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Predicting creatinine clearance and renal drug clearance in obese patients from estimated fat-free body mass cheap minomycin online visa antibiotics for uti amoxicillin. Erratum in: Obstet complaints related to central or peripheral nervous system or Gynecol 2007;109:788 buy 50 mg minomycin mastercard virus ebola. Ext • Develop a plan for managing each problem that includes plans Mild bilateral foot and ankle edema for monitoring patient response to interventions purchase 100mg minomycin fast delivery best antibiotics for mild acne. Dialyze 4 hours per session, three times per week (M, W, F morning Develop a therapeutic plan for the use of vancomycin in this shift) patient, including a monitoring plan. Indicate the advantages and disadvan- clinical practice recommendations for diabetes and chronic kidney tages of each option. What clinical and laboratory parameters would you recommend 52 to evaluate the desired and undesired consequences of each of your recommended interventions? What information should be provided to the patient to enhance compliance, ensure successful therapy, and minimize adverse effects? Kevin was driving himself and four other passengers home from a Neuro party when he swerved off the road and hit a tree. What information (signs, symptoms, laboratory values) indi- A & O × 3 but disoriented about recent events. Hyponatremia, fluid-electrolyte disorders, and the syn- Optimal Plan drome of inappropriate antidiuretic hormone secretion: diagnosis and 4. What clinical and laboratory parameters are necessary to evaluate the therapy for achievement of the desired therapeutic outcome and to detect or prevent adverse effects? What information should be provided to the patient to enhance 53 compliance, ensure successful therapy, and minimize adverse effects? At that time, the patient admitted that he and his friends had been taking the Maintaining Homeostasis on an drug “ecstasy” at the party before the car accident. Perform a literature or Internet search to identify the vasopressin • Recommend a patient-specific therapeutic plan for treating receptor antagonist agents available and those under investigation. Hyponatremia: evaluating the past 5 years with a high-flux cellulose triacetate membrane; he correction factor for hyperglycemia. What information should be provided to the patient to help cates the presence or severity of hyperkalemia? Formulate a Therapeutic Alternatives treatment plan for the patient’s anemia of chronic kidney disease. What feasible pharmacotherapeutic alternatives are available Time (g/dL) (ng/mL) Saturation Dosage for treating hyperkalemia? What drug, dosage form, dose, schedule, and duration of therapy are best for treating hyperkalemia in this patient? What clinical and laboratory parameters are necessary to evaluate be prevented in dialysis patients by lowering dialysate potassium or the therapy for achievement of the desired therapeutic outcomes calcium concentrations. What information should be provided to the patient regarding Compare the cost of a 1-month supply of calcium carbonate, nonprescription medications that could reduce the risk of hyper- calcium acetate, sevelamer, and lanthanum carbonate using usual kalemia? What information (signs, symptoms, laboratory values) indi- cates the presence or severity of hyperphosphatemia and hyper- 1. What are the clinical consequences of hyperphosphatemia and bone metabolism and disease in chronic kidney disease. What pharmacotherapeutic alternatives are available for treat- treated with erythropoietin: a meta-analysis. What drugs, dosage forms, schedules, and duration of therapy are best for treating this patient’s hyperphosphatemia and hypercal- cemia? What clinical and laboratory parameters are necessary to evaluate the therapy for achievement of the desired therapeutic outcome Laura L. Gen • Evaluate laboratory data and clinical symptoms for assessment Patient is pale; does not appear to be in any discomfort and monitoring of hypercalcemia, hypercalcemia treatment, and complications of hypercalcemia. Skin • Recognize and develop management strategies for toxicities Dry with tenting on the dorsal surfaces of both hands; slow capillary associated with treatment options for hypercalcemia. He reports that his wife’s last bowel movement was 5 days ago despite administration of a stool softener and enema. S/P left breast lumpectomy and axillary Normal female genitalia; normal rectal tone; stool heme (–) lymph node dissection with two of 22 lymph nodes positive. Bentley has no other complaints except a history of í Chest X-Ray sharp aching pain near her left clavicle that began 2 months ago. Normal saline at 150 mL/h is initiated, and she is admitted to the inpatient oncology service for further management. Bentley’s husband is unfamiliar with the neurologic side Problem Identification effects of hypercalcemia