Part A: Comprehensive Health History

Identifying Data And Source Of The History

The case study involves Mr. Porter who is a 59 years old male. He is the primary source of data for this case. Other data are obtained observations done and also the measurements recorded.

Chief Complaint(s)

The patient complains of mild central chest pain radiating to the left arm with severe shortness of breath while doing some boxing training. The pain was of sudden onset. He now he complains that he feels his heart racing.

Present Illness

Mr. Porter came looking sweaty and pale complaining of mild central chest pain radiating to the left arm with severe shortness of breath while he is doing his boxing training and he also feels his heart racing. On examination his blood pressure(BP) is 130/90 mmHg which is under the normal range of 90/60 mm Hg to120/80 mm Hg , heart rate 181 b/min which is high above the normal average range of 60 to 100 b/min in adults, respiration rate 24 breaths per minute, oxygen saturation 98% and electrocardiogram(ECG) findings showed ventricular tachycardia.

Past History

The patient was admitted six years ago due to myocardial infarction. He was done percutaneous coronary intervention (PCI) whereby stent was put in place to keep the coronary arteries open thus improving blood supply to the myocardium which will result in chest pain reduction. The patient also has type 2 diabetes mellitus and hypertension. He does not have any known drug allergies.

Personal And Social History

Mr. Porter is active in exercise because he actively participates in boxing training. The patient also sort immediate health care intervention on feeling mild central chest pain.

Review Of Systems

Cardiovascular System

On inspection the patient looked sweaty and pale due to decreased blood supply to the peripheral tissues. Also electrocardiogram findings showed ventricular tachycardia due to heart overworking to pump more blood to meet oxygen supply to the tissues (Chummun, 2009). .On auscultation the pulse rate was 181 beats per minute which is high due to tachycardia. Normal average is about 72 beats per minute. Blood pressure is 130/90 mmHg which is slightly higher than the normal (120/80 mm Hg). Cardiology review shows that the patient has a new bundle branch block which leads to altered ventricular depolarization and conduction of impulses. This leads to impulses directed to muscles or different direction decreasing cardiac output.

Respiratory System

On inspection respiratory rate was 24 breaths per minute. The client also presents with shortness of breath while he was doing his boxing training. This is due to th radiating pain that he felt and thus he responds by having shallow breaths. Oxygen saturation was 98% which is within the normal range (95%-100%).

Musculoskeletal System

On investigations show that Mr. Porter has elevated troponin levels of 230. This is due to necrosis of cardiac cells due to oxygen deprivation. This leads to high troponin levels. The pain also radiates to the left arm and this in turn interferes with functioning of the arm hence his daily activities impaired.

Part B: Medicines Profile

Current Management Plan

Mr. Porter has to be under prolonged bed rest so that the pain can be alleviated. This helps because it reduces oxygen consumption by other organs and tissues and thus increasing oxygen supply to vital organs such as the heart. Resting also reduces heart workload and hence lower oxygen consumption. It is important to nurse the patient in left lateral. He also has to be advised and monitored closely to avoid strenuous exercises such boxing as it requires more oxygen.

Teach the patient on breathing exercises and pattern. This involves the client taking shallow breaths but faster. This will increase oxygen supply to the tissues and also reduce pain.

Give aspirin 300 mgs as it is an antiplatelet hence it will prevent platelet aggregation and formation of clots in the coronary vessels. This ensures that blood is supplied to all cells in the heart and thus the occurrence of cardiac cells necrosis is minimized.

Analgesics can also be administered if necessary. Also administer glyceride trinitrate spray which acts as a vasodilator reducing both pre-load and stroke volume. This reduces myocardial oxygen consumption.

Mr. Porter should also be taught about his medication, this includes the dosage and side effects to be expected. He should be informed the importance of adhering to the medications prescribed and to report any abnormal changes experienced while undergoing his treatment.

The client should also be counseled and reassure concerning his condition as this would help alleviate any worries or anxiety that he is experiencing (Pincus, Holt, Vogel, Underwood, Savage, Walsh & Taylor, 2013). This also is important in improving the patient’s conditioning and even enhancing his cooperation throughout his management. Reassuring can also at times helps ease the pain being felt according to (Linton, McCracken & Vlaeyen, 2008).

