Dyslipidemia
-
Upload
jay-jay-dizon -
Category
Healthcare
-
view
327 -
download
1
Transcript of Dyslipidemia
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 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 doesn’t 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.
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 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 patient’s 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
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, Crohn’s)
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.