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Concomitant administration of drugs known to inhibit the activity of cytochrome P450 isozymes may increase the plasma levels of clozapine butenafine 15mg amex fungus gnat nepenthes. Cimetidine order 15 mg butenafine mastercard fungus ergot, caffeine buy 15mg butenafine visa fungus gnats get rid, and erythromycin may increase plasma levels of clozapine discount butenafine 15 mg with visa fungus gnats yellow sticky cards, potentially resulting in adverse effects. Skin Rash Haematological System Leukopaenia, neutropaenia, agranulocytosis, eosinophilia Clozapine! Gastrointestinal System: Nausea, vomiting, abdominal pain or diarrhoea may be particularly troublesome in the presence of peptic ulcer or spastic colon. Infuse over 60 to 90 minutes Fluid restriction or high dose infusion: 1 vial (5ml) diluted with 75ml of 5% glucose 6 vials (30ml) diluted with 500ml of 5% glucose More than 6 vials diluted with 1000ml of 5% glucose Inspect for signs of turbidity or precipitation – if present, discard. Infuse over a period not exceeding 60 minutes and flush line thoroughly after drug administration. When diluted in Hartmann’s, the prepared solution is stable for 8 hours at a 1 in 25 dilution and for 24 hours at a 1 in 35 dilution. Trimethoprim blocks the production of tetrahydrofolic acid from dihydrofolic acid by binding to and reversibly inhibiting the required enzyme, dihydrofolate reductase. Thus, sulfamethoxazole; trimethoprim blocks two consecutive steps in the biosynthesis of nucleic acids and proteins essential to many bacteria. The following organisms are usually susceptible: Escherichia coli, Klebsiella species, Enterobacter species, Morganella morganii, Proteus mirabilis, indole-positive Proteus species including Proteus vulgaris, Haemophilus influenzae (including ampicillin- resistant strains), Streptococcus pneumoniae, Shigella flexneri and Shigella sonnei. The overall prevalence of sulfite sensitivity in the general population is unknown and probably low. Sulfite sensitivity is seen more frequently in asthmatic than in nonasthmatic people. It has been reported that sulfamethoxazole; trimethoprim may prolong the prothrombin time in patients who are receiving the anticoagulant warfarin. This interaction should be kept in mind when sulfamethoxazole; trimethoprim is given to patients already on anticoagulant therapy, and the coagulation time should be reassessed. Allergic Reactions: Stevens-Johnson syndrome, toxic epidermal necrolysis, anaphylaxis, allergic myocarditis, erythema multiforme, exfoliative dermatitis, angioedema, drug fever, chills. Henoch-Schoenlein purpura, serum sickness-like syndrome, generalized allergic reactions, generalized skin eruptions, conjunctival and scleral injection, photosensitivity, pruritus, urticaria and rash. In addition, periarteritis nodosa and systemic lupus erythematosus have been reported. Gastrointestinal: Hepatitis (including cholestatic jaundice and hepatic necrosis), elevation of serum transaminase and bilirubin, pseudomembranous enterocolitis, pancreatitis, stomatitis, glossitis, nausea, emesis, abdominal pain, diarrhoea, anorexia. Neurologic: Aseptic meningitis, convulsions, peripheral neuritis, ataxia, vertigo, tinnitus, headache. Diuresis and hypoglycaemia have occurred rarely in patients receiving sulfonamides. Cyclizine may be mixed with morphine in a syringe immediately before use If cyclizine must be diluted in a syringe, either water for injection or 5% dextrose is recommended as the diluent rather than normal saline. In such patients, cyclizine may cause a fall in cardiac output associated with increases in heart rate, mean arterial pressure and pulmonary wedge pressure. Because of its anticholinergic activity cyclizine may enhance the side-effects of other anticholinergic drugs. Respiratory System: dryness of the mouth, nose and throat Cardiovascular System: tachycardia Gastrointestinal System: Cholestatic jaundice, constipation, hypersensitivity hepatitis Haematological System: agranulocytosis Urogenital System: Urinary retention, Skin: Urticaria, drug rash Cyclizine! Patients admitted to the intensive care unit may be on cyclosporin at the time of admission for the following indications: 1. Ensure concentrate is well mixed in diluent fluid