56 years old man (weight 75 kg, body surface 1.96m2) without previous health problems was admitted in 4th stage of diffuse Hodgkin lymphoma. Therapy was started with 4 cycles of rituximab, doxorubicin, cyclophosphamide, bleomycin, vincristine, and prednisolone with a good therapeutic answer. To prevent metastases in CNS one cycle of high-dose methotrexate (3 g/m2) was administered in 30 minutes i.v. infusion followed by hyperhydratation (3L/24h 5% dextrose) and 210 mmol of sodium bicarbonate. Urine pH was corrected by infusion of 140 mmol of sodium bicarbonate before methotrexate administration.
Biochemistry results: creatinine 78 μmol/l, liver enzymes without pathology.
", qs: [ { task: "What are modes of action of drugs administered?
", }, { task: "Why was sodium bicarbonate administered together with methotrexate and also after its administration?
", } ] }, { text: "24h after administration of methotrexate creatinine levels were measured with the result 167 μmol/l.
", qs: [ { task: "Calculate creatinine clearances before and after methotrexate treatment by Cockroft-Gault equation (physiological clearance in men is 97-137 ml/min):
ClCR= ((140-age)x weight x 1,23)/( cCR in μmol/l) (in women = 0.85 x creatinine clearance in man)
", }, { task: "What can you conclude from calculated clearances?
", }, { task: "Which drug could be used to reduce methotrexate toxicity?
", } ] }, { text: "Acute kidney failure was diagnosed 24 hours after administration of methotrexate. Therapy with calcium folinate was started (50 mg and later 200 mg), and another doses of sodium bicarbonate were administered.
3 days after methotrexate administration the pH was again low (6.5 pH instead of desired 8.5). It was found out, that patient bought and consumed large amount of Coca-Cola from hospital cafeteria. Patient was asked to stop drinking such beverages. Therapy of hyperhydratation, sodium bicarbonate, and folinate was ended on the 12th day. Kidney functions were normal on the 56th day.
", qs: [ { task: "How could coke interfere with urinary pH?
", } ] } ], biblio: ["Santucci, R, Levêque, Herbrecht R. Cola beverage and delayed elimination of methotrexate. British Journal of Clinical Pharmacology, 2010; 70, (5): 762-764.
http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2125.2010.03744.x/full
"], editors: '0', index: 58 }, { title: 'Kinetics 2', cathegory: 4, keywords: ["clarithromycin", "spironolactone", "digoxin", "captopril", "pravastatin", "isosorbide mononitrate", "furosemide", "bisoprolol", "interaction", "P-glycoprotein"], parts: [ { text: "A 83-year-old patient, previously stable without complications, was suddenly hospitalized due to fatigue, dyspnea on exertion, cough, nausea, loss of appetite, and lightheadedness. It was found that the patient had started using clarithromycin (500 mg orally twice daily) for the treatment of possible pneumonia three days before his presentation.
Case history of the patient includes hypertension, dyslipidemia, myocardial infarction, left ventricular dysfunction, and chronic obstructive pulmonary disease. His cardiac medications included daily digoxin 0.125 mg, spironolactone 25 mg, captopril 25 mg b.i.d., pravastatin 40 mg, isosorbide mononitrate 30 mg, furosemide 60 mg, bisoprolol 2.5 mg, and potassium 20 mmol.
Biochemistry results on the day of hospitalization: Biochemistry results 3 weeks ago:
What are the modes of action and indications of administered drugs?
", }, { task: "Impairment of which organ led to patient\'s biochemistry results?
", }, { task: "Is any of drugs administered nephrotoxic?
", } ] }, { text: "Initial medical examination was performed after the 5th dose of clarithromycin. The patient was feeling unwell and he was afebrile. His blood pressure and heart rate were 124/50 mm Hg + 68 bpm (supine) and 105/40 mm Hg + 82 beats per minute (standing), respectively. His respiratory rate was 16/min with an oxygen saturation of 99 % (room air). Levels of digoxin were 4.6 nM (5 hours postdose) and 4.7 nM (18 hours postdose). His electrocardiogram showed normal sinus rhythm, complete right bundle branch, and left anterior hemiblock and evidence of prior anteroseptal and inferior infarctions (no significant changes from previous electrocardiogram).
