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DYSLIPIDAEMIAS

Content
 Lipid metabolism
 Dyslipidaemias
 Laboratory measurement of lipids and lipoproteins
 Management of dyslipidaemias
Lipid Metabolism
 Lipids include (1) triglycerides, (2) phospholipids, (3) cholesterol and (4) a few others
of less importance.
 Chemically, the basic lipid moiety of the triglycerides and the phospholipids is fatty
acids, which are long-chain hydrocarbon organic acids.
 Cholesterol sterol nucleus is synthesized from portions of fatty acid molecules.
 The triglycerides are used in the body mainly to provide energy for the different
metabolic processes.
 Cholesterol, the phospholipids, and small amounts of triglycerides, are used to form
the membranes of all cells of the body and to perform other cellular functions.
Transport of Lipids in the Body Fluids

 Transport of Triglycerides and Other Lipids from the Gastrointestinal Tract by


Lymph—the Chylomicrons
 Removal of the Chylomicrons from the Blood
 “Free Fatty Acids” Are Transported in the Blood in Combination with Albumin
 Lipoproteins—Their Special Function in Transporting Cholesterol and Phospholipids
Lipoproteins

 Chylomicrons
 Very low density lipoproteins (VLDLs)
 Intermediate-density lipoproteins (IDLs)
 Low-density lipoproteins (LDLs)
 High-density lipoproteins (HDLs)
 Lipoprotein (a)
++++++++++++++++++++++++++++++++++++
++++++++++++++++++++++++++++++++++++
++++++++++++++++++++++
Lipoproteins
Transport of Lipids in the Body Fluids
Cholesterol
 Exogenous cholesterol & endogenous cholesterol
 Factors That Affect Plasma Cholesterol Concentration—Feedback Control of Body
Cholesterol.
1. An increase in the amount of cholesterol ingested each day increases the plasma
concentration slightly
2. A highly saturated fat diet increases blood cholesterol concentration 15 to 25 percent,
especially when this is associated with excess weight gain and obesity
3. Ingestion of fat containing highly unsaturated fatty acids usually depresses the blood
cholesterol concentration a slight to moderate amount.
4. Lack of insulin or thyroid hormone increases the blood cholesterol concentration, whereas
excess thyroid hormone decreases the concentration
5. Genetic disorders of cholesterol metabolism may greatly increase plasma cholesterol levels
DEVELOPMENT OF ATHEROSCLEROTIC
PLAQUE
A, Attachment of a monocyte to an adhesion molecule on
a damaged endothelial cell of an artery. The monocyte
then migrates through the endothelium into the intimal
layer of the arterial wall and is transformed into a
macrophage. The macrophage then ingests and oxidizes
lipoprotein molecules, becoming a macrophage foam
cell. The foam cells release substances that cause
inflammation and growth of the intimal layer.
B, Additional accumulation of macrophages and growth
of the intima cause the plaque to grow larger and
accumulate lipids. Eventually, the plaque could occlude
the vessel or rupture, causing the blood in the artery to
coagulate and form a thrombus.
Dyslipidaemias
 Lipid by itself and through interaction with other cardiovascular (CV) risk factors
may affect the development of atherosclerosis.
 Therefore, dyslipidaemias cover a broad spectrum of lipid abnormalities, some of
which are of great importance in CVD prevention. Dyslipidaemias may be related
to other diseases (secondary dyslipidaemias) or to the interaction between genetic
predisposition and environmental factors.
 Elevation of total cholesterol (TC) and low-density lipoprotein-cholesterol (LDL-
C) has received most attention.
 Abnormal lipoprotein metabolism is a major predisposing factor to
atherosclerosis. It is estimated that a dyslipidaemias is present in over 70% of
patients with premature CHD.
Cholesterol and atherosclerosis

 LDL-C is strongly associated with an increased risk of


atherosclerosis and CVD events.

1% decrease
in LDL-C
reduces CHD
risk by 1%
Laboratory measurement of lipids and
lipoproteins
 Baseline lipid evaluation: TC, TG, HDL-C, and LDL-C, calculated with the
Friedewald formula unless TG are elevated (> 4.5 mmol/L or greater than 400
mg/dL), non HDL-C, ApoB, Lp(a)
 Friedewald formula
in mmol/L: LDL-C = TC - HDL-C - TG/2.2;
in mg/dL: LDL-C = TC - HDL-C - TG/5.
 Fasting or non-fasting?
Clinical classification of dyslipidaemias:
Fredrickson
Secondary causes of dyslipidaemia
 Diabetes mellitus
 Cholestatic liver disease
 Nephrotic syndrome
 Chronic renal disease
 Hypothyroidism
 Obesity
 Cigarette smoking
 Excessive alcohol consumption
 Medications
Guideline
Management of dyslipidaemias

 Total cardiovascular risk estimation


 Primary prevention/ secondary prevention
 Treatment targets and goals
 Lifestyle modifications to improve the plasma lipid profile
 Drugs for treatment of dyslipidaemias
ĐỐI TƯỢNG NGUY CƠ CẦN TẦM SOÁT
RLLM VÀ BĐMDXV
ĐỐI TƯỢNG NGUY CƠ CẦN TẦM SOÁT
RLLM VÀ BĐMDXV
ƯỚC TÍNH NGUY CƠ TIM MẠCH
ƯỚC TÍNH NGUY CƠ TIM MẠCH
ƯỚC TÍNH NGUY CƠ TIM MẠCH CHO
NGƯỜI TRẺ < 40T
ƯỚC TÍNH NGUY CƠ BỆNH TIM MẠCH
CHO NGƯỜI LỚN TỪ ≥ 40T
ƯỚC TÍNH NGUY CƠ BỆNH TIM MẠCH
CHO NGƯỜI MẮC BỆNH ĐTĐ
PHÂN TẦNG NGUY CƠ TIM MẠCH

 Nguy cơ rất cao


 Nguy cơ cao
 Nguy cơ trung bình
 Nguy cơ thấp
Conclusion

 The effect of LDL-C on the risk of ASCVD appears to be determined by both


the absolute magnitude and the total duration of exposure to LDL-C.
 Total cardiovascular risk estimation for treatment targets

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