Essay On Dyslipidemia


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Dyslipidemia


Dyslipidemia is a condition characterized by abnormally high levels of lipids in the blood (Edmunds & Mayhew, 2013). The condition can either involve low or high levels of lipoproteins. Low Density Lipoprotein refers to the bad cholesterol while High Density Lipoprotein is a term that can be used to refer to good cholesterol. The condition of dyslipidemia occur in patients with Type Two diabetes mellitus and is a trigger factor to coronary heart disease (Edmunds & Mayhew, 2013). Lipids are diverse molecules that have both structural and functional role in the body. When metabolized they are used as a source of energy while at the same time forming the lipid bilayer of the cell membrane (Baliga & Cannon, 2012). The diverse groups of lipids include fats, waxes, steroid and phospholipids among others. Dyslipidemia involves either elevated levels of HDL or LDL. LDL serves in the conveyance of fat molecules in the interstitial fluid. It is the primary transporter of cholesterol consisting of the hydrophobic core mainly the cholesteryl esters and triglycerides encased by a monolayer of phospholipid and free cholesterol (Edmunds & Mayhew, 2013). HDL helps in the removal of cholesterol from the arteries and transportation to the liver for excretion. Dyslipidemia has been associated with the development of atherosclerosis and coronary heart disease.

It has been observed that obesity, dyslipidemia, hypertension and diabetes occur in many people simultaneously. All these conditions have been given various guises such as Syndrome X, Insulin Resistance Syndrome or Metabolic Syndrome (Edmunds & Mayhew, 2013). Metabolic Syndrome increases the chances of contracting cardiovascular disease and type 2 diabetes mellitus. Metabolic syndrome is a pathophysiologic entity that designates a cluster of related abnormalities of body metabolism inclusive of dyslipidemia (Karapetrovič & Ačimovič, 2012). Metabolic syndrome and dyslipidemia are related in that the presence of free fatty acids has an inhibitory effect on post-insulin receptor contributing to insulin resistance. Resistance of insulin action or rather the deprivation leads to lipolysis and metabolically activates intra-abdominal fat (Edmunds & Mayhew, 2013).

Free Fatty Acids are released in the portal circulation where they are converted to triglycerides (Edmunds & Mayhew, 2013). This explains the relationship between dyslipidemia and metabolic syndrome. Increased glucose levels in the blood and overproduction of VLDL raises the concentration triglyceride particles resulting in reciprocal exchange of FFA: triglycerides are transferred to LDL and HDL forming both small dense LDL and HDL (Baliga & Cannon, 2012). These are the major indicators of dyslipidemia. Obesity and high concentration of abdominal fat remain the major risk factor associated with dyslipidemia. Insulin resistance a condition leading to Type 2 diabetes mellitus contributes to dyslipidemia (Baliga & Cannon, 2012). Individuals who lead a sedentary life and take alcoholic beverages are at risk of developing dyslipidemia. There are genetic predisposing factors that contribute to the development and advancement of dyslipidemia (Edmunds & Mayhew, 2013). These factors are associated with deformed genes that play a critical role in lipid metabolism.

Laboratory testing is essential before instituting drug therapy (Karapetrovič & Ačimovič, 2012). They are conducted both for fasting and non-fasting individuals. The laboratory tests aim at valuing the levels of lipids in the blood of the patient. The tests aim at measuring cholesterol levels, triglycerides, HDL and LDL levels in the blood (Edmunds & Mayhew, 2013). There have been no exact numeric values for dyslipidemia. In the appraisal of dyslipidemias, laboratory tests confirm the levels of serum cholesterol, HDL-cholesterol, LDL-cholesterol and triglycerides. These measurements are sufficient in diagnosis of dyslipidemia (Edmunds & Mayhew, 2013). Ultracentrifugation is helpful in determining VLDL and LDL cholesterol. Lipoprotein electrophoresis is handy when diagnosing Type III dyslipidemia and detecting chylomicrons (Edmunds & Mayhew, 2013). Apolipoprotein B-100 tests are useful in young adults with coronary heart disease. In diagnostic testing, the doctor can recommend an assay of alkaline phosphatase and transaminases such as AST and ALT for the overall management of dyslipidemia (Karapetrovič & Ačimovič, 2012).

Effective treatment administered for dyslipidemia helps in improving the prognosis. Statin therapy is documented as the main treatment for dyslipidemia. Combination therapy has also found great relevance for the treatment of dyslipidemia. Adjunctive omega-3 supplementations find great relevance in patients diagnosed with elevated levels of triglyceride (Edmunds & Mayhew, 2013). Statins are HMG-CoA reductase inhibitors with the major target being the reduction of LDL levels in the blood. HMG-CoA is a rate determining enzyme in the second step of cholesterol formation. Bile acid sequestrants form another class of drugs that helps in the treatment of hyperlipidemia (Edmunds & Mayhew, 2013). These are resins hence do not undergo intestinal absorption. They are primary agents in the drug therapy when the patient does not tolerate statins. Niacin or nicotinic acid and their derivatives play a crucial role in treating lipid related problems. These class of drugs address dyslipidemia by treating hypertriglyceridemia, low levels of HDL and elevated levels of LDL (Edmunds & Mayhew, 2013).

Finally, Fibrates are cholesterol lowering drugs whose mechanism of action remains elusive. They have potential impacts at all the levels of dyslipidemia, but their primary role is lowering triglycerides while increasing HDL (Baliga & Cannon, 2012). Examples of fibrates include Clofibrate and Gemfibrozil.

The medications used in treating dyslipidemia have adverse effects. Hepatotoxicity and myopathy are significant adverse effects associated with statin (Edmunds & Mayhew, 2013). These effects are likely in situations when there are high doses of statin drugs. Since they are not absorbed in the intestines, constipation and bloating problems are associated with bile acid sequestrants when used as second line agents for dyslipidemia (Edmunds & Mayhew, 2013). Niacin and nicotinic acid contribute to side effects such as flushing and GI upset which may make the patient lack the will to continue with the therapy (Edmunds & Mayhew, 2013).

References
Baliga, R. R., & Cannon, C. P. (2012). Dyslipidemia. Oxford: Oxford University Press.
Edmunds, M. W., & Mayhew, M. S. (2013). Pharmacology for the primary care provider. St. Louis, Mo: Elsevier-Mosby.
Karapetrovič, M., & Ačimovič, Z. (2012). Dyslipidemia: Causes, diagnosis and treatment. New York: Nova Science Publishers.