Metoprol

Indications; hypertension, myocardial infarction, angina, tachyarrhythmia and also in prevention of migraine

Mechanism of action;

Metoprolol act by blocking beta 1 adrenergic receptors in the muscles of the heart, therefore it has antihypertensive effect due to reduction of cardiac output without increasing peripheral resistance. Also acts on central nervous system by reducing renin secretion. It has antianginal effect by reducing left ventricular oxygen consumption and also reduces the rate of contraction of heart muscles. (Gorre &  Vandekerckhove, 2010).

Pharmacokinetic and pharmacodynamics

It is taken orally dosage initially 25 to 50mg and maintenance dose of 50 to 100mg at least twice daily. It is absorbed and broken down by enzymes CYP2D6 and CYP3A4 through alpha hydroxylation and O-demethylation as a substrate into inactive metabolites. It is the excreted through urine (Goryachkina, Burbello, Boldueva, Babak, Bergman& Bertilsson, 2008)

Iatrogenic diseases associated with metoprolol.

This includes; Diaphoresis, confusion, dizziness, chest pain, sweating, unusual tiredness, noisy breathing and irregular heartbeats.

Contraindications

It is known to worsen symptoms of heart failure in some patients such as chest pains, fatigue, and shortness of breath, irregular heartbeats and dilated neck veins. It may also cause changes in blood sugar levels and therefore such signs of hypoglycemia such as rapid heart rate may be covered up. Therefore, reduce dose in patients with heart failure and diabetes.

Part C: Medicines Profile Scenarios

Clopidogrel

Clopidogrel is an antiplatelet agent and it is an example of Thienopyridine. It is used in secondary prevention of stroke and myocardial infraction, non –ST- segment elevation acute coronary syndrome (with aspirin).

MOA

It reduces platelet aggregation by irreversibly inhibiting the ADP receptors of platelets which induces platelet aggregation.

Pharmacokinetics And Pharmacodynamics

It is a prodrug which when taken orally it is rapidly absorbed. Maximal platelet inhibition is 8 to 10 days after therapy is started and this effect persists for a few days after therapy is stopped. It is less leukopenia and thrombocytopenic.

Iatrogenic diseases

Includes; GI ulcer, thrombotic thrombocytopenic purpura, aplastic anemia, thrombocytopenia and neutropenia.

Contraindications

Metoprolol is contraindicated in brain tumors, head trauma, intracranial bleeding, metastatic cancer, history of cerebrovascular accident, patients with healing wounds and pregnancy. Usually give with aspirin for improved performance.

Clopidogrel resistance has however been associated with elevated risk of recurrent Atherothrombotic events in patients having Acute Myocardial Infarction (Matetzky, Shlomi, Boris Shenkman, Victor Guetta, Michael Shechter, Roy Beinart, Ilan Goldenberg, Ilya Novikov et al). Mr porter having myocardial infarction may therefore be at high risk should he develop resistance to this drug.

Cilazapril

Cilazapril is an angiotensin converting enzyme inhibitor and it is used in heart failure, hypertension, diabetic neuropathy and myocardial infarction. Its mechanism of action is blocking the conversion of angiotensin I to angiotensin II which is a potent vasoconstrictor and causes sodium retention and release of aldosterone.  Also prevents the breaking down of bradykinins.

Pharmacokinetics And Pharmacodynamics

It is a pro-drug which is taken orally and 60% of it is absorbed, duration of action is about 12 to 24 hours, its onset of action is about one hour, its peak effect is about 4 to 6 hours (Paszun & Stanisz, 2013).

Iatrogenic diseases

Increase in serum creatinine levels, may cause low blood pressure, also angioedema which may present by swelling of face and lips causing obstruction of the airway

Contraindications

In patients with angioedema, it may increase the risk. Dehydration and hypovolemia increases the risk of hypotension, using together with potassium sparing diuretics may cause hyperkalemia hence the levels of potassium should be monitored.

Glyceryl trinitrate / GTN spray

Glyceryl trinitrate is a vasodilation agent. It is indicated for treatment of acute angina pectoris and also for prevention of inducible angina, that is, angina that can result from physical effort, exposure to cold and even emotional stress(Abrams, 2011)..

Mechanisms of action

Glyceryl trinitrate causes the arteries and veins to vasodilate by acting on the vascular smooth muscles. This in turn leads to reduce in venous return and improvement in myocardial perfusion together with a decrease in the work done by the heart and thus there will be reduce in oxygen demand.

