NURS 6521 Assignment: Pharmacotherapy for Cardiovascular Disorders Advanced Pharmacotherapy How the factor I chose (Obesity) might influence the pharmacokinetic and pharmacodynamic processes in the patient
Numerous interrelated mechanisms play a role in the development of high blood pressure in obesity, often leading to end organ damage including chronic kidney disease and cardiovascular disease. The mechanism of hypertension in non-obese individuals is different from the mechanism of hypertension in obesity. According to Cataldi et al. (2019), the major determinants of hypertension in non-obese individuals in peripheral vasoconstriction, while obesity-related hypertension relies on hyperactivation of the sympathetic nervous system (SNS) along with the resulting rise in aldosterone and rennin release and cardiac output.
The mechanism responsible for hyperactivation of the SNS is connected to the release of substances such as free fatty acids, inflammatory cytokines, and adipokines from adipose tissue. These substances might indirectly or directly activate autonomic neurotransmission, by affecting insulin sensitivity. Moreover, the syn
Assignment Pharmacotherapy for Cardiovascular Disorders
thesis of both aldosterone and angiotensin II that causes a rise in blood pressure and promotes retention of sodium ions occurs in the adipose tissue. Nonalcoholic-fatty liver disease (NAFLD) that usually coexists with obesity additionally has a crucial role in causing insulin resistance and also activating the renin-angiotensin-aldosterone (RAA) system (Cataldi et al., 2016).
The psychologic complexity of obesity-related to hypertension presents numerous challenges in its pharmacological management. According to Cohen (2017), there is a strong correlation between obesity and treatment resistant hypertension, which requires the additive and synergistic effects of numerous antihypertensive drugs to adequately control blood pressure. As explained by Sharid and McKenzie (2020), treatment resistant hypertension is blood pressure that remains above goal despite being concurrently managed by three antihypertensive drugs of different classes, or blood pressure that is controlled with more than three medications.
The etiology of resistant hypertension in patients with obesity is a result of several factors, including dysfunctional neurohormonal pathways, especially increased secretion of aldosterone, and also the systemic effect of adipokines suck as adiponectin and leptin. Although obesity does not change the oral absorption of medications, the pharmacodynamics and pharmacokinetics of numerous drugs are affected by excess adiposity. These changes are mediated via a range of pathophysiologic mechanisms such as increased neurohormonal activity, altered renal and hepatic clearance, and expanded volume of distribution (Cohen, 2017).
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