to reduce risk of an initial bolus of heavier non-solubilised polyoxyethylated castor oil, which carries an increased risk of anaphylactoid reactions. Visually inspect infusion concentrated and infusion solution for particulate matter and / or discolouration. Laboratory Tests: Cyclosporin has a narrow therapeutic index and variable pharmacokinetics and so monitoring of therapy is mandatory in the critically ill. C0 sampling has been widely used although it appears that C0 is only a weak indicator of absorption of drug. Moreover, the results are assay-dependent as samples of this type contain a large proportion of metabolite that may interfere. Moreover, most of the measured drug found at this time is parent drug, making the measurement relatively free of interference from metabolites. A disadvantage of C2 is the need for samples to be taken close to the 2-hour time-point (+ or -15 minutes). Factors affecting the target ranges for treatment include time of sampling (C0 or C2), organ transplanted, time since transplantation, and other medications. More specific recommended target concentrations for transplant patients are as follows. They may vary in individual cases on the basis of age, gender, renal function, number of episodes of rejection, and concomitant immunosuppressive medication. Target trough (C0) ranges are as follows: Liver: Induction 225-300 ng/mL Maintenance 100-150 ng/mL Heart: Induction 250-325 ng/mL Maintenance 125-175 ng/mL Kidney: Induction 150-225 ng/mL Maintenance 100-180 ng/mL Bone Marrow: Induction 95-205 ng/mL Maintenance 95-205 ng/mL Autoimmune indications: Induction 150-200 ng/mL Maintenance 100-150 ng/mL Target C2 ranges are as follows: Liver: 0-3 months post transplant 800-1200 ng/mL 3-6 months post transplant 640-960 ng/mL >6 months post transplant 480-720 ng/mL Renal: 1 months post transplant 1360-2040 ng/mL 2 months post transplant 1200-1800 ng/mL 3 months post transplant 1040-1560 ng/mL 4-6 months post transplant 880-1320 ng/mL 7-12 months post transplant 720-1080 ng/mL >12 months post transplant 640-960 ng/mL Lung: 0-2 days post transplant >800 1-7 days post transplant 1200 1-4 weeks post transplant 1200-1700 2 months post transplant 1000-1500 3 months post transplant 800-1200 4-6 months post transplant 700-1000 7-12 months post transplant 600-900 >12 months post transplant 600-800 Cyclosporin! Drugs That Alter Cyclosporin Concentrations Cyclosporin is extensively metabolized cytochrome P-450 3A. Substances that inhibit this enzyme could decrease metabolism and increase cyclosporin concentrations. Substances that are inducers of cytochrome P-450 activity could increase metabolism and decrease cyclosporin concentrations. Monitoring of circulating cyclosporin concentrations and appropriate dosage adjustment are essential when these drugs are used concomitantly. Drugs That Increase Cyclosporin Concentrations Calcium Channel Blockers: Diltiazem, nicardipine, verapamil. Other Drugs: Allopurinol, bromocriptine, danazol, metoclopramide, colchicine, amiodarone. Severe digitalis toxicity has been seen within days of starting cyclosporin in several patients taking digoxin. There are also reports on the potential of cyclosporin to enhance the toxic effects of colchicine such as myopathy and neuropathy, especially in patients with renal dysfunction. Cyclosporin should not be used with potassium-sparing diuretics because hyperkalaemia can occur. A large bore, vented needle (as found in the malignant hyperthermia box in theatre) will hasten the transfer of diluent and reconstituted solution. Reconstituted solution should be stored at room temperature and must be protected from direct light. The usual dose for chronic spasticity is between 25mg daily and 50mg four times a day. It is hypothesized that addition of dantrolene to the "triggered" malignant hyperthermic muscle cell! Inhibition of calcium release from the sarcoplasmic reticulum by dantrolene re-establishes the myoplasmic calcium equilibrium, increasing the percentage of bound calcium. These measures must be individualized, but it will usually be necessary to discontinue the suspect triggering agents, attend to increased oxygen requirements, manage the metabolic acidosis, institute cooling when necessary, monitor urinary output, and monitor for electrolyte imbalance.

