Essay Sample on Angiotensin-Converting-Enzyme Inhibitor

Introduction

ACE inhibitors are a pharmaceutical drug that is used for treating elevated blood pressure (hypertension) and congestive heart failure (CHF). The drug operates by causing relaxation of the blood vessels as well as reducing the volume of blood which in turn reduces the oxygen demand of the heart and consequently reduces blood pressure. ACE inhibitors inhibit the activity of the angiotensin-converting enzyme one of the core components of the renin-angiotensin system responsible for causing increase in blood volume (Dundas, Harris & Narasimhan, 2007). The drug is used alongside other drugs especially for patients who have diabetes.

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Mechanism in use is renin-angiotensin-aldosterone system. The release of enzyme renin from the kidney cells is as a result of sodium and water imbalance in the body. Other factors include hypertension, decreased blood volume and high sympathetic tone trigger. Renin activates the circulation of angiotensin I which causes amino acid imbalance (Dundas, Harris & Narasimhan, 2007). ACE enzymes inhibits conversion of angiotensin I (ATI) to angiotensin II (ATII).

Effects: ACE inhibitors restrict the conversion of ATI to ATII thus lowering resistance in the blood vessels while increasing the venous capacity. A decrease in the cardiac index, cardiac output volume and stroke work which lower resistance by the blood vessels hence increased natriuresis.

Patient education needed is to observe doctor's recommendation and prescriptions to avoid rapidly decreasing blood pressure as a result of using a maximum dose of the ACE inhibitors for controlling blood pressure.

Beta-Blockers

Beta blockers are medications that are applied to reduce blood pressure for patients with CHF. The medication works by blocking the epinephrine hormone and its effects commonly known as adrenaline. By blocking the release and effects of adrenaline, beta blockers slow down the heart rate of the patient which reduces the demand for oxygen by the heart hence reducing high blood pressure on patients. Beta blockers treat high blood pressure, heart failure, angina, heart attack and abnormal heart rhythms (Volmink, Bradley, Maroney, Mbewu & Opie, 2017).

Mechanism used by beta blockers is signal transduction mechanism. This mechanism is responsible for regulating the entropy. Beta brokers manages the systolic dysfunction which comes from the loss of viable contracting muscle. It also manages the diastolic dysfunction which occurs when there is a stiff ventricle hence impairing ventricular filling process.

Common side effects include fatigue, weight gain and cold feet and hands. Other mild side effects include trouble sleeping, depression and shortness of breath.

Patient education should be to educate the patients who suffer or have had asthma to avoid beta blockers because it can trigger severe asthmatic attacks on the patients thus worsening the situation and making it rather difficult to solve.

When not properly used, beta blockers can affect a person's triglyceride and cholesterol levels by increasing the amount of harmful triglyceride and reducing the amount of lipoprotein a good type of cholesterol.

Diuretics

Heart failure causes the renin-angiotensin-aldosterone to activate and which is responsible for the increase in the retention of sodium and water in the kidneys. Sodium and water retention are the major causes of chronic heart failure because they cause an increase in the blood volume which leads to the rise in venous pressures a major phenomenon in heart failure and subsequently the cause of systematic and pulmonary edema. The application of diuretics is to reduce the pulmonary and systematic edema and an additional clinical symptoms associated with edema such as dyspnea (Fiuzat & Califf, 2011). When used for long-term cure, diuretics may also promote systemic vasodilation thus reducing the afterload on the heart. Systemic vasodilation is key in improving ventricular ejection.

Non-compliance: when dealing with diuretics to heal heart failure, the patient must be careful not to overdose the drugs because it can depress cardiac output. In systolic dysfunction over reducing the diuretics will cause the heart to operate in ascending limb of the frank-starling relationship while in diastolic dysfunction misuse may impair ventricular filling.

Advice: patients are advised to use loop diuretics as opposed to thiazide diuretics because they are more effective in reducing heart failure through unloading sodium and water.

