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Pharmacokinetic Interactions of Omeprazole, Cardiprin, Endone, Coversyl, Lasix, and Other Drugs - Case Study Example

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The paper “Pharmacokinetic Interactions of Omeprazole, Cardiprin, Endone, Coversyl, Lasix, and Other Drugs” is a meaningful variant of a case study on nursing. Probitor 20mg According to the Australian Department of Health [ADH], its generic name is omeprazole 20mg…
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AN INTEGRATED CLINICAL CASE By (Name) The Name of the School (University) Tutor (Professor) The City and State where it is located The Date Answers 1. Probitor 20mg: a. According to Australian Department of Health [ADH], its generic name is omeprazole 20mg (2013). b. The Joint Formulary Committee [JFC] classifies it as a “Proton Pump Inhibitor” (2009, p.49). c. Its indications include treatment and management of “benign gastric ulcers, duodenal ulcers”, diseases associated with Non-Steroidal Anti-Inflammatory Drugs [NSAIDs] use and Helicobacter pylori, Zollinger-Ellison syndrome, decreasing gastric acid in the course of general anesthesia, management of gastro-oesophageal reflux disease, acid reflux disease, dyspepsia and severe ulcerating reflux oesophagitis (JFC, 2009, p. 49). d. It is under regulatory schedule 4 according to National Drugs and Poisons Schedule Committee [NDPSC] (2008). Cardiprin 100mg: a. Its generic name is Acetyl Salicylic Acid 100mg [ASA 100mg] (ADH, 2013). b. It is classified under NSAIDs (JFC, 2009, p.233). c. Its indications include “headache, transient musculoskeletal pain, dysmenorrhea and pyrexia” (JFC, 2009, p.233). It is also useful for prophylaxis against thrombotic events due to its antiplatelet properties. d. It is under schedule 4 (NDPSC, 2008). Zocor 40mg: a. Its generic name is simvastatin 20mg (ADH, 2013). b. It is classified under statins (JFC, 2009, p.143). c. It is indicated for the management of combined hyperlipidemia, primary hypercholesterolemia, homozygous familial hypercholesterolemia and prophylaxis in the case of cardiovascular events (JFC, 2009, p.145). d. It is under schedule 4 (NDPSC, 2009). Endone 5mg: a. Its generic name is oxycodone 5mg (ADH, 2013). b. It is classified under opioid analgesics (JFC, 2009, p.237). c. It is indicated for “the control of pain in palliative care” (JFC, 2009, p.237). d. It is under schedule 8 (NDPSC, 2009). Coversyl 5mg: a. Its generic name is perindopril 5mg (ADH, 2013). b. Perindopril is classified under Angiotensin Converting Enzyme Inhibitors [ACE-Inhibitors] (JFC, 2009, p.102). c. Its indications include hypertension, as an adjunct in heart failure and as prophylactic treatment after myocardial infarction (JFC, 2009, p.106). d. It is scheduled under schedule 4 (NDPSC, 2009). Lasix 40mg: a. Its generic name is furosemide 40mg (ADH, 2013). b. Lasix falls under the class of loop diuretics (JFC, 2009, p.76). c. It is useful in the treatment of oedema and management of resistant hypertension (JFC, 2009, p.77). d. It is classified under schedule 4 (NDPSC, 2009). Noten 50mg: a. Its generic name is atenolol 50mg (ADH, 2013). b. It is in the class of beta-blockers (JFC, 2009, p.87). c. It is indicated for the management of hypertension, arrhythmias and angina. d. It is under schedule 4 (NDPSC, 2009). Diaformin 850mg: a. Its generic name is metformin 850mg (ADH, 2013). b. Metformin is classified under biguanides (JFC, 2009, p.382). c. Its indication includes management of diabetic mellitus and polycystic ovary syndrome (JFC, 2009, p.383). d. It is under schedule 4 (NDPSC, 2009). 2. Each tablet of Blackmore Joint Formula contains 250mg of chondroitin sulfate-bovine sodium 90%, 942mg of glucosamine sulfate sodium chloride complex, 8.8mg of manganese gluconate and 8.8mg of borax (Blackmores, 2013). A tablet of nature’s Way Brain and Memory Supplement contains 180mg of eicosapentanoic acid [EPA], 120mg of Docosahexaenoic acid [DHA], 10mg of pyridoxine hydrochloride, 100mg of glutamine, 100mcg of folic acid, 100mcg of cyanocobalimin and Ginkgo biloba extract equivalent to 3000mg of dry leaf, 14.4mg of ginkgo flavonglycoside and 3.6 mg of ginkgolides and bilobalide (Nature's Way, 2013). Finally, a tablet of Blackmores Mood Support St John’s Wort supplement contains 1800mg of ” Hypericum perforatum (St John’s Wort) extract equivalent to dry flowering herb top (standardized to contain hypericin derivatives 990mcg)” (Blackmores, 2013). 