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Mixed Drug Abuse
Published in Frank Lynn Iber, Alcohol and Drug Abuse as Encountered in Office Practice, 2020
Cross tolerance is the basis of some but not all of the use of drugs in sequence or combination. Thus cocaine and amphetamines produce marked cross tolerance; opiates abusers have cross tolerance for nearly all sedatives and alcohol. In other cases opposite effects are used to produce a prolonged “high”. Amphetamine use with opiates is probably the most widely abused pair among the major drugs. More recently, intravenous cocaine has been used by opioid addicts.4 Desipramine treatment has been proposed for such users.5
Historical Notes
Published in Albert A. Kurland, S. Joseph Mulé, Psychiatric Aspects of Opiate Dependence, 2019
Albert A. Kurland, S. Joseph Mulé
Some resolution of the confusion and controversy concerning tolerance may be achieved by describing the phenomenon quantitatively, utilizing the criteria suggested by Hugg:43Relationship to dosageTime courseDegree of toleranceExtent of cross-toleranceResidual effects (i.e., whether all the manifestations of tolerance are completely reversible)
Characteristics and Theories Related to Acute and Chronic Tolerance Development
Published in S.J. Mulé, Henry Brill, Chemical and Biological Aspects of Drug Dependence, 2019
Cross tolerance may be defined as diminished responsiveness of the system to one drug, induced by the development of tolerance to another drug of a similar or dissimilar chemical structure or pharmacological action.298Specific cross tolerance denotes the fact that the test compound has the ability to evoke the same adaptive change (tolerance) as the original drug and that the two substances are mutually interchangeable in maintaining a state of tolerance. Generally, cross tolerance develops among drugs of the same pharmacological class.74,151,295,370 Within each phar-malogical class, cross tolerance may develop more readily among compounds from the same chemical class,295 although the latter is not always true. Nonspecific cross tolerance, in contrast, is usually a low-grade tolerance evident for compounds of different pharmacological classes (e.g., tolerance to general anesthetics in chronic alcoholics.6,120,181)
Green tobacco sickness: mecamylamine, varenicline, and nicotine vaccine as clinical research tools and potential therapeutics
Published in Expert Review of Clinical Pharmacology, 2019
The extent to which tobacco use (i.e. cigarette smoking) protects against green tobacco sickness is equivocal. Smokers were reported to be less susceptible to green tobacco sickness than non-smokers in cases reported in Florida [2], Kentucky [8] and North Carolina [3,5]. The implication is that tolerance to tobacco from cigarette smoking produces cross-tolerance to the effects of chemicals absorbed from tobacco leaves. In both cases the chemical to which tolerance develops is very likely to be nicotine. However, even cigarette smokers become ill with green tobacco sickness; urine nicotine measured in afflicted smokers can exceed nicotine measured in smokers who are not ill [11]. Protection in cigarette smokers is not universally reported or accepted. Some accounts even suggest that the prevalence of green tobacco sickness is greater in smokers as compared with non-smokers [12,13]. This has led some to question whether the behaviorally active tobacco alkaloids normally inhaled in cigarette smoke are the main causal factor in green tobacco illness. Some chemical insecticides sprayed onto tobacco plants, such as organophosphate and carbamate, have been identified as possible causes of reported symptoms. Some insecticides contain nicotine and related chemicals that target nAChRs [14], which could potentially be a source of nicotine and nicotine-like poisoning in tobacco farm workers. Nicotine poisoning from insecticide exposure has been documented previously [6]. However, green tobacco sickness is reported to occur on farms that do not use insecticides [3].
Promoting a comprehensive understanding of the opioid epidemic
Published in International Review of Psychiatry, 2018
The term ‘opioid’ broadly refers to licit products, such as the prescription opioid medications that are a mainstay for pain management throughout the world, and illicit products, such as heroin. Opioids confer effects on the human body by engaging the endogenous opioid system, which initially produces positive feelings such as euphoria and pain relief, but can, following extended exposure to either prescribed or illicit opioids, produce a physical dependence that is characterized by patterns of tolerance (e.g. the need to consume more opioids to get the same effect) and an aversive withdrawal syndrome. Opioids also produce high levels of cross-tolerance, which allows individuals to substitute different opioids to achieve the same effects. Although heroin has traditionally been the predominant opioid of abuse, an aggressive emphasis on treating pain in the 1990s (Baker, 2017) led to a thriving market for prescription opioids, and an eventual abundance of potential opioid products to use, misuse, and substitute. By the early 2010s, the US was consuming 43,879 doses of opioids per million individuals a day, which far exceeded all other countries examined, and almost doubled the consumption of the 2nd country in the list (Germany, with 23,352 units per day) (Berterame et al., 2016). Given this context, the quiet but steady increase in the misuse and abuse of prescription opioids and heroin over the past decade is perhaps not surprising. However, the magnitude of morbidity and mortality that has been associated with chronic opioid exposure was certainly unexpected and alarming. The US, as well as other parts of the world, has now recognized opioid misuse as an epidemic.
Impact of chronic medications in the perioperative period –anesthetic implications (Part II)
Published in Postgraduate Medicine, 2021
Ofelia Loani Elvir-Lazo, Paul F White, Hillenn Cruz Eng, Firuz Yumul, Raissa Chua, Roya Yumul
Methadone has been used for managing pain in patients with chronic pain syndromes and treating OUD for over 50 years. When used in combination with other CNS depressants, including other opioids, sedative or hypnotic drugs, or alcohol it can be toxic. Psychiatric prescribed medications (e.g. fluoxetine, amitriptyline, quetiapine, and alprazolam) also can increase methadone accumulation and risk of toxicity. In general, 4 to 5 half-lives (∼5 days) are required to reach steady state at a given methadone dose. Adjusting the dose in increments of 5 to 10 mgs every 3 to 5 days (based on symptoms of withdrawal or sedation) usually is adequate[51]. For patients taking methadone on a chronic basis for OUD, they should continue with the same methadone dose during the acute postoperative period to maintain a stable baseline opioid level and multimodal nonopioid analgesic techniques should be utilized. When acute pain decreases, they should be rapidly tapered off the supplemental opioid medication. Incomplete cross-tolerance with other opioids and/or addition of sedatives may increase side effects such as respiratory depression [52,53]. For patients who are on methadone maintenance therapy (MMT), methadone should be continued as described previously. If oral medication is contraindicated, the IV or subcutaneous route of administration can be used. Optimize non-opioid analgesic multimodal strategies as appropriate (e.g. non-opioid analgesics, adjuvant medications, regional anesthesia techniques, physical measures, integrative therapies, and psychosocial or behavioral management strategies). For ambulatory pain management, administer a nonopioid pain medication (e.g. ketorolac) prior to discharge [52,53]. When methadone dose has been interrupted for more than 5 days, an experienced provider with MMT should be consulted before restarting the treatment [54,55].