Optimal LDL cholesterol levels Essays

Optimal LDL cholesterol levels Essays Optimal LDL cholesterol levels Paper Optimal LDL cholesterol levels Paper Dyslipidemia came from the words â€Å"dys-â€Å" plus â€Å"lipid† which means fat and â€Å"-emia† which means in the blood. Altogether it means essentially, disordered lipids in the blood. According to Merck Co. 2008, Dyslipidemia is a disorder of lipoprotein metabolism, including lipoprotein overproduction or deficiency. Dyslipidemias may be manifested by elevation of the total cholesterol, the bad low-density lipoprotein (LDL) cholesterol and the triglyceride concentrations, and a decrease in the good high-density lipoprotein (HDL) cholesterol concentration in the blood. Dyslipidemia is a condition wherein it comes under consideration in many situations including diabetes, a common cause of lipidemia. For adults with diabetes, it has been recommended that the levels of LDL, HDL, and total cholesterol, and triglyceride be measured every year. Optimal LDL cholesterol levels for adults with diabetes are less than 100 mg/dL (2. 60 mmol/L), optimal HDL cholesterol levels are e4qual to or greater than 40 mg/dL (1. 02 mmol/L), and desirable triglyceride levels are less than 150 mg/dL (1. 7 mmol/L). Dyslipidemias were traditionally classified by patterns of elevation in lipids and lipoproteins. A more practical system categorizes dyslipidemias as primary or secondary and characterizes them by increases in cholesterol only (pure or isolated hypercholesterolemia), increases in TGs only (pure or isolated hypertriglyceridemia), or increases in both cholesterol and TGs (mixed or combined hyperlipidemias). This system does not take into account specific lipoprotein abnormalities (eg, low HDL or high LDL) that may contribute to disease despite normal cholesterol and TG levels. Dyslipidemia is a condition marked by abnormal concentrations of lipids or lipoproteins in the blood. (Merriam- Webster’s Medical Dictionary 2006) The Primary cause of dyslipidemia are single or multiple genetic mutations that result in either overproduction or defective clearance of TG and LDL cholesterol, or in underproduction or excessive clearance of HDL Primary lipid disorders are suspected when a patient has physical signs of dyslipidemia, onset of premature atherosclerotic disease less than 60 years old, a family history of atherosclerotic disease, or serum cholesterol 240 mg/dL ( 6. 2 mmol/L). Primary disorders, the most common cause of dyslipidemia in children, do not cause a large percentage of cases in adults. The names of many reflect an old nomenclature in which lipoproteins were detected and distinguished by how they separated into ? (HDL) and ? (LDL) bands on electrophoretic gels. The Secondary cause of this disease contributes to most cases of dyslipidemia in adults. The most significant secondary cause in developed countries is a sedentary lifestyle with excessive dietary intake of saturated fat, cholesterol, and trans fatty acids (TFAs). TFAs are polyunsaturated fatty acids to which hydrogen atoms have been added; they are commonly used in many processed foods and are as atherogenic as saturated fat. Other frequent secondary causes include diabetes mellitus, alcohol overuse, chronic renal insufficiency and/or failure, hypothyroidism, primary biliary cirrhosis and other cholestatic liver diseases, and drugs, such as thiazides, ? -blockers, retinoids, highly active antiretroviral agents, estrogen and progestins, and glucocorticoids. Diabetes is most common significant secondary cause because patients tend to have an atherogenic arrangement of high TGs; high small, dense LDL fractions; and low HDLs (diabetic dyslipidemia, hypertriglyceridemic hyperapo B). Patients with type 2 diabetes are especially at risk. The combination may be a consequence of obesity and/or poor control of diabetes, which may increase circulating FFAs, leading to increased hepatic VLDL production. TG-rich VLDL then transfers TG and cholesterol to LDL and HDL, promoting formation of TG-rich, small, dense LDL and clearance of TG-rich HDL. Diabetic dyslipidemia is often exacerbated by the increased caloric intake and physical inactivity that characterize the lifestyles of some patients with type 2 diabetes. Women with diabetes may be at exceptional risk for cardiac disease from this form. B. Signs and Symptoms Dyslipidemia itself can cause no symptoms but can lead to symptomatic vascular disease, including coronary artery disease and peripheral arterial disease. High TGs ( 1000 mg/dL [ 11. 3 mmol/L]) can cause acute pancreatitis. Extremely high levels of LDL can cause eyelid xanthelasmas; arcus corneae; and tendinous xanthomas found at the Achilles, elbow, and knee tendons and over metacarpophalangeal joints. Patients with the homozygous form of familial hypercholesterolemia may have the above findings plus planar or cutaneous xanthomas. Patients with severe elevations of TGs can have eruptive xanthomas over the trunk, back, elbows, buttocks, knees, hands, and feet. Patients with the rare dysbetalipoproteinemia can have palmar and tuberous xanthomas. Another one is severe hypertriglyceridemia which is ( 2000 mg/dL [ 22. 