and thinks his wife is “dopey” from pain 1. What information (signs, symptoms, laboratory values) indi- because his wife has no pain at this time. She is discharged from the Desired Outcome hospital on the same pain regimen she was taking prior to admis- sion. The last two episodes were separated by 2 weeks, and both were treated by her outpatient Therapeutic Alternatives oncologist with normal saline rehydration and zoledronic acid. What are the therapeutic options for the acute and chronic week after her last treatment with zoledronic acid, Mrs. Her pain was controlled with sus- tained-release morphine sulfate 30 mg po Q 12 h, immediate-release 2. The sustained-release morphine sulfate was subse- cemia in patients receiving calcitriol for anticancer therapy? Her use of immediate-release morphine When evaluating a patient for hypercalcemia, a corrected calcium dropped from four times a day to zero over a period of 3 days. Management of the adverse effects associated Seizure disorder (last seizure approximately 8 months ago) with intravenous bisphosphonates. Extensive alcohol history: drank up to two cases pooled analysis of two randomized, controlled clinical trials. Appears older than stated age; cachectic; oriented to self only; confused and uncooperative; stated the year is 2002 and that he is at • Monitor patients receiving electrolyte replacement therapy for Al’s Bar. What information (signs, symptoms, laboratory values) indi- Genit/Rect cates the presence and severity of the electrolyte abnormalities? What additional information is needed to satisfactorily assess Upper and lower extremities reveal pallor in the nail beds and this patient’s electrolyte disorders? What feasible pharmacotherapeutic alternatives are available for Neuro treatment of dehydration, hypokalemia, and hypomagnesemia? What medical options are available for treating this patient’s he- í Abdominal Ultrasound patic encephalopathy? What changes should be made to the patient’s medication patic biliary ductal dilatation; spleen enlarged at 18. Describe how a patient’s acid–base status can affect serum Blood cultures drawn × 2 electrolyte concentrations. How might the patient’s buffer therapy requirement change if she is started on sevelamer to prevent dietary phosphorus absorption? Differentiate between the bone disease of metabolic acidosis versus that associated with chronic renal failure and osteoporosis. Which information obtained from the patient’s symptoms, it does not appear to be progressive unless the patient’s renal physical examination, and laboratory analysis indicates the function worsens.
The 4th arch on the right becomes the brachiocephalic and right subclavian artery; on the left purchase discount minomycin line antibiotics for acne when pregnant, it differentiates into the deﬁnitive aortic arch discount 50mg minomycin visa natural treatment for dogs fleas, gives off the left subclavian artery and links up distally with the descending aorta best 100mg minomycin antibiotic resistance funding. When the truncus arteriosus splits longitudinally to form the ascending aorta and pulmonary trunk, the 6th arch, unlike the others, remains linked with the latter and forms the right and left pulmonary arteries. This diagram explains the relationship of the right recurrent laryngeal nerve to the right subclavian artery and the left nerve to the aortic arch and the ligamentum arteriosum (or to a patent ductus arteriosus). This asymmetrical development of the aortic arches accounts for the different course taken by the recurrent laryngeal nerve on each side. In the early fetus the vagus nerve lies lateral to the primitive pharynx, separated from it by the aortic arches. What are to become the recurrent laryngeal nerves pass medially, caudal to the aortic arches, to supply the developing larynx. With elongation of the neck and caudal migration of the heart, the recurrent nerves are caught up and dragged down by the descending aortic arches. On the right side the 5th and distal part of the 6th arch absorb, leaving the nerve to hook round the 4th arch. On the left side, the nerve remains looped around the persisting distal part the 6th arch (the ligamentum arteriosum) which is overlapped and dwarfed by the arch of the aorta. Relatively little mixing of oxygenated and deoxygenated blood occurs in the right atrium since the valve overlying the oriﬁce of the inferior vena cava serves to direct the ﬂow of oxygenated blood from that vessel through the foramen ovale into the left atrium, while the deoxygenated stream from the superior vena cava is directed through the tricuspid valve into the right ventricle. From the left atrium the oxy- genated blood (together with a small amount of deoxygenated blood from the lungs) passes into the left ventricle and hence into the ascending aorta for the supply of the brain and heart via the vertebral, carotid and coronary arteries. As the