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Dyslipidemia
Introduction
 Classes of lipids
 Cholesterol
 Triglycerides
 Phospholipids
 Plasma cholesterol and TG :Clinically important risk factors for
atherosclerosis.
 LIPOPROTIEN
 Poorly water soluble
 Absorbed from GIT
 Consist of hydrophobic core and less hydrophobic surface coat
 TYPES :
 Chylomicrons
 VLDL
 LDL
 HDL
Transport and storage of lipids
1. Exogenous (dietary ) lipid pathway
2. Endogenous pathway
3. Reverse cholesterol transport
Exogenous lipid pathway
Small intestine
Blood circulation
Fatty acids
Dietary lipids
Chylomicrons
Energy
production
Stored as TG
Endogenous pathway
 Fasting : liver is the source of plasma lipids
 TGs and Cholesterol ester : synthesised by liver and secreted as VLDL
 VLDL > hydrolysis by LPL > fatty acids to tissues + IDL
 IDL converted to LDL by hepatic lipase
 LDL : atherogenic lipo protein
 Regulation of plasma LDL concentration: Receptor mediated endocytosis in
cells or liver
 Supply of cholesterol through this pathway downregulates further expression
of LDL receptor gene > Decreases synthesis and activity of HMG CoA reductase
 This negative feedback loop along with modulation of cholesterol
esterification controls the intracellular free cholesterol level.
Reverse cholesterol transport
 Process in which cholesterol is removed from the peripheral tissues and
returned to liver.
 HDL are the main lipoprotein along with lipid poor Apo A1 are involved in this
process.
 HDL produced in liver and catabolized in intestine
 HDL able to accept more free cholesterol from atherogenic lipoproteins and
peripheral tissues to the liver
 A circulating enzyme called LCAT (lecithin cholesterol acyltransferase)
esterifies these HDL.
Dyslipidemia
 Dyslipidemia refers to levels that are either higher or lower.than the normal range of blood
fats.Among these hyperlipidemia is most commonest cause.
 Characterised by an abnormalities in the lipid profile,consisting of a variety
of disorders with raised total cholesterol, LDL or TG or conversely ,lower
levels of HDL
Classification and causes
 Primary hyperlipidemia : Genetic disorder of lipid metabolism
,characterised by genetic mutation which causes impaired clearance of LDL
from the circulation due to absence of LDL receptors.
Eg : familial hypercholesterolemia.
 Secondary hyperlipidemia : hyperlipidemia secondary to a disease /
disorder other than genetic defect.
Dyslipidemia symptoms
 Dyslipidemia doesn't have symptoms at all, but it can cause othersymptomatic
vascular disease, like coronary artery disease.
 Eyelid xanthelasmas, tendinous xanthomas at the elbow, kneetendons and
Achilles and arcus cornea are caused by high levels ofLDL.
 Acute pancreatitis is caused by high levels of TGs.Patients that have familial
hypercholesterolemia in homozygous formcan have the above findings with
planar xanthomas.
 Patients that have elevation of TGs in severe condition can expect having
eruptivexanthomas over their elbow, back, trunks, knees, buttocks, feet and
hands.
 Those with rare dysbetalipoproteinemia can expect having palmar xanthomas
and tuberous xanthomas.
 Retinal arteries and veins can have a creamy white appearance dueto the
severe hypertriglyceridemia. You can also have a milkyappearance in your
blood plasma when you have high lipid levels.You can expect symptoms like
paresthesias, confusion and dypsnea.
Thank you

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Dyslipidemia-1.pptx

  • 2. Introduction  Classes of lipids  Cholesterol  Triglycerides  Phospholipids  Plasma cholesterol and TG :Clinically important risk factors for atherosclerosis.  LIPOPROTIEN  Poorly water soluble  Absorbed from GIT  Consist of hydrophobic core and less hydrophobic surface coat  TYPES :  Chylomicrons  VLDL  LDL  HDL
  • 3. Transport and storage of lipids 1. Exogenous (dietary ) lipid pathway 2. Endogenous pathway 3. Reverse cholesterol transport
  • 4. Exogenous lipid pathway Small intestine Blood circulation Fatty acids Dietary lipids Chylomicrons Energy production Stored as TG
  • 5. Endogenous pathway  Fasting : liver is the source of plasma lipids  TGs and Cholesterol ester : synthesised by liver and secreted as VLDL  VLDL > hydrolysis by LPL > fatty acids to tissues + IDL  IDL converted to LDL by hepatic lipase  LDL : atherogenic lipo protein  Regulation of plasma LDL concentration: Receptor mediated endocytosis in cells or liver  Supply of cholesterol through this pathway downregulates further expression of LDL receptor gene > Decreases synthesis and activity of HMG CoA reductase  This negative feedback loop along with modulation of cholesterol esterification controls the intracellular free cholesterol level.
  • 6. Reverse cholesterol transport  Process in which cholesterol is removed from the peripheral tissues and returned to liver.  HDL are the main lipoprotein along with lipid poor Apo A1 are involved in this process.  HDL produced in liver and catabolized in intestine  HDL able to accept more free cholesterol from atherogenic lipoproteins and peripheral tissues to the liver  A circulating enzyme called LCAT (lecithin cholesterol acyltransferase) esterifies these HDL.
  • 7. Dyslipidemia  Dyslipidemia refers to levels that are either higher or lower.than the normal range of blood fats.Among these hyperlipidemia is most commonest cause.  Characterised by an abnormalities in the lipid profile,consisting of a variety of disorders with raised total cholesterol, LDL or TG or conversely ,lower levels of HDL
  • 8. Classification and causes  Primary hyperlipidemia : Genetic disorder of lipid metabolism ,characterised by genetic mutation which causes impaired clearance of LDL from the circulation due to absence of LDL receptors. Eg : familial hypercholesterolemia.  Secondary hyperlipidemia : hyperlipidemia secondary to a disease / disorder other than genetic defect.
  • 9.
  • 10. Dyslipidemia symptoms  Dyslipidemia doesn't have symptoms at all, but it can cause othersymptomatic vascular disease, like coronary artery disease.  Eyelid xanthelasmas, tendinous xanthomas at the elbow, kneetendons and Achilles and arcus cornea are caused by high levels ofLDL.  Acute pancreatitis is caused by high levels of TGs.Patients that have familial hypercholesterolemia in homozygous formcan have the above findings with planar xanthomas.  Patients that have elevation of TGs in severe condition can expect having eruptivexanthomas over their elbow, back, trunks, knees, buttocks, feet and hands.  Those with rare dysbetalipoproteinemia can expect having palmar xanthomas and tuberous xanthomas.  Retinal arteries and veins can have a creamy white appearance dueto the severe hypertriglyceridemia. You can also have a milkyappearance in your blood plasma when you have high lipid levels.You can expect symptoms like paresthesias, confusion and dypsnea.
  • 11.
  • 12.