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Pharmacotherapy for Cardiovascular Disorders


Among the leading causes of death in the United States, cardiovascular disorders are fatal, worse than even AIDS and cancer combined. Statistics shows that approximately 1 million victims die of these disorders annually (Arcangelo & Peterson, 2013, p. 213). As such, a person dies of these disorders after every 33 seconds. The reason for this shocking revelation is that the disorder demands extensive treatment and nursing care post-diagnosis. Nonetheless, even with these statistics there is something to smile about since there has been a significant decline in the number of deaths since 1960s.

This is owed to the fact that practitioners take into consideration the patient’s medical history together with the risk factors before administering treatment. Such factors as the patient’s gender, age, ethnicity and genetics have an influence on a patient’s pharmacokinetic and pharmacodynamics. As such, an advanced nursing practitioner (ANP) needs to fathom this for the sake of effective treatment. In this essay, a victim of cardiovascular disorder undergoes examination prior to recommendation of an appropriate treatment course.

Patient’s condition and drug therapy

In this case study, the victim is suffering from atrial fibrillation (AF) and transient ischemic attack (TIA) both of which are cardiovascular disorders. Apart from this, the patient has been diagnosed with ischemic disease, type 2 diabetes, hypertension and hyperlipidemia. In this condition, the patient is under this dosage: 5 mg of warfarin on Mondays, Wednesdays and Fridays and 2.5 mgs of warfarin on the other days; 81 mg of aspirin daily; 1000 mg of metformin po bid; 10 mg of glyburide bid; 100 mg of atenolol daily; and 200 mg of motrin after every 6 hours.

How genetics influences pharmacokinetics/pharmacodynamics

Among the risk factors that might influence the both pharmacokinetics and pharmacodynamics of this patient is genetics. Humans respond differently to drugs owing to variability in the genetic makeup. As such, up to 95% of the variability in drug response is genetically-based, which is responsible for drug efficacy as regards drug-metabolism and excretion (Amudha, Wong, Choy, & Lang, 2003, p. 1692).

On narrowing down to pharmacokinetics study, the focus is on the drug’s efficacy rate until excretion. Once ingested, the drug takes this course: metabolism usually in the liver, before excretion via the kidney. Genetic profiling of many drug-metabolizing enzymes is available. This is inclusive of the p450 enzymes, the main drug-metabolizing enzyme in humans. As such, a variety of humans with distinct phenotypic information exhibiting abilities to metabolize drugs at different rates exist. This differs among ethnics. Moreover, intrinsic and extrinsic factor e.g. smoking influences pharmacokinetics.

With regards to pharmacodynamics, the focus is on the effect the drug has on the biological system. The relationship pitting drug concentration and biological drug response is dependent on the drug’s mode of action (Koopmans, Insel, & Michel, 2003, p. 707). The mode of action of the drug in the body may be direct, for instance, through binding a particular receptor, or indirect via inhibition. Enzyme profiling of genes responsible for hypertension reveals blacks as more prone to severe cases of hypertension than their whites’ counterparts.

This reflects on the polymorphism in their genes. To this end, the drug therapy for blacks ought to have lower dosage of diuretics, or high-dosage of ACE (angiotensin-converting enzyme) inhibitors (Trotta, Donati, & Iacoviello 2004, p. 355). Hyperlipidemia is a gene-related cardiovascular disorder, a consequence of mutation of the gene responsible for reducing the low-density lipoproteins in the blood stream. Other extrinsic factors e.g. lifestyle contribute to this condition.


In view of a patient of blacks’ ethnicity, and exhibiting the aforementioned conditions, lower dosages of diuretics combined with high levels of any ACE drug e.g. captopril, or ARBs would work best for the patient since he/she is diabetic. The ACE will also work well to mitigate hyperlipidemia condition.


Amudha, K., Wong, L. P., Choy, A. M., & Lang, C. C. (2003). Ethnicity and drug therapy for hypertension. Curr Pharm Des., 9 (21),1691–1701.

Arcangelo, V. P., & Peterson, A. M. (2013). Pharmacotherapeutics for advanced practice: A practical approach (3rd ed.). Ambler, PA: Lippincott Williams & Wilkins.

Koopmans, R. P., Insel, P. A., & Michel, M. C. (2003). Pharmacogenetics of hypertension treatment: a structured review. Pharmacogenetics, 13 (12), 705– 713.

Trotta. R., Donati, M. B., & Iacoviello, L. (2004). Trends in pharmacogenomics of drugs acting on hypertension. Pharmacol Res., 49 (4), 351–356.

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StudyKraken. (2022, August 26). Pharmacotherapy for Cardiovascular Disorders.

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"Pharmacotherapy for Cardiovascular Disorders." StudyKraken, 26 Aug. 2022,

1. StudyKraken. "Pharmacotherapy for Cardiovascular Disorders." August 26, 2022.


StudyKraken. "Pharmacotherapy for Cardiovascular Disorders." August 26, 2022.


StudyKraken. 2022. "Pharmacotherapy for Cardiovascular Disorders." August 26, 2022.


StudyKraken. (2022) 'Pharmacotherapy for Cardiovascular Disorders'. 26 August.

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