Pharmacology. Case Study

Pharmacology. Case Study

What is happening to Elliot

What is happening to Elliot is a condition known as hypokalemia. This is associated with potassium loss in the body. The signs and symptoms linked with this condition include nausea, weakness, visual disturbances as well increased fatigue(Turakhia et al., 2014). Hypokalemia is referred generally as serum potassium level that is less than 3.5 mEq/L. The potassium homeostasis plays a significant role in the body. For instance, the potassium homeostasis maintains the cellular function especially the muscle and nerve cells. Ion specific exchange pumps such as adenosine triphosphate ATPase pumps regulate the potassium homeostasis tightly. The renal secretion regulation, the pancreas, and potassium adrenal gland play a paramount role in maintaining the potassium homeostasis(Shah et al., 2014). The low potassium intake in patients places the patient at a risk of developing hypertension. It is also linked with hypertensive end-organ damage. Hypokalemia may result in the altered vascular activity as a result of the depletion of potassium on mediators of vascular relaxation, angiotensin receptor, and the adrenergic receptors. The impaired relaxation and vasoconstriction is enhanced and may play a paramount role in diverse clinical sequelae development.

For his hypertension, Eliot is using hydrochlorothiazide, a drug that tends to minimize potassium levels. Thus when taking thiazide, it is also recommended that he incorporates potassium supplements, eat diet rich in potassium and also decrease the amount of salt intake. Eliot is also taking digoxin(Vamos et al., 2015). The combination of the two drugs, thiazide and digoxin, worsens cardiac arrhythmias. While thiazides work by inhibiting sodium chloride transport in the distal tubules, digoxin increases force of contraction. This is due to inhibition of the NA-K-ATPase activity of the myocardial cells leading to overload of sodium in the cells and an increase in sarcoplasmic calcium content mediated by Na/Ca exchange.

Elliot may be experiencing digoxin toxicity also. The common symptoms and signs associated with the problem include cardiac arrhythmias which are severe, visual changes, weakness, fatigue, decreased appetite, vomiting, and nausea. Elliot is complaining of more than one of these symptoms. The symptoms and signs may be as a result of the interaction between amlodipine, lisinopril, and digoxin(Maury et al., 2016)

. The Digoxin inhibits the Na-K-ATPase  membrane pump. This is associated with the increased intracellular levels of sodium concentration.  The increased concentration of sodium intracellular level stimulates the sodium-calcium exchange.  This result in the increase in the concentration of sodium as well. The contractile protein activation is increased. The force and velocity of myocardial contraction are increased as well (Physician Desk Reference, 2017). The toxicity occurs when the concentration of calcium is above the storage capacity. The excess calcium concentration activates depolarizing current that is in correspondence with the sodium-calcium exchange. The current generated delayed after depolarization that is associated with ventricular arrhythmias.

In the treatment of severe digoxin toxicity, digibind is used.  Performing more blood work on Elliot is important. This is important to assess the current digoxin level in Elliot case. It is also important to hold the digoxin medication for several days before restarting the medication on Elliot(Shah et al., 2014). It is important also to evaluate the digoxin toxicity levels to make sure they are within the normal act before starting any form of medication.  Monitoring Elliot digoxin toxic level should be a continuous process.  If the drug fails to work, it is important to start Elliot on another type of medication.  The newly introduced medication should be effective on Elliot hypertension. It is also important to monitor Elliot closely.



Maury, P., Rollin, A., Galinier, M., &Juillière, Y. (2014). Role of digoxin in controllingthe ventricular rate during atrial fibrillation: a systematic review anda rethinking. Research Reports In Clinical Cardiology, 593-100.doi:10.2147/RRCC.S44919

Shah, M., Tsadok, M. A., Jackevicius, C. A., Essebag, V., Behlouli, H., &Pilote, L. (2014). Relation of digoxin use in atrial fibrillation and the risk of all-cause mortality in patients≥ 65 years of age with versus without heart failure. The American journal of cardiology114(3), 401-406.

Turakhia, M. P., Santangeli, P., Winkelmayer, W. C., Xu, X., Ullal, A. J., Than, C. T., …& Yang, F. (2014). Increased Mortality Associated with Digoxin in Contemporary Patients with Atrial Fibrillation: Findings from the TREAT-AF Study. Journal of the American College of Cardiology64(7), 660.

Vamos, M., Erath, J. W., &Hohnloser, S. H. (2015). Digoxin-associated mortality: a systematic review and meta-analysis of the literature. European heart journal36(28), 1831-1838.

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