Some people have a low HDLC ( less than 35 mg / dL) and other disorders of lipid metabolism. These disorders are called "fat" or "dyslipoproteinemias" and are most likely caused by genetic defects deterioration of poor nutrition (obesity can cause serious some of these problems). Dyslipidemia is an increase in plasma cholesterol and / or TG or low HDL level that contributes to the development of atherosclerosis. Causes may be primary (genetic) or secondary. The diagnosis is the measurement of total cholesterol, triglycerides and lipoproteins individual. treatment changes in diet, exercise and lipid-lowering drugs.
Dyslipidemia currently affects approximately 10% of the world population. It is becoming more frequent and medically necessary for the modification of lipid medications in obese patients and patients with type 2 A large proportion of patients with type 2 diabetes have abnormal levels of lipoproteins. In the U.S., Japan and Europe there are over 240 million people with abnormal levels of lipoproteins. Of these, more than 55 million high lipoprotein (HDL) and / or high triglycerides.
There is no natural border between normal and abnormal, because the measures of lipids in lipid levels are continuous. There is probably a linear relationship between lipid levels and cardiovascular risk, as people with "normal" cholesterol benefit of reaching a level even lower. Therefore, there is no numerical definition of dyslipidemia is used in relation to serum lipids, whose treatment has been beneficial. Evidence of benefit is the greater reduction of high levels of LDL, is a smaller reduction in TG high and low HDL cholesterol increased, partly because of high TG and low HDL are methods of cardiovascular risk in women than among men. This scanning electron microscope shows a cross section of color coronary atherosclerosis, fatty plaque (in yellow). diet rich in cholesterol may reduce the blood flow and lead to blood clots or blockages.
The Etiology and Classification
Dyslipidemia traditionally been classified according to the design elevation of lipids and lipoproteins. A more practical categorizes primary or secondary dyslipidemias are characterized only by increasing the concentration of cholesterol (hypercholesterolemia pure or simple), only an increase in triglyceride levels (hypertriglyceridemia pure or isolated), an increase in both cholesterol and TG (mixed or combined hyperlipidemia).
This system does not take into account the specific lipoprotein abnormalities (eg, low HDL or high LDL), which may contribute to disease despite normal cholesterol and TG. The main reason they are single or multiple genetic mutations that lead either to overproduction or defective clearance of TG and LDL cholesterol, or shortages or excessive play in HDL cholesterol. The primary lipid disorders are suspected when a patient has physical symptoms of dyslipidemia (see lipid disorders: symptoms), the premature onset of atherosclerosis ( less than 60 years), family history of atherosclerosis, or cholesterol serum more than 240 mg / dl ( more than 6.2 mmol / L). primary disorder, the most common cause of dyslipidemia in children, do not cause a significant proportion of adults. Reflecting the names of several of the old nomenclature, in which lipoproteins have been detected and identified by how divided the α (HDL) and β (LDL) teams gel electrophoresis.
Dyslipidemia currently affects approximately 10% of the world population. It is becoming more frequent and medically necessary for the modification of lipid medications in obese patients and patients with type 2 A large proportion of patients with type 2 diabetes have abnormal levels of lipoproteins. In the U.S., Japan and Europe there are over 240 million people with abnormal levels of lipoproteins. Of these, more than 55 million high lipoprotein (HDL) and / or high triglycerides.
There is no natural border between normal and abnormal, because the measures of lipids in lipid levels are continuous. There is probably a linear relationship between lipid levels and cardiovascular risk, as people with "normal" cholesterol benefit of reaching a level even lower. Therefore, there is no numerical definition of dyslipidemia is used in relation to serum lipids, whose treatment has been beneficial. Evidence of benefit is the greater reduction of high levels of LDL, is a smaller reduction in TG high and low HDL cholesterol increased, partly because of high TG and low HDL are methods of cardiovascular risk in women than among men. This scanning electron microscope shows a cross section of color coronary atherosclerosis, fatty plaque (in yellow). diet rich in cholesterol may reduce the blood flow and lead to blood clots or blockages.
The Etiology and Classification
Dyslipidemia traditionally been classified according to the design elevation of lipids and lipoproteins. A more practical categorizes primary or secondary dyslipidemias are characterized only by increasing the concentration of cholesterol (hypercholesterolemia pure or simple), only an increase in triglyceride levels (hypertriglyceridemia pure or isolated), an increase in both cholesterol and TG (mixed or combined hyperlipidemia).