lungs of the fetus are inactive, most of the deoxygenated blood from the right ventricle is short-circuited by way of the ductus arteriosus from the pulmonary trunk into the descending aorta. This blood supplies the abdominal viscera and the lower limbs and is shunted to the placenta, for oxygenation, along the umbilical arteries arising from the internal iliac arteries. At birth, expansion of the lungs leads to an increased blood ﬂow in the pulmonary arteries; the resulting pressure changes in the two atria bring the overlapping septum primum and septum secundum into apposition which effectively closes off the foramen ovale. At the same time active contraction of the muscular wall of the ductus arteriosus results in a functional closure 40 The Thorax of this arterial shunt and, in the course of the next 2–3 months, its complete obliteration. Similarly, ligature of the umbilical cord is followed by throm- bosis and obliteration of the umbilical vessels. Congenital abnormalities of the heart and great vessels The complex development of the heart and major arteries accounts for the multitude of congenital abnormalities which may affect these structures, either alone or in combination. Dextro-rotation of the heart means that this organ and its emerging vessels lie as a mirror-image to the normal anatomy. It may be associated with reversal of all the intra-abdominal organs; I have seen a student correctly diagnose acute appendicitis as the cause of a patient’s severe left iliac fossa pain because he found that the apex beat of the heart was on the right side! Septal defects At birth, the septum primum and septum secundum are forced together, closing the ﬂap valve of the foramen ovale. If the septum secundum is too short to cover the foramen secundum in the septum primum, an atrial septal defect persists after the septum primum and septum secundum are pressed together at birth. This results in an ostium secundum defect, which allows shunting of blood from the left to the right atrium. A more serious atrial septal defect results if the septum primum fails to fuse with the endocardial cushions. This ostium primum defect lies immediately above the atrioventricular boundary and may be associated with a defect of the pars membranacea septi of the ventricular septum. Occasionally the ventricular septal defect is so huge that the ventricles form a single cavity, giving a trilocular heart. Congenital pulmonary stenosis may affect the trunk of the pulmonary artery, its valve or the infundibulum of the right ventricle. If stenosis occurs in conjunction with a septal defect, the compensatory hypertrophy of the right ventricle (developed to force blood through the pulmonary obstruc- tion) develops a sufﬁciently high pressure to shunt blood through the defect into the left heart; this mixing of the deoxygenated right heart blood with the oxygenated left-sided blood results in the child being cyanosed at birth. This results from unequal division of the truncus arteriosus by the spinal septum, resulting in a stenosed pul- monary trunk and a wide aorta which overrides the oriﬁces of both the ven- tricles. The displaced septum is unable to close the interventricular septum, which results in a ventricular septal defect. Cyanosis results from the shunting of large amounts of unsaturated blood from the right ventricle through the ventricular septal defect into the left ventricle and also directly into the aorta. If left uncorrected, it causes progressive work hypertrophy of the left heart and pulmonary hypertension. There may be an extensive obstruction of the aorta from the left subclavian artery to the ductus, which is widely patent and maintains the circulation to the 42 The Thorax lower parts of the body; often there are multiple other defects and fre- quently infants so afﬂicted die at an early age. More commonly there is a short segment involved in the region of the ligamentum arteriosum or still patent ductus. In these cases, circulation to the lower limb is maintained via collateral arteries around the scapula anastomosing with the intercostal arteries, and via the link-up between the internal thoracic and inferior epi- gastric arteries. Clinically, this circulation may be manifest by enlarged vessels being palpable around the scapular margins; radiologically, dilatation of the engorged intercostal arteries results in notching of the inferior borders of the ribs. Abnormal development of the primitive aortic arches may result in the aortic arch being on the right or actually being double. An abnormal right subclavian artery may arise from the dorsal aorta and pass behind the oesophagus—a rare cause of difﬁculty in swallowing (dysphagia lusoria). Rarely, the division of the truncus into aorta and pulmonary artery is incomplete, leaving an aorta–pulmonary window, the most unusual congeni- tal ﬁstula between the two sides of the heart. The superior mediastinum This