1. Chapter 3. lipids

Dyslipidemia

Disorder of plasma lipoprotein metabolism.

Common causes of dyslipidemia

Diet, obesity, physical inactivity, genetics, and secondary diseases.

Secondary causes of dyslipidemia

Diabetes mellitus, hypothyroidism, renal disease, cholestasis, and pregnancy.

Fredrickson classification

Classification of dyslipidemia by elevated lipoproteins, cholesterol, triglycerides, serum appearance, and atherogenicity.

Type I dyslipidemia

Increased chylomicrons, very high triglycerides, creamy layer, not directly atherogenic.

Type IIa dyslipidemia

Increased LDL, high cholesterol, strong atherogenicity.

Type IIb dyslipidemia

Increased LDL and VLDL, high cholesterol and triglycerides, strong atherogenicity.

Type III dyslipidemia

Increased IDL/remnants, high cholesterol and triglycerides, strong atherogenicity.

Type IV dyslipidemia

Increased VLDL, high triglycerides, mild atherogenicity.

Type V dyslipidemia

Increased VLDL and chylomicrons, very high triglycerides, mild atherogenicity.

Lipoprotein lipase deficiency

Autosomal recessive disorder causing severe hyperchylomicronemia and pancreatitis risk.

Apo C-II function

Activates lipoprotein lipase.

Apo C-II deficiency

Causes hyperchylomicronemia because lipoprotein lipase activation is impaired.

Dysbetalipoproteinemia

Caused by defective removal of chylomicron remnants and IDL.

Apo E2

Poor receptor binding, causing remnant accumulation.

Familial hypercholesterolemia

LDL receptor defect causing very high LDL and very high atherosclerosis risk.

Familial defective apo B-100

Reduced LDL receptor binding causing high LDL and increased atherogenic risk.

Hypoalphalipoproteinemia

Low HDL-cholesterol with increased atherosclerosis risk.

Atherosclerosis

Lipid accumulation in the arterial wall leading to fatty streaks, plaques, and possible plaque rupture.

Most important atherogenic lipoprotein

LDL.

Why is LDL atherogenic?

It enters the arterial wall, becomes oxidized, and is taken up by macrophages to form foam cells.

Foam cells

Macrophages filled with lipids from oxidized LDL.

Small dense LDL

Especially atherogenic because it is more easily oxidized.

Atherogenic lipid triad

High triglycerides, low HDL, and small dense LDL.

Remnant lipoproteins

Atherogenic lipoproteins such as chylomicron remnants and IDL.

HDL

Anti-atherogenic lipoprotein that helps remove cholesterol from tissues.

Why are chylomicrons not directly atherogenic?

They are too large to enter the subendothelial space.

Basic lipid profile

Total cholesterol, triglycerides, HDL-cholesterol, and LDL-cholesterol.

Why are total cholesterol and triglycerides alone insufficient?

They do not show the distribution between atherogenic LDL and protective HDL.

Total cholesterol target/reference value

4.1–5.2 mmol/L.

LDL-cholesterol target value

<2.6 mmol/L.

Triglyceride reference value

0.3–1.7 mmol/L.

HDL-cholesterol reference value

1.00–2.00 mmol/L.

Fasting before lipid profile

12–14 hours.

How often should lipid profile be checked in adults over 20?

At least once every 5 years.

Friedewald formula in mmol/L

LDL = total cholesterol − HDL − triglycerides/2.2.

Friedewald formula condition

Only valid if triglycerides are <4.0 mmol/L and chylomicrons are absent.

Apo A-I

Main protein of HDL and activator of LCAT.

Low Apo A-I

Indicates increased atherosclerosis risk.

Apo B-100

Main protein of LDL, IDL, and VLDL.

High Apo B-100

Indicates increased atherosclerosis risk.