Aldosterone Antagonists

These drugs include eplerenone (Inspra) and spironolactone (Aldactone). These drugs contain potassium-sparing diuretics which can help people with severe systolic heart failure to keep living for a longer time. Heart failure is the functional inability of the ventricle to meet the body's metabolic needs. Renal hypoperfusion is a characteristic that occurs as a result of minimum cardiac output thus the activation of angiotensin-aldosterone system to cover for the renal hypoperfusion (Kosaka et al., 2010). Aldosterone antagonist is responsible for inhibiting the release of aldosterone which is a cause of cardiac hypertrophy, coronary inflammation, and necrotic lesions.

The mechanism in use is receptor antagonist. The antagonism of these receptors is vital for inhibiting sodium resorption in the kidney's nephron collecting duct (Kosaka et al., 2010). As a result, the receptor antagonism interferes with the sodium/potassium exchange and minimizes the excretion of urinary potassium while increasing the diuresis weakly.

Effects of misuse: can raise the amount of potassium in the blood to levels that pose danger. Patients should seek the doctor's prescription before using the drugs.

Patients should be educated on the best practices to observe in their dietary practices as a way to avoid over accumulation of potassium in the kidney during treatment. The intake of food should be modified to manageable levels of potassium supplements.

Salmeterol Inhalers

In clinical studies, the patients with asthma who used salmeterol experienced more severe asthma episodes that required specialized medication in the hospital and even led to death compared to patients who did not use salmeterol over the same period. Salmeterol is used in applications in moderate-to-severe asthma after a previous treatment (Tamura, 2017). Salmeterol is a long-acting v2 adrenergic receptor agonist (LABA) that prevents asthma symptoms. Being a LABA, it should not be used for monotherapy rather; it should be accompanied by an inhaled corticosteroid such as a fluticasone propionate or a beclometasone dipropionate during the treatment of asthma because it minimizes the serious reactions such as deaths.

The warning is heard in commercials for products with salmeterol because LABAs should be applied when dealing with acute conditions of Asthmatic infections. The difference between SABAs and salbutamol is the duration the salmeterol lasts. Since there is a variation in time, patients are warned of the side-effects that result from this reaction. While albuterol lasts for 4-6 hours, SABAs last up to 12 hours which may result in unforeseen side effects on the patient.

Patients should get sensitization on the different uses of salmeterol. First, the patient should tell the doctor or pharmacist about any allergies they may be suffering. Also, the patient should tell the physician about any other LABA combinations they are using (Ambrose et al., 2012). Furthermore, the patient should tell the doctor about any supplements and prescription medication they are taking. In case of pregnancy, breastfeeding or planning to become pregnant, the patient should let the doctor know before administering salmeterol.

References

Ambrose, H., Lawrance, R., Cresswell, C., Goldman, M., Meyers, D., & Bleecker, E. (2012). Effect of v2-adrenergic receptor gene (ADRB2) 3 untranslated region polymorphisms on inhaled corticosteroid/long-acting v2-adrenergic agonist response. Respiratory Research, 13(1), 37. doi: 10.1186/1465-9921-13-37

Dharmarajan, K., & Rich, M. (2017). Epidemiology, Pathophysiology, and Prognosis of Heart Failure in Older Adults. Heart Failure Clinics, 13(3), 417-426. doi: 10.1016/j.hfc.2017.02.001

Fiuzat, M., & Califf, R. (2011). Conduct of Clinical Trials in Acute Heart Failure: Regional Differences in Heart Failure Clinical Trials. Heart Failure Clinics, 7(4), 539-544. doi: 10.1016/j.hfc.2011.06.004

Guazzi, M. (2008). Clinical Use of Phosphodiesterase-5 Inhibitors in Chronic Heart Failure. Circulation: Heart Failure, 1(4), 272-280. doi: 10.1161/circheartfailure.108.802116

Tamura, G. (2017). Comparison of the aerosol velocity of two Respimat soft mist inhalers and two pressurized metered-dose inhalers for short-acting muscarinic antagonists. Respiratory Investigation, 55(4), 287-288. doi: 10.1016/j.resinv.2017.03.003