Pharmacogenomics Report: Metoprolol (Lopressor)
1. Mechanism of action/indications and use
Metoprolol is a common drug utilized to treat a range of cardiovascular problems including hypertension, heart failure, acute myocardial infarction, arrhythmia and tachycardia among others (Sagent, 2016). It acts as a beta blocker that specifically targets beta-1 adrenergic receptors found in the heart. Stimulation of beta-1 adrenergic receptors causes an increase in cardiac output by increasing heart rate (through action on receptors in the SA node) and contractility (by acting on the receptors in the myocardium). As a result, blocking these receptors with metoprolol would cause a decrease in heart rate, contractility, and blood pressure, ultimately alleviating some of the problems mentioned above (Brodde, 2008).
2. Pharmacokinetics
Metoprolol and other lipid soluble beta blockers undergoes hepatic as opposed to renal metabolism. The former process boasts a shorter half life than the latter through which metoprolol is quickly eliminated from the body (BHS, 2008).
The drug is primarily administered to a patient orally and the majority of the dosage is rapidly absorbed in the GI tract. Once ingested and absorbed, metoprolol quickly disperses throughout the body. Approximately 10% of metoprolol in the blood binds to serum albumin. Metabolism of the drug in the body occurs through the combination of alpha-hydroxylation, O-demethylation, and N-dealkylation via oxidative deamination.
The aspirin starts begins to dissolve by the enzymes and are soaked in while traveling down to the stomach. They then are distributed to the areas that need the pain relief.
Absorption – “How the drugs enter the circulation process through the body, and how they resist general breakdown by the stomach, liver, and the intestines”. Some of the factors that affect the absorption of drugs in the body is as follows, “acidity of the stomach, Physiochemical properties, Presence of food in the stomach or intestine, and Routes of administration”,
Patients who have congestive heart failure and do not respond to diuretics may benefit from a combination of several types of diuretic medication, each with a different system of action. Another medication for someone that has congestive heart failure can take Beta-blockers. Side effects include fatigue, cold hands, headache, upset stomach, constipation, diarrhea, dizziness, and shortness of breath. Data reported from 17 studies, researchers came to the conclusion that the risk of death from all causes was 31 percent lower in patients with heart failure who were treated with beta-blockers than in those not receiving such medications. Aldosterone blockers is a form of medication one may take to help slow down the rate of congestive heart failure.This medication can sometimes affect kidney function and can also increase potassium levels. Aldosterone blockers are prescribed to individuals who develop heart failure after a heart attack. Studies show that these medications can reduce the risk of hospitalization and death from cardiovascular disease. The last form of medication is BiDil (isosorbide
Depending on the rehabilitation facility, patients may be given medication to help combat the effects of an addiction. Individuals who are wondering, “What is naltrexone?” can ask their doctor or addiction specialist for help understanding the uses and side effects of the medication. While some detox facilities do not use any medication, others offer help to combat the addiction.
Well written paper on beta blockers in controlling hypertension. In my experience, I had seen more than 80% of patients are prescribed with antihypertensive drugs in their medical chart. A beta blocker is one of the most common drugs in a geriatric setting especially atenolol. Beta blockers are the standard of therapy for many cardiovascular conditions and it is the main line of treatment in decreasing risk of stroke. According to Ladage, Schwinger, and Brixius (2013) beta blocker was more effective in decreasing mortality and morbidity rate in acute coronary syndrome patients. Atenolol is a water soluble and had longer half-lives with non-metabolized actions and excreted via the kidneys (Ladage et al., 2013). The exercise capacity increases in patients who are on beta-blockers, like bisoprolol, nebivolol, carvedilol (Ladage et al., 2013). A recent meta-analysis study showed patients who are untreated with hypertension, they are at risk of developing chronic kidney diseases, cardiovascular complications, and cerebrovascular complications (Butt & Harvey, 2015). In one study, mainly geriatric population who are taking atenolol had shown greater mortality rate and increase arterial pressure (Testa et al., 2014).
Beta Blockers are known as a medicine that used to treat a person who has a blood pressure. By blocking the effect of adrenaline and noradrenaline, this drug can lower blood pressure, slow down the heart rate and lessen the force of the blood impelled in the body. While taking this drug, it requires to check the pulse daily and when it is slower than it was supposed to be, ask the doctor if the medication needs to take that day. Sometimes, the beta blocker doesn’t work right while the person is also using another drug. The person who is taking this medication should avoid caffeine and alcohol and for those whom this drug may not work with them are older people and people with asthma, for those who has a low blood pressure, and person who has
Metoprolol is a selective β1 receptor blocker.1 It is used to treat high blood pressure or hypertension, myocardial infarction (MI), heart failure and angina pectoris.2 Metoprolol was first made in 1969 and is on the World Health Organization’s list of essential medicines.3 Metoprolol is available only in its salt form due to its low melting point, such as metoprolol tartrate or metoprolol succinate. Its salt form, metoprolol tartrate was first developed by Novartis and was approved by FDA on August 7, 1978.4 Metoprolol is also available as a generic drug.1
Propranolol is a beta-blocker. Beta-blockers affect the heart and circulation (blood flow through arteries and veins).
