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Dyslipidemia
Introduction
 Cardiovascular dse affects >70 mil Americans
- underlying dse largely preventable
 Increasingly aggressive approach in the treatment of
cholesterol
- NCEP ATP III guidelines
Epidemiology
 Total cholesterol & LDL Cholesterol increase
throughout life
- Atherogenic pattern characteristic of Western
society diets
 More than 50% of American adults 20y of age or older
have elevated total cholesterol
- 1/3 are aware of it
 Dyslipidemia  (aka hyperlipidemia, aka
hypercholesterolemia) is a disorder of elevated or
abnormal levels of lipids and/or lipoproteins in the
blood, characterized by high cholesterol, triglycerides
(TGs) or both, or low HDL levels.
- a complex disease caused by the interplay of
genetic, dietary and physiologic factors
- LDL  130mg/dl (borderline high or higher)
Diagnosis - by using fasting lipoprotein profiles and
measuring plasma levels (total cholesterol, TGs,
Lipoproteins)
Classification of Dyslipidemia
 Phenotype. Dyslipidemia is present in the body. You
can easily see that the type of lipid that has been
increased.
 Etiology. This classification tackles more on the reason
why the condition has happened. The reasons may
include genetic or secondary to another conditions.
LIPID METABOLISM (Normal Physiology)
Dyslipidemia
Dyslipidemia Cause
 Primary Causes. (Familial) Overproduction and defective
clearance of the cholesterols TG and LDL is the result of the
mutations of single or multiple genes. The primary disorders
are the common dyslipidemia causes to the children,
although it may not affect in the most cases of adult
dyslipidemia.
 Secondary Causes. Adults are the most affected ones
when it comes to secondary causes. The causes contribute
a lot on how an adult will be affected with dyslipidemia. The
sedentary lifestyle is the most essential secondary cause.
The lifestyle includes excessive dietary intake of cholesterol,
trans fats and saturated fats. Trans fats are the fatty acids
that are either polyunsaturated or monounsaturated, in
which there are added hydrogen atoms. Trans fats are
usually used in a lot of processed foods.
Other secondary causes are:
 Alcohol overuse Cigarette smoking
 Inactivity
 Diabetes mellitus
 Hypertension & Obesity
 Chronic kidney disease
 Hypothyroidism, Liver disease
 Low HDL < 40mg/dl
 Age and Gender ( Men >45yo, Women >55yo )
 Other cholestatic liver diseases and primary biliary cirrhosis.
 Drugs like thiazides, retinoids, estrogens and glucocorticoids,
among others.
 Dyslipidemia Symptoms
 Dyslipidemia doesnt have symptoms at all, but it can cause other
symptomatic vascular disease, like coronary artery disease.
 Eyelid xanthelasmas, tendinous xanthomas at the elbow, knee
tendons and Achilles and arcus cornea are caused by high levels of
LDL. Acute pancreatitis is caused by high levels of TGs.
 Patients that have familial hypercholesterolemia in homozygous form
can have the above findings with planar xanthomas. Patients that
have elevation of TGs in severe condition can expect having eruptive
xanthomas 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 due
to the severe hypertriglyceridemia. You can also have a milky
appearance in your blood plasma when you have high lipid levels.
You can expect symptoms like paresthesias, confusion and dypsnea.
Dyslipidemia
Dyslipidemia
Dyslipidemia
Determining Goal
 Identify presence of clinical atherosclerotic dse (high
risk)
 Determine presence of major risk factors
 Cigarette smoking
 HTN (BP 140/90 or uncontrolled or on meds)
 Low HDL (<40mg/dl)
 Family history of premature CHD
 Age ( men  45 , women  55)
 Determine Framingham risk
Dyslipidemia
Dyslipidemia
Dyslipidemia
Dyslipidemia
Dyslipidemia Treatment
A. Non-Pharmacologic Treatment
 Therapeutic Lifestyle Change- diet plans include foods that are low
in cholesterol and calories and trans-fat free. Foods that are sugary
and fried must be avoided. Dairy products and red meat are taken in
moderation. In order to lower their cholesterol level, it is
recommended that patients should eat fish, vegetables, nuts and
fruits.