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The Port officer should examine B/E and should decide at this stage whether:- a) Labelling & marking need to be checked by the port officers and samples may be drawn (If the drug imported is in small container of 5 kg or less than the original container may be called for to check the markings/label) b) When required Samples to be sent for testing / analysis to the Government / Approved testing lab cheap butenafine 15mg on line fungus gnats vinegar. However order butenafine 15mg on line fungus gnats arizona, the port officer may draw more samples depending on the previous test reports cheap 15 mg butenafine with mastercard antifungal drops for ears, number of consignments and the reputation of the manufacturer/ importer butenafine 15mg on line antifungal questions. There are no proper labels/markings or no markings on the containers or the markings are illegible. Drugs imported from a supplier/manufacturer have been reported to be not of standard quality/spurious etc at this port or any other port in India. The price of the drug imported is abnormally low as compared with the previous imports. Pending testing report, to avoid demurrage if the importer gives an undertaking (Rule 40 (1)) in writing not to dispose of the drugs without the consent of Customs commissioner etc. Drugs requiring cold storage such as sera, vaccines, may be released forthwith conditionally on L/G for test etc. If there are any labelling defects and importer desire to rectify the defects at their place, they may be allowed to be clear the consignment on L/G for rectification of labelling and/or test. Samples are drawn as far as possible under the direct supervision of a technical representative of the port office. Also, sampling should invariably be carried out in the presence of the importer‘s representative. In case of drugs requiring special precautions due to their hygroscopic, thermo labile nature etc. If the drug is sterile, the importers should be asked to make arrangement for drawing of samples under sterile conditions. Usually √n+1 number of 417 samples may be drawn, where n is number of containers / batches as per requirements. No samples should be drawn from the consignments imported for the purpose of registration only. It is responsibility of the Port Officer to ensure that all samples intended for test, are sent to laboratory as early as possible. The first part of the sample (original) is for test, the second part (Duplicate) is to be retained in the Port Office. Samples drawn from bulk containers to be sent to the laboratories with a code number in order to maintain secrecy. Port officer should ensure that the seal of the samples should remain intact at required temperature / cold chain shall be maintained during the transportation. If the goods on test by the laboratory are found to be of standard quality and are labelled as prescribed, they may be released. If the goods, on test, are declared to be not of standard quality, the Customs Commissioner is informed about this along with 2 copies of the test Report. The proforma of the Communication for action under Rule 41(1) used is given in Annexure: P-7, intimation about such imports are made to the Deputy Drugs Controller (India) with copies to the other Port Offices, the proforma used for such communication is given in Annexure: P-8. On the basis of the advice of the Port Officers the Customs will issue a show Cause memo to the firm concerned. On the basis of the party‘s reply the case will be finally adjudicated after ascertaining views of the Port Officers. In case the importers appeal for a retest by submitting sufficient evidence like manufacturer‘s protocols of test on the items in question, the case should be referred to the Deputy Drugs Controller (India) for orders along with comments of the Port Officer. If the Deputy Drugs Controller (India) so directs, a fresh sample shall be drawn, should be sent for retest to the laboratory. The orders passed by the Deputy 419 Drugs Controller (India) on the basis of such retest are final. Where the defect is such, that the importers undertake to recondition the goods up to the required standard, they must submit along with their appeal - a) The method that will be adopted for re-processing of Bulk Drugs. In case of grossly substandard / spurious / adulterated drugs, Commissioner of customs is to be informed stating that the import of these goods constitutes an offence u/s. In case of not of standard quality, other than those mentioned in point 6 above, the importers may be given the option to reship the goods to the country of origin if they so desire or forfeit them to the Central Government for destruction. For the import of non-notified diagnostic kits/reagents, only import license in Form-10 is required. The product label should comply with Rule 96 of Drugs and Cosmetics Rules including name and address of the manufacturer as stated in the Form-10, import license number. There are substances which are covered under the definition of the drug but are not used for medicinal purpose and are used in other industries like textile industries, chemical industries and food industries etc. After release of the goods, the same to be informed to the concerned State Drug Controller and the Zonal officer for post import check. The procedure to be followed in case of imports for personal use is detailed under Rule 36 of Drugs & Cosmetics Rule 1945. Other documents may be asked