Hyperlipidemias Flashcards
(26 cards)
Name the HMG COA Reductase Inhibitors
End in -statin
Name the Fibrates
Gemfibrozil
Fenofibrate
Name the Bile Acid Sequestrants
Cholestyramine
Colesevelam
Colestipol
Name the Cholesterol Absorption Inhibitors
Ezetimibe
Niacin
Used to decrease hyperlipidemia
Name the Omega 3 Fatty Acids
Docosahexaenoic Acid
Eicosapentaenioc Acid
Hyperlipidemia
Elevation in lipoproteins
5 types of lipoproteins
Chylomicrons VLDL LDL IDL HDL
Lipoproteins
Transport cholesterol and triglycerides because they can’t dissolve in blood.
Chylomicrons
Transport dietary lipids (cholesterol and triglycerides) from intestine to liver.
Can deposit triglycerides in organs and body as travels to liver.
VLDLs
Made in liver and transport triglycerides (TG) to tissues.
Once TG are removed and it’s only Cholesterol, becomes LDL
LDLs
Transports cholesterol (C) to tissues Deposits C in artery wall forming an atheroma. (Atherosclerosis) Return to liver after done circulating
HDLs
Made by liver and intestine
Picks up cholesterol in body and takes it to the liver
Cleans up atheromas
Results of Hyperlipidemia
Acute Pancreatitis
Atherosclerosis
-Leading cause of death for males and females in US
-Correlated with high LDL and low HDL
-High cholesterol can be caused by lifestyle AND genetics
Type 1 (Familial Hyperchylomicronemia)
Increased chylomicron level
No effective drug tx
Only diet therapy
Treatment goals for hyperlipidemia
Less than 200 Total Cholesterol
Less than 130 LDL
Greater than 60 HDl
Treatment options for hypercholesterolemia
If moderate hyperlipidemia: changes in diet, exercise and weight reduction
LDL>160 plus additional risk factor: Drug therapy
If 2 or more risk factors, tx is aggressive. May need to get LDL as low as 70.
Treatment options for hypertriacylglycerolemia
Diet and exercise
Niacin and fibrates are most effective drugs to decrease triglyceride levels
MOA of HMG CoA Reductase Inhibitors
Analog of HMG
Competes for the HMG CoA reductase, inhibiting cholesterol synthesis.
Lower cholesterol levels in liver causes an increase in LDL receptors to take in more LDL from blood
Prevents release of VLDL
MOA of Niacin (Nictotinic acid)
Increases HDL levels
Inhibits lipolysis in adipose tissues (reduces circulating triglycerides)
Increases secretion of tissues plasminogen activator and decreases plasma fibrinogen levels (helps reverse endothelial damage and platelet cascade)
Fibrates
Increases genetic expression of lipoproteins.
Results in lowered trigylceride (TG) concentration and increased HDL levels
Used to treat high TG levels
MOA of Bile Acid Sequestrates
Bile Acid-Binding Resins
Binds to bile in the intestines and prevents from being reabsorbed. (The liver needs cholesterol to make bile)
Since it can’t recycle the bile, it uses more cholesterol to make more. LDL receptors are increased and cholesterol is taken in from the plasma. Doesn’t work if homozygous for type IIA (familial hypercholesterolemia) since no LDL receptors
Cholesterol Absorption Inhibitor
Ezetimibe
Inhibits absorption of cholesterol from diet.
Liver will use stores, produce C and take up from blood.
Very long half life (22 hours) so can’t use if liver problems
Therapeutic Uses and Adverse Effects of HMG CoA Reductase Inhibitor
Not as effective for those homozygous for familial hypercholesterolemia since they don’t have LDL receptors
Excreted by bile and feces so kidney issues aren’t a problem. Adverse Effects:
Dissolution of muscle (rare)
Can’t use for pregnant, kids or teens