is bounded in front by the manubrium sterni and behind the ﬁrst four thoracic vertebrae (Fig. Above, it is in direct continuity with the root of the neck and below it is continuous with the three compartments of the inferior mediastinum. Its principal contents are: the great vessels, trachea, oesophagus, thymus—mainly replaced by fatty tissue in the adult, thoracic duct, vagi, left recurrent laryngeal nerve and the phrenic nerves (Fig. The arch of the aorta is directed anteroposteriorly, its three great branches, the brachiocephalic, left carotid and left subclavian arteries, ascend to the thoracic inlet, the ﬁrst two forming a V around the trachea. The brachio- cephalic veins lie in front of the arteries, the left running almost horizontally across the superior mediastinum and the right vertically downwards; the two unite to form the superior vena cava. Posteriorly lies the trachea with the oesophagus immediately behind it lying against the vertebral column. The oesophagus The oesophagus, which is 10in (25cm) long, extends from the level of the lower border of the cricoid cartilage at the level of the 6th cervical vertebra to the cardiac oriﬁce of the stomach (Fig. Course and relations Cervical In the neck it commences in the median plane and deviates slightly to the left as it approaches the thoracic inlet. The trachea and the thyroid gland are its immediate anterior relations, the 6th and 7th cervical vertebrae and pre- The mediastinum 43 Fig. On the left side it is also related to the subclavian artery and the terminal part of the thoracic duct (Fig. From being somewhat over to the left, it returns to the midline at T5 then passes downwards, forwards and to the left to reach the oesophageal opening in the diaphragm (T10). Anteriorly, it is crossed by the trachea, the left bronchus (which 44 The Thorax constricts it), the pericardium (separating it from the left atrium) and the diaphragm. Posteriorly lie the thoracic vertebrae, the thoracic duct, the azygos vein and its tributaries and, near the diaphragm, the descending aorta.
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Paracetamol is an effective value; if it lies above a semi-logarithmic graph joining treatment for mild-moderate pain and for relieving fever order minomycin us antibiotic resistance animal agriculture. Paracetamol has analgesic efficacy equivalent to patic damage is likely (plasma concentrations measured aspirin discount minomycin 100 mg on line antibiotics for uti nitrofurantoin, but in therapeutic doses it has only weak anti- earlier than 4 h are unreliable because of incomplete ab- inflammatory effects buy minomycin online from canada antimicrobial 10, a functional separation that reflects sorption). Patients who are malnourished are regarded as its differential inhibition of enzymes responsible for pros- being at risk at 50% of these plasma concentrations. It is inactivated in the liver, principally by the smaller, is thought to have been ingested within the conjugation as glucuronide and sulphate. This substance is normally Specific therapy involves replenishing stores of liver glu- rendered harmless by conjugation with glutathione. Maximal, long- most effective if administered within 8 h of the overdose, term, daily dosing may predispose to chronic renal disease. Her husband said that his wife ‘knew that too much paracetamol was In the 18th century, the Reverend Edmund Stone wrote dangerous but she did not realise there was paracetamol in [the about the value of an extract of bark from the willow tree proprietary preparation]’ which she bought at a supermarket that did not have a dispensary counter where she could have received advice. Aspirin is a common cause of allergic or proved highly successful in the treatment of rheumatic fe- pseudoallergic symptoms and signs. The new preparation proved acceptable aspirin use to the development of the rare Reye’s tohisfatherandpavedthewayfortheproductionofaspirin. Platelets cannotregeneratethe enzyme comfort, tinnitus, deafness, sweating, pyrexia, restlessness, and the resumption of thromboxane A2 production is tachypnoea and hypokalaemia. A large overdose (plasma dependent on the entry of new platelets into the salicylate concentration above 750 mg/L) may result in circulation (platelet lifespan is 7 days). Thus a pulmonary oedema, convulsions and coma, with severe de- continuousantiplateleteffectisachieved withlow doses. Bleeding is unusual, despite the anti- • Respiratory stimulation is a characteristic of aspirin platelet effect of aspirin. In • Although aspirin in high dose reduces renal tubular children under 4 years, severe metabolic acidosis is more reabsorption of uric acid so increasing its elimination, likely than respiratory alkalosis, especially if the drug has other treatments for hyperuricaemia are preferred. Indeed aspirin should be avoided in gout as low doses Serial measurements of plasma salicylate