Pharmacokinetics

GTN is absorbed rapidly through the sublingual and buccal mucus. Its peak concentrations in plasma are achieved after around four minutes of administrations. Its bioavailability is around 39% and is metabolized by liver enzymes (especially by denitration). The plasma half-life of GTN is 1-3 minutes (Abrams, 2011).

Toxicity

Overdose of glyceryl trinitrate spray may cause face flushing, severe headache, tachycardia, hypotension, fainting and rarely cyanosis and methaemoglobinaemia. Few patients may also experience nausea, vomiting, weakness, sweating and syncope.

Metformin

Metformin is a drug suited for treatment of individuals with type II diabetes (non-insulin dependent diabetes mellitus.

Mechanism of actions

 Metformin works by lowering the liver glucose production, decreasing intestinal absorption of glucose and improves sensitivity by increasing peripheral glucose uptake utilization (Rena, Pearson & Sakamoto, 2013).  

Pharmacokinetics

It has an oral bioavailability of approximately 60% and is absorbed slowly. It reaches its peak plasma concentrations within one to three hours. It has a high apparent volume of distribution of about 300-1000 after a single dose and hence a negligible plasma protein binding (Gong, Goswami, Giacomini, Altman & Klein, 2012).

Adverse effects

 The most common adverse effects associated with metformin include diarrhea, cramps, nausea, vomiting and flatulence increase. Rare and serious one is lactic acidosis.

Contraindications

 Metformin is contraindicated in individuals with any condition that could increase the risk lactic acidosis and also lung and liver disease. Heart failure especially congestive heart failure increases risk of lactic acidosis with this drug.

Gliclazide

Like metformin, gliclazide is also indicated for use together with diet and exercise regimens to control high blood sugar in type II diabetes.

Mechanism of actions

 It acts by binding to the beta cell sulfonyl urea which in turns blocks the ATP sensitive potassium channels. Closure of the channels results from this binding and hence leading to a decrease in potassium efflux which causes depolarization of the beta cells. This opens voltage-dependent calcium channels in the beta cells and calmodulin is activated, which in turn causes exocytosis of insulin containing secretorty granules (Bösenberg, & van Zyl,2008).

Pharmacodynamics and pharmacokinetics

Overall, it potentiates insulin release and improves its dynamic. Gliclazide is well absorbed rapidly and peak plasma concentrations occur within 4-6 hours of oral administration. It is metabolized in the liver and eliminated primarily by the kidneys and also in the feces. Its half-life is 10.4 hours and duration of action is 10-24 hours (Resztak, Hermann,  Sawicki,  & Danielak, 2014).  

Side effects

Side effects associated with this medication are nausea, stomach upset and diarrhea initially before the body adapts. It also causes hypoglycemia and its symptoms include dizziness, fatigue, drowsiness, headache and sweating.

Contraindications

Gliclazide is contraindicated in severe hepatic and renal dysfunction.

Chronic kidney impairment

Chronic kidney failure is known to significantly lead to reduce renal clearance of drug which may in turn cause toxicity of the drugs. This may then lead to adverse reactions associated with the drugs. Some drugs even cease to function when there kidney impairment.

Chronic liver impairment

The ability of the liver to metabolise drugs depends on hepatic blood flow and liver enzyme activity, both of which can be affected by liver disease. Liver failure can also influence the plasma binding of a drug to plasma proteins. These alterations may occur singly or in combination; when they occur at once their effect on drug kinetics is synergistic, not simply additive

Heart failure

Heart failure is most commonly known to cause alteration in cardiac output, autonomic nervous system activity, central and systemic venous pressures, and sodium and water metabolism (Benowitz,  & Meister, 2009) These changes in turn influence the degree and pattern of tissue perfusion  land likely to lead to tissue hypoxia and visceral congestion, and may also alter gastrointestinal motility. By these mechanisms, cardiac failure likely disturbs absorption and distribution of drugs. This will require adjustment in dosage regimen for best therapy.

Citalopram and fluoxetine

Citalopram and fluoxetine are selective serotonin reuptake inhibitors. They specifically inhibit serotonin reuptake into the synaptic nerve terminal hence increase serotonin in the synaptic cleft (Böer, Noll, Cierny, Krause, Hiemke,  & Knepel, 2010).  They have fewer anticholinergic and cardiotoxicity effect and commonly used to treat depression that is accompanied by agitation, anxiety and insomnia. It inhibits various drug metabolizing enzymes therefore interact with several drugs. Its main adverse effect is nausea, decreased libido and serotonin syndrome due to interaction with monoamine oxidase inhibitors which leads to increased serotonin in the synapses.