-eat in smaller portions and avoid their cravings.
- 3 months trial for all patients
 Smoking Cessation
 Physical Activity
 Weight Loss
 Dietary Modification
 -Reduce saturated and trans fats
 Increase Fiber (25g/day) and complex carbohydrates
 Diet remains cornerstone of therapy
 LDL lowering of 25%
 Exercise to increase HDL
 Cardioprotective affect
 Non-prescription agents
 Garlic (-6%)
 Soy protien (-9%)
 Vitamin E reduces efficacy of statins and niacin
 Regular Exercise- regular exercises help the patients
in losing weight, improve the functions of their lungs
and heart and to stabilize their blood pressure.
Exercise routines are adjusted to fit in the patients
ability level. If the patient is physically able, they are
encouraged to take walk regularly and ride bicycles.
Other activities like Pilates, Yoga, Workout classes and
weightlifting are also suggested.
*If TLC are not effective or pts. are at high CV risk or
extremely elevated LDL ( >200mg/dl ) then, TLC is
applied concurrently with Pharmacologic Tx
Dyslipidemia
Lipid lowering drugs
B. Pharmacologic Treatment
Omega-3 fatty acids (fish oil)
Statin
 Synthesis of LDL cholesterol
 LDL lowering 10-70%
 Other benefits
 Reduce plasma viscosity
 Decrease platelet aggregation
 Decrease C-reactive protein levels
Adverse effect
- Elevated LFT  obtain LFT at baseline, routine monitoring is
necessary
- Rhabdomyolysis w/ acute renal failure and or myopathy 
baseline CPK and recheck CPK if symptoms suggest myopathy;
patient should be instructed to report unexplained muscle pain,
tenderness, weakness, brown urine; d/c if CPK is markedly elevated
or myopathy is suspected
Bile Acid Sequestrants
 Rarely used
 Bind bile acids in the intestinal lumen
 Increased clearance of cholesterol from blood
 Poorly tolerated (GI effects, Constipation, aggravate GI
conditions  IBS, Crohns)
 Mild LDL lowering
 Increase HDL
Nicotinic acid (Niacin)
 Modifies plasma lipoproteins and lipids favorably
 Effects on lipids
 LDL: dec 14%
 HDL: inc 25%
 TGs: dec 30%
 Preferred agent for patients with low HDL in whom therapeutic lifestyle
changes have already been tried
 Niacin 500-1000mg PO QHS
 Pre-treat w/ ASA 325mg PO 1-2hrs before dose to avoid ADRs (flushing,
pruritus, Gi distress)
Adverse Effect
- Flushing  taking aspirin 30 mins before aspirin, taking niacin at bedtime w/
food, avoid hot beverages, spicy foods and hot shower at time of
administration
- Hyperglycemia  caution w/ diabetes
- Upper GI Distress
- Hepatotoxic  monitor LFT 6-12 weeks
Fibrates
 Regulate genes that control lipid metabolism
 Indicated for hypertriglyceridemia with low LDL
 GI disturbances
Adverse Effect
- Gallstones  increase fluid intake, d/c if gallstones are found
- Myopathy  baseline CPK
- - Increase hepatic transaminase  monitor LFT every 3
months
Fish Oil
 Omega-3 fatty acids
 Decrease triglycerides by 20-50%
 1-4g PO QD
 Chill capsules to increase palatability
Long-term intake results in increased HDL
Cholesterol absorption
inhibitor
 MOA  intestinal absorption of cholesterol
 Dyslipidemia in Diabetes
Diabetics with dyslipidemia are diagnosed to have low HDL
cholesterol and too many triglycerides. Patients of type 2
diabetes have higher risk of having this condition. The risk
factors are having high blood glucose, being obese, and
resistant to insulin. And with the combination of these two
conditions, there is a consequence of having poor control of
their diabetes. Those diabetics with no dyslipidemia can
develop one for no apparent reasons like kidney diseases and
hypothyroidism. Patients with dyslipidemia can develop
diabetes in the future, according to studies. Female patients
that have diabetes can have higher risk of cardiac disease
because of this form.
