CBL Case Presentation - Essay Example

Hypertension in past 12 months. Mrs MJ’s medications are: Lercanidipine 20mg D Metoprolol 50mg BD Furosemide 160mg BD Cholecalciferol 25mcg D Predinsolone 12.5mg D Azathioprine 80mg D 1. Lercanidipine: is a dihydropyridine calcium-channel blocker. Mode of Action (MOA): In deforming the channel, preventing the ion-control gating mechanisms, and/or interfering with the release of calcium from the sarcoplasmic reticulum, this drug prevents the influx of extracellular calcium within the myocardial and vascular smooth muscle cell membranes.

The reduction in the intracellular calcium prevents the contraction of processes of the myocardial smooth muscle cells, leading to the dilation of the coronary and systemic arteries, leading to improved oxygen delivery to the myocardial tissues and decreased after load (1). Pharmacokinetic (PK): Completely absorbed after oral administration with bio-availability of 10%. Distribution: protein binding is 99%. Metabolised by CYP3A4, and 50% of the drug is excreted in the urine unchanged. The therapeutic activity lasts for 24 hours due to binding to lipid membrane.

In severe renal dysfunction or dialysis-dependent patient - plasma level increases (2). Therefore, this drug should be contraindicated in severe renal impairment as in our patient’s case. . : This drug particularly inhibits beta1-adrenergic receptors; which are mainly found on the cardiac muscles cells; therefore it has a highly selective activity towards the heart with little or no activity on beta 2 adrenegeric receptors in therapeutic doses. By blocking the beta 1- adrenergic receptors on cardiac muscles cells it causes reduction in heart rate and contractility leading to reduced cardiac output(4).

PK: Almost completely absorbed >95% from GI tract. 95% is metabolised by the liver; less than 5% of an oral dose eliminated unchanged in the urine with half life of 4 hours. Since Metoprolol mainly metabolised by liver, there should not be any concern regarding use in this patient. Side effects include bradycardia, postural hypotension, cold hands and feet, palpitations (5). Pharmacogenetic: Therapeutic dose recommendations have been evaluated based on CYP2D6 genotype, and as a result, for poor and intermediate metabolisers, change of selection or dose reduction has been recommended (6).

Furosemide: MOA, Loop diuretic. The molecular target is sodium – potassium -2 chloride co transporter (NKCC2), which transports 1Na, 1K, 2CL ions. The activity of this transporter is blocked by furosemide leading to increases diuresis (7). PK: Well absorbed from GI tract (more than 60%). Distribution: binds to protein mainly albumin (95%). Only small amount hepatically metabolised with the majority excreted unchanged through urine. Half life: up to 2 hours. Excretion: 80% is excreted in urine unchanged through both glomerular filtration and proximal tubular secretion (8).

Side effects include electrolyte imbalance, decreased serum potassium; excessive diuresis, headache, dry mouth, visual impairment, hypotension (9). Pharmacogenetics: renal and hepatic furosemide