The Implications of Prescribing Oral Lactose, Oral Frusemide, Multi-Vitamin B Forte for Patient with Reference to the Pharmacodynamics of Each Medication - Case Study Example

Name Pathophysiology and Pharmacology Course Date Pathophysiology and Pharmacology Question 3 Margaret is prescribed oral lactulose 45 ml QID and oral Frusemide 40 mg BD. Discuss the implications of prescribing these medications for Margaret with reference to the pharmacodynamics and pharmacokinetics of each medication Oral lactose 45 ml QID The oral lactose 45 ml QID was prescribed due to constipation Margaret had and for prevention and treatment of portal-systemic encephalopathy due the liver failure. In treating Margaret’s constipation, lactulose has a laxative action. Lactulose is a synthetic disaccharide osmotic laxative made up of galactose and fructose. The breakdown of lactulose to lactic and acetic acid causes elevated osmotic effect which results to elevated fecal bulk, softened stool as well as reduced transit time (Skidmore-Roth, 2013). Lactulose cannot be digested and hence it passes via the gastro intestinal tract to the colon without being changed where it is digested by bacteria that are naturally within the gastro intestinal tract forming low molecular weight acids that acidify the colon contents. This leads to production of weak acids which increases the fluid content of the stool causing distention of GI tract and hence promotes peristalsis and bowel evacuation as well (Skidmore-Roth, 2013). Additionally, lactulose will also lower serum ammonia levels in Margaret due to the liver failure. The breakdown of lactulose will acidify colon and as a result ammonia (NH3) will be converted to ammonium (NH4+), which cannot be absorbed and hence will be excreted in the stool. Still, since the colon contents are more acidic than blood, ammonia migrates from the blood into the colon forming ammonium ion and the laxative action of the lactulose metabolites then removes the trapped ion from the colon where the ion-trapping effect will cause the ammonia to diffuse from the blood into the colon where ammonia excretion will also occur because lactulose will reduce the concentration of ammonia in the blood as well as reduce the degree of portal-systematic encephalopathy. Excretion of urine is lower or at 3 percent and is basically complete in 24 hours (Skidmore-Roth, 2013). Oral Frusemide 40 mg BD Oral Frusemide 40 mg BD was prescribed to treat ascites which is typified by excessive accumulation of fluid within the abdominal cavity. In Margaret, this is manifested by worsening fatigue and bilateral edema. Frusemide is a diuretic and hence it will increase the amount of urine that Margaret passes from her kidneys. Frusemide will clear the excess fluid from her body because Margaret is retaining more fluids than the body needs and the excess fluid is what is causing worsening fatigue and bilateral edema (Brown & Cadogan, 2011). Frusemide will also prevent Margaret from developing further encephalopathy and also reduce the portal hypertension. The hyperdynamic circulation starts within the portal venous bed due to portal hypertension resulting from elevated increased resistance to flow from altered hepatic vascular morphology of the liver disease (Brown & Cadogan, 2011). Therefore, the oral frusemide will work by causing the kidneys to pass out more fluid through interfering with the transportation of salt and water across the cells in the loops of Henle in the kidneys. As the amount of fluids passed out by the kidney increases, lower amount of fluids remain within the bloodstream. Therefore, any fluids that have built up in the tissues and body as well will be drawn back in the bloodstream for the replacement of the extra fluids passed out through the kidneys. This will manage and treat symptoms such as worsening fatigue, tachycardia as well as bilateral edema in Margaret which was being caused by accumulation of extra fluid (Brown & Cadogan, 2011). In addition, frusemide will increase the excretion of urine of water and electrolytes by inhibiting reabsorption of electrolyte from the nephron lumen which will increase osmolarity and excretion of water. Since frusemide is a diuretic, it will inhibit the Na+-K+-2Cl– symporter from the luminal surface of the medullary and cortical segments of the thick ascending extremity of the loop of Henle through a competitive bi excretion, whereby there is also increased tubular flow and also an increased volume of urine is excreted (Brown & Cadogan, 2011). Question 4 Multi vitamin B Forte Margaret has liver failure which is an advanced liver disease and thus she has developed deficiency of fat soluble vitamins making it necessary for her to have multi vitamin B Forte to prevent and treat deficiency of vitamin B and vitamin C. normally, deficiencies in vitamins such as Vitamin B are common in liver disease. Additionally, the risk of encephalopathy increases when a patient has liver disease in patient deficient in thiamine. B-complex vitamins mostly affected by liver disease consist of B1, B-6 and B-12 and also liver damage reduces B-12 store in the liver (Victor, 2009). Therefore, Margaret should take multi vitamin B Forte to improve nutritional deficiencies that normally develop when a person has liver disease. Margaret shows symptoms of severe B-1 deficiency which is manifested by her increasing mental confusion and poor coordination indicated by calling her plate a cup and wanting sit on the table while pointing at the chair. Taking the multi vitamin B Forte that has B-1 can assist in reversing these symptoms. Similarly, deficiency of vitamin B-6 due to her liver damage can damage the nerves while deficiency in Vitamin B-12 and folate can result to anemia which could be contributing to her persistent headache. Taking the multi vitamin B forte can reverse these symptoms (Victor, 2009). Vitamin B4 which is present in the multi vitamin B forte is very effective in reducing harmful levels of homocysteine which is an amino acid that contains sulfur which is a major contributing factor in heart disease and Margret is showing a symptom of heart disease with the developing tachycardia. Normally, homocysteine plays an important part in the biosynthesis of cysteine, which helps the glutathione in the liver in detoxification