3. Chondroitin sulfate has antithrombotic activity partly mediated by anti-thrombin III activity (Fonseca and Mourao, pp.822-9). This may lead to pharmacodynamics interaction with aspirin, which also has antithrombotic activity. However, aspirin acts through a different mechanism by inhibiting thromboxane A2 synthesis thereby preventing platelet adhesion. Consequently, a combination of these drugs may lead to increased risk of bleeding. St John’s Wort has a pharmacokinetic type of drug-interaction with simvastatin. According to Zhou et.al’s article (2004, pp.262-276), St John’s Wort potently induces CYP 3A4, a liver enzyme that activates the pro-drug simvastatin to some of its active metabolites. The clinical case reported an increase in the active metabolites of simvastatin which may precipitate hepatic toxicity. Ginko biloba has pharmacodynamics interactions with aspirin. Its antithrombotic effects are due to its ability to inhibit platelet-activating factor which can lead to decreased platelet mediated thrombosis (Sierpina, Wollschlaeger and Blumenthal, 2003, pp.923-926).This interaction may result in increased bleeding risk as explained in the above clinical case source. 4. Omeprazole is a proton pump inhibitor. Its mechanism of action involves inhibition of the H+,K+-ATPase [proton pump in the gastrointestinal tract] (Brunton, 2006, ch.36). The pro-drug is absorbed into the bloodstream and “diffuses into the parietal cells of the stomach” to accumulate “in the acid secretory canaliculi” where “it is activated by proton catalyzed formation of a tetracycline sulfonamide”. The activated form covalently binds “with the sulfhydryl groups of cysteines in the” proton pump “irreversibly inactivating the pump molecule” (Brunton, 2006, ch.36). This inhibits H+ secretion and consequently preventing acid formation resulting in prolonged 24-48hr suppression of acid secretion. Omeprazole is useful in management of the patient’s gastro-oesophageal reflux disease [GERD], a condition precipitated by acid reflux into the oesophagus. Since the proton pump is a significant contributor to acid secretion, its inhibition greatly decreases the amount of acid in the stomach and prevents reflux into the lower oesophagus. This offers symptomatic relief to the patient. 5. Pouchain, et al. in his article titled “Gaviscon vs. omeprazole in symptomatic treatment of moderate GERD”, published by Biomed Central Ltd in 2012 in BMC Gastroenterology journal vol.12 Issue 18, compares the effects of omeprazole and an alginate for 14 days in management of GERD. It was a randomized double-blind non-inferiority trial and his study proved that gaviscon, an alginate, was not “inferior to omeprazole in achieving a 24hr heartburn-free period”. The definition of the study method was met. However, in his design, “all patients were duly informed of the trial objectives”. The extent to which the study participants comprehended the trial beats the logic of it being double-blind. In the trial, omeprazole was compared to a specific brand of alginates called gaviscon. There is a possibility that the results would be different if another brand of alginate with different additional active ingredients was used. There were 278 participants in the study but a larger sample would be more appropriate. The results obtained demonstrated omeprazole to be slightly better to alleviate pain for a short period but the alginate was equally effective in reduction of pain intensity. Both drugs were well tolerated. Omeprazole’s clinical significance in humans was also studied by Ricardo Pereira. His article titled “Regression of GERD symptoms using dietary supplementation with melatonin, vitamins and amino acids: comparison with omeprazole”, was published in 2006 in the Journal of Pineal Research, vol.41, pp.195-200. It was a “randomized parallel group comparative, single blind, single center study”. The actual randomization fits the description of the study type. However, the single blind study introduces some element of bias. Pereira did not mention whether it was the study participants or outcome assessors that were blinded. If the outcome assessors or investigators were not blinded, they may have known the type of treatment allocated to each study participant resulting in a possible compromise on the impartiality of the assessment. In the study, the regression observed with omeprazole and the supplements are compared thus helping to determine which treatment has better outcomes. Pereira used a sample size of 351 study participants but the number increased over time. This empowered the research outcome in terms of its applicability to a larger population. Omeprazole’s effectiveness was assessed by observing the extent of ulcer regression using endoscopic examination. This was an effective method of monitoring the outcome since the ulcer’s physical improvement was observed by comparing the initial and final picture after treatment. Omeprazole was not as good as the supplements in management of GERD as only 65.7% of patients reported marked improvement of symptoms compared to 100% on the supplement. From these two studies, omeprazole is effective in the management of GERD and can be relied upon although better alternative medicines can be used in refractory cases. 