Drug action

Drug action Mr is a 60 year old gentleman who lives with his partner. Mr has smoked 10 cigarettes per day for 30 years and has recently been screened for bowel cancer with a positive result. Lipitor which is also known as atorvastatin is one of the medications that Mr Jones is having. The purpose of this paper is to introduce the clinical use of atorvastatin and explore the anatomy, physiology and pathophysiology associated with the action of atorvastatin. Also, the reason why atorvastatin is being given to Mr Jones will be demonstrated.

Clinically, the primary uses of atorvastatin are for the treatment of dyslipidemia and the prevention of cardiovascular diseases. People with high blood cholesterol or at risk of stroke, heart attack, or other heart complications in people with type 2 diabetes, coronary heart disease would receive atorvastatin (Atorvastatin Calcium 2013). Mr Jones might have atorvastatin because he has Ischaemic Heart Disease (IHD) and he is at risk of Transient Ischaemic Attack (TIA). Atorvastatin is recommended to be used in conjunction with some other nondrug therapies such as diet, exercise, and weight reduction (Atorvastatin Calcium 2013).

The recommended starting dose of atorvastatin is 10 or 20 mg once daily. Patients who require a large reduction in LDL-C may be started at 40 mg once daily. The dosage range of atorvastatin is 10 to 80 mg once daily (Atorvastatin Calcium 2013). A brain, with billions of neurons, continuously demands for adequate blood supply which contains nutrients and oxygen. The network of blood vessels in the brain carries blood supply to the brain (Martini, Nath & Bartholomew 2012, pp. 454-455).

In a person with hypercholesterolemia, the excessive LDLs cannot be removed from the blood by receptor-mediated mechanisms. Subsequently, it can cause the accumulation of cholesterol on cerebral arterial wall and development of atherosclerosis (Pathophysiology 2011, p. 422). When a blood vessel in the brain is blocked by a clot, the blood supply to the brain is interrupted and a TIA can occur (Martini, Nath & Bartholomew 2012, pp. 454-455). In the case of Mr Jones, he might have had the TIA because of atherosclerosis causing narrowing vessels in the cerebral blood supply.

Atorvastatin is a HMG-CoA reductase inhibitor which can lower plasma LDL and total cholesterol (pharmacology p. 603). The effect of atorvastatin begins with inhibition of hepatic HMG-CoA reductase which is an enzyme found in liver and required for cholesterol biosynthesis. Subsequently, cholesterol biosynthesis in the liver is inhibited. Furthermore, for reasons that are not fully understood, the inhibition of cholesterol biosynthesis causes liver cells to synthesize more LDL receptors (pharmacology p. 604).

LDL receptors on the surface of liver cell can recognise apoprotein B100 which is embedded in the outer layer of LDL particles and bind to LDL particles (Goldstein & Brown 2009, pp. 431-438). As a result, more LDLs can be removed from the blood. In terms of pharmacokinetics, Atorvastatin is rapidly absorbed by the patients after oral administration. The plasma concentration reaches maximum concentration within 1 to 2 hours. Taking atorvastatin with food can reduce the rate of absorption by decreasing peak concentration (Lennernas 2003, p.1141).

The absorbed amount of atorvastatin ranges between 30% and 90%. Regardless of how much atorvastatin has been absorbed, most of the atorvastatin is extracted from the blood when it first passes the liver. Atorvastatin and its metabolites are eliminated primarily in bile following hepatic metabolism (pharmacology p. 606). In the case of Mr Jones, atorvastatin can lower the LDL and total cholesterol in his blood and prevent the accumulation of cholesterol on his cerebral arterial wall. The risk of getting a TIA can be decreased.

Pathophysiology in Jones` vessels. When administering atorvastatin, safety of the patient must be taken into account. Contraindications of atorvastatin include pregnancy, breastfeeding, hypersensitivity to atorvastatin, and active liver diseases such as viral or alcoholic hepatitis (Atorvastatin Calcium 2013). In addition, when atorvastatin is used on liver transplant patients, extra caution should be taken if they are on other drugs that inhibit drug-metabolizing enzymes (Tandra & Vuppalanchi 2009, pp. 272–278).

Furthermore, although atorvastatin is generally well tolerated, patients still have a chance to develop some side effects. Mild side effects of atorvastatin include constipation, diarrhea, fatigue, heartburn, and headache (pharmacology, p. 606). When used alone and particularly when used with other drugs that are myotoxic or that raise the concentrations of atorvastatin, atorvastatin can cause myopathy and rhabdomyolysis (Murty, McMorran & Vu 2002, pp. 85-86).

Several factors including advanced age, small body frame, chronic renal insufficiency, and hypothyroidism increase the risk of myopathy and rhabdomyolysis (Murty, McMorran & Vu 2002, pp. 85-86).

Besides, atorvastatin has hepatotoxicity. 0. 5% to 2% of the patients who have been using atorvastatin for 1 year or longer may develop liver injury (pharmacology, p. 606). In terms of nursing practice, nurses must ensure that patients do not have contraindications of atorvastatin before administering atorvastatin. It is recommended that atorvastatin is initiated at lower therapeutic doses because evidence suggests that myopathy is dose-dependent (Murty, McMorran & Vu 2002, pp. 85-86).

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