by the port officer to ensure the authenticity and quality of the cosmetics 4. Sample to be drawn at random and sent for test to Government appoved Testing Laboratories only. As regard to testing and follow up action is provided under Rule 131, the guidelines 424 and protocols to be followed is very much similar to the Drugs, only sections and rules to be changed. Simultaneously, the matter to be informed to the concerned State Drug Controller / Zonal Officer for the re- import check. Export permissions issued by the Deputy Drugs Controller for / fixed dose combinations / medicines beyond Schedule V limits / unapproved/approved new drugs/banned drugs under 26-A / without labels etc. Rule 94 violations – In case of export by loan licensee, the name and any address of manufacturer mentioned on the license may be acceptable. In case of neutral code, the consignment may be allowed as long as the identity of the manufacturer is ascertained with licence / code number available on the label. Aurvedic Drugs In case of export of ayurvedic drugs following documents are to be examined before release i) shipping bill, ii) Invoice, iii) packing list , iv) Mfg‘s test report of ayurvedic items for presence of heavy metals, Pb As, Sb, Hg within permissible limits (as per ayush guidline),specimen label/specimen sample, valid mfg. Licence with list of approved items labelling provision of ayurvedic drugs for export should comply with Rule 161A of D&C Rule. Subsequent to the above Notification, representations have been received from various Drug Manufacturers Associations requesting for exemption from registration requirements of the Drugs & Cosmetics Act for imports under the Advance Licensing Scheme. The requests have been considered and It has been decided that import of approved & unapproved drugs under the Advance Licensing Scheme will not be subjected to the Registration procedure and the imports will be permitted subject to the following conditions: i. Import license will only be given against an existing valid export order and to the extent raw material is required as per that order. A copy of the license would be endorsed to the Drug Controller and the concerned State Drug Controller. Any violation is punishable under the Foreign Trade Development and Regulation Act and the Customs Act. The Drug Controller could also make provisions for penalizing the Drug Manufacturing Units in terms of suspension or cancelling of his license.

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In the same studies purchase butenafine 15 mg fungus gnat spray uk, didanosine was more cytotoxic and less muta- genic than zidovudine buy discount butenafine 15mg on-line fungus underarm. There is inadequate evidence in experimental animals for the carcinogenicity of didanosine purchase butenafine overnight fungal watch. Overall evaluation Didanosine is not classifiable as to its carcinogenicity to humans (Group 3) purchase butenafine 15 mg on-line fungus link to cancer. A review of its antiviral activity, pharmaco- kinetic properties and therapeutic potential in human immunodeficiency virus infection. The gelatin capsules may also contain citric acid, gelatin, glycerol, iron oxide, parabens (ethyl and propyl), polyethylene glycol 400, sorbitol and titanium dioxide. Etoposide concentrate for injection is a sterile, non-aqueous solution of the drug in a vehicle, which may be benzyl alcohol, citric acid, ethanol, polyethylene glycol 300 or polysorbate 80. Etoposide phosphate for injection is a sterile, non-pyrogenic, lyophilized powder containing sodium citrate and dextran 40; after reconstitution of the drug with water for injection to a concentration of 1 mg/mL, the solution has a pH of 2. The following impurities are limited by the requirements of The British Pharma- copoeia: 4′-carbenzoxy ethylidene lignan P, picroethylidene lignan P, α-ethylidene lignan P, lignan P and 4′-demethylepipodophyllotoxin (British Pharmacopoeia Commission, 1994). Trade names for etoposide phosphate include Etopofos and Etopophos (Swiss Pharmaceutical Society, 1999). Methods for the analysis of etoposide and its metabolites in plasma, serum and urine have included reversed-phase high-performance liquid chromatography with oxidative electrochemical detection, fluorescence detection and ultraviolet detection. Podophyllotoxin is isolated from the dried roots and rhizomes of species of the genus Podophyllin, such as the may apple or American mandrake (Podophyllin peltatum L. Etoposide can be synthesized from naturally occurring podophyllotoxin by first treating the podophyllotoxin with hydrogen bromide to produce 1-bromo-1-deoxyepi- podophyllotoxin, which is demethylated to 1-bromo-4′-demethylepipodophyllotoxin. The bromine is replaced by a hydroxy group, resulting in 4′-demethylepipodo- phyllotoxin. After protection of the phenolic hydroxyl, the 4-hydroxy group is coupled with 2,3,4,6-tetra-O-acetyl-β-D-glucopyranose. The protecting group at the 4′- hydroxy is removed by hydrogenolysis and the acyl groups by hydrolysis, and the cyclic O-4,6 acetal is formed by reaction with acetaldehyde dimethyl acetal (Holthuis et al. During early clinical trials for cancer chemotherapeutic use, podophyllotoxin proved to be too toxic and, in the 1960s, two epipodophyllotoxins were described, teniposide (see monograph, this volume) and etoposide (Keller-Juslén et al. The first clinical trial of etoposide was reported in 1971, and etoposide entered routine use after 1981 (Oliver