From the case study the drug is advisable for Mr Porter as it does not cause increase in cardiac activity or muscarinic effects such as urinary retention. Hence it will help relieve the depression that he has been diagnosed with and also improve his energy levels and how he feels about his health. It is however advisable to try other remedies like counseling the client and maintain low doses of this medication because he is already on several medications.

Erythromycin

Erythromycin is a macrolide drug that is bacterialstatic. It acts on 50s ribosomal subunit by inhibiting bacteria protein synthesis (Anderson, Groundwater, Todd, & Worsley, 2012). Erythromycin is used mostly in treatment of hospital acquired pneumonia. It is also indicated in treatment of lower respiratory tract infections and also in rheumatic fevers to those who are allergic to penicillin. It is also used in treatment of acne.

This drug is taken orally and is activated easily by gastric acid and rapidly absorbed. It is metabolized in the liver by hepatic enzymes and eliminated by bile. It has a half-life of 1.5 to 2 hours and prolonged in patients with end stage renal disease

Its adverse effects include; arrhythmias which has a prolonged QT intervals. It also inhibits cytochrome P450 enzyme system which affects the metabolism of certain drugs like warfarin.

Mr. porter is diagnosed with lower respiratory pneumonia which is likely to be hospital acquired pneumonia since he acquires it while under care in the hospital setting (Torres, Ewig, Lode, Carlet, & European HAP Working Group. (2009)). It is therefore advisable for him to take this medication to curb his condition. This drug is suitable for this patient because it does not interfere with metabolism of the other drugs being taken. It should also be infused slowly when given through intravascular in order to minimize cardiac arrhythmias and thrombophlebitis.

Amitriptyline

Amitriptyline is a tricyclic antidepressant used to treat endogenous depression and some episodic phobias. It acts by blocking the norepinephrine, serotonin and dopamine reuptake into the synaptic nerve terminal. It also blocks the serotonergic, alpha adrenergic, histamine and muscarinic receptors. It thus increases the concentration of monoamines in the synaptic cleft. This therefore elevate mood, improve mental alertness and reduce morbid .Also increases physical activity. Its adverse effects are blurred vision, xerostomia (dry mouth), urinary retention, constipation and aggravation of glaucoma. This is due to blockage of muscarinic receptors. Also it increases cardiovascular activity resulting in cardiac overstimulation which can be fatal. It also causes orthostatic hypotension and reflex tachycardia due to alpha adrenergic receptor blockade. It can also cause sedation.

From the case study this drug is not suitable for the client due to its mechanism of action and side effects. Mr. Porter has been prescribed this drug in order to treat neuropathy pain, however the drug has different mechanism of actions and hence not suitable and thus should be stop and another medication considered.  Amitriptyline increases physical activity and mental alertness and also increases cardiac activity. Mr Porter needs to reduce oxygen consumption by the myocardial muscles and also in activity. Therefore using the drug may elevate chances of angina occurring and also myocardial infarction. Moreover, urinary retention and constipation will affect elimination of such drugs such as aspirin increasing their half-life and hence their side effects like bleeding.

Metformin

Metformin is the only oral hypoglycaemic agent which is currently known to reduce cardiovascular risk and is used as a drug of choice for treatment of type II diabetes patients. However accumulation of this drug has been known to lead to lactic acidosis but less evidence has been found. Metformin does not alter lactate concentrations in patients with type2 diabetes, it is eliminated through the kidney and has a short half-life. Therefore accumulation rarely occurs unless in advance renal failure. I would therefore advise Mr Porter to use this medication for watch out for any change as the dosage is being increased. This includes suspected tissue hypoxia due to myocardial infarction. According to Lexis, Wieringa, Hiemstra, van Deursen, Lipsic, van der Harst & van der Horst, (2014), chronic metformin treatment reduces the size of MI in type 2 diabetes as compared to other diabetic patients managed with non- metformin therapies.

Fluoxetine discontinuation.