are necessary to inhibit uric acid secretion and on balance its effects on monitor the course of the overdose, for the concentration uric acid elimination are adverse. The main use of aspirin is as an antiplatelet agent to agement of overdose applies, but the following are relevant prevent arterial thrombotic events due to atherosclerosis. Gastric lavage or the use in Kawasaki disease, in combination with intravenous im- of an emetic is no longer recommended. Hydrolysis removes is treated with sodium bicarbonate, which alkalinises the acetyl group, and the resulting salicylate ion is inacti- the urine and accelerates the removal of salicylate in the vated largely by conjugation with glycine. Doses of 75–150 mg/day are used to prevent throm- Colchicine is derived from the autumn crocus (Colchicum botic vascular occlusion; 300 mg as immediate treatment for autumnale). Its anti-inflammatory properties have long myocardial infarction; 300–900 mg every 4–6 h for analgesia. Effects particularly associated with aspi- tion to relieving inflammation in acute gout attacks, it is rin are: used to treat other inflammatory disorders including Beh- • Salicylism (the symptoms of an excessive dose): tinnitus c¸et’s syndrome and the hereditary fever syndrome familial and hearing difficulty, dizziness, headache and Mediterranean fever. The most common adverse effect of colchicine is diar- Most conventional immunomodulatory agents act by rhoea, due to its effects on rapidly proliferating gastrointes- inhibiting activation or reducing proliferation of lympho- tinal epithelial cells. Many have more than one mechanism of action may follow and it is therefore a sign to stop the drug and often the precise way in which they exert their effects and restart at a lower dose. Methotrexate, azathioprine, mycophenolate mofetil and Immunomodulatory drugs are used both to control symp- leflunomide are antimetabolites, interfering with the de toms and to retard or arrest the progression of chronic in- novo synthesis of purines and pyrimidines, on which pro- flammatory diseases. Metho- variety of ways, and reduce the proliferation and activation trexate is thought to have additional anti-inflammatory of lymphocytes. The calcineurin antagonists (ciclosporin and tacro- The terminology surrounding immunomodulatory drugs limus) and sirolimus selectively inhibit T-cell activation has evolved separately in different specialties, although the and proliferation, by inhibiting cytokine expression and underlying management principles are similar. Intravenous immuno- disease progression in illnesses such as rheumatoid or psori- globulin has immunomodulatory effects through interfer- aticarthritis. Treatmentregimensforsystemicvasculitisorse- ence with Fcg receptor signalling, among other vere organ involvement in the connective tissue diseases mechanisms. The precise mechanisms of action of sulfasa- make use of terminology drawn from oncology, with ‘remis- lazine, hydroxychloroquine, thalidomide, dapsone and sion induction’ followed by ‘maintenance’ phases. Many of gold are less clear, but they have been shown to influence thesedrugsaredescribedas‘steroid-sparing’astheirconcom- the expression of a range of pro-inflammatory cytokines. All should only be initiated under specialist hazardous than rash or arthritis and therefore a more supervision and all call for close monitoring, for example of potent but potentially more toxic drug regimen is bone marrow, liver, kidney or other organs, as known tox- justified. Live vaccines in general should not be given to • Adverse-effect profile: both the probability and severity immunosuppressed patients as there is a risk of dissemi- of potential adverse effects need to be considered. Methotrexate was first developed as an anticancer drug • Co-morbidity: drugs causing hypertension or adverse 50 years ago. Many conventional immunomodulatory drugs used in rheumatology practice are anti-metabolites, inhibiting de novo synthesis of purines or pyrimidines; pathways upon which activated lymphocytes are particularly dependent. The mechanisms of action of sulfasalazine, hydroxychloroquine and thalidomide appear to involve inhibition of expression of pro-inflammatory cytokines. Methotrexate is usually prescribed orally, thritis, and in the maintenance phase of therapy for sys- starting at 7. Folic acid is usually prescribed (variably inhibits folate-dependent enzymes involved in purine bio- 5 mg weekly, three times weekly or on all days apart from synthesis, thus reducing lymphocyte proliferation, and this on the methotrexate dosing day), in order to mitigate the was originally thought to be its principal mechanism of ac- adverse effects. This appears to have little effect on the tion (and is likely to be the source of many of its toxic ef- blockade of de novo purine synthesis, unlike folinic acid fects). Increased plasma concentra- Mouth ulcers and nausea occur