et al. Etoposide is one of the most widely used cytotoxic drugs and has strong anti- tumour activity in cases of small-cell lung cancer, testicular cancer, lymphomas and a variety of childhood malignancies. It is one of the most active single agents in the treatment of small-cell lung cancer (Slevin et al. For testicular germ-cell tumours, etoposide is used in combination with bleomycin and cisplatin. Durable complete responses were achieved in about 80% of patients with disseminated germ-cell tumours; in a randomized trial, the combination resulted in longer overall survival and less toxicity than the standard cisplatin–bleomycin– vinblastine regimen (Williams et al. Three or four cycles of etoposide with cisplatin and bleomycin are now generally regarded as the standard treatment for this disease (Nichols, 1992). Etoposide is active as a single agent in non-Hodgkin lymphoma, with response rates of 17–40% in previously treated patients (O’Reilly et al. It has been investigated for use in combination with the widely used cyclophosphamide–doxo- rubicin–vincristine–prednisone regimen and in a number of new combinations. Etoposide is less commonly used in a number of other tumour types, including non-small-cell lung cancer, breast, ovarian and gastric cancer, leukaemias, Kaposi sarcoma and in histiocytosis (Joel, 1996; Okada et al. The efficacy of etoposide is clearly schedule-dependent, longer exposures of three to five days being more active than a single dose (Slevin et al. A typical intra- venous dose is 375–500 mg/m2 over three to five days days (90–120 mg/m2 per day), repeated every three weeks. Owing to its poor solu- bility, a more water-soluble pro-drug, etoposide phosphate, was developed for clinical use. Once this drug enters the systemic circulation, the phosphate is rapidly and com- pletely cleaved by circulating phosphatases. Studies of Cancer in Humans Several factors make it difficult to evaluate etoposide with respect to the incidence of second malignancies. First, most cancer patients are treated with combined treatment modalities (chemotherapy and radiotherapy), and multiple antineoplastic drugs are usually administered within combination chemotherapy regimens. The administration of possibly carcinogenic drugs other than etoposide was adjusted for in only a few studies. For example, there is now general agreement that the development of leukaemia in patients with mediastinal germ-cell cancer should be regarded as part of the natural history of the disease (Nichols et al. In studies of the risk for treatment-related leukaemia, patients with mediastinal germ-cell cancer should therefore be excluded. In studies in which patients were treated with etoposide and/or teniposide (see monograph, this volume), the authors used various conversion factors to derive an ‘equivalent dose’ of etoposide from that of teniposide. The conversions were based, however, on the therapeutic effects with regard to the possible leukaemogenic potency at a given dose rather than on metabolic considerations. In all of these, however, the development of leukaemia followed the administration of etoposide in combination with other cytostatic drugs and/or irradiation. Since several cohort studies of patients with various malignancies have been conducted to estimate the risk for second malig- nancies after exposure to etoposide, this section includes only case reports of the specific group of patients with Langerhans cell histiocytosis and metastatic germ-cell tumours who received etoposide. Langerhans cell histiocytosis entails proliferation of connective tissue cells which originate in the bone marrow. An eight-year-old Peruvian girl with Langerhans cell histiocytosis of the bone who had been treated according to an Italian protocol for this disease, consisting of etoposide at a dose of 200 mg/m2 for three consecutive days every three weeks with 15 courses administered in one year for a cumulative dose of 8400 mg/m2, was hospi- talized for acute promyelocytic leukaemia 18 months after discontinuing therapy. Eto- poside was the only cytotoxic agent that had been used before the onset of acute myeloid leukaemia. This patient was one of 26 treated only with an epipodophyllo- toxin for Langerhans cell histiocytosis; their follow-up periods ranged between 11 and 44 months, with a median of 29. The first case was a four-year-old girl, in whom the disease was diagnosed in bone in July 1988. She initially received intravenous vin- blastine and oral prednisolone, followed by etoposide injections alone at 200 mg/m2 weekly, between June 1989 and January 1990. The second case was in a five-month-old girl with Langerhans cell histiocytosis diagnosed in June 1987 who was treated with intravenous etoposide (100 mg/m2 eight doses, two or three times a week), in addition to bolus vincristine, intravenous cyclophosphamide at doses unlikely to be leukaemogenic, intra- venous methotrexate and oral prednisolone. The total doses of etoposide and cyclo- phosphamide administered were 1860 mg (4800 mg/m2) and 4070 mg (10 800 mg/m2), respectively. The first patient, aged 34, developed acute myeloid leukaemia 63 months after treatment with bleomycin, cisplatin and etoposide. The other patient, aged 36, developed acute myelomonocytic leukaemia 27 months after radiotherapy and bleomycin, etoposide, vinblastine and cisplatin. Thus, the observed cumulative inci- dences in most studies are clearly higher than the incidence in the general population.

