Article Contents ::
- 1 Dyslipidemias Causes Risk Factors Epidemiology Etiology
- 2 Dyslipidemias Risk Factors
- 3 Epidemiologyof Dyslipidemias
- 4 Hypercholesterolemia
- 5 hypertriglyceridemia
- 6 Morbidity and Mortality due to Dyslipidemias
- 7 Etiology of Dyslipidemias
- 8 Fat intake increases plasma levels of factor VII and VIla – thus increasing coagulability.
- 9 Lipoproteins
- 10 Physical Exam
- 11 Pregnancy Considerationsfor Dyslipidemias
- 12 Clinical Considerations for Dyslipidemias
- 13 Lipoproteins are essential for transport of :
- 14 Transport of cholesterol:
- 15 Apolipoproteins
Dyslipidemias Causes Risk Factors Epidemiology Etiology
- It initiates atherosclerosis. It causes plaque formation. Alters endothelial functions.
- It enhances coagulability of blood.
- major classes of lipids are Chylomicrons
- Very low density lipoproteins (VLDL) Intermediate density lipoproteins (IDL) Low density lipoproteins (LDL)
- High density lipoproteins (HDL).
- Serum cholesterol >200 mg/dL (5.18 mmol/L):
- Due mainly to lifestyle habits in Westernized countries; however, genetic and secondary causes should be considered.
Dyslipidemias Risk Factors
- Obesity (BMI >30 kg/m2)
- Physical inactivity
- Diet rich in saturated fat and cholesterol
- Heredity
Epidemiologyof Dyslipidemias
- Predominant age: Increases with age (female onset delayed by 10–15 years compared with males)
- Predominant sex: Male = Female
Hypercholesterolemia
- LDL (Low density lipoproteins) cholesterol is increased.
- Combined Hyperlipidemia Increased LDL and triglycerides.
hypertriglyceridemia
- increased Triglycerides.
- any blockages can be cleared or stabilized by Iowering drugs
- modification of serum lipid profile prevents and controls CAD.
- lipid levels are controlled, a patient of myocardial infarction does not develop reinfarction.
- ngina pectoris can be cured by lowering the lipids to normal.
Morbidity and Mortality due to Dyslipidemias
- number of deaths due to CAD and complications diabetes can be reduced by maintaining a normal lipid profile.
- morbidity due to CAD and diabetes is reduced the control of lipids by lifestyle changes and _ ugs.
- Lipoprotein subpopulations are commonly used to augment risk prediction, favoring the term dyslipidemia, which encompasses:
- High-density lipoprotein fraction of cholesterol (HDL): Atheroprotective
- Low-density lipoprotein (LDL): Atherogenic
- Triglycerides
- Reduction in plasma LDL cholesterol causes regression of coronary atherosclerosis.
Etiology of Dyslipidemias
Primary: |
Heredity |
Diet/sedentary lifestyle/obesity |
Secondary: |
Anabolic steroids |
Beta-blockers, except those with intrinsic sympathomimetic activity |
Chronic renal failure |
Cirrhosis |
Corticosteroids |
Diabetes mellitus |
Diuretics, except indapamide (Lozol) |
Estrogens |
Glycogen storage disorders |
Hypothyroidism |
Nephrotic syndrome |
Obstructive liver disease |
Progestins |
Retinoic acid derivatives |
Some immunosuppressants (e.g., cyclosporine |
Fat intake increases plasma levels of factor VII and VIla – thus increasing coagulability.
- By reducing dietary fat intake thrombogenic risk in CAD is reduced quickly.
- A single high fat meal can impair endothelial function and blood flow within 1 hour.
- A low fat diet improves blood flow and endothelial function.
Lipoproteins
- Proteins are large coml2.lexes that transport
- lipids through body flued
Physical Exam
- Few specific findings, most secondary to atherosclerotic disease
- Genetic familial hypercholesterolemia:
- Corneal arcus age <50 years
- Xanthomata
Pregnancy Considerationsfor Dyslipidemias
- Fetal nutritional demands may alter diet and drug treatment.
- Statins contraindicated in pregnancy – Class X
- Lactation: Possibly unsafe
Clinical Considerations for Dyslipidemias
- Though very low cholesterol readings have been associated with higher mortality (J-curve phenomenon),
- this epidemiologic finding is likely due to confounding disease processes associated with low cholesterol levels,
- such as cancer and liver disease, rather than a primary effect of low cholesterol itself. A lower limit of cardiovascular benefit has not been established.
Lipoproteins are essential for transport of :
- · Cholesterol
- · Triglycerides
- ·Fat soluble vitamins.
Transport of cholesterol:
- · Triglycerides, cholesterol and fat soluble vitamins are transported from liver to peripheral tissues.
- · Cholesterol is transported from peripheral tissues to liver.
Apolipoproteins
- Are required for assembly and structure of lipoproteins.
- Activate enzymes for Lipoprotein metabolism. , Mediate binding of Lipoprotein to receptors.