Pharmacological Management of the Disease Paper

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Pharmacological Effects of Anti-Hyperlipidemia Medications in the Management of Hyperlipidemia

Managing diseases, especially chronic conditions, is a critical part of healthcare delivery for providers like nurses. Pharmacological interventions entail use of medications to treat and manager conditions like hyperlipidemia that affect millions of individuals. According to the Centers for Disease Control and Prevention (CDC) hyperlipidemia is a risk factor for heart disease and should be controlled or treated to reduce its effects on one’s health. A core feature of this condition is high levels of cholesterol in the blood.

The CDC (2023b) asserts that close to 25 million adults in the U.S. have high cholesterol levels that constitute hyperlipidemia. Again, about 7% of children and adolescents also suffer from this condition. As such, it is critical to explore the medications used to manage and treat hyperlipidemia to reduce its effects like increasing the risk for other conditions like heart disease. The purpose of this paper is to discuss the pharmacological management of hyperlipidemia, especially the effects of anti-hyperlipidemia medications.

Disease Process of Hyperlipidemia

Having high lipid levels or fats in the blood, including cholesterol and triglycerides entails hyperlipidemia. This disease can increase one’s risk of getting heart attack, strokes, and other complex problems as it leads to the narrowing of vessel wall and obstruction to the flow of blood. High cholesterol implies that one has too many fats or lipids in their blood. The liver creates cholesterol to help the body digest food and make other components like hormones.

However, people also get cholesterol from food like meat and dairy aisles. The cholesterol consumed by people is extra and leads to building up of fatty plaques. The recommended cholesterol level should be about 150 mg/dL. However, having cholesterol levels of between 200 mg/dL and 239 mg/dL means implies bad levels since the level can create roadblocks in the arterial highways and this damages organs since they do not get sufficient blood.

There are three types of cholesterol levels (CDC, 2023). These include low-density lipoprotein (LDL) which is classified as bad cholesterol, very low-density lipoprotein (VLDL) or triglycerides, and high-density lipoprotein (HDL) which is considered good cholesterol. LDL is called bad cholesterol since it clogs arteries and ranges about 100 mg/dL (Wang et al., 2019). Triglycerides are bad cholesterol since they add to artery plaque.

High-density lipoprotein (HDL) is considered optimal cholesterol since it carries cholesterol from the liver and helps in formation of components required by the body like hormones. The implication is that having high bad cholesterol levels leads to hyperlipidemia which blocks blood vessels and places one at increased risk of complex health issues like heart disease and stroke.

Hyperlipidemia is a chronic, progressive disease which demands behavioral changes among the affected individuals that include lifestyle changes and dietary modifications as well as the possible need for lipid-reducing medications. Patients with premature coronary artery disease (CAD) have increased chances of suffering from hyperlipidemia. Estimates demonstrate that over 50% of Americans adults have elevated LDL levels, with close to 35% sufficiently managing their conditions (Hill et al., 2022). This means that in most cases, hyperlipidemia is undertreated by those diagnosed.

Hyperlipidemia exits in two broad categories that include primary or familial and secondary or acquired. Primary hyperlipidemia is usually hereditary emanating from a plethora of genetic disorders which one can acquire from birth. Secondary hyperlipidemia originates from other underlying etiology like having unhealthy diet, certain medications such as amiodarone, uncontrolled diabetes and having poor lifestyle. Studies show that existing lipoprotein metabolism disturbances are mainly familial, which make an individual’s family history more critical Wang et al., 2019; Hill, 2022).

For instance, studies show that close to 54% of individuals with a history of coronary artery disease had other hereditary disorders. In many individuals, hyperlipidemia demonstrates a polygenic inheritance pattern while manifestations of the disease are mainly influenced by secondary aspects like obesity, intake of saturated fats, and the level of cholesterol that one has in their diet.

Overview of Pathophysiology of Hyperlipidemia

The pathophysiology of hyperlipidemia entails looking at two main classifications of condition. The core pathophysiology of hyperlipidemia entails idiopathic hyperchylomicronemia where defects in lipid metabolism causes hypertriglyceridemia. Hyperchylomicronemia is caused by defects in lipoprotein lipase activity or the lack of surface apoprotein substance CII31. Further, hyperchylomicronemia among individuals with autosomal recessive defects in lipoprotein lipase (LPL) activity leads to primary hyperlipidemia.