6. An article by Antoni, Szwed and Sadowski titled “Anti-ischaemic response to sublingual nitroglycerin during oral administration of isosorbide dinitrate in patients with stable angina pectoris: when does cross-tolerance occur?” was published by Kluwer Academic Publishers in 2004 in vol.18 of Cardiovascular Drugs and Therapy journal pp.47-55. It was a double-blind crossover type of study. It would have been more appropriate if the authors defined their study as being a controlled trial since they used placebos in assessing the efficacy of sublingual glyceril trinitrate [GTN]. The trial was conducted in two phases; phase one lasting seven days and phase two lasting six weeks where the study participants were careful monitored and results were recorded. This duration of study was enough to observe the pharmacological effects of sublingual GTN and the development of tolerance. However, a relatively small sample size of 38 male patients was used and the authors did not consider the possibility of different results if a larger sample size incorporating women was used. The outcome measures were assessed by analyzing the time it took a study participant to develop ischaemia while walking, a suitable method of finding out angina pectoris’ response to therapy. In a different article by Henrikson, et al. titled “Chest pain relief by nitroglycerin does not predict active coronary artery disease” published in the year 2003 in Annals of Internal Medicine journal vol.139 pp.979-986, sublingual GTN only relieved pain in 35% of patients with active coronary artery disease. It was a case-control study since it only included study participants that had experienced “documented chest pain while under medical supervision”. 459 study participants were used. It was not a big number but the results obtained are an acceptable indicator of the effectiveness of GTN in controlling chest pain associated with coronary artery disease chest pain. The outcome measure was based on chest pain relief which was “defined as a decrease of at least 50% in patient’s self-reported pain within 5minutes of the initial dose of sublingual“ GTN. The ability of the patients to report that the pain they were experiencing had dropped by 50% is debatable. The two research articles proved that though sublingual GTN is useful in relieving pain associated with ischaemic heart disease, it might not be effective in all cases. Evidence of its efficacy in reducing mortality is not forthcoming. 7. Before administration of GTN, the patient should have his blood pressure taken to ensure it is not leading to a hypotensive state. Patient’s history should be examined to exclude any previous hypersensitivity to nitrates. Clinical assessment is necessary to exclude any presence of pulmonary oedema, head trauma or marked anaemia. Consideration of the patient’s medication is important especially the use of anti-hypertensive such as atenolol, perindopril and furosemide as these may precipitate a hypotensive state. GTN aggravates pulmonary oedema and head trauma. Antihypertensive drugs can interact with GTN causing additional lowering of blood pressure, which leads to hypovolemic shock if blood pressure is not monitored and their doses adjusted accordingly. In addition, reflex sympathetic stimulation after sudden lowering of blood pressure may aggravate the prevailing angina. Assessment of the risks associated with discontinuation of the antihypertensives over lowering their doses is important. Blood pressure monitoring especially when increasing the dose of GTN is essential and, regular check of radial pulse is useful in identifying any reflex sympathetic stimulation of the heart. 