This system does not take into account the specific lipoprotein abnormalities (eg, low HDL or high LDL), which may contribute to disease despite normal cholesterol and TG. The main reason they are single or multiple genetic mutations that lead either to overproduction or defective clearance of TG and LDL cholesterol, or shortages or excessive play in HDL cholesterol. The primary lipid disorders are suspected when a patient has physical symptoms of dyslipidemia (see lipid disorders: symptoms), the premature onset of atherosclerosis ( less than 60 years), family history of atherosclerosis, or cholesterol serum more than 240 mg / dl ( more than 6.2 mmol / L). primary disorder, the most common cause of dyslipidemia in children, do not cause a significant proportion of adults. Reflecting the names of several of the old nomenclature, in which lipoproteins have been detected and identified by how divided the α (HDL) and β (LDL) teams gel electrophoresis.
Secondary causes contribute to most of dyslipidemia in adults. The leading causes of school in developed countries is a sedentary lifestyle, excessive consumption of cholesterol, fat, saturated fat and trans fatty acids (TFA). TFA are polyunsaturated fatty acids with added hydrogen atoms, are widely used in many processed foods and saturated fats in atherosclerosis. Other common secondary causes are diabetes, alcohol abuse, chronic renal failure and / or failure, hypothyroidism, primary biliary cirrhosis and other cholestatic liver diseases and medications such as diuretics thiazide, β-blockers, retinoids, very active antiretroviral agents, estrogen and progestin, and glucocorticoids.
Diabetes is particularly important that the secondary cause of atherosclerosis in patients also have a combination of high TG, high small dense LDL and low HDL fractions (dyslipidemia, hypertriglyceridemia hyperapo B). Patients with type 2 diabetes are particularly at risk. The connection may be a consequence of obesity and / or poorly controlled diabetes, which can increase traffic AGL, which results in increased hepatic VLDL production. TG-rich VLDL TG and then transmits the LDL and HDL to promote the establishment of TG-rich, small dense LDL and HDL clearance of TG-rich. Diabetic dyslipidemia is a significant increase in caloric intake and physical inactivity, which are characteristic of the style of life in patients with type 2 among women with diabetes may be at particular risk for heart disease with this form.
Symptoms may
Dyslipidemia himself no symptoms but can lead to symptomatic vascular disease, including coronary artery disease and peripheral arterial disease. High TG ( more than 1000 mg / dL [ more than 11.3 mmol / L]) can cause acute pancreatitis. High levels of LDL can cause eyelid xanthelasma, corneal arcus and tendon xanthomas located in the Achilles, elbow, knee and tendon and metacarpophalangeal joints. Patients with homozygous familial hypercholesterolemia can form above and flat or cutaneous xanthomas. Patients with elevated TG are serious eruptive xanthomas on the trunk, shoulders, knees, buttocks, knees, hands and legs. Patients may have rare dysbetalipoproteinaemia hands and tuberous xanthomas.
Severe hypertriglyceridemia (more than 2000 mg / dL [more than 22.6 mmol / l]) gives the retinal arteries and veins creamy white appearance (lipemia retina). Very high concentrations of lipids also provide nursing care (milky) appearance of blood plasma.
Treatment
When a diagnosis of genetic disease of lipid metabolism, you must adhere to a diet very strict and complex, and perhaps also take drugs. This is a situation where it must be perceived by experts like Dr. Tapp lipid rather than a GP. Because each of these disorders is very unique and manifests itself differently in different patients, you must work with the healthcare provider to develop an optimal plan. The treatment is based on a combination of different strategies:
- The loss of weight. This is the most important strategy for overweight people
- Low calorie diet, rich in nutrients, essential fatty acids. adequate vitamins and minerals
- Exercise
- Combinations of drugs
Medicines are in several categories, each category is particularly useful for the type of disorder. Some increase in HDL cholesterol and TG decline in aid, others to reduce total cholesterol and LDL. Your doctor must spend considerable time analyzing problems to determine the cause of their lipid disorders and the best types of drugs for the disease.
Once a decision is reached on the types of drugs to use, we must decide in each type of drug and dose. These decisions relate to the finer aspects of each state. Sometimes you try drugs for a while, then switch to another type to see which one works better and has fewer side effects. Furthermore, drugs can change minimize side effects.
The drug combination may allow a physician to prescribe lower doses of both drugs, thereby reducing the risk of side effects. Remember: all drugs have side effects, and many long-term adverse effects can not be known, because each person has different genes and probably everyone reacts differently to medicine.
via tappmedical
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