Pharmacology Case Study Example | Topics and Well Written Essays - 500 words

Pharmacology - Case Study Example Applicable to patients who were diagnosed with hypertension, OConnell (2014: 12) pointed out the idea that â€Å"calcium channel blockers† should be given to those with African origin. Since the patient is an African man, the administration of â€Å"calcium channel blockers† is much better as compared to Maxzide 37.5/25 mg each morning. As such, the best option to improve CF’s blood pressure is to change the patient’s current medication to calcium channel blockers and ACE inhibitors (i.e. Lotrel – amlodipine and benzepril, Teczem – diltiazem and enalapril, or Lexxel – felodipine and enalapril) (Makani et al., 2011). Calcium channel blockers can effectively reduce the patient’s blood pressure by purposely dilating the arteries (Elliott & Ram, 2011). The main reason behind the need to combine the use of calcium channel blockers with ACE inhibitor is not only to increase its effectiveness in treating hypertension but also to prevent the risks of developing peripheral edema caused by the use of calcium channel blocker monotherapy (Makani et al., 2011). The following are the initial dosage of each alternative medication: BMI between 30 to 34 is classified as â€Å"obese 1† whereas BMI between 35 to 40 is classified as either â€Å"obese II or III† (University of Vermont, 2015). The fact that the patient’s BMI is 32 strongly suggests that the patient is obese. To prevent the risks of developing serious organ damage (i.e. stroke or heart failure); patient teaching should focus on the need to encourage the patient to change or modify his lifestyle. In general, BP of more than 140/90 is classified as â€Å"Stage 1† hypertension (OConnell, 2014: 12). Given the fact that obesity is one of the possible causes of hypertension (OConnell, 2014), patient teaching should include weight control through proper diet and

The genetic basis of glucose-6-phosphate dehydrogenase (G6PD) Essay

The genetic basis of glucose-6-phosphate dehydrogenase (G6PD) deficiency - Essay Example 008, pp.64, define G6PD deficiency as â€Å"an X-linked, hereditary genetic defect due to mutations in the G6PD gene, which cause functional variants with many biochemical and clinical phenotypes†. Most of the mutations are single base changes that result in amino acid substitutions. G6PD deficiency presents itself clinically in the form of acute haemolytic anaemia (Capellini & Fiorelli, 2008). The gene responsible for the production of the enzyme G6PD is the G6PD gene G6PD is the catalyst responsible for oxidising glucose-6-phosphate to 6-phosphogluconate, while at the same time it is also responsible for the reduction of the oxidised form of nicotanamide adenine dinucleotide phosphate (NADP+) to nicotinamide adenine dinucleotide phosphate (NADPH). This function of G6PD in the production of NADPH is important, as it is NADPH that plays a role as a cofactor in many biosynthetic reactions and maintaining glutathione in its reduced form (Carter & Gross, 2008). Reduced glutathione functions as a scavenger within cells, removing the dangerous oxidative metabolites in the cells. In addition with assistance from the enzyme glutathione peroxidase, it neutralizes hydrogen peroxide, which is harmful to the cell, by converting it to water. G6PD and its role in the production of NAPDH is important to red blood cells, as NAPDH is the sole contributor of protection to the red blood cells against oxidative stresses, The importance of G6PD to the red blood cells lies in it being the sole source of NAPDH and the protection NAPDH offers the red blood cells (Carter & Gross, 2008). The G6PD gene that is responsible for the enzyme Glucose-6-Phosphate Dehydrogenase is found on the terminal region of the long arm of the X chromosome (Xq28), at a distance of less than 2 centi-Morgan centrometric to the Factor VIII gene. G6PD deficiency is a genetic condition, wherein the molecular grounds for the disease stems from mutations in the G6PD locus at Xq28. The length of the gene is 18