", qs: [ { task: "What is digoxin therapeutic range and what are typical symptoms of digoxin intoxication?
", }, { task: "What is the mode of interaction between digoxin and clarithromycin?
", } ] }, { text: "The digoxin and clarithromycin was discontinued immediately, and patient’s rehydration was started. In addition, medications that could raise serum potassium levels were discontinued on a temporary basis.
", qs: [ { task: "Which drugs used by the patient may increase potassium levels in the blood?
", }, { task: "What are the therapeutic approaches in case of digoxin intoxication?
", } ] }, { text: "Blood tests on day 2 of hospitalization showed a slow decrease of level of creatinine (154 μM) to normal level. The patient was discharged from the hospital 10 days later (creatinine 103 μM) with optimized medication.
", qs: [ { task: "Which drugs used by the patient do have a similar effect on the excretion of digoxin as clarithromycin does?
", } ] } ], biblio: ["Lee CYW, et al. Digoxin toxicity precipitated by clarithromycin use: case presentation and concise review of the literature. Canadian Journal of Cardiology. 2011; 27(6): 870. e15-870. e16.
http://www.sciencedirect.com/science/article/pii/S0828282X11003618
"], editors: '04', index: 59 }, { title: 'Kinetics 3', cathegory: 4, keywords: ["valsartan", "fenofibrate", "rhabdomyolysis", "sodium bicarbonate"], parts: [ { text: "A 26-year-old male patient was admitted to hospital because of fatigue and severe myalgia. His medical history revealed hypertension and chronic renal failure which was diagnosed 3 years ago (due to focal segmental glomerulosclerosis). The patient had been treated with valsartan (80 mg p.o. daily) for 2 years, and he had started using fenofibrate one week before his presentation. On physical examination the patient was normal (body temperature 37.2 °C, blood pressure 90/60 mm Hg, and HR 84/min) except for diffuse muscle tenderness and pretibial edema. The patient reported that did not ingest any alcohol, did not have any strenuous physical exertion, trauma, surgery, or recent viral infection.
Biochemistry results on the day of hospitalization:
What are the modes of action and indications of administered drugs?
", }, { task: "Which drugs used by the patient did probably cause the patient\'s clinical symptoms?
", }, { task: "How would you call the patient\'s pathophysiological state?
", }, { task: "What other drugs or substances can cause the same pathophysiological state?
", } ] }, { text: "The fenofibrate therapy was discontinued and intravenous fluid replacement with sodium bicarbonate was started. Clinical and laboratory findings of the patient began to improve on the third day after admission, and after one month, his symptoms had completely disappeared, and blood tests for muscle enzymes had returned to normal levels.
", qs: [ { task: "Why was sodium bicarbonate used besides rehydration?
", } ] } ], biblio: ["Erdur FM, et al. Fenofibrate-induced rhabdomyolysis in a patient with chronic renal failure due to nephrotic syndrome: A rare case report. Clinical biochemistry. 2012; 45(1): 162-164.
http://www.sciencedirect.com/science/article/pii/S0009912011026889
"], editors: '04', index: 60 }, { title: 'Kinetics 4', cathegory: 4, keywords: ["fentanyl"], parts: [ { text: "In parenteral administration of fentanyl there can develop a suppression of breathing in some patients in several hours.
In the graph 1 you can see plasma levels of fentanyl in a rat. In the graph 2 you can see changes in the respiratory response to CO2. Notice corresponding changes in 90 minutes after the administration.
Graph 1. Plasma concentrations of parenterally administered fentanyl in a rat.
[[Graf_1_kinetika4.png]]
Graph 2. Respiratory response to CO2 in a rat.
[[Graf_2_kinetika4.png]]
", qs: [ { task: "Try to explain an unusual concentration curve of fentanyl.
", }, { task: "How can you treat respiratory depression caused by fentanyl?