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When n (the number of doses given) is sufficiently large (>4 or 5 doses) 15mg butenafine sale fungus gnats houseplants, the equation above simplifies to: We can estimate the minimum or trough concentration at steady state cheap butenafine generic yates anti fungal. The trough concentration occurs just before the administration of the next dose (at t = τ) purchase 15mg butenafine with amex antifungal under breast. In this situation purchase butenafine on line amex antifungal liver, the general equation for the equation for Cn(t) becomes: Note the similarity between the equations for Cpeak(steady state) and Ctrough(steady state). The expression for -Kt Ctrough(steady state) simplifies to Cpeak(steady state) times e. An almost identical equation (below) can be used to calculate the concentration at any time after the peak. The only difference is that t is replaced by the time elapsed since the peak level. Clinical Correlate In most clinical situations it is preferable to wait until a drug concentration is at steady state before obtaining serum drug concentrations. Use of steady-state concentrations are more accurate and make the numerous required calculations easier. If two drug concentrations and the time between them are known, K can be calculated. Because is independent of any pharmacokinetic model, it is helpful to the practicing clinician (model assumptions do not have to be made). Several mathematical methods may be used to calculate the average drug concentration, but only one is presented here. Therefore: and since: The equation: 4-3 is very useful, particularly with drugs having a long half-life, in which the difference between peak and trough steady-state levels may not be large. It is important to recognize from the equations that at steady state is determined by the clearance and drug dose (dose/τ). Also, changes in V or K that are not related to a change in clearance would not alter. With multiple drug dosing at steady state, changes in τ, K, or V (with no change in clearance) would alter the observed peak and trough drug concentrations but not. In dealing with such equations, it is helpful to remember that the units of measure on both sides must be the same. For example, in the equation above, should be in micrograms per milliliter, milligrams per liter, or similar concentration units. Therefore, the right side of the equation must have the same units, as is the case when: • dose is in a consistent mass unit, such as milligrams, • clearance is in liters per hour or milliliters per minute, and • dosing interval is in hours. So dose/(Cl × τ) has the following units: Then, as both hour terms cancel out, we see that amount per volume (concentration) is left. For example, most patients with normal renal function will have a gentamicin V of 0. A patient receives 500 mg of drug X intravenously every 6 hours until steady state is reached. Just after the dose is injected, a blood sample is drawn to determine a peak plasma concentration. Using the two plasma concentrations, we first calculate K, as described previously: Then we insert the known Cpeak, K, X0, and τ values in the equation for Cpeak. By rearranging the equation to isolate the only remaining unknown variable, we can then use it to calculate V: Now we know the values of all the variables in the equation (V, K, Cpeak, X0, and τ) and can use this information to calculate a new Cpeak if we change the dose (e. For example, if we want the peak level to be higher and wish to calculate the required dose to reach this new peak level, we can rearrange our equation: -Kτ X0 = V × Cpeak(steady state)(1 - e ) and substitute our calculated V and K and the desired Cpeak. Or we can choose a new dose (X0) and calculate the resulting Cpeak by inserting the calculated K and V with τ into the original equation: Remember that each time we calculate a peak plasma level (Cpeak), the trough plasma level also can be calculated if we know K and τ: -Kτ Ctrough = Cpeake If the dosing interval is not changed, new doses and concentrations are directly proportional if nothing else changes (i. What is the maximum concentration after 15 doses if the dose (X0) is 800 mg and the volume of -1 distribution (V) is 20 L? When multiple drug doses are given and steady state is reached, the amount of drug eliminated during one dosing interval (τ) is equal to the drug dose. A drug with a relatively small K (long T1/2) takes a longer time to reach steady state than a drug with a large K. If a drug with a T1/2 of 12 hours is