Analysis Pharmacokinetics Related to the Patient - Case Study Example

Author’s Name: Instructor’s Name: Course Details: Institutional Affiliation: Date of Submission: Appendix B-Proforma for pharmacology table Note: All medications need to be on one table so any drug interactions etc can be obvious to the student or marker. This table should be written in size 9 font & please ensure that headings are repeated on each page (if you don’t know how to do this ask your lecturer). Names of medication and Dosage Mode of Action & why is it ordered for this patient Pharmakinetics related to the patient A Absorption D Distribution M Metabolism E Excretion HL Half life P Peak Main side-effects related to patient Contraindications and Drug interactions related to patient Frusemide Administration of fruseimide is either conducted orally of through the intravascular and intramuscular routes. However, the intravascular doses ought to e administered at a rate not exceeding 4mg/min to avoid ototoxicity (MIMS, 2012). In oral administration, the dosage is 20-40mg once or twice daily. However this dosage is adjusted basing on the clinical response of the patient to the maintenance dose and can reach a maximum of 400mg daily (MIMS, 2012). Frusemide mediates its functions by increasing the elimination of water from the body through urine. Frusemide inhibits the absorption of sodium and chloride ions at the ascending loop of henle. As a result the reabsorbtion of water by the kidneys is inhibited. Frusemide is a loop diuretic that is used in edema resulting from liver failure. The patient has bilateral edema as well as ascitis. Frusemide is used in this patient to correct the bilateral edema and ascitis. Frusemide necessitates the loss of water by inhibiting its reabsorbtion in the loop of henle (MIMS, 2012). Frusemide is rapidly absorbed within the gastrointestinal tract. The efficacy in the absorption of frusemide within the gastrointestinal tract ranges between 60 to 70% in the patients with liver failure (MIMS, 2012). Distribution Frusemide is distributed in the body while bound to the plasma proteins mainly albumin (MIMS, 2012). Excretion The excretion of frusemide occurs through the renal system in the patients with a normal renal function. However some minimal amounts of frusemide are excreted though the faeces (MIMS, 2012). Half life The half life of frusemide in plasma ranges up to 100 minutes. However, hepatic insufficiency prolongs the half life of frusemide (MIMS, 2012). Peak The effects of frusemide start taking toll between one to two hours after its administration (MIMS, 2012). The patient encountered headache episodes after the use of frusemide (MIMS, 2012). --- Lactulose The administration of Lactulose is administered orally or through the rectal route. The dosage of lactulose is 20-30 mg 6 hourly. However the dose will be adjusted with every one to two days in order to achieve the production of two to three stools per day (MIMS, 2012). Lactulose prevents hepatic encephalopathy from occurring. Lactulose is metabolised by the colonic bacteria to form short chained fatty acids and produce lactic and acetic acids respectively. This leads to acidification of the contents within the gut by increasing the concentration of the hydrogen ions. The acidification of the gut attracts ammonia from the blood stream making it to become trapped in the stool. At the same time, the hydrogen ions lead to the formation of the non absorbable ammonium ion from ammonia. This leads to the reduction of the concentration in the plasma concentrations of ammonia. Lactulose was given to the patient to reduce the effects of nitrogenous wastes which is characteristic of liver failure. This is attributed to the fact that the patient had features that suggested the building up of nitrogenous wastes which includes confusion, disorientation and being in high spirits. Lactulose increases the transit time of the contents within the gut hence reducing the amount of nitrogenous wastes being formed and their absorption (MIMS, 2012). Absorption Lactulose is absorbed in minimal amounts of nearly 3%. Lactulose is absorbed within the gastrointestinal tract (MIMS, 2012). Excretion Lactulose is excreted in urine unchanged (MIMS, 2012). Half life Lactulose has a half life of 1.7 to 2 hours (MIMS, 2012). Peak Peak of lactulose is at 100 minutes (MIMS, 2012). Headaches, nausea (MIMS, 2012). --------- Omeprazole Omeprazole is given at a dose of 20 mg once daily and is administered orally or though the intravenous route (MIMS, 2012). Omeprazole mediates its functions by inhibiting the acid pump that is located within the parietal cells. Omeprazole is basic in nature and it becomes active in the acidic environment found within the parietal cells. Omeprazole effects this by inhabiting the proton pumps that are found within the parietal cells. The inhibition of the proton pumps thus prevents the secretion of basal acid and the stimulated acid secretion. Omeprazole is given to reduce the secretion of excess acid by the parietal cells (MIMS, 2012). Administration Omeprazole is administered administration orally or through the intravenous route (MIMS, 2012). Absorption Omeprazole is a weak base that is effectively absorbed within the gastrointestinal tract (small intestines) (MIMS, 2012). Distribution Omeprazole is distributed in the body while bound to plasma (MIMS, 2012). Excretion 80% of omeprazole is excreted through urine whereas the remaining is excreted in faeces (MIMS, 2012). Half life The half life of omeprazole is usually less than one hour. However, the half life of omeprazole will be increased in this patient due to liver failure (MIMS, 2012). Half life The half life of omeprazole is usually within three to six hours (MIMS, 2012). Peak The peak plasma level of omeprazole is after four hours (MIMS, 2012). Headaches, nausea (MIMS, 2012). --------------- Metoclopramide Metoclopramide is given at a dose of 20mg once daily (MIMS, 2012). Metoclopramide increases the, motility of contents within the gastrointestinal tract. The increase in