Fluoxentine is a drug used to treat depression and panic attacks. It is also indicated for obsessive compulsive disorder and bulimia. It is not advisable to stop fluoxetine treatment immediately on completion due to antidepressant discontinuation syndrome which is usually an adverse effect of second generation antidepressants. Rapid discontinuation of such drugs as fluoxetine can lead to such symptoms as dizziness, disturbance of balance, headache, vivid dreams, nausea electric shock like sensation ,numbness, hallucinations and irritability. It is therefore important to taper off the drug over a period of about four weeks before stopping the drug. (Blum, Maldonado, Meyer, & Lansberg, 2008)

Warfarin

Warfarin is anticoagulant used to prevent clot formation and clot enlargement. It is a vitamin k epoxide reductase inhibitor and a coumarin anticoagulant. It is 100% bioavailable and 99% protein bound. It blocks y-carboxylation of factors II, VII, IX, X, protein C and protein which is a vitamin K dependent process. This prevents metabolism of inactive vitamin K epoxide. It is always necessary to monitor warfarin by prothrombin time(INR) to reduce its side effects. The main side effect of warfarin is bleeding and skin necrosis. Also when given with non steroidal anti-inflammatory drugs it increases the risk of gastrointestinal bleeding.

Mr. Porter having been diagnosed with deep vein thrombosis should therefore take warfarin, however heparin could have been prescribed first as it works immediately to prevent further clotting and thereafter warfarin can be taken to prevent other clots forming.

Conclusion

In conclusion, Mr. Porter’s case needs urgent actions and management so that it cannot worsen further. Collaborative management for this case is of high value. The various health care staff who can take part in this management may include; a doctor, nurse, medical laboratory technologist, cardiologist, counselor, physiotherapist among others. Mr Porter’s family members must also be involved in his management as they are the ones who he constantly feel so close to as compared to other management personnel. This may be of great importance even when passing some information to him like even importance of adhering to medications which would eventually enhance his cooperation throughout the management. This will in turn lead to better health for him.

References

Abrams, J. (2011). Glyceryl trinitrate (nitroglycerin) and the organic nitrates. Drugs, 34(3), 391-403.

Anderson, R. J., Groundwater, P. W., Todd, A., & Worsley, A. J. (2012). Macrolide Antibiotics. Antibacterial Agents: Chemistry, Mode of Action, Mechanisms of Resistance and Clinical Applications, 173-196.

Blum, D., Maldonado, J., Meyer, E., & Lansberg, M. (2008). Delirium following abrupt discontinuation of fluoxetine. Clinical neurology and neurosurgery, 110(1), 69-70.

Boden, W. E., Finn, A. V., Patel, D., Frank Peacock, W., Thadani, U., & Zimmerman, F. H. (2012). Nitrates as an integral part of optimal medical therapy and cardiac rehabilitation for stable angina: review of current concepts and therapeutics. Clinical cardiology, 35(5), 263-271.

Böer, U., Noll, C., Cierny, I., Krause, D., Hiemke, C., & Knepel, W. (2010). A common mechanism of action of the selective serotonin reuptake inhibitors citalopram and fluoxetine: reversal of chronic psychosocial stress-induced increase in CRE/CREB-directed gene transcription in transgenic reporter gene mice. European journal of pharmacology, 633(1-3), 33-38.

Bösenberg, L. H., & van Zyl, D. G. (2008). The mechanism of action of oral antidiabetic drugs: a review of recent literature. Journal of Endocrinology, Metabolism and Diabetes of South Africa, 13(3), 80-88.

Chummun, H. (2009). Understanding changes in cardiovascular pathophysiology. British Journal of Nursing, 18(6), 359-364.

Fan, M. I., Mitchell, M., & Cooke, M. (2009). Cardiac patients’ knowledge and use of sublingual glyceryl trinitrate (SLGTN). Australian Journal of Advanced Nursing, The, 26(3), 32.

Gong, L., Goswami, S., Giacomini, K. M., Altman, R. B., & Klein, T. E. (2012). Metformin pathways: pharmacokinetics and pharmacodynamics. Pharmacogenetics and genomics, 22(11), 820.

Gorre, F., & Vandekerckhove, H. (2010). Beta-blockers: focus on mechanism of action Which beta-blocker, when and why?. Acta cardiologica, 65(5), 565-570.

Goryachkina, K., Burbello, A., Boldueva, S., Babak, S., Bergman, U., & Bertilsson, L. (2008). CYP2D6 is a major determinant of metoprolol disposition and effects in hospitalized Russian patients treated for acute myocardial infarction. European journal of clinical pharmacology, 64(12), 1163.