", } ] } ], biblio: ["Stoeckel H, Hengstmann J H, Schüttle, J. Pharmacokinetics of fentanyl as a possible explanation for recurrence of respiratory depression. British journal of anaesthesia. 1979; 51(8): 741-745.
http://bja.oxfordjournals.org/content/51/8/741.short
"], editors: '07', index: 61 }, { title: 'Kinetics 5', cathegory: 4, keywords: ["disulfiram", "alcoholism", "disulfiram-like reaction", "bisoprolol", "quetiapine", "lamotrigine"], parts: [ { text: "A 46-year-old artist came to the attention of an internist during an admission for acute relapse of his alcoholism. His pattern was one of prolonged abstinence interrupted by binge drinking. He is treated by Antabus 100 mg per a day.
", qs: [ { task: "What is an active substance in Antabus?
", }, { task: "What is the mechanism of action of this substance?
", } ] }, { text: "Patient gave a 2 year history of unexplained malaise. He reported a cyclical pattern of nausea on waking, palpitations, left-sided chest discomfort, paraesthesia on the left side of his head and upper limb fatigability. He describes himself feeling ‘poisoned’ with a permanent hangover. These cycles lasted ~ 1 week and were unpredictable. He described his quality of life as ‘poor’ although notably during a break from work the previous summer he had felt better.
Past history included partial gastrectomy for peptic ulcer disease 13 years previously, requiring iron and vitamin B12 supplementation and aortic valve disease diagnosed 3 years previously. He had been prescribed bisoprolol for palpitations and more recently quetiapine 100 mg for nocturnal sedation and lamotrigine 100 mg as a mood stabilizer.
Physical examination and serum biochemistry, including liver function, were unremarkable, except for a low serum testosterone, for which he was prescribed testosterone undecanoate 1000 mg monthly. Tests in the month prior to admission showed no detectable blood alcohol on two occasions and negative drug screens. An organic solvent screen found a slightly elevated urinary acetone concentration.
He appeared fully aware of the mechanism of disulfiram and reported discontinuation of disulfiram prior to binge relapses of which there had been two in the past year and none in the previous year. He reported also stopping the use of deodorants because of possible alcohol content.
", qs: [ { task: "What is the mode of action and indications of co-administered drugs?
", }, { task: "Is there any interaction between co-administered drugs with disulfiram?
", } ] }, { text: "Patient worked as a self-employed artist, painting and fabricating fiberglass structures on commission. He worked 7 days a week, 12 h a day using a range of solvent containing materials:
Product Relevant solvent components
Methylated spirits ethanol and methanol
Paint/vanish removers methanol and dichlormethane
Lacquer spray paints toluene and xylene
Lacquer thinners methanol, acetone, toluene, xylene and isopropyl alcohol
Metal polish isopropyl alcohol
Spray glue acetone, hexane and cyclohexane
", qs: [ { task: "Why patient experienced alcohol intoxication, although he intentionally did not use any?
", }, { task: "Find another drugs which can cause disulfiram-like reaction.
", } ] }, { text: "", qs: [ ] } ], biblio: ["Ehrlich RI, Woolf DCS, Kibel DA. Disulfiram reaction in an artist exposed to solvents. Occupational medicine. 201; 62(1): 64-66.
http://occmed.oxfordjournals.org/content/early/2011/11/07/occmed.kqr172.full
"], editors: '07', index: 62 }, { title: 'Kinetics 6', cathegory: 4, keywords: ["urinary tract infection", "co-trimoxazole"], parts: [ { text: "48 years old woman is coming to a doctor’s office with typical symptoms of urinary tract infection. Laboratory tests confirmed a bacteriuria. Twice a day 1 tablet of Co-trimoxazole 80 mg/400 mg was prescribed to the patient. It was recommended not to eat and drink any acidic food, do not take any non-steroidal anti-inflammatory drugs and to keep an optimal drinking regime. Patient does not take any other drugs.
", qs: [ { task: "What active compound contains Biseptol and what is its mechanism of action?
", }, { task: "Why is it recommended not to use NSAIDs or “acidic” food or beverages (cola, juices etc.) together with co-trimoxazole?