of carcinogens as well as other toxins but without sufficient methylation, this cannot occur. Folic acid and other vitamin B vitamins facilitate the methylation process and hence deficiency of these biochemical reactions resulting from methylation of homocysteine cannot take place (Ronald, 2014). Additionally, low amount of vitamin B4 results to high levels of lipoperoxidases which indicates an elevated oxidative stress. Accordingly, vitamin B4 has a likelihood of benefiting Margaret during her early stages of acute liver disease and also to prevent further oxidative damage that occurs as the process of liver damage continues (Ronald, 2014). Studies have shown that vitamin B4 improves liver chemistry measurements during the recovery duration after the sickness. This improvement is associated with the impact of nucleotide synthesis. Studies have also shown that reduced levels of folic acid which a vitamin B complex resulted to increased levels of homocysteine and thus elevated oxidative stress as well as liver peroxidation (Dancygier, 2009). The B vitamins have a very important role in several metabolic functions that consist of enzymatic activities. The enzyme activities play numerous roles and are also metabolize carbohydrates and fats and assist in the function of the nervous and digestive system, red blood cells production as well as have synergistic influence on each other. The B vitamins are in big quantities in the liver and hence when the liver is damaged as in case of Margaret, these vitamins are affected and therefore the necessity of Margaret to be administered with multi vitamin B Forte (Dancygier, 2009). Question 5 How would Margaret’s pathophysiology be different if her BMI was 45? If the BMI of Margaret was 45, it would mean that she is obese and hence her liver damage would have resulted from building up of fatty acids in the liver. Amassing of fatty acids on the liver makes the liver to be fatty. Pathogenesis occurs in two ways where in the first way the hepatic steatosis due a fatty liver renders the liver venerable to some hepatic insults resulting to inflammation of the liver as well as steato-necrosis and fibrosis (Loomba & Lutchman et al., 2009). Hepatic steatosis is linked with insulin resistance in which the tissues attempt to protect themselves from increasing fat. The free fatty acids stimulate an enzymatic cascade that results to the impairment of usual normal tyrosine phosphorylation of insulin receptor substrates. This results an impaired transportation of glucose in the cell. Factors that contribute to the disruptions in physiologic pathways include fatty diets and cholesterol, a decreased capacity of insulin to hamper lipolysis as well as reduced protein levels that are involved in the metabolism of VLDL (Taheri & Khedmat, 2011). The second way in which pathogenesis of liver damage occurs in people with high BMI encompass too much quantities of oxidative stress and pro-inflammatory cytokines with reduced hepatic ATP production. Amassing of fat within the liver and increased quantities of free fatty acids are the key contributing factors in the pathogenesis. Large quantities of fat in the liver can take place because of the liver absorbing increased quantities of free fatty acids, reduced oxidation of the free fatty acids, too much synthesis of the fatty acids in the liver, in addition to reduced generation of VLDL cholesterol by the liver (Khoshbaten, Aliasgarzadeh, Masnadi K, et al., 2010). When the free fatty acids are metabolized in the liver, this stimulates oxygen species involved in the production of free radicals. The free radicals are extremely reactive and they consequently stimulate a damaging metabolism for free fatty acids called lipid peroxidation that causes cellular membranes to be disrupted and faulty cellular. Injection of insulin causes steatohepatitis within the liver (Taheri & Khedmat, 2011). This suggests that insulin contributes to the liver damage associated with excess body weight. Insulin does this by reducing metabolism of free fatty acids which causes an increase of the quantities of toxic free fatty acids within the liver. In addition, overweight people are resistant to insulin and have increased quantities of free fatty acids. Insulin levels in overweight people are enough to hinder the liver from delivering free fatty and hence increased insulin levels results to building up of free fatty acids within the liver, and as a result causing liver damage (Loomba & Lutchman et al., 2009). Mechanisms that elucidate the pathogenesis encompass absorption of bacterial products from the blind loop and also absorption of the bile acids, deficiency of protein-energy, deficiency of vitamins, in addition to pathologic activation of free fatty acids when an overweight person loses weight drastically. When overweight individuals stay for a long time without food for weight decrease, the level of insulin reduces; nonetheless, the level of insulin in overweight patients who previously had a gastrointestinal bypass surgery to reduce weight increases because they go on receiving starches which stimulate production of insulin. Similarly, the elevated quantities of insulin in these people results to building up of free fatty acids within the liver and consequently causing liver damage (Taheri & Khedmat, 2011). Bibliography Brown, A & Cadogan, M, 2011, Marshall and Ruedy's on Call Principles and Protocols, Sydney: Elsevier Australia. Dancygier H, 2009, Clinical Hepatology: Principles and Practice of Hepatobiliary Diseases: Volume 2, Melbourne: Springer. Khoshbaten M, Aliasgarzadeh A, Masnadi K, et al., 2010, N-Acetylcysteine Improves Liver Function in Patients with Non-Alcoholic Fatty Liver Disease, Hepat Mon, 10 (1):12-6. Loomba R & Lutchman G, et al., 2009, Clinical trial: pilot study of metformin for the treatment of non-alcoholic steatohepatitis, Aliment Pharmacol Ther. 29 (2):172-82. Ronald, J, 2014, Liver Disease in Children, Cambridge: Cambridge University. Skidmore-Roth, L, 2013, Mosby's 2014 Nursing Drug Reference, Austria: Elsevier Health Sciences. Taheri S & Khedmat, H, 2011, Non-alcoholic steatohepatitis: An update in pathophysiology, diagnosis and therapy, Hepatitis Monthly, 11 (2): 74-85. Victor, P, 2009, Nutrition, Diet Therapy, and the Liver, New Jersey: CRS Press. Read More