given every 6 hours and a peak concentration at steady state is 10 mg/L, what will be the approximate peak concentration just after the fifth dose is administered? Which patient (A or B) is likely to achieve higher steady-state plasma concentrations? Decreasing the dosing interval while keeping the dose constant will result in lower steady-state concentrations. Which of the following dosage techniques results in the greatest difference between maximum (peak) and minimum (trough) concentrations after a dose? A 500-mg dose of drug X is given every 6 hours until steady-state levels are reached. After steady state is reached, a peak level of 15 mg/L is determined; the level 4 hours after the peak is 4. For the example given in the last question, when the peak plasma level is 35 mg/L, what will the trough plasma level be? When steady state is reached, the amount of drug eliminated over one dosing interval is equal to the dose. A longer half-life (lower K) will mean that more time is required to reach steady state. After one half-life, the peak concentration would be 50% of steady-state concentration; at two half-lives, it would be 75%. By decreasing the dosing interval the amount of drug administered per unit of time will increase and steady state concentrations will increase. A small dose given very frequently results in less of a change from peak to trough concentrations. Doubling the dose would result in a doubling of the steady-state peak concentration to 30 mg/L. To answer this question, K must first be calculated: -1 K = (ln C4hr - ln Cpeak) / 4 = 0. Explain the relationships of pharmacokinetic parameters and how changes in each parameter affect the others. Calculate an appropriate loading dose to achieve therapeutic range at onset of infusion. Changes in Elimination Rate Constant If the dose, the volume of distribution, and the dosing interval (τ) all remain the same but the elimination rate constant (K) decreases (as with decreasing renal or hepatic function), the curve should change as shown in Figure 5-2. The difference between peak and trough levels at steady state is smaller because the elimination rate is lower. Because K is decreased in this situation, the half-life (T1/2) is increased and, therefore, the time to reach steady state (5 × T1/2) is also lengthened. This concept is important in designing dosing regimens for patients with progressing diseases of the primary organs of drug elimination (kidneys and liver).

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If you’re taking sulfonamides buy butenafine no prescription fungus vinegar, you’d better be Pharmacodynamics drinking lots of fluids! Sulfonamides are bacteriostatic drugs that prevent the growth of microorganisms by inhibiting folic acid production order 15mg butenafine amex fungus diabetes. The decreased folic acid synthesis decreases the number of bacterial nucleotides and inhibits bacterial growth buy butenafine 15mg line fungus gnats tea tree oil. Therefore buy butenafine 15mg with mastercard fungus gnats vegetable seedlings, the choice of therapy should be based on bacteria susceptibility tests. Infectious behavior Sulfonamides also are used to treat infections caused by Nocardia asteroides and Toxoplasma gondii. Co-trimoxazole (a combina- tion of a sulfa drug and a folate antagonist) is used for a variety of other infections, such as Pneumocystis carinii (Pneumocystis jiroveci) pneumonia, acute otitis media (due to H. Sulfonamides exhibit a wide spectrum of activity against gram-positive and gram-nega- tive bacteria. Adverse reactions to sulfonamides Excessively high doses of less water-soluble Is it serum sickness? This complication isn’t a problem chospasm, and leukopenia (reduced white with the newer water-soluble sulfonamides. Hypersensitivity reactions may occur and ap- Photo finish pear to increase as the dosage increases. It isn’t useful in treating pyelonephritis or perinephric (around the kid- ney) diseases. Metabolism and excretion Nitrofurantoin is partially metabolized by the liver, and 30% to 50% is excreted unchanged in urine. Pharmacodynamics Usually bacteriostatic, nitrofurantoin may become bactericidal, depending on its urinary concentration and the susceptibility of the infecting organism. Nitrofurantoin isn’t effective against systemic bacterial in- • anorexia fections. The drugs keep viruses from major antiviral drug classes used to treat systemic infections in- multiplying. Drugs in this class include: • acyclovir • famciclovir • ganciclovir • valacyclovir • valganciclovir. Valacy- clovir is