DEFINITION

Hyperlipidemia is abnormally elevated levels of any or all lipid or lipoprotein in the

blood. It is the most common form of dyslipidemia (which includes any
abnormal lipid levels).
Or Elevation of measured serum lipid components:
- Total cholesterol
- LDL cholesterol
Friedewald formula is LDL = total cholesterol - HDL - (triglycerides/5)
- Triglycerides (TGs)
- low HDL
The main types of lipid : Cholesterols functions: it plays a role in the structure of cell
membranes, in the synthesis of steroid hormones, and in the formation of bile
acids, Triglycerides functions of are energy storage (in fat) and energy use (by
muscle)..
Lipoprotein is lipid that binds to certain protein in order to dissolve in blood.
Because lipid is water-insoluble molecule. The main types of lipoprotein :
Chylomicron, VLDL, LDL, HDL.
Apolipoprotein (Apos) is proteins that bind to and help solubilize hydrophobic lipids
in the blood. It locates on the surface of lipoprotein.
Apolipoproteins- Protein constituents of lipoproteins that add structural stability;
may help mediate catabolism.
Lipid catabolism - 70% LDL removed in liver by LDL receptors.
Chylomicrons transport lipids absorbed from the intestine to adipose, cardiac, and
skeletal muscle tissue exogenously, where their triglyceride components are
hydrolyzed by the activity of the lipoprotein lipase, allowing the released free fatty
acids to be absorbed by the tissues. When a large portion of the triacylglycerol
core have been hydrolyzed, chylomicron remnants are formed and are taken up by
the liver, hereby transferring dietary fat also the liver.
VLDL/Very Low Density Lipoprotein transport lipids absorbed from the intestine
to adipose, cardiac, and skeletal muscle tissue endogenously. They contain higher
triglyceride than cholesterol. In blood circulation, VLDL will contact with
lipoprotein lipase, allowing the released free fatty acids to be absorbed by the
tissues. The composition of the molecule changes, it becomes IDL (intermediate
Density Lipoprotein) and are taken up by the liver. IDL will become LDL because
they contain a large amount of cholesterol.
LDL /Low Density Lipoprotein is often referred
to as “bad cholesterol”. LDL is taken into a cell
via the LDL receptor via endocytosis then
cholesteryl ester is hydrolyzed into FFA (Free
Fatty Acid) to cell membrane synthesis or
converted into other products such as steroid
hormones or bile acids.

HDL /High Density Lipoprotein is

often referred to as “good
cholesterol” . HDL picks up excess
cholesterol in blood and take it
back to liver where is broken down
and removed from body.
 Cholesterol Biosynthesis
• Liver and intestines - major sources of
endogenously derived cholesterol.
• Diet - exogenously derived cholesterol.
• In liver- rate limiting step is converting
HMG CoA to mevalonic acid by HMG CoA
Reductase (role of “STATINS”).
• Increase intake in dietary cholesterol - down
regulation of LDL receptors  subsequent
elevation of serum LDL cholesterol.

5
 CLASSIFICATION

Primary (Familial)
Fredrickson-Levy-Lees Classification of Hyperlipoproteinemia
Secondary (acquired)
RISK FACTORS
SIGN & SYMPTOM
DIAGNOSIS
 TREATMENT

Non-Pharmacologic therapy

Therapeutic Lifestyle Changes (TLC)

• Diet control eg. High antioxidant, high fiber fruits vegetables, low-cholsterol
saturated fat& trans fats diet
• Weight reduction
• Regularly exercise
• Smoking cessation
• Decrease sodium intake
• control of risk factors eg. DM, HTN, renal disease, obesity, etc.
• Stop drinking alcohol
• Avoid drugs that can increase plasma lipids ; contraceptive pills, b-blockers,
thiazide, corticosteroids
Pharmacologic therapy

Drug Class Agents Effects (% change) Side Effects

HMG CoA reductase Lovastatin LDL (18-55), HDL (5- Myopathy, increased liver
inhibitors Pravastatin 15) enzymes
Rosuvastatin (Crestor)  Triglycerides (7-30)
Simvastatin (Zocor)
Cholesterol Ezetimibe  LDL( 14-18),  HDL Headache, GI distress
absorption inhibitor (1-3)
Triglyceride (2)
Nicotinic Acid niacin LDL (15-30),  HDL Flushing, Hyperglycemia,
(15-35) Hyperuricemia, GI distress,
 Triglyceride (20-50) hepatotoxicity
Fibric Acids Gemfibrozil LDL (5-20), HDL (10- Dyspepsia, gallstones,
Fenofibrate 20) myopathy
Triglyceride (20-50)

Bile Acid Cholestyramine  LDL GI distress, constipation,

sequestrants Resins  HDL decreased absorption of
Colesevelam No change in other drugs
Colestipol triglycerides
Guarrem