Henderson, R. A., & O’flynn, N. (2012). Management of stable angina: summary of NICE guidance. Heart, 98(6), 500-507.

Hyttel, J. (2008). Citalopram—pharmacological profile of a specific serotonin uptake inhibitor with antidepressant activity. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 6(3), 277-295.

ISHAQ, M., & JAMAL, Q. (2012). TREATMENT OF HEART FAILURE UNDER CURRENT GUIDELINES. Pakistan Heart Journal, 34(1-4).

Khazaie, H., Rahimi, M., Tatari, F., Rezaei, M., Najafi, F., & Tahmasian, M. (2011). Treatment of depression in type 2 diabetes with fluoxetine or citalopram. Neurosciences (Riyadh), 16(1), 42-45.

Lexis, C. P., Wieringa, W. G., Hiemstra, B., van Deursen, V. M., Lipsic, E., van der Harst, P., … & van der Horst, I. C. (2014). Chronic metformin treatment is associated with reduced myocardial infarct size in diabetic patients with ST-segment elevation myocardial infarction. Cardiovascular drugs and therapy, 28(2), 163-171.

Linton, S. J., McCracken, L. M., & Vlaeyen, J. W. (2008). Reassurance: help or hinder in the treatment of pain. Pain, 134(1), 5-8.

Matetzky, Shlomi, Boris Shenkman, Victor Guetta, Michael Shechter, Roy Beinart, Ilan Goldenberg, Ilya Novikov et al. “Clopidogrel resistance is associated with increased risk of recurrent atherothrombotic events in patients with acute myocardial infarction.” Circulation 109, no. 25 (2004): 3171-3175.

Moore, R. A., Derry, S., Aldington, D., Cole, P., & Wiffen, P. J. (2012). Amitriptyline for neuropathic pain and fibromyalgia in adults. Cochrane Database Syst Rev, 12(12).

Paszun, S. K., & Stanisz, B. J. (2013). Cilazapril decomposition kinetics and mechanism in the solid state versus stability of the other ester pro-drug angiotensin converting enzyme inhibitors. Reaction Kinetics, Mechanisms and Catalysis, 109(2), 285-300.

Pincus, T., Holt, N., Vogel, S., Underwood, M., Savage, R., Walsh, D. A., & Taylor, S. J. C. (2013). Cognitive and affective reassurance and patient outcomes in primary care: a systematic review. Pain®, 154(11), 2407-2416.

Rena, G., Pearson, E. R., & Sakamoto, K. (2013). Molecular mechanism of action of metformin: old or new insights?. Diabetologia, 56(9), 1898-1906.

Resztak, M., Hermann, T. W., Sawicki, W., & Danielak, D. Z. (2014). Pharmacokinetics and Pharmacodynamics of Gliclazide from Immediate and Modified Release Formulation Tablets in Rats. Iranian journal of pharmaceutical research: IJPR, 13(1), 29.

Sahra, I. B., Laurent, K., Loubat, A., Giorgetti-Peraldi, S., Colosetti, P., Auberger, P., … & Bost, F. (2008). The antidiabetic drug metformin exerts an antitumoral effect in vitro and in vivo through a decrease of cyclin D1 level. Oncogene, 27(25), 3576.

Salpeter, S. R., Greyber, E., Pasternak, G. A., & Salpeter, E. E. (2010). Risk of fatal and nonfatal lactic acidosis with metformin use in type 2 diabetes mellitus. The Cochrane Library.

Siempos, I. I. (2013). Hospital-acquired pneumonia. Future Medicine Ltd.

Sarkar, A., Tiwari, A., Bhasin, P. S., & Mitra, M. (2011). Pharmacological and Pharmaceutical Profile of Gliclazide: A Review.

Skinner, N., & Moran, P. (2008). Deep vein thrombosis (DVT).

Venecourt-Jackson, E., & Maharaj, I. (2009). A rare complication of wireless capsule endoscope. The New Zealand Medical Journal (Online), 122(1289).

Yoon, I. S., Choi, M. K., Kim, J. S., Shim, C. K., Chung, S. J., & Kim, D. D. (2011). Pharmacokinetics and first-pass elimination of metoprolol in rats: contribution of intestinal first-pass extraction to low bioavailability of metoprolol. Xenobiotica, 41(3), 243-251.