Dyslipidaemias Flashcards

Flashcards on Dyslipidaemias

Major Lipids in Serum

The major lipids present in the serum are fatty acids, triglycerides, cholesterol, and phospholipids.

Lipids and Atherosclerosis

Elevated lipid concentrations, particularly cholesterol, are generally related to the pathogenesis of atherosclerosis.

Apolipoprotein AI

Apolipoprotein that activates LCAT; structural in HDL

Apolipoprotein AII

Apolipoprotein that inhibits hepatic triglyceride lipase (HTGL) at high concentration; structural in HDL

Apolipoprotein B100

Apolipoprotein that is structural (in LDL and VLDL) receptor binding

Apolipoprotein B48

Apolipoprotein that is structural in chylomicrons

Apolipoprotein CII

Apolipoprotein that is an activator of LPL

Apolipoprotein CIII

Apolipoprotein that inhibits LPL and clearance of chylomicrons and VLDL remnants

Apolipoprotein E

Apolipoprotein with binding to LDL and remnant receptors

Chylomicrons

Dietary lipids absorbed as monoglycerides, fatty acids, and cholesterol are assembled in the enterocyte with apo B48 to form…

Lipoprotein Lipase (LPL)

Hydrolyzes triglycerides and the fatty acids are taken up by peripheral tissues (mainly adipose tissue and muscle)

High-Density Lipoproteins (HDL)

Transports cholesterol from periphery to the liver.

LDL

Main carrier of cholesterol (loosely: “bad” cholesterol)

HDL

Carries cholesterol from non-hepatic tissues to liver (loosely: “good” cholesterol)

Chylomicron LP Function

Transport of dietary TG plus the cholesterol absorbed from gut

VLDL LP Function

Main carrier of endogenous TG

IDL LP Function

Remnant of TG-rich lipoproteins (CM and VLDL)

Primary Dyslipidaemias

Dyslipidaemias that occur as a result of a genetically determined disorder

Secondary Dyslipidaemias

Dyslipidaemias that occur as a result of an acquired condition

Familial Hypercholesterolaemia (FH)

Characterized by high cholesterol levels present from early in childhood and inherited as an autosomal dominant characteristic

Familial Defective apo B 100

Mutation in the apo B gene decreases the avidity of LDL for its receptor

Familial dysbetalipoproteinaemia

Clinically characterised by the presence of fat deposits in the palmar creases and tuberous xanthomata

The Framingham risk score

Used to determine LDL cholesterol treatment target, defines the risk for suffering any CVS event (MI, stroke, heart failure, TIA) in the next 10 yr without treatment

Calculated LDL

Formula to calculate LDL = Total Chol – (HDL chol + TG/2.2); when expressed in mmol/L. This formula is invalid if TG concentration > 4.5 mmol/L