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Summary of cocaine during pregnancy In summary quality 52.5 mg nicotinell, the epidemic use of cocaine during pregnancy has resulted in an alarming number of individuals with serious adverse outcomes in mothers discount 52.5mg nicotinell with mastercard, fetuses, and newborns. The use of cocaine is often compounded by frequent concomitant heavy use of other illicit drugs and alcohol. Women who use cocaine during pregnancy are at significant risk for no prenatal care, shorter gestations, premature rupture of membranes, prema- ture labor and delivery, spontaneous abortions, abruptio placentae, decreased uterine blood flow, and death. The fetuses of these women who use cocaine are growth-retarded or severely distressed, and have an increased mortality risk. Fetal and maternal cere- brovascular accidents, with attendant profound morbidity and mortality, occur in asso- ciation with maternal cocaine use during pregnancy. Major congenital anomalies involv- ing the brain, genitourinary tract, bowel, heart, limbs, and face occur with significantly increased frequency among infants whose mothers used cocaine during gestation. Use of hallucinogens during pregnancy 319 Hence, cocaine use during pregnancy is very probably teratogenic and fetotoxic. The mechanisms of cocaine’s adverse effects are vascular disruption and hypoperfusion for gross abnormalities, but molecular level mechanisms are yet to be determined. Some hallucinogens are assumed to exert their effect by displacing this or other neurotransmitters, but the molecular basis for the action of hallucinogens is not established. Tolerance of hallucinogens is rapidly devel- oped and chronic users must increase doses rapidly over the course of the drug’s use to maintain desired effects (Carroll, 1990). Hallucinogens or psychedelic drugs are not nearly as popular in 2006 as they were 30 or so years ago. Less than 2 percent of the general population uses psychedelic drugs, based upon data that are not partitioned by sex, ethnicity, or pregnancy status. Under medical supervision lysergide has been used to treat psy- chiatric illness, and ergotamine is a closely related drug. The most frequently observed malfor- mation among exposed infants are limb defects, but the defect types were highly vari- able (i. However, lifestyle practices associated with drug abuse during pregnancy are probably harmful to intrauterine development. Human toxic exposures to lysergic acid are rare, but among cattle and sheep that consumed wheat grain affected with the fungus Claviceps pupurea, which produces lysergic acid, peripheral neuropathy, gangrene, and necrosis were observed. As with most illegal drugs, no quality control or assurance measures are taken to assure drug purity. Flattened dried seed pods from this plant, called ‘buttons’ or ‘peyote,’ are ingested for recreational use and are used in Native American religious rituals. Members of the Native American Church use mesca- line legally in their ceremonies. Naturally mescaline is often contaminated with strych- nine and is associated with severe nausea and vomiting. The user also often experiences episodes of severe vomiting and nausea following ingestion of the drug. The hallucino- genic effects usually last about 12 h and sometimes much longer (20–40 hours) depend- ing upon dose. No published studies of congenital anomalies in infants born to mothers who used mescaline during pregnancy are available. In an animal study, neural tube defects were increased in frequency among the offspring of hamsters whose mothers were given mescaline during pregnancy at one-tenth to one-fifth the dose usually ingested by humans, but the effect was not dose related (Geber, 1967). Neonatal weight was decreased among hamsters born to mothers injected with mescaline during pregnancy (Geber and Schramm, 1974). Moreover, no such abnormalities were seen in animal stud- ies by other investigators who employed doses three to six times those used by humans (Hirsch and Fritz, 1981). Psilocin mexicana is the classic source of the drug and is known as the magic mushroom. Psilocybin typically grows in highly organic Opiate abuse during pregnancy 321 media, such as cow feces (cow patties) and usually in the springtime. Ingestion of these hallucinogenic mushrooms has become a popular form of sub- stance abuse among some adolescents and young adults (Schwartz and Smith, 1988). The effects of psilocybin ingestion include hallucinogenic visions, altered states of conscious- ness, and a pronounced pyrogenic effect. The frequency of congenital anomalies in the offspring of mothers who ingested psilo- cybin during pregnancy has not been published for human studies or animal experi- ments. Summary of hallucinogens Hallucinogen use during pregnancy is not well studied and unknown risks may exist. The pyrogenic effects of hallucinogens and non- medical use of other substances may be cause for concern. However, any concern is based upon theoretical grounds and not published information. Opiates (natural and synthetic) are pharmacologi- cal narcotics, not to be confused with the legally defined narcotic class which includes such drugs as marijuana, amphetamines, and methamphetamines.