8. In vol.3 issue 10 of the Thrombosis Journal, an article by Borna, et al. titled “Resistance to aspirin is increased by ST- elevation myocardial infarction and correlates with adenosine diphosphate level” was published in 2005. It was an explanatory type of study hence the study participants were highly selected. This is justified since the selection had to include merely patients experiencing chest pain. No control group was used. This might be attributed to the high mortality risks associated with not using aspirin at all in STEMI patients. The tests for the study were initiated on patient admission and the results were released in less than a week. Simple, short-lived chemical tests and assays were used to quantify aspirin resistance. The outcome measure was the extent of platelet aggregation among the three specified groups; patients with no sign of cardiac disease, non-STEMI and STEMI patients. This measure was quite appropriate since the aim of the study was to investigate the resistance of aspirin in these patients. STEMI patients exhibited more aspirin resistance at 83.3% compared to other groups of study participants. Hurlwn, et al, also demonstrated the significance of aspirin after myocardial infarction in the article titled “Warfarin, aspirin, or both after myocardial infarction” published in 2002 in New England journal of medicine vol.347 pp.969-974. In design, it was a randomized, open-label, multicenter study. The randomization utilized permuted blocks. This probably introduced some selection bias associated with the permuted block method of administering randomization. The study took six years with recruitment stopping at the fourth year. The study duration was sufficient to observe a substantial number of the predetermined outcomes of reinfarction, death or thromboembolic stroke. There were 3630 study participants. This was an adequate number to optimize the outcomes. The outcome measures were the number of ”death, nonfatal reinfarction, or thromboembolic stroke”. The results show the benefits of aspirin alone in reducing the risks associated with myocardial infarction with a 19% risk reduction although warfarin alone had better risk reduction at 29%. In summary, aspirin is still significant in prevention of platelet aggregation and consequently prevent the thrombotic events that would otherwise aggravate myocardial infarction or angina. Addition of anticoagulant therapy such as warfarin or clopidogrel offers better prophylaxis against thrombosis in STEMI patients. 9. Figure 1: Metabolic activation of clopidogrel in the liver hepatocytes (Alquatani and Alnabti, 2009, p.111). 1 represents absorbed but intact clopidogrel molecule. 2 represents 2-oxo-clopidogrel. 3 represents the active thiol metabolite of clopidogrel. Clopidogrel is a pro-drug that requires hepatic activation before it exerts its activities. After absorption into the bloodstream, it diffuses into the liver parenchyma. Here, cytochrome P450 enzymes activate it, mainly the CYP2C19. The activation is a two-step oxidation. First, the thiophene ring is oxidized forming 2-oxo clopidogrel before opening up the ring forming the active thiol metabolite as shown above. Only 15% of the pro-drug forms the active metabolite (Alqatani and Alnabti, 2009, p110-111). As explained by Alqatani and Alnabti, the active thiol metabolite forms a disulfide bridge with the cysteine residues of the P2Y12 receptor on platelet membrane. This irreversibly inhibits the G1-protein coupled P2Y12 receptor. Activation of this receptor usually results in the release of alpha1 and beta1 subunits of G1. The former inhibits adenylate cyclase while the latter activates phosphatidylinositol. Both of these activities lead to GP IIb/IIIa receptor activation and consequently platelet aggregation. 10. Clopidogrel may interact with omeprazole. A research done by Juurlink et al. showed that omeprazole can decrease clinical effectiveness of clopidogrel (2009, p718). It is a pharmacokinetic type of interaction. CYP2C19 enzyme partially metabolises both drugs. Metabolism of omeprazole by this enzyme presents a competitive type of inhibition to clopidogrel activation. This may lower therapeutic concentrations of the active metabolite of clopidogrel and restrict clopidogrel’s efficacy when co-administered with omeprazole hence the need to monitor the patient’s response to the anticoagulant. The research done by Juurlink et al. was a controlled clinical case study. The study participants were Ontario residents aged 66 years and above “discharged from hospital between Apr. 1, 2002, and Dec. 31, 2007”. Since the study was done on humans and not animals, it strengthens the evidence obtained and its application to medical practice. 11. a. Temazepam has 96% of the drug in the body bound to plasma proteins (Schwarz, 1979) b. The unbound fraction is calculated by: (100 -96)%/100= 1/25=0.04 c. The decrease in plasma albumin may increase temazepam’s unbound fraction that may consequently lead to an increase in clearance. 