commonly but may be im- tions of adenosine are thought to mediate many anti- proved by co-prescription of folic acid. Lastly, co-prescription of angiotensin- scribed to patients with moderate to severe renal impair- converting enzyme inhibitors and azathioprine increases ment, liver disease or an active infection. Because of its the risk of myelosuppression; the mechanism is incom- teratogenicity it must not be prescribed for women who pletely understood but has assumed greater importance are or may become pregnant or who are breast feeding. Experience with azathioprine in pregnant women with renal transplants indicates that Azathioprine it is relatively safe, probably because the fetus cannot me- Azathioprine is another antimetabolite which acts by inhi- tabolise 6-mercaptopurine. Although a teratogenic metab- biting purine biosynthesis, thus preferentially acting on olite is present in breast milk, its concentration is low and proliferating lymphocytes. Besides its use to prevent rejec- no evidence for harm exists; nevertheless, breast feeding tion in organ transplant recipients, it has a well established while taking azathioprine is best regarded as unsafe. It is licensed for the prophy- in the presence of glutathione to 6-mercaptopurine and laxis of acute rejection following organ transplantation then to 6-thioguanine. These are similar to azathioprine and in- 25–50 mg and rising over the course of several weeks to clude gastrointestinal disturbances (diarrhoea is particularly a daily dose of 1. The major serious reactions are bone mar- row suppression resulting in leucopenia, anaemia and Leflunomide thrombocytopenia; hepatotoxicity; increased susceptibility to infection; and in the long term an increased risk of neo- The active metabolite of leflunomide (A77 1726) inhibits plasia. As with methotrexate, regular monitoring of full dihydro-orotate dehydrogenase,a mitochondrial enzymere- quired for the synthesis of pyrimidines.
Computerized methods that incorporate expected population pharmacokinetic characteristics (Bayesian pharmaco- kinetic computer programs) can be used in difficult cases where serum concentrations are obtained at suboptimal times or the patient was not at steady state when serum con- centrations were measured order minomycin amex antibiotic of choice for uti. An additional benefit of this method is that a complete pharmacokinetic workup (determination of clearance purchase 50mg minomycin with amex antibiotic resistance can boost bacterial fitness, volume of distribution purchase generic minomycin online antibiotic vaginal itching, and half- life) can be done with one or more measured concentrations that do not have to be at steady state. Because nonlinear pharmacokinetics for pro- cainamide has been observed in some patients, suggested dosage increases greater than 75% using this method should be scrutinized by the prescribing clinician, and the risk versus beneﬁt for the patient assessed before initiating large dosage increases (>75% over current dose). Using linear pharmacokinetics, the new dose to attain the desired concentration should be proportional to the old dose that produced the measured concentration. The patient would be expected to achieve steady-state conditions after the ninth day (5 t1/2 = 5 ⋅ 13. Using linear pharmacokinetics, the new dose to attain the desired concentration should be proportional to the old dose that produced the measured concentration. The patient would be expected to achieve steady-state conditions after the second day (5 t1/2 = 5 ⋅ 5. Using linear pharmacokinetics, the new dose to attain the desired concentration should be proportional to the old dose that produced the measured concentration: Dnew = (Css,new / Css,old)Dold = (8 μg/mL / 4. Pharmacokinetic Parameter Method The pharmacokinetic parameter method of adjusting drug doses was among the ﬁrst techniques available to change doses using serum concentrations. The pharmacokinetic parameter method requires that steady state has been achieved and uses only a steady-state pro- cainamide concentration (Css). During a continuous intravenous infusion, the following equation is used to compute procainamide clearance (Cl): Cl = k0 / Css, where k0 is the dose of procainamide in mg/min. If the patient is receiving oral procainamide therapy, pro- cainamide clearance (Cl) can be calculated using the following formula: Cl = [F(D/τ)] / Css, where F is the bioavailability fraction for the oral dosage form (F = 0. Because this method also assumes linear pharmacokinetics, procainamide doses computed using the pharmacokinetic parameter method and the linear pharmacokinetic method should be identical. Procainamide clearance can be computed using a steady-state procainamide concentra- tion: Cl = [F(D/τ)] / Css = [0. A steady-state procainamide serum concentration could be measured after steady state is attained in 3–5 half-lives. The patient would be