", } ] }, { text: "After 3 days women is coming back to a doctor’s office and is complaining about impairment of symptoms in a form of unilateral pain radiating to a groin. Laboratory tests are negative for bacteriuria and positive for hematuria and crystalluria. After the talk with the doctor patient states long-term use of food supplement containing an extract from cranberries as a prevention of urinary infection.
", qs: [ { task: "Try to explain the mechanism involved in the actual complications of therapy with co-trimoxazole.
", } ] } ], biblio: [], editors: '07', index: 63 }, { title: 'Kinetics 7', cathegory: 4, keywords: ["furosemide", "digoxin", "levothyroxine", "myxedema", "quinidine", "P-glycoprotein"], parts: [ { text: "An older man (69 years old) with a history of IHD and myxedema wad admitted to hospital with left ventricular failure. Patient takes medication regularly as follows: furosemide, digoxin, potassium chloride and levothyroxine. Plasma level of digoxin is maintained at 1 nmol/L. Now his ECG shows atrial flutter and quinidine sulfate was added to his drug regimen to control the dysrhythmia. After the stabilization of ECG, patient was discharged.
Two weeks later, the patient was readmitted to the hospital after five-day history of vomiting. ECG showed atrial flutter with ventricular premature beats. Plasma level of digoxin was 2.4 nmol/L. No kidney dysfunction was found and non-compliance was excluded.
", qs: [ { task: "What are the mechanisms of action and typical indications of the drugs used?
", }, { task: "What is digoxin therapeutic range?
", answer: "0.8‒2.0 ng/mL (1.2‒2.0 nmol/L)
" }, { task: "Why were digoxin levels elevated?
", }, { task: "What other adverse effects (except for vomiting and flutter) could possibly manifest?
", } ] }, { text: "Symptoms disappeared when quinidine and digoxin were withdrawn. After stabilization, digoxin was added again to the drug regimen at the previous dose, while long-term plasma concentrations were maintained around 1 nmol/L. Patient was discharged.
", qs: [ { task: "What other drugs could possibly interact with digoxin by the same mechanism?
", }, { task: "What are other drugs (apart from digoxin) whose plasma levels could be altered by the same mechanism?
", } ] }, { text: "The mechanism mentioned in questions 2 and 3 plays a significant role in the cancer treatment. Substances able to block this mechanism are being developed, or are tested in clinical trials. Some compounds of natural origin with the same effect are also examined.
", qs: [ { task: "What is the clinical significance of this mechanism in the chemotherapy (treatment of cancer with cytostatics)?
", } ] } ], biblio: ["Holt DW, et al. Clinically significant interaction between digoxin and quinidine. British medical journal. 1979; 2(6202): 1401.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1597102/
", "Fromm MF, et al. Inhibition of P-glycoprotein–mediated drug transport a unifying mechanism to explain the interaction between digoxin and quinidine. Circulation. 1999; 99(4): 552-557.
http://circ.ahajournals.org/content/99/4/552.short
"], editors: '06', index: 64 }, { title: 'Kinetics 8', cathegory: 4, keywords: ["phenprocoumon", "cholestyramine", "heparin"], parts: [ { text: "A women with prosthetic bileaflet aortic valve (implanted 5 years ago) is nowadays on chronic anticoagulant treatment with phenprocoumon. According to the last medical check-up, the treatment is correctly dosed (INR 3.0). All previous check-ups had shown normal valve function.
", qs: [ { task: "What is the mechanism of action of phenprocoumon? How it is metabolized and excreted?
", } ] }, { text: "During a routine cardiologic check-up, patient reports mild dizziness and progressive fatigue during the last few weeks. She had recognized a change in the valve’s ‘click’ and was worried because the ‘click’ had disappeared completely 2 days before. Her cardiologist recommended the admission to the hospital. Examination at the hospital showed tachycardia (115 bpm) and mild hypertension (150/90 mm Hg) with normal routine laboratory values. INR was 1.1 showing inadequate anticoagulant therapy. Transesophageal echocardiography demonstrated a non-functioning anterior leaflet of the aortic valve, presumably caused by thrombosis. The cardiologist at hospital found that the patient had started taking cholestyramine due to the hypercholesterolemia a week before the admission to hospital.