In secondary hyperlipidemia, the postprandial absorption of chylomicrons from the gastrointestinal tract happens between 30 and 60 minutes upon ingestion of food having fat that leads to elevated serum triglycerides for about 3 to 10 hours (Hill et al., 2022). Patients with diabetes have low LPL activity that leads to high production of VLDL cholesterol by the live that ultimately leads to hyperlipidemia. Again, hypothyroidism-induced low LPL activity and lipolytic activity reduce hepatic degradation of cholesterol to bile acids. Additionally, hyperadrenocorticism elevates the synthesis of VLDL by the liver causing the development of both hypercholesterolemia and hypertriglyceridemia.

According to the response-to-injury model, risk factors like oxidized LDL, mechanical injury to endothelium, immunologic attack and infection-induced changes in the endothelial as well as intimal function cause dysfunction of endothelial and a number of cellular interactions that cause atherosclerosis (Wang et al., 2019). Again, hyperlipidemia, inflammatory and immunological factors, hypertension, smoking and the plaque erosion or rupture contribute to the development of atherosclerosis which remains asymptomatic until plaque stenosis gets to about 70% and 80% of the vessel’s diameter.

The damage of the endothelial leads to increased inflammation around the site of dysfunction, allowing lipids to accumulate within its innermost layers’ walls. The lipids are then surrounded by macrophages, resulting to the establishment of “foam cells.” The implication is that the cholesterol build-up in these cells leads to mitochondrial dysfunction, apoptosis, and necrosis of the underlying tissues. Additionally, the process leads to encapsulation of the pack of “foam cells” or debris, that creates a fibrotic plaque which hinders the underlying lipid debris from being destroyed (Hill et al., 2022).

The clinical manifestation of hyperlipidemia entails several aspects, from familial hypercholesterolemia to type V hyperlipoproteinemia. For instance, familial hypercholesterolemia involves a selective elevation in plasma LDL and deposition of LDL arising from cholesterol in tendons and arteries. Again, massive accumulation of chylomicrons and a related rise in plasma triglycerides or type I lipoprotein pattern are the main features of familial lipoprotein lipase disorder.

Effects of Anti-Hyperlipidemia Medications

The treatment of hyperlipidemia entails mainly using drugs or medications. The primary drug in the treatment of this disease is statin. Statin works mainly to inhibit conversion of HMG-CoA to mevalonate. There are several Reductase inhibitors that include Lovastatin, Rosuvastatin and Simvastatin. These medications mediate the functions of the liver in controlling high cholesterol levels to reduce the possible diagnosis of hyperlipidemia. As such, statin reduces the synthesis of LDL and enhances catabolism of LDL mediated through its receptors to lower the effects of the extra lipids in the blood.

When used alone, statins at the most effective potent total and LDL cholesterol-reducing agents and the most tolerated. Statins reduce total and LDL cholesterol through a dose-related approach by about 30% or more when used in dietary therapeutic (Reijman et al., 2021). When used alongside other medications like BAR (Bile acid resins), the combination increases the LDL receptors leading to higher degradation of cholesterol and inhibition of intracellular synthesis of cholesterol while also interrupting enterohepatic recycling of bile acids.

Again, it is rational to combine a statin and ezetimibe since ezetimibe hinders cholesterol absorption across the gullet border and reduces the effects by between 12% and 20%. The main effect of using statin is constipation that occurs in less than 10% of patients. Other effects may include elevated serum aminotransferase, increased creatine kinase levels, and myopathy as well as very rare cases of rhabdomyolyis.

Bile acid resins (cholestyramine, colestipol, colesevelam) (BARs) bind acids found in the intestinal lumen to reduce bile acid pool size and stimulate hepatic production of bile acids from cholesterol. The process leads to depletion of hepatic cholesterol pool resulting in a rise in cholesterol biosynthesis and a rise in the amount of LDL receptors on the hepatocyte membrane, which stimulates the increased catabolism from plasm and a decline in the LDL levels. Of concern is that the rise in hepatic cholesterol biosynthesis may lead to parallel increase in hepatic VLDL production (Wang et al., 2021).

