-CoA (Hydroxylmethylglutaryl-Coenzyme A) reductase inhibitors (-statins)
*most effective
A. AKA: Statins
B. MOA: decreases the rate of cholesterol production. Liver requires HMG-CoA to
produce cholesterol. Statins inhibit HMG-CoA. When less cholesterol is produced the
liver increases the recycling of LDL from the circulation. LDL needed for synthesis
of steroids, bile acids, and cell membranes. Metabolized by the liver. Excreted by the
kidneys.
C. Therapeutic uses: hyperlipidemia
D. SE and Adverse Effects: GI, rash, HA, myopathy and rhabdomyolysis;  LFTs;
dizziness, blurred vision, fatigue, insomnia, myalgias, skin rashes
E. Interactions: Statins don’t always play well with others! Digoxin (toxicity)
Warfarin ( effect); fibrinic acid or niacin ( risk of rhabdomylosis); macrolide
antibiotics; -azole antifungals; grapefruit juice; calcium channel blockers; protease
inhibitors (HIV, Hep. C); quinidine, amiodarone, cyclosporine.
F. Drug Profiles
 Lovastatin (Mevacor)
 Simvastatin (Zocor)
 Fluvastatin (Lescol
 Pravastatin (Pravachol)
 Atorvastatin (Lipitor)
F. Contraindications: liver dysfunction and bile acid sequestrants
II.
Bile Acid Sequestrants
A. MOA: bile acids needed for cholesterol; by binding to bile acids removal of LDL
from blood ’s.
B. Drug Effects: breakdowns cholesterol into bile acids and excreted in fecal matter.
C. Therapeutic uses: hyperlipoproteinemia
D. SE and Adverse Effects: GI: Constipation, Gas-take with meals
E. Interactions
1. Drugs should be take 1 hours before or 4-6 hours after dose
2.  absorption of fat-soluble vitamins ADEK
F. Drug Profiles
 Cholestyramine (Questran)
 Colestipol (Colestid)
 Colesevelam (WelChol)
V. Fibric acid derivatives
A. MOA: activate lipoprotein lipase which breaks down cholesterol, inhibits
triglyceride synthesis
B. Drug Effects:  triglyceride levels;  HDL;  LDL
C. SE and Adverse Effects: GI, GU, prolonged PT; LFT; dizziness, HA
D. Interactions: anticoagulants, HMG-CoA inhibitors
E. Drug Profiles
 Clofibrate (Atromid-S)
 Gemfibrozil (Lopid)
VI. Niacin; Vitamin B3
A. MOA: believed to inhibit lipolysis in adipose tissue, and increase lipase
B. Drug Effects:  LDL;  triglyceride levels;  HDL
C. Therapeutic uses: Vitamin supplement needed for bodily processes
D. SE and Adverse Effects: Flushing, pruritus, GI distress; vasodilation r/t
prostaglandins & histamine (can reduce this by taking NSAIDS and by taking with
meals).
E. Interactions: with HMG-CoA increase risk of myopathy; Anti-HTN/ B/P
F. Drug Profiles
 Niacin (Niacor, Nicolar)
 Immediate release (OTC, cheap)
 SR (Rx,  SE)
VII. Cholesterol absorption inhibitor
A. Ezetimibe (Zetia)
B. MOA: prevents cholesterol and related sterols from being absorbed in the small
intestine.
C. Therapeutic uses:  total cholesterol,  LDL,  triglycerides
D. Reserved to patients who do not respond to other drugs.