", qs: [ { task: "What is the mechanism of action of cholestyramine?
", } ] }, { text: "General practitioner which had prescribed cholestyramine was aware of a potential interaction between cholestyramine and phenprocoumon. In accordance with the recommendations, the patient ingested cholestyramine in the morning, at least 1 h before taking phenprocoumon and had a good compliance to this regime.
", qs: [ { task: "By which mechanism could cholestyramine influence the absorption of other drugs and how can we prevent it?
", }, { task: "What is biological half-life of phenprocoumon?
", }, { task: "What was the mechanism of drug-drug interaction in this case? Why was the time interval not a sufficient protection against the interaction?
", } ] }, { text: "Thrombosis was treated with rt-PA (thrombolytic) and heparin (anticoagulant). Despite the therapy, electromechanical dissociation occurred 2 hours later. Cardiopulmonary resuscitation was started immediately, but was unsuccessful. Autopsy findings confirmed the clinical and echocardiographic diagnosis of aortic valve thrombosis with severely impaired leaflet motion.
", qs: [ { task: "What is electromechanical dissociation and what is its prognosis?
", } ] } ], biblio: ["Balmelli N, et al. Fatal drug interaction between cholestyramine and phenprocoumon. European journal of internal medicine. 2002; 13(3): 210-211.
http://www.sciencedirect.com/science/article/pii/S0953620502000262
", "Delgado C, et al. Intermittent electromechanical dissociation as an unusual sign of prosthetic valve thrombosis in a patient with prosthetic fibrous ingrowth. Journal of the American Society of Echocardiography. 2000; 13(7): 685-689.
http://www.sciencedirect.com/science/article/pii/S0894731700848348
"], editors: '06', index: 65 }, { title: 'Kinetics 9', cathegory: 4, keywords: ["Parkinson’s disease", "pregnancy", "levodopa", "benserazide", "selegiline", "bromocriptine"], parts: [ { text: "A 34-year-old woman diagnosed with Parkinson\'s disease (PD) found that she became pregnant. The disease of the patient had already started 8 years ago with symptoms that include progressive bilateral tremor during rest and action (left/sided dominance), combined with mild hypokinesia/bradykinesia, and a minor rigidity. Up to now, the patient responded well to treatment, which included Madopar 250 (21/4 a day) and Eldepryl 5mg (2 a day) preparations.
", qs: [ { task: "What are the active substances contained in these preparations and what mechanisms of action they have?
", }, { task: "For what reason are there two active substances in Madopar?
", } ] }, { text: "Eldepryl 5 mg administration was discontinued after finding out that the patient is pregnant. The dose of Madopar 250 was reduced (1 a day), and new preparation containing bromocriptine (7.5 mg a day) was started. The aim was to switch to bromocriptine monotherapy, but these changes of medication made symptoms of PD worse. Therefore, preparation containing bromocriptine was discontinued, and dose of Madopar 250 was increased to the original one (21/4 a day). This dosage was kept unchanged until delivery.
", qs: [ { task: "Why was medication of the patient changed, and why the physician aimed for the bromocriptine monotherapy?
", }, { task: "What is the mechanism of action of bromocriptine?
", } ] }, { text: "The patient did not experience any complications of pregnancy (during the treatment by Madopar 250), except for very mild transient depressive tendencies. Her PD did not worsen during pregnancy. In gestation week 39, the patient delivered a normal and healthy boy (weight 3050 g and length, 49 cm) by an uncomplicated elective caesarean section. After the delivery, Eldepryl 5 mg was reintroduced (2 a day) and Madopar 250 increased (from 21/4 a day to 23/4 a day). The child was developing normally 32 months after delivery.
", qs: [ { task: "Would you recommend to the patient breast-feeding of the baby?