12. a. Temazepam has a volume of distribution (Vd) of 1.4L/kg (Divoll et al., 1981, p.1105). b. It is a small volume of distribution. c. This small Vd signifies that the drug accumulates more in blood while bound to plasma proteins than in body tissues. 13. a. It is calculated by: % excreted unchanged/100% , (Schwarz, 1979, p.25S). =1.8/100 =0.018 b. About 80% of the metabolites are excreted in urine while 13% in feces (Schwarz, 1979, p.28S). 14. Figure 2: Secretion and elimination of inactive temazepam metabolites in the kidney Temazepam is primarily excreted via the kidney (Schwartz, 1979, p23S). The O-conjugated temazepam and O-conjugated N-desmethyltemazepam are the inactive metabolites. They are secreted in the proximal convoluted tubule into the glomerular filtrate before excretion in urine. 15. a. Temazepam has low extraction ratios and systemic clearance (Verbeeck, 2008, 1149). Hepatic clearance (CLh) = Qh*Eh =1000ml/min/*0.0002 =0.2ml/min. Renal clearance (CLr) = f*GFR =0.04*61ml/min =2.44ml/min. Qh is hepatic blood flow, Eh is extraction fraction and f is unbound fraction. b. Temazepam has a low hepatic clearance. c. The clearance is not dependent on hepatic blood flow but on the unbound fraction. Increasing this fraction may increase clearance. 16. Temazepam has an almost 100% oral bioavailability (Schwarz, 1979, 23S). This is due to its complete absorption across the gastrointestinal wall and very low, almost negligible, hepatic extraction ratio. For this patient, the bioavailability shall remain constant since his gastrointestinal tract has no known dysfunction and the hepatic functionality does not affect the drug’s bioavailability. 17. Temazepam is O-conjugated in the liver before excretion via the kidney. According to this patient’s Child-Pugh score of six, he has a mild liver disease that cannot substantially affect temazepam’s metabolism. However, the decrease in plasma albumin would increase the unbound fraction that may lead to an increase in clearance. Therefore, adjustment of temazepam’s dose may be necessary. 18. Temazepam use in this patient can be continued because the hepatic and renal dysfunctions are not severe enough to affect the metabolism and elimination of the drug respectively. In addition, the patient’s temazepam dose is only 10mg OD. This is a relatively small dose and may not elicit any toxicity even with current renal and hepatic states of the patient. However, the patient should be familiarized with common side effects of the drug such as confusion, dizziness, drowsiness and hangover. Monitoring the state of consciousness and deterioration of the hepatic and renal functions are paramount. References Alqahtani, A. and Alnabti, A. 2009. Clopidogrel Hyporesponsiveness. Heart Views, 10(3), pp.110-20. Australian Department of Health, 2013. Pharmaceutical Benefits Scheme. [Online] Available at: [Accessed 13th October 2013]. Blackmores, 2013. Blackmores. [Online] Available at: [Accessed 14 October 2013]. Brunton, L., ed., 2006. Goodman & Gilman's The Pharmacological basis of Therapeutics. 11th ed. New York: McGraw-Hil. Divoll, M., Greenblatt, D.J., Harmatz, J.S. and Shader, R.I. 1981. Effect of Age and Gender on Disposition of Temazepam. Journal of Pharmaceutical Science, 70(10), pp.1104-1107. Fonseca R.J. and Mourao, P.A., 2006. Fucosylated Chondroitin Sulfate as a new Oral Anticoagulant. Haemostasis and Thrombosis, 96(6), pp.822-29. Available at: [Accessed 14 October 2013]. Juurlink, D.N.,Gomes, T., Ko, D.T., Szmitko, P.E., Austin, P.C., Tu, J.V., Henry, D.A., Kopp, A. and Mamdani, M.M. 2009. A Population-Based Study of The Drug Interaction Between Proton Pump Inhibitors and Clopidogrel. Canadian Medical Association Journal, 180(7), pp.713-718. Joint Formulary Committee, 2009. British National Formulary. 58th ed. London: BMJ Group & RPS Publishing. National Drugs and Poisons Schedule Commitee, 2008. Poisons Standard 2008. [print] Canberra, Australia: Australian Government Available at: [Accessed 13 October 2013]. Nature's Way, 2013. Nature's Way. [Online] Available at: [Accessed 14 October 2013]. Schwarz, H.J., 1979. Pharmacokinetics and Metabolism of Temazepam in Man and Several Animal Species. British Journal of Clinical Pharmacology, 8, pp.23S-9S. Sierpina, S.V., Wollschlaeger, B. and Blumenthal, B., 2003. Ginko Biloba. American Family Physician, 68(5), pp.923-26. Verbeeck, R.K., 2008. Pharmacokinetics and Dosage Adjustment in Patients with Hepatic Dysfunction. European Journal of Clinical Pharmacology, 64, pp.1147-61. Zhou, S., Chan, E., Pan, S.Q., Huang, M. and Lee, E.J., 2004. Pharmacokinetic Interactions of Drugs with St John's Wort. Journal of Pychopharmacology, 18(2), pp.262-76. Read More

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