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 2

Dyslipidemias Causes Risk Factors Epidemiology Etiology

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


  • LDL (Low density lipoproteins) cholesterol is in­creased.
  • Combined Hyperlipidemia Increased LDL and triglycerides.


  • 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

Diet/sedentary lifestyle/obesity
Anabolic steroids
Beta-blockers, except those with intrinsic sympathomimetic activity
Chronic renal failure
Diabetes mellitus
Diuretics, except indapamide (Lozol)
Glycogen storage disorders
Nephrotic syndrome
Obstructive liver disease
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.


  • 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.


  • Are required for assembly and structure of lipo­proteins.
  • Activate enzymes for Lipoprotein metabolism. , Mediate binding of Lipoprotein to receptors.


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