W1_CaseStudy_Kattakayam_Jaya (1)

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South University, Savannah *

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NSG6001

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Health Science

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Feb 20, 2024

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1 Advanced Pharmacology Jaya Aju Kattakayam South University NSG6005 Dr Olson December 2, 2023

2 Advanced Pharmacology A 58-year-old post Myocardial infarction and angioplasty started on metoprolol for hypertension. He has a history of coronary artery disease, diabetes, asthma, and hypertension. The 2020 International Society of Hypertension Global Hypertension Practice Guidelines – recommend the use of selective ß1-receptor agonists in patients diagnosed with coronary heart disease, hypertension diabetes, and asthma. American Heart Association - https://www.ahajournals.org/doi/epub/10.1161/HYPERTENSIONAHA.120.15026 Clinical guidelines also help us to determine the best medication for patients with heart disease, and comorbidities like asthma, diabetes, and hypertension. Q 1: Metoprolol is a cardioselective ß1-adrenergic receptor antagonist, primarily blocking the ß1 receptors in the heart (Rosenthal & Burchum, 2020). This selectivity helps reduce the heart rate and blood pressure by blocking the effects of catecholamines adrenaline and noradrenaline specifically on the heart. Beta-blockers bind with beta-adrenergic receptors, competing with catecholamines causing negative chronotropic and ionotropic effects. By blocking ß1 receptors in the juxtaglomerular cells, ß blockers lower blood pressure by decreasing the activity of the renin-angiotensin activation system (Martínez et al., 2023). There are three types of β-adrenoceptors, β 1 -, β 2 - and β 3 -adrenoceptors. Beta 1 - adrenoceptors are found mainly in the cardiac muscles and stimulation of catecholamines causes positive chronotropic and ionotropic effects (Bennett et al., 2021). Beta 2 -adrenoceptors are present in bronchial smooth muscle, cardiac, and skeletal muscle, and blood vessels. Beta 3 - adrenoceptors are seen in bladder muscles and adipose tissue (Bennett et al., 2021). Different hormones act on different β-adrenoceptors. Binding with Beta 1 -adrenoceptors, catecholamines like norepinephrine and epinephrine increase cardiac automaticity and velocity of conduction.

3 Beta-1 receptors also cause the release of renin from the kidneys. Catecholamines binding to beta-2 receptors induce smooth muscle relaxation and increased metabolic effects like glycogenolysis. Beta-receptor antagonists or beta blockers block the effects of epinephrine and norepinephrine by binding to beta-receptors, reducing the availability of these receptors through competitive inhibition (Martínez et al., 2023). Beta-blockers bind to the beta-1 and beta-2 receptors, inhibit the chronotropic and inotropic effects, and the heart rate and force of contraction slow down. Beta-blockers also decrease blood pressure by decreasing renin and reducing cardiac output. The negative chronotropic and inotropic effects relieve angina symptoms by decreasing cardiac oxygen demand. Beta-blockers also prolong the atrial refractory periods and cause a potent antiarrhythmic effect (Martínez et al., 2023). Metoprolol is a second generation β blocker, which does not cause β2 blockade at therapeutic doses but can block β2 receptors at higher doses (Rosenthal & Burchum, 2020). With minimal β2 blockade, metoprolol rarely causes adverse effects of bronchoconstriction and hypoglycemia. Q 2: Metoprolol, second generation ß1-selective blockers, and cardioselective beta- blockers exert several cardiovascular effects. By blocking ß1 receptors in the myocardium, metoprolol lowers the heart rate and reduces the force of contraction. Metoprolol, by blocking ß1 receptors in the heart, decreases the velocity of AV node conduction. Metoprolol reduces cardiac output, leading to a decrease in blood pressure. It also reduces blood pressure by decreasing the renin secretion by the kidneys and reducing peripheral vascular resistance. Metoprolol decreases the oxygen demand of cardiac muscles by blocking ß1 receptors in the heart. It increases exercise tolerance by decreasing the intensity and frequency of angina and reducing the risk of death in post-myocardial infarction patients. However, metoprolol is not

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