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getcustomessay comcustom essay Arch intern med. 2002;162:1117–1121. 24. Day e, bentham p, callaghan r, et al. Thiamine for wernickekorsakoff syndrome in people at risk from alcohol abuse. Cochrane database syst rev. 2004;(1):Cd004033. 25. Lingford-hughes ar, welch s, nutt dj. Evidence-based guidelines for the pharmacological management of substance misuse, addiction and comorbidity. Recommendations from the british association for psychopharmacology. J psychopharmacol. 2004;18:293–335. 26. Blondell rd. Ambulatory detoxification of patients with alcohol dependence. Am fam physician. 2005;71(3):495–502. 27. Mayo-smith mf, beecher lh, fischer tl, et al.

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http://projects.csail.mit.edu/courseware/?term=sporting-spirit-essay sporting spirit essay Chapter 9  |  arrhythmias  157 vf/pulseless vt some drugs that have been reported to cause torsades de pointes1,50 amiodarone amitriptyline arsenic chloroquine chlorpromazine ciprofloxacin citalopram clarithromycin disopyramide dofetilide doxepin droperidol erythromycin famotidine flecainide fluconazole fluoxetine haloperidol ibutilide indapamide ketoconazole call for help. Initiate cpr. Give oxygen. Attach defibrillator obtain iv or io access defibrillation attempts × 2 epinephrine 1 mg every 3–5 minutesa or vasopressin 40 mga (can replace first or second dose of epinephrine) amiodarone 300 mg iva amiodarone 150 mg iva figure 9–9. Decision algorithm for resuscitation of vf or pulseless vt. (cpr, cardiopulmonary resuscitation. Io, intraosseous. Iv, intravenous. Vf, ventricular fibrillation. Vt, ventricular tachycardia. ) adefibrillation attempt should be made after every dose of drug. Torsades de pointes torsades de pointes (tdp) is a specific polymorphic vt associated with prolongation of the qt interval in the sinus beats that precede the arrhythmia. 1,50 »» epidemiology and etiology the incidence of tdp in the population at large is unknown. The incidence of tdp associated with specific drugs ranges from less than 1% to as high as 8% to 10%, depending on dose and plasma concentration of the drug and the presence of other risk factors for the arrhythmia. Tdp may be inherited or acquired. Patients with specific genetic mutations may have an inherited long qt syndrome, in which the qt interval is prolonged, and these patients are at risk for tdp. Acquired tdp may be caused by numerous drugs (table 9–15);1,50 the list of drugs known to cause tdp continues to expand. »» pathophysiology tdp is caused by circumstances, often drugs, that lead to prolongation in the repolarization phase of the ventricular action potential (see figure 9–2) manifested on the ecg by prolongation of the qt interval. Prolongation of ventricular repolarization occurs via inhibition of efflux of potassium through potassium channels. Therefore, drugs that inhibit conductance through potassium channels may cause qt interval prolongation and tdp. Prolongation of ventricular repolarization promotes the development of early ventricular afterdepolarizations during the relative refractory period, which may provoke reentry leading to tdp. Table 9–15  levofloxacin levomethadyl methadone metoclopramide moxifloxacin ondansetron pentamidine pimozide procainamide propafenone quetiapine quinidine risperidone sertraline sotalol tacrolimus thioridazine trazodone voriconazole ziprasidone drug-induced tdp rarely occurs in patients without specific risk factors for the arrhythmia (table 9–16). 1,50 in most cases, administration of a drug known to cause tdp is unlikely to cause the arrhythmia. However, the likelihood of the arrhythmia increases in patients with concomitant risk factors. The onset of tdp associated with oral drug therapy is somewhat variable and in some cases may be delayed. Often, a patient can be taking a drug known to cause tdp for months or longer without problem until another risk factor for the arrhythmia becomes present, which then may trigger the arrhythmia. In some patients, tdp may be of short duration and may terminate spontaneously. However, tdp may not terminate on its table 9–16  risk factors for drug-induced torsades de pointes1,50 qtc interval > 500 ms increase in qtc interval by > 60 ms compared with the pretreatment value female sex age > 65 years heart failure electrolyte abnormalities. Hypokalemia, hypomagnesemia, hypocalcemia bradycardia elevated plasma concentrations of qt interval-prolonging drugs due to drug interactions or absence of dose adjustment for organ dysfunction rapid iv infusion of torsades-inducing drugs concomitant administration of more than one agent known to cause qt interval prolongation/torsades de pointes concomitant administration of loop diuretics genetic predisposition previous history of drug-induced torsades de pointes iv, intravenous.

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thesis statement generator owl High total cortisol levels are also observed in the presence of increased cortisol binding globulin (the carrier protein for 80% of circulating cortisol molecules), which is seen in pregnancy or other high-estrogen states (eg, exogenous estrogen administration). 2 cortisol is converted in the liver to an inactive metabolite known as cortisone. The zona reticularis produces the androgens androstenedione, dehydroepiandrosterone (dhea), and the sulfated form of dehydroepiandrosterone (dhea-s). Only a small amount of testosterone and estrogen is produced in the adrenal glands. Androstenedione and dhea are converted in the periphery, largely to testosterone and estrogen. Adrenal hormone production is controlled by the hypothalamus and pituitary. Corticotropin-releasing hormone (crh) is secreted by the hypothalamus and stimulates secretion of adrenocorticotropic hormone (acth. Also known as corticotropin) from the anterior pituitary. Acth in turn stimulates the adrenal cortex to produce cortisol. When sufficient or excessive cortisol 695 696  section 7  |  endocrinologic disorders h3c h3c h3c h ch3 h h3c h h ho cholesterol glucocorticoid precursors cyp11a1 adx o h3c h3c o ch3 h3c h3c h h o progesterone h3c o ch3 h3c h h3c h h por cyp17a1 h3c h3c o 17-hydroxyprogesterone (17ohp) por cyp17a1 h h h3c o androstenedione dhea papss2 sult2a1 o 11deoxycortisol o h3c h3c h adrenal androgen precursors o testosterone h o hsd11b2 h3c h o oh cortisone zona fasciculata glucocorticoids h h srd5a oh oh hsd11b1 cortisol h3c o aldosterone h h h6pdh h h hsd17b h3c o h3c h h adx cyp11b1 h o oh oh h o h h hsd3b2 h3c h3c h3c h ho h o por cyp21a2 h o o h3c h adx cyp11b2 18oh-corticosterone h3c ho h h o 17-hydroxy- hsd3b2 pregnenolone h h 5-dihydrotestosterone zona reticularis - androgens h h ho h3c h h o oh oh oh h3c h adx cyp11b2 corticosterone o cho ho oh h3c o h3c oh ho h h deoxycorticosterone cyp11b1 h h h ho h ch3 h3c oh oh h adx o cyp11b2 por cyp17a1 por cyp17a1 h3c por o cyp21a2 hsd3b2 pregnenolone oh o ho h3c ho h h o o h3c h h h ho o ch3 h3c h zona glomerulosa - mineralcortocoids mineralocorticoid precursors h dheas figure 45–1. The adrenal cortex consists of three histologically distinct zones.

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