There are no great limits to growth because
there are no limits of human intelligence,
imagination, and wonder.
Ronald Reagan
Thank you.

More Related Content

Dyslipidemia

  • 2. Introduction Cardiovascular dse affects >70 mil Americans - underlying dse largely preventable Increasingly aggressive approach in the treatment of cholesterol - NCEP ATP III guidelines
  • 3. Epidemiology Total cholesterol & LDL Cholesterol increase throughout life - Atherogenic pattern characteristic of Western society diets More than 50% of American adults 20y of age or older have elevated total cholesterol - 1/3 are aware of it
  • 4. Dyslipidemia (aka hyperlipidemia, aka hypercholesterolemia) is a disorder of elevated or abnormal levels of lipids and/or lipoproteins in the blood, characterized by high cholesterol, triglycerides (TGs) or both, or low HDL levels. - a complex disease caused by the interplay of genetic, dietary and physiologic factors - LDL 130mg/dl (borderline high or higher) Diagnosis - by using fasting lipoprotein profiles and measuring plasma levels (total cholesterol, TGs, Lipoproteins)
  • 5. Classification of Dyslipidemia Phenotype. Dyslipidemia is present in the body. You can easily see that the type of lipid that has been increased. Etiology. This classification tackles more on the reason why the condition has happened. The reasons may include genetic or secondary to another conditions.
  • 8. Dyslipidemia Cause Primary Causes. (Familial) Overproduction and defective clearance of the cholesterols TG and LDL is the result of the mutations of single or multiple genes. The primary disorders are the common dyslipidemia causes to the children, although it may not affect in the most cases of adult dyslipidemia. Secondary Causes. Adults are the most affected ones when it comes to secondary causes. The causes contribute a lot on how an adult will be affected with dyslipidemia. The sedentary lifestyle is the most essential secondary cause. The lifestyle includes excessive dietary intake of cholesterol, trans fats and saturated fats. Trans fats are the fatty acids that are either polyunsaturated or monounsaturated, in which there are added hydrogen atoms. Trans fats are usually used in a lot of processed foods.
  • 9. Other secondary causes are: Alcohol overuse Cigarette smoking Inactivity Diabetes mellitus Hypertension & Obesity Chronic kidney disease Hypothyroidism, Liver disease Low HDL < 40mg/dl Age and Gender ( Men >45yo, Women >55yo ) Other cholestatic liver diseases and primary biliary cirrhosis. Drugs like thiazides, retinoids, estrogens and glucocorticoids, among others.
  • 10. Dyslipidemia Symptoms Dyslipidemia doesnt have symptoms at all, but it can cause other symptomatic vascular disease, like coronary artery disease. Eyelid xanthelasmas, tendinous xanthomas at the elbow, knee tendons and Achilles and arcus cornea are caused by high levels of LDL. Acute pancreatitis is caused by high levels of TGs. Patients that have familial hypercholesterolemia in homozygous form can have the above findings with planar xanthomas. Patients that have elevation of TGs in severe condition can expect having eruptive xanthomas 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 due to the severe hypertriglyceridemia. You can also have a milky appearance in your blood plasma when you have high lipid levels. You can expect symptoms like paresthesias, confusion and dypsnea.