6 mmol/L]) it can give retinal arteries and veins a creamy white appearance (lipemia retinalis). Extremely high lipid levels also give a lactescent (milky) appearance to blood plasma. Dyslipidemias are usually asymptomatic; it may cause xanthelesmas and xanthelamata, and after a prolonged period it may result into Ischemic heart disease, Peripheral vascular disease, Cerebrovasular disease and kidney disease C. Physical Exam Findings It is usually diagnosed by measuring serum lipids, though it may be suspected in patients with characteristic physical findings. Routine measurements also known as lipid profile, includes total cholesterol (TC), TGs, HDL, and LDL. TC, TGs, and HDL are measured directly; TC and TG values reflect cholesterol and TGs in all circulating lipoproteins, including chylomicrons, VLDL, IDL, LDL, and HDL. TC values vary by 10% and TGs by up to 25% day-to-day even in the absence of disease. TC and HDL can be measured in the nonfasting state, but most patients should have all lipids measured while fasting for maximum accuracy and consistency. Testing of the disease should be postponed until after resolution of acute illness, because TGs increase and cholesterol levels decrease in inflammatory states. Lipid profiles are generally reliable within the first 24 h after an acute MI but then change. LDL values are most often calculated as the amount of cholesterol not contained in HDL and VLDL, where VLDL is estimated by TG ? 5; ie, LDL = TC ? [HDL + (TGs ? 5)] (Friedewald formula). VLDL cholesterol is estimated by TG ? 5 because the cholesterol concentration in VLDL particles is usually 1? 5 of the total lipid in the particle. This calculation is valid only when TGs are 400 mg/dL and patients are fasting, because eating increases TGs. The calculated LDL value incorporates measures of all non-HDL, nonchylomicron cholesterol, including that in IDL and Lp(a). LDL can also be measured directly using plasma ultracentrifugation, which separates chylomicrons and VLDL fractions from HDL and LDL, and by an immunoassay method. Direct measurement may be useful in some patients with elevated TGs to determine if LDL levels are also high, but these direct measurements are not routinely necessary. The role of apo B testing is under study because values reflect all non-HDL cholesterol (in VLDL, VLDL remnants, IDL, and LDL) and may be more predictive of coronary artery disease (CAD) risk than LDL alone. (Brunner Suddhart’s Textbook of Medical-Surgical Nursing 10th edition 2004) A fasting lipid profile (TC, TGs, HDL, and calculated LDL) should be obtained in all adults ? 20 yr and should be repeated q 5 yr. Lipid measurement should be accompanied by assessment of other cardiovascular risk factors, defined as diabetes mellitus, cigarette use, hypertension, and family history of CAD in a male 1st-degree relative before age 55 or a female 1st-degree relative before age 65. A definite age after which patients no longer require screening has not been established, but evidence supports screening of patients into their 80s, especially in the presence of atherosclerotic cardiovascular disease. Indications for screening patients 20 yr are atherosclerotic risk factors, such as diabetes, hypertension, cigarette smoking, and obesity; premature CAD in a parent, grandparent, or sibling; or a cholesterol level 240 mg/dL ( 6. 2 mmol/L) or known dyslipidemia in a parent. If information on relatives is unavailable, as in the case of adopted children, screening is at the discretion of the health care practitioner. Patients with premature atherosclerotic cardiovascular disease, cardiovascular disease with normal or near-normal lipid levels, an extensive family history of heart disease, or high LDL refractory to drug therapy should probably have Lp(a) levels measured. Lp(a) levels may also be directly measured in patients with borderline high LDL to determine if drug therapy is warranted. C-reactive protein and homocysteine measurement may be considered in the same populations. Tests for secondary causes of dyslipidemia- including measurements of fasting glucose, liver enzymes, creatinine, thyroid stimulating hormone (TSH), and urinary protein- should be performed in most patients with newly diagnosed dyslipidemia, and when a component of the lipid profile has inexplicably changed for the worse. D. Treatment Prognosis The prognosis of this disease varies with lipid levels and other cardiovascular risk factors. Treatment for dyslipidemia is indicated for all patients with cardiovascular disease (secondary prevention) and for some without (primary prevention). The National Institutes of Healths National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATPIII) guidelines are the most common reference for deciding which adults should be treated The guidelines focus primarily on reducing elevated LDL levels and secondarily on treating high TGs, low HDL, and metabolic syndrome (see Obesity and the Metabolic Syndrome: Metabolic Syndrome). An alternate treatment guide (the Sheffield table) uses TC: HDL ratios combined with presence of CAD risk factors to predict cardiovascular risk, but this approach probably leads to undertreatment. E. Bibliography Anne Hackman, MD; Yasunori Abe, MD; William Insull, Jr, MD; Henry Pownall, PhD; Louis Smith, PhD; Kay Dunn, PhD; Antonio M. Gotto, Jr, MD, DPhil; Christie M. Ballantyne, MD; 1996 Levels of Soluble Cell Adhesion Molecules in Patients With Dyslipidemia; Circulation. 1996;93:1334-1338 Brunner Suddhart’s Textbook of Medical-Surgical Nursing 10th edition 2004 Frick MH, Elo O, Haapa K, Heinonen OP, Heinsalmi P, Helo P, Huttunen JK, Kaitaniemi P, Koskinen P, Manninen V 1987 Nov 12;317(20):1237-45. Helsinki Heart Study: primary-prevention trial with gemfibrozil in middle-aged men with dyslipidemia. Safety of treatment, changes in risk factors, and incidence of coronary heart disease. et al. 1: N Engl J Med. Haffner SM 1998 Jan; 21(1):160-78. Management of dyslipidemia in adults with diabetes. PMID: 9538988 [PubMed indexed for MEDLINE] Jonathan Valabhji, Robert S Elkeles 2003; Dyslipidemia in Type 2 Diabetes: Epidemiology and Biochemistry Medicine Net, Inc. 1996-2008; Dyslipidemia definition: medterms. com/script/main/art. asp? articlekey=33979 Merck Manual Professional 1995-2008; Dyslipidemia: Lipid Disorders: merck. com/mmpe/sec12/ch159/ch159b. html Merriam- Webster’s Medical Dictionary 2006