stimulation thus results in the reduction of the transit time of the gastric contents. Metoclopramide increases motility of contents in the gastrointestinal tract by increasing the tone and amplitude of gastric contractions. Therefore, metoclopramide produces the anti-emetic properties which antagonise the effects of the central as well as the peripheral dopamine receptors (MIMS, 2012). Administration Metoclopramide is administered through oral, intramuscular and intravascular routes. Absorption The absorption of the Metoclopramide occurs within the gastrointestinal system (small intestines). The absorption of omeprazole is influenced by the gastric acidity (MIMS, 2012). Half life The half life of Metoclopramide ranges between 2.5 to 6 hours (MIMS, 2012). Excretion Metoclopramide is excreted through the urine (MIMS, 2012). Headaches (MIMS, 2012). --------------------- Critique Omeprazole has positive effects to the patient which include reducing the transit time for gastric contents and diminish the amount of gastric acid secreted into the stomach. Even though omeprazole mediates these positive activities, its administration also comes with negative effects. The administration of omeprazole leads to the inhibition of the activity of other drugs. This is because omeprazole mediates its functions by inhibiting the action of the liver enzymes. Omeprazoles effect of inhibiting the liver enzymes reduces the breakdown of medication by the liver. The inhibition thus aggravates liver failure since the other medications given to the patient become more potent hence subjecting the liver to further insults or injury (MIMS, 2012). Pathophysiology of Ascitis Ascitis arises from the accumulation of fluids within the peritoneal cavity. The accumulation of fluids within the peritoneal cavity takes place following a cascade of events. In this patient, the ascitis is caused by portal hypertension. Portal hypertension is responsible for triggering the vasoconstrictor system as well as the retention of sodium. At the same time, portal hypertension leads to the elevation of the capillary hydrostatic pressures within the beds of the splachnic circulation. The occurrence of ascitis takes place in stages. The first stage involves the vasodilatation of the splachnic circulation. The progressive splachnic vasodilatation results in the decrease of the plasma volume. This means that various vital organs such as the liver, heart and the kidney are deprived the normal blood flow. The vasodilatation is activated by the decrease in arterial blood volume brought about by the severe arterial vasodilatation. Splachnic circulation vasodilatation leads to the hyperactivity of the endogenous systems of vasoconstriction. At the same time, splachnic vasodilatation leads to the increased retention of sodium and water by the kidneys. The initial phases of splachnic vasodilatation are well compensated by the body increasing its cardiac output. However, the continued splachnic vasodilatation leads to a marked decrease in arterial blood supply as well as the arterial blood pressures. in an attempt to maintain the normal arterial blood supply, the rennin-angiotensin , sympathetic and nervous systems respectively are activated. In addition, arganine and vasopressin are also activated. This leads to the retention of sodium and water. The condition is further made worse by the continued increase in capillary hydrostatic pressures within the splachnic circulation that further leads to sequestration of fluids within the abdomen. The accumulation of fluids within the peritoneal cavity is further aggravated by the low albumin levels due to the liver having lost its integrity. The low albumin levels aggravate the patient’s condition by allowing more fluids to be drawn into the peritoneal cavity due to low hydrostatic pressures. The accumulation of fluids within the peritoneal cavity continues gradually thus giving rise to ascitis (Porth & Matfin 2010, p. 969). The increase in body mass index aggravates liver failure. An increase in body mass index brings about retention of the drugs within the body for longer periods. In addition, the increment in body mass index brings about the increase in the deposition of fat on the liver cells. This in turn increases the susceptibility of the liver to injuries as well as limits its capabilities of regenerating (Hanley, Abernethy & Greenblatt 2010, p. 74). Continued injuries subjected to the liver and the inability to regenerate makes the liver to lose its integrity. The normal functioning of the liver is thus affected since its integrity is greatly interfered with. The patients with increased body mass index thus have poor outcomes in the management of liver failure (Singer, Attal-Singer & Shapiro 2008 p. 523). Apart from the increase in body mass exacerbating liver failure, the body mass index also affects the pharmacokinetics of the drugs within that body. For instance, the rate at which drugs are metabolized and cleared from the body is greatly affected by increase in body mass index certainly affects the time that the drug remains retained within the body (Hanley, Abernethy & Greenblatt 2010, p. 78). The elevation of the body mass index increases the time taken for the drugs to be eliminated from the body. The increase in body mass index increases the quantity of body fat. The increase in the amounts of fat slows down the rate at which metabolism and distribution of drugs is mediated (Singer, Attal-Singer & Shapiro 2008, p. 525). Reference List Porth, C, & Matfin, G, 2009, Pathophysiology concepts of altered health states, 8th edn, Lippincott, Williams & Wilkins, Philadelphia. Singer, P, Attal-Singer, J, and Shapiro, H, 2008, Body Mass Index and Weight Change: The Sixth Vital Sign, The Israel Medical Association journal, 10:523–525. Hanley, M, Abernethy, D, Greenblatt, D, 2010, Effect of obesity on pharmacokinetics of drugs in humans, Journal on clinical pharcokinetics: 49(2): 71-87. MIMS, 2012, pharmacology tables, retrieved on 12th June, 2012 from http://www.mims.co.uk/mims_specialist/. Read More