  • 14. Determining Goal Identify presence of clinical atherosclerotic dse (high risk) Determine presence of major risk factors Cigarette smoking HTN (BP 140/90 or uncontrolled or on meds) Low HDL (<40mg/dl) Family history of premature CHD Age ( men 45 , women 55) Determine Framingham risk
  • 19. Dyslipidemia Treatment A. Non-Pharmacologic Treatment Therapeutic Lifestyle Change- diet plans include foods that are low in cholesterol and calories and trans-fat free. Foods that are sugary and fried must be avoided. Dairy products and red meat are taken in moderation. In order to lower their cholesterol level, it is recommended that patients should eat fish, vegetables, nuts and fruits. -eat in smaller portions and avoid their cravings. - 3 months trial for all patients Smoking Cessation Physical Activity Weight Loss Dietary Modification -Reduce saturated and trans fats Increase Fiber (25g/day) and complex carbohydrates
  • 20. Diet remains cornerstone of therapy LDL lowering of 25% Exercise to increase HDL Cardioprotective affect Non-prescription agents Garlic (-6%) Soy protien (-9%) Vitamin E reduces efficacy of statins and niacin
  • 21. Regular Exercise- regular exercises help the patients in losing weight, improve the functions of their lungs and heart and to stabilize their blood pressure. Exercise routines are adjusted to fit in the patients ability level. If the patient is physically able, they are encouraged to take walk regularly and ride bicycles. Other activities like Pilates, Yoga, Workout classes and weightlifting are also suggested. *If TLC are not effective or pts. are at high CV risk or extremely elevated LDL ( >200mg/dl ) then, TLC is applied concurrently with Pharmacologic Tx
  • 23. Lipid lowering drugs B. Pharmacologic Treatment Omega-3 fatty acids (fish oil)
  • 24. Statin Synthesis of LDL cholesterol LDL lowering 10-70% Other benefits Reduce plasma viscosity Decrease platelet aggregation Decrease C-reactive protein levels Adverse effect - Elevated LFT obtain LFT at baseline, routine monitoring is necessary - Rhabdomyolysis w/ acute renal failure and or myopathy baseline CPK and recheck CPK if symptoms suggest myopathy; patient should be instructed to report unexplained muscle pain, tenderness, weakness, brown urine; d/c if CPK is markedly elevated or myopathy is suspected
  • 25. Bile Acid Sequestrants Rarely used Bind bile acids in the intestinal lumen Increased clearance of cholesterol from blood Poorly tolerated (GI effects, Constipation, aggravate GI conditions IBS, Crohns) Mild LDL lowering Increase HDL
  • 26. Nicotinic acid (Niacin) Modifies plasma lipoproteins and lipids favorably Effects on lipids LDL: dec 14% HDL: inc 25% TGs: dec 30% Preferred agent for patients with low HDL in whom therapeutic lifestyle changes have already been tried Niacin 500-1000mg PO QHS Pre-treat w/ ASA 325mg PO 1-2hrs before dose to avoid ADRs (flushing, pruritus, Gi distress) Adverse Effect - Flushing taking aspirin 30 mins before aspirin, taking niacin at bedtime w/ food, avoid hot beverages, spicy foods and hot shower at time of administration - Hyperglycemia caution w/ diabetes - Upper GI Distress - Hepatotoxic monitor LFT 6-12 weeks
  • 27. Fibrates Regulate genes that control lipid metabolism Indicated for hypertriglyceridemia with low LDL GI disturbances Adverse Effect - Gallstones increase fluid intake, d/c if gallstones are found - Myopathy baseline CPK - - Increase hepatic transaminase monitor LFT every 3 months
  • 28. Fish Oil Omega-3 fatty acids Decrease triglycerides by 20-50% 1-4g PO QD Chill capsules to increase palatability Long-term intake results in increased HDL
  • 29. Cholesterol absorption inhibitor MOA intestinal absorption of cholesterol
  • 30. Dyslipidemia in Diabetes Diabetics with dyslipidemia are diagnosed to have low HDL cholesterol and too many triglycerides. Patients of type 2 diabetes have higher risk of having this condition. The risk factors are having high blood glucose, being obese, and resistant to insulin. And with the combination of these two conditions, there is a consequence of having poor control of their diabetes. Those diabetics with no dyslipidemia can develop one for no apparent reasons like kidney diseases and hypothyroidism. Patients with dyslipidemia can develop diabetes in the future, according to studies. Female patients that have diabetes can have higher risk of cardiac disease because of this form.
  • 31. There are no great limits to growth because there are no limits of human intelligence, imagination, and wonder. Ronald Reagan