That is detectable using controlled study design methods but is of no clinical importance under usual therapeutic cir- cumstances because (1) the interaction purchase nicotinell 52.5 mg overnight delivery, while statistically significant buy nicotinell 35 mg low cost, is not large enough in magnitude to produce a clinically important change in dynamics of the victim drug; (2) the therapeutic index of the victim drug is large enough that even a substantial change in plasma levels of the victim will not alter therapeutic effects or toxicity; or (3) kinetics and response to the victim drug is so variable that changes in plasma levels due to the drug interaction are far less important than inherent variability. Even less common are clinically important interactions that require modification in dosage of the perpetrator, the victim, or both. The most unusual consequence of a drug interaction is a situation in which the drug combination is so hazardous as to be contraindicated, as in the case of ketoconazole and terfenadine (71). These situations are rare, but unfortunately they receive disproportionate attention in the public media. Many secondary sources are available to clinicians as guidelines to anticipate and avoid drug interactions. These compendia often serve as excellent and comprehensive collections of published data on drug interactions, but they generally are less helpful to clinicians in critically sorting out the literature and deciding what interactions are actually of real concern in the course of drug therapy. A useful general guideline for clinicians is that drug interactions are more likely to be important when (1) the perpetrator drug produces a very large change in the kinetics and plasma levels of the victim drug, that is, the perpetrator is a powerful inducer or inhibitor and (2) the therapeutic index of the victim is narrow. The second case is exemplified by victim drugs such as phenytoin, warfarin, and digoxin, for which small changes in plasma levels could have important clinical consequences. The intrinsic kinetic properties of the victim drug also influence the potential clinical consequences of an interaction. For triazolam (a high-extraction compound), the effect is evident as reduced presystemic extraction, increased Cmax, and prolonged half-life. However, for alprazolam (a low- extraction compound), the effect of ketoconazole is evident only as a prolongation of half- life. However, alprazolam is a low-extraction compound with bioavailability ordinarily in the range of 90% (75). As such, the reduction in alprazolam clearance caused by ketoconazole was evident mainly as prolonged elimination half-life but without a significant change in Cmax. The level of complexity of an integrated kinetic-dynamic study depends on the nature of the pharmacody- namic actions of the drug under study as well as the type of pharmacodynamic outcome measures that are required. For this category of drugs, a variety of outcome measures is available, but the approaches may differ substantially in their relevance to the principal thera- peutic actions of the drug, the stability of the measure in terms of response to placebo or changes caused by practice or adaptation, the objective or sub- jective nature of the quantitative assessment, and the comparability of results across different investigators and different laboratories (Table 3). The extent to which the various pharmacodynamic measures provide unique information, as opposed to being overlapping or redundant, is not clearly established. Clinical Application The kinetic and dynamic interaction of the triazolobenzodiazepine triazolam with various macrolide antimicrobial agents illustrates a number of these principles (77). Recovery from inhibition depends on the normal process of enzyme turn- over and regeneration (83). The following study of a drug interaction with macrolide antimicrobial agents illustrates the link between in vitro and in vivo findings as well as methods to define the pharmacodynamic consequences of a pharmacokinetic interaction (77). Rates of formation of the metabolites with coaddition of inhibitor were expressed as a percentage of the control velocity with no inhibitor present. Reaction velocities when preparations were preincubated with the macrolide agents are expressed as a percentage of the control velocity with no inhibitor present (inhibitor ¼ 0). However, azithromycin was a very weak inhibitor of triazolam in vitro and is anticipated to produce no significant interaction in vivo. The clinical pharmacokinetic-pharmacodynamic study had a double blind, randomized, five-way crossover design, with at least seven days elapsing between trials. Following each dose of triazolam (or placebo to match triazolam), multiple venous blood samples were drawn over a period of 24 hours and multiple phar- macodynamic testing procedures were performed. This would have required three additional trials—triazolam placebo plus azithromycin, triazolam placebo plus erythromycin, and triazolam placebo plus clarithromycin. Triazolam plasma concentrations were determined by gas chromatography with electron capture detection (73,95). The pharmacokinetic results demon- strated that mean clearance during Trials B and C were nearly identical (413 and 416 mL/min, respectively); that is, coadministration of azithromycin had no effect on the pharmacokinetics of triazolam (Fig. However, triazolam clearance was significantly reduced to 146 mL/min by erythromycin (Trial D) and to 95 mL/min by clarithromycin (Trial E). The pharmacodynamic data indicated that the benzodiazepine agonist effects of triazolam plus placebo (Trial B) and of triazolam plus azithromycin (Trial C) were similar to each other and greater than the effects of placebo plus placebo (Trial A). However, coadministration of erythromycin (Trial D) or Drug-Drug Interactions: Clinical Perspective 655 Figure 6 Mean changes over baseline in observer-rated sedation during each of the five trials, as described in the text and in Fig. Kinetic-dynamic modeling indicated that the augmentation in benzodiazepine agonist effects of triazolam caused by coadministration of erythromycin or clarithromycin was fully consistent with the increase in triazolam plasma concentrations (Fig. As anticipated, there was some redundancy among the various pharmacodynamic measures, in that the changes in these outcome measures at corresponding times were signi- ficantly intercorrelated (Fig. The line represents a function of the form y ¼ BxA determined by nonlinear regression. Ideally, the approach should incorporate the collaborative participation of individuals with expertise in molecular phar- macology, cytochrome biochemistry, in vitro metabolism, clinical pharmacoki- netics-pharmacodynamics, and clinical therapeutics. The ultimate goal should be the informed and safe use of drug combinations in clinical practice. The line represents a function of the form y ¼ BxA determined by nonlinear regression. Human cytochromes and some newer antidepressants: kinetics, metabolism, and drug interactions.
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