used to treat herpes zoster, genital herpes, and herpes labialis. Pharmacokinetics Each of these antiviral drugs travels its own route through the body. Slow by mouth When given orally, acyclovir absorption is slow and only 10% to 30% complete. It’s distributed throughout the body and metabo- lized primarily inside the infected cells; the majority of the drug is excreted in urine. More than 90% of ganciclovir isn’t metabolized and is excreted unchanged by the kidneys. Metabolic changes Valacyclovir is converted to acyclovir during its metabolism and has pharmacokinetic properties similar to those of acyclovir. Val- ganciclovir is metabolized in the intestinal wall and liver to ganci- clovir; however, interchanging the two drugs isn’t effective. Presto change-o Acyclovir enters virus-infected cells, where it’s changed through a series of steps to acyclovir triphosphate. Adverse reactions to synthetic nucleosides Treatment with these drugs may lead to particular adverse reactions. Acyclovir Famciclovir and valacyclovir Reversible kidney impairment may occur with rapid I. Oral history Valganciclovir Common reactions to oral acyclovir include headache, nausea, Common adverse reactions to valganciclovir include vomiting, and diarrhea. Ganciclovir The most common adverse reactions to ganciclovir are granu- locytopenia and thrombocytopenia. Adverse reactions to Pharmacokinetics foscarnet Foscarnet is poorly bound to plasma proteins. In patients with normal kidney function, the majority of foscarnet is excreted un- Adverse reactions to changed in urine. It’s also used in combination therapy with gan- • granulocytopenia, ciclovir for the patient who has relapsed with either drug. Because of the risk of kidney toxicity, the pa- tient should be aggressively hydrated during treatment. Ribavirin is administered by nasal or oral inhalation and is rimantadine well absorbed. Ribavirin capsules are rapidly absorbed after admin- Adverse reactions in- istration and are distributed in plasma. Pharmacotherapeutics Rimantadine Amantadine and rimantadine are used to prevent and treat respi- Adverse reactions to ri- ratory tract infections caused by strains of the influenza A virus. In the meantime These drugs also protect the patient who has received the influen- za vaccine during the 2 weeks needed for immunity to develop as well as the patient who can’t take the influenza vaccine because of hypersensitivity. Drugs in this class include: • abacavir • didanosine • emtricitabine • lamivudine • stavudine • zidovudine. It’s distributed in the extravascular space, and about 50% binds with plasma proteins. Abacavir is metabolized by the cy- tosolic enzymes and excreted primarily in urine with the remain- der excreted in stool. Gastric Lamivudine and stavudine are rapidly absorbed after adminis- acid rapidly tration and are excreted by the kidneys. Buffer needed Because didanosine is degraded rapidly in gastric acid, didanosine tablets and powder contain a buffering drug to increase pH. Abacavir Zidovudine • Headache, peripheral neuropathy, dizziness levels increase • Blood-related reactions • Muscle weakness, rash, itching, muscle with alcohol • Headache and dizziness pain, hair loss consumption. All three drugs are metabolized by the cytochrome P-450 liver enzyme system and excreted in urine and stool. Monotherapy (using a single drug) isn’t rec- ommended for human Pharmacodynamics immunodeficiency virus Nevirapine and delavirdine bind to the reverse transcriptase en- infection. Efavirenz competes for the enzyme through non- antiretroviral agents is competitive inhibition. Me- tabolism isn’t thought to be mediated by cytochrome P-450 liver enzymes, and the drug is excreted by the kidneys. Adverse • Potentially fatal lactic acidosis and severe hepatomegaly with steatosis have occurred in patients taking tenofovir alone or with reactions to other antiretrovirals. Patients Adverse reactions to the with preexisting liver disease should take this drug with caution. Drugs in liver) this group include: • lactic acidosis (in- • amprenavir creased lactic acid pro- • atazanavir • darunavir duction in the blood). Pharmacokinetics Protease inhibitors may have different pharmacokinetic proper- ties. Active and inactive Amprenavir is metabolized in the liver to active and inactive metabolites and is minimally excreted in urine and stool. Availability unknown Nelfinavir’s bioavailability (the degree to which it becomes avail- able to target tissue after administration) isn’t determined.

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