The result is that BARs can aggravate hypertriglyceridemia in individuals having combined hyperlipidemia. BARs can also help treat primary hypercholesterolemia, especially familial hypercholesterolemia. Individuals using BARs experience gastrointestinal complaints that include constipation, bloating of the stomach, nausea, epigastric fullness and flatulence. Individuals with these adverse effects can moderate and manage them through taking more fluids, dietary modifications that entails increasing bulk and using stool softeners.

These individuals may also experience impaired absorption of fat-soluble vitamins that include A, D, E and K. They may also have hypercholoremia and gastrointestinal obstruction as well as lowered bioavailability of acidic medications like thyroxine and warfarin among others.
Niacin, especially nicotinic acid, reduces the hepatic synthesis of VLDL that in turn lowers the synthesis of LDL. It also increases HDL by reducing its metabolism. The main use of niacin is mixed hyperlipidemia and in some instances as a second-line agent when combining therapy to address hypercholesterolemia (Wang et al., 2019).

The implication is that with even its effects like adverse drug effects, the pharmacological working is effective in treatment of hypertriglyceridemia and even diabetic dyslipidemia. The other medication is fibrate acids that effectively lowers VLDL but may lead to a rise in the LDL and overall cholesterol values. The HDL in the plasma may increase by between 10% and 15%. Adverse effects may include gastrointestinal complaints that occur in about 5% of patients, rash in 2% of patients and dizziness (Yandrapalli et al., 2019). As such, it is essential to understand the underlying effects of the pharmacological effects of the medications used in treating hyperlipidemia.

Importance of the Information for Advanced Practice Nurses

Advanced practice nurses should have information on the pharmacological agents that they can use in treatment of hyperlipidemia so that they develop effective care and management plans. The information concerning the side effects, and the mechanism of the working of these medications is essential to managing the condition. By understanding the adverse effects of the medications, nurses can educate patients and their families about the most effective approaches to the condition.

The information allows nurses to know the adverse effects of each drug as well as the pathophysiology of the condition. Advanced practice nurses can then implement evidence-based practices to reduce the effects of the condition and help patients implement dietary and lifestyle modifications appropriately.

Conclusion

Hyperlipidemia, like other chronic diseases, increases the risk of getting heart disease and stroke as well as hypertension. Understanding the disease process and its pathophysiology is essential in developing sufficient interventions to reduce its effects and help patients manage it, especially through behavioral changes and dietary modifications. Advanced practice nurses require this information to develop customized care plans for patients based on their condition.

References

• Centers for Disease Control and Prevention (CDC). (2023 May 15). High Cholesterol Facts.
  https //www.cdc.gov/cholesterol/facts.htm
• Centers for Disease Control and Prevention (CDC) (2023b March 20). About Cholesterol.
  https //www.cdc.gov/cholesterol/about.htm
• Hill, M. F. & Bordoni, B. (2022 August 8). Hyperlipidemia.
  https //www.ncbi.nlm.nih.gov/books/NBK559182/
• Patti, A. M., Giglio, R. V., Papanas, N., Rizzo, M., & Rizvi, A. A. (2019). Future perspectives of the pharmacological management of diabetic dyslipidemia. Expert Review of Clinical Pharmacology, 12(2), 129-143.
• Reijman, M. D., Kusters, D. M., & Wiegman, A. (2021). Advances in familial
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• Yandrapalli, S., Gupta, S., Andries, G., Cooper, H. A., & Aronow, W. S. (2019). Drug therapy of dyslipidemia in the elderly. Drugs & aging, 36, 321-340.
  DOI 10.1007/s40266-018-00632-x.
• Wang, F., Wang, J., Cai, H., Yuan, L., Sun, C., Peng, X., … & Zhang, J. (2021). Network pharmacology combined with metabolomics to investigate the anti-hyperlipidemia mechanism of a novel combination. Journal of Functional Foods, 87, 104848. https //doi.org/10.1016/j.jff.2021.104848