", } ] } ], biblio: ["Hagell P; Odin P; Vinge E. Pregnancy in Parkinson's disease: a review of the literature and a case report. Movement disorders. 1998; 13(1): 34-38.
http://onlinelibrary.wiley.com/doi/10.1002/mds.870130110/epdf
"], editors: '04', index: 66 }, { title: 'Kinetics 10', cathegory: 4, keywords: ["lamotrigine", "phenobarbital", "phenytoin", "amoxicillin", "diazepam", "cytochrome P450"], parts: [ { text: "A 44-year-old man presented to the emergency department (ED) with complaints of headache, clumsiness, and decreased co-ordination. Apart from a long-standing seizure disorder, his past medical history was unremarkable, except for right arm amputation following a fall. Medications prior to admission included lamotrigine 100 mg twice daily, phenobarbital 60 mg in the morning and 120 mg at supper and phenytoin 300 mg in the morning and 400 mg at supper. This medication regimen had been unchanged for almost 5 months.
The last seizure the patient experienced occurred approximately 2 weeks prior to admission.
", qs: [ { task: "What are the indications and modes of action of administered drugs?
", }, { task: "Are doses in accordance to recommended doses in SmPC?
", }, { task: "Which from the drugs administered probably evoked current symptoms?
", }, { task: "Is any from the drugs used recommended for TDM?
", } ] }, { text: "The only known total phenytoin concentration had been determined by his family physician shortly before the seizure occurred and was 8 μg/mL. No changes in the regimen were made at that time.
", qs: [ { task: "What is phenytoin’s therapeutic range?
", } ] }, { text: "Two days prior to admission, the patient had visited his family physician following 1 week of cough with purulent sputum. He was prescribed amoxicillin 500 mg/d for treatment of a presumed upper respiratory tract infection and diazepam for insomnia.
", qs: [ { task: "What are indications and modes of action of amoxicillin and diazepam?
", }, { task: "What are the risks of diazepam chronic use?
", } ] }, { text: "When interviewed by the pharmacist in the ED, the patient reported taking 10 mg of diazepam at bedtime the day it was prescribed. However, the next day he felt confused, with poor memory recall (he could not remember names or numbers) and slurred speech. He decided to reduce the diazepam dose himself to 5 mg that night. Again, he felt drowsy and unwell the next day (the day of admission) and stopped taking diazepam altogether. He also took the amoxicillin for the 2 days prior to and on the day of admission. He reported adherence to his antiepileptic drugs regimen and denied the use of any nonprescription or herbal medication. He did not smoke or consume alcohol.
On physical examination, the patient’s vital signs were stable, he was in no acute distress, and was alert and oriented. The fundi were normal, and pupils were equal and reactive to light and accommodation, and were 3 mm, but he had nystagmus and reported diplopia. His gait was markedly ataxic. The patient’s cardiac, respiratory, and abdominal examinations were unremarkable, as were his electrolyte levels and complete blood cell count.
", qs: [ { task: "Interaction of which drugs led to the present symptoms?
", } ] }, { text: "The total phenytoin concentration drawn on hospital admission was 37 μg/mL; he had no history of prior documented phenytoin toxicity. The phenobarbital concentration (23 μg/mL) was within the normal range. No lamotrigine concentration was determined.
", qs: [ { task: "What is the therapeutic range of phenobarbital and lamotrigine?
", }, { task: "What is the probable mechanism of phenytoin and diazepam interaction?
", } ] }, { text: "", qs: [ ] } ], biblio: ["Murphy A, Wilbur K. Phenytoin-diazepam interaction. The Annals of Pharmacotherapy. 2003, 37°: 659-663.
http://aop.sagepub.com/content/37/5/659.full.pdf+html
"], editors: '0', index: 67 }, { title: 'Kinetics 11', cathegory: 4, keywords: ["cyclosporine A", "prednisone", "orlistat", "microemulsion"], parts: [ { text: "Man (65 years old, BMI 28) is treated with cyclosporine A (CsA, 250 mg/day) and prednisone (6 mg/day) in a standard immunosuppressant regime after heart transplantation. Plasma level of CsA is chronically maintained at 150 ± 20 ng/mL.
", qs: [ { task: "What is the mechanism of action and indications of cyclosporine A?