Carvedilol (CAR, Figure 1) is a racemic mixture in which nonselective β-adrenoreceptor blocking action resides in the (-) enantiomer whereas blocking α1-adrenergic receptors is due to both (+) and (-) enantiomers at the same potency. The (-) isomer of CAR is administered in congestive heart failure in combination with diuretic therapy and ACE inhibitors. (-) CAR reduces lipid peroxidation level, as is
Diclofenac is 100% absorbed after oral administration compared to IV administration as measured by urine recovery. However, due to first-pass metabolism, only about 50% of the absorbed dose is systemically available .Food has no significant effect on the extent of diclofenac absorption. However, there is usually a delay in the onset of absorption of 1 to 4.5 hours and a reduction in peak plasma levels of < 20%. Diclofenac is primarily metabolized by CPY2C9. Diclofenac is eliminated through metabolism and subsequent urinary and biliary excretion of the glucuronide and the sulfate conjugates of the metabolites
especially in patients with a history of asthma. β-Blockers will have no effect on the patient’s
BB have been shown to be effective in treating people with PAD as well as those with undergoing any vascular surgery. For instance, after vascular surgery, the chance for myocardial infarction ranges from 5-24% after the surgery (Mostafaie et al., 2015). The aim of the study is to investigate the role of metoprolol and its effects on cardiac complications after vascular surgery in reducing cardiac mortality, myocardial infarction, and other cardiac problems. This was shown in a study by the Colcharne Collaboration. It is a double blind random control trial with one group (298 people) receiving a placebo, while the other group (301 people) received some type of beta blocker. To measure the results, a meta-analysis was done with an odds ratio (OR) and Confidence Interval (CI) (Mostafie et al., 2015). There was no evidence that perioperative beta-adrenergic blockade reduced all-cause mortality (OR 0.62, 95% CI 0.03 to 15.02), non-fatal myocardial infarction (OR 0.83, 95% CI 0.46 to 1.49; P value = 0.53), heart failure (OR 1.71, 95% CI 0.40 to 7.23), stroke (OR 2.67, 95% CI 0.11 to 67.08), or composite cardiovascular events (OR 0.87, 95% CI 0.55 to 1.39; P value= 0.57). However, there was strong evidence that BB increased the odds of intra-operative bradycardia (OR 4.97, 95% CI 3.22 to 7.65; P value < 0.00001) and intra-operative hypotension (OR 1.84, 95% CI 1.31 to 2.59; P value = 0.0005)
Carvedilol provides benefits through a balance in blocking beta receptors, which as a result on one hand reduce cardiac work and on other produce peripheral vasodilation. This drug ensures cardiovascular protection through their anti-proliferative, anti-atherogenic, anti-ischemic, anti-hypertrophic and antiarrhythmic actions. These actions are a consequence of their potent antioxidant effects, decreased lipid metabolism, glucose, insulin sensitivity, modulating neurohormones factors and modulation of cardiac electrophysiological properties (Andersson et al., 2014). By reducing the heart rate, the myocardial metabolism is decreased, the ventricular diastole filling is prolonged, and thus the infusion time, increase coronary flow, and also streamlines
as “Predictors of Success of Methotrexate Treatment in Women with Tubal Ectopic Pregnancies.”7 The objective of this study is determining the institutional success rate with single-dose intramuscular methotrexate therapy for the treatment of ectopic pregnancy and to identify predictors of treatment outcome. This research was a retrospective study which reviewed consecutive patients who were treated with methotrexate from 2000 to 2002. Their treatment success was defined as complete resolution of ectopic pregnancy without the need for surgical intervention. The result of the study was success rate of 85% (69/81 patients). Women in which their treatment was successful their pretreatment serum beta-human chorionic gonadotropin (HCG) level was lower compared to those were treatment was not successful (793 vs 3804 mIU/mL, P 2000mIU/mL), history of
Metformin transporter genes have been studied in vivo in rodents to explain metformin pharmacodynamics. The distribution of metformin to the liver in Oct1 −/− mice was reduced 30-fold compared with wild-type mice [6], and the glucose-lowering effects of metformin