expected to achieve steady-state conditions after the ninth day (5 t1/2 = 5 ⋅ 13. Procainamide clearance can be computed using a steady-state procainamide concentra- tion: Cl = [F(D/τ)] / Css = [0. A steady-state procainamide serum concentration could be measured after steady state is attained in 3–5 half-lives. The patient would be expected to achieve steady-state conditions after the second day (5 t1/2 = 5 ⋅ 5. Procainamide clearance can be computed using a steady-state procainamide concentra- tion: Cl = k0/Css = (1 mg/min)/(4. A steady-state procainamide serum concentration could be measured after steady state is attained in 3–5 half-lives. In this situation, two pro- cainamide serum concentrations obtained at least 4–6 hours apart during a continuous infusion can be used to compute procainamide clearance and dosing rates. In addition to this requirement, the only way procainamide can be entering the patient’s body must be via intravenous infusion. Once procainamide clearance (Cl) is determined, it can be used to adjust the procainamide salt infusion rate (k0) using the following relation- ship: k0 = Css ⋅ Cl. Additionally, the time difference between t2 and t1, in minutes, was determined and placed directly in the calculation. Additionally, the time difference between t2 and t1, in minutes, was determined and placed directly in the calculation. The most reliable computer programs use a nonlinear regression algorithm that incorporates components of Bayes’ theorem. Nonlinear regression is a sta- tistical technique that uses an iterative process to compute the best pharmacokinetic parameters for a concentration/time data set. The computer program has a phar- macokinetic equation preprogrammed for the drug and administration method (oral, intra- venous bolus, intravenous infusion, etc. Typically, a one-compartment model is used, although some programs allow the user to choose among several different equations. Using population estimates based on demographic information for the patient (age, weight, gender, liver function, cardiac status, etc. Kinetic parameters are then changed by the computer program, and a new set of estimated serum concentrations are computed. The pharmacokinetic parameters that generated the estimated serum concentrations closest to the actual values are remem- bered by the computer program, and the process is repeated until the set of pharmacoki- netic parameters that result in estimated serum concentrations that are statistically closest to the actual serum concentrations are generated. Bayes’ theorem is used in the computer algorithm to balance the results of the computations between values based solely on the patient’s serum drug concentrations and those based only on patient population parameters. Results from studies that compare various methods of dosage adjustment have consistently found that these types of computer dosing programs per- form at least as well as experienced clinical pharmacokineticists and clinicians and better than inexperienced clinicians. Some clinicians use Bayesian pharmacokinetic computer programs exclusively to alter drug doses based on serum concentrations. An advantage of this approach is that consis- tent dosage recommendations are made when several different practitioners are involved in therapeutic drug monitoring programs. However, since simpler dosing methods work just as well for patients with stable pharmacokinetic parameters and steady-state drug concentrations, many clinicians reserve the use of computer programs for more difﬁcult situations. Those situations include serum concentrations that are not at steady state, serum concentrations not obtained at the speciﬁc times needed to employ simpler meth- ods, and unstable pharmacokinetic parameters. Many Bayesian pharmacokinetic com- puter programs are available to users, and most should provide answers similar to the one used in the following examples. He started taking procainamide sustained-release tablets 500 mg four times daily at 0700, 1200, 1800, and 2200 H. Enter patient’s demographic, drug dosing, and serum concentration/time data into the computer program. In this patient’s case, it is unlikely that the patient is at steady state so the linear phar- macokinetics method cannot be used. The pharmacokinetic parameters computed by the program are a volume of distribu- tion of 152 L, a half-life equal to 3. The oral one-compartment model equation used by the program to compute doses indicates that 2000 mg of procainamide every 6 hours will produce a steady-state trough concentration of 6. On the second day of therapy before the morning dose is administered, the procainamide serum concentra- tion equals 4. Enter patient’s demographic, drug dosing, and serum concentration/time data into the computer program. In this patient case, it is unlikely that the patient is at steady state so the linear pharma- cokinetics method cannot be used.