", } ] }, { text: "A year ago patient started to use orlistat (3× 120 mg/day) to decrease his body weight. After 6 months of this therapy, level of CsA decreased to 50 ng/mL. The dosing was therefore increased to 300 mg/day, but plasma levels raised only to 65 ng/mL. Thus a change in CsA dosage form was made – a microemulsion in gelatin capsules was started at the dose of 350 mg/day. In a week, plasma concentration of CsA increased to 125 ng/mL. After another adjustment of the dose to 375 mg/day, the plasma concentration finally reached 160 ng/mL.
[[Kinetics_11.jpg]]
", qs: [ { task: "What is the mechanism of action of orlistat? Is it an OTC, or a prescription drug?
", }, { task: "Is cyclosporine A lipophilic, or hydrophilic molecule?
", }, { task: "By which mechanism could orlistat influence the absorption of other drugs?
", } ] }, { text: "Medical preparations in the form of emulsion consist of the active substance, hydrophilic and lipophilic solvent, and excipients – surfactants (emulsifiers). In the microemulsion form, the oil particles are very small (tens of nanometers), therefore with the naked eye a microemulsion is not distinguishable from a solution.
", qs: [ { task: "What are advantages of using microemulsion dosage form of ciclosporin A?
", } ] } ], biblio: ["Le Beller C, et al. Co-administration of orlistat and cyclosporine in a heart transplant recipient. Transplantation-Baltimore. 2000; 70(10): 1541-1541.
", "Evans S, et al. Drug interaction in a renal transplant patient: Cyclosporin-neoral and orlistat. American Journal of Kidney Diseases. 2003; 41(2): 493-496.
http://www.sciencedirect.com/science/article/pii/S0272638602691632
"], editors: '06', index: 68 }, { title: 'Kinetics 12', cathegory: 4, keywords: ["intoxication", "wintergreen oil", "methylsalicilate", "activated charcoal"], parts: [ { text: "A man (80 years old) with end-stage diabetic nephropathy was cared by a live-in attendant. The patient requires hemodialysis three times per week. His medical history included diabetes mellitus and severe coronary artery disease. He had a pacemaker. The live-in attendant rubbed regularly patient’s lower extremities with the oil of wintergreen (or eastern teaberry, Gaultheria procumbens, Ericaceae).
", qs: [ { task: "What is the active substance of wintergreen oil?
", } ] }, { text: "One day, the attendant spread the oil to patient’s legs and left the bottle on the nightstand. The patient mistakenly drank a mouthful of it. Even if the patient vomited the oil immediately, two hours later he had symptoms of poisoning (seizures). The oil contained 35 % of active substance (1 teaspoon is equivalent to 1600 mg of acetylsalicylic acid). The patient was admitted to the Emergency Department unresponsive, with apnoe and strongly smelling of wintergreen oil. He was dialyzed one day prior to the poisoning. His ECG showed a wide complex QRS, his blood pressure was 146/66 mm Hg, palpable pulse was 55 bpm. Blood biochemistry showed pH of arterial blood 6.95 and plasma concentration of salicylates was 74.8 mg/dL.
", qs: [ { task: "How are salicylates eliminated? Can renal or kidney disease significantly influence their elimination?
", }, { task: "How to increase excretion of salicylates via urine in a healthy person?
", } ] }, { text: "The patient was intubated and then followed gastric lavage and administration of activated charcoal. Immediate hemodialysis was initiated upon transfer to the Intensive Care Unit. Approximately 9 h after admission, the patient had another generalized tonic-clonic seizure, which responded to diazepam. However, because the patient desired no other resuscitative efforts, he passed away soon. An autopsy revealed a plasma concentration of salicylates post mortem of 82.6 mg/dL.
", qs: [ { task: "Why was the activated charcoal administered?
", }, { task: "How can you explain the fact, that patient had higher plasma levels of salicylates after hemodialysis than before the procedure?
", }, { task: "What could influence the absorption of salicylates through skin?
", }, { task: "How is chronic poisoning with salicylates called and what are the symptoms?
", } ] } ], biblio: ["Chin RL; Olson KR; Dempsey D. Salicylate toxicity from ingestion and continued dermal absorption. The California Journal of Emergency Medicine. 2007; 8(1): 23.
"], editors: '06', index: 69 } ]