China
Africa
Explore chapters and articles related to this topic
Diagnosis and evaluation of poisoning
Published in Bev-Lorraine True, Robert H. Dreisbach, Dreisbach’s HANDBOOK of POISONING, 2001
Bev-Lorraine True, Robert H. Dreisbach
(See tables at the ends of chapters for toxic blood levels of chemicals and drugs.) Bromide – Serum chloride is spuriously increased in bromism because the standard tests (e.g. AutoAnalyzer) measure total halides.Glucose (whole blood) – Increased after thiazide diuretics or adrenal glucocorticoids; decreased after salicylates, lead, or ethanol.Potassium (serum or plasma) – Decreased after salicylates, thiazide diuretics, adrenal glucocorticoids, excessive rhubarb ingestion, oral podophyllum.Uric acid (serum) – Increased after thiazide diuretics or ethanol.
Psychiatric Emergencies Associated with Drug Overdose
Published in R. Thara, Lakshmi Vijayakumar, Emergencies in Psychiatry in Low- and Middle-Income Countries, 2017
S. Haque Nizamie, Sai Krishna Tikka, Nishant Goyal
A clinician dealing with psychiatric emergencies related to drug overdose must have a good idea of the psychiatric manifestations of overdose of various drugs, whether clinically prescribed (Table 6.1) or clinically not prescribed/poisons (Table 6.2), and dietary supplements (Table 6.3). Psychiatric manifestations can be caused either by acute ingestion of a drug in excessive dose or excess accumulation of a drug due to the long-term and chronic use of the drug. Altered mental status, seizures, psychosis, and agitation are the commonest presentations of drug overdose. All these generally occur as acute effects. The other psychiatric manifestations reported are emotional changes such as euphoria and anxiety, as observed in the case of amphetamine overdose; speech disturbances such as becoming over-talkative, again as observed in the case of amphetamine overdose, and slurred speech, as seen in the case of gabapentin overdose; and sleep disturbances, including nightmares, as seen in the case of amantadine and efavirenz overdose. Overdose due to the chronic use of a drug is by and large relatively rare, and there are only a few drugs that cause such overdose. Bromism, chronic overdose of bromides, was at one time responsible for 5%–10% of admissions to psychiatric facilities because it causes frank psychosis. Certain interesting and some of the rarest manifestations are associated with chronic drug overdose, for example, carbon monoxide overdose may cause subtle personality disorder; amphetamine chronic overdose is associated with stereotypical behavior in the form of skin-picking; and nitroprusside overdose may cause hyperventilation (Tables 6.1 and 6.2). Late or chronic overdose of caffeine is termed caffeinism, which is characterized by nervousness, irritability, anxiety, tremulousness, twitching of muscles, insomnia, and palpitations. Table 6.3 presents the psychiatric manifestations of overdose of dietary supplements such as anabolic steroids and vitamins.
Pharmacokinetics and pharmacodynamics of dextromethorphan: clinical and forensic aspects
Published in Drug Metabolism Reviews, 2020
Ana Rita Silva, Ricardo Jorge Dinis-Oliveira
Since DXM can be found in the form of a bromide salt, bromide poisoning may occur if large quantities are taken. Bromide poisoning, known as bromism, is primarily a chronic neuropsychiatric disorder manifested by behavior changes, headaches, apathy, irritation, slurred speech, psychosis, tremors, ataxia, hallucinations, and coma (James et al. 1997; Frances et al. 2003; Hsieh et al. 2007). It can also cause weight loss and bromoderma characterized as an acneiform rash mimicking a pyoderma gangrenosum (Kunze 1976; Battin and Varkey 1982; Hung 2003; Maffeis et al. 2008; Oda et al. 2016).
Pharmacokinetic and pharmacodynamic of bupropion: integrative overview of relevant clinical and forensic aspects
Published in Drug Metabolism Reviews, 2019
Rafaela Costa, Nuno G. Oliveira, Ricardo Jorge Dinis-Oliveira
Since its introduction in the market in 1989, bupropion has been proposed for several clinical conditions, namely depression and in the treatment of smoking cessation aid. However, with over 40 million patients worldwide prescribed with bupropion (Fava et al. 2005), understanding the possible causes of intersubject complex pharmacokinetic and pharmacodynamic variability is critical to assure safety and efficacy. Figure 3 highlights major clinical, pharmacokinetic and pharmacodynamic aspects of bupropion. Bupropion is a synthetic cathinone that exerts its effects through inhibition of dopamine, noradrenaline reuptake and inhibition of nicotinic receptors (Damaj et al. 2004; Shalabi et al. 2017). Bupropion is cleared via oxidation by cytochrome P450 to hydroxybupropion and 4’-hydroxybupropion and via reduction by 11β-HSD-1 and aldoketoreductase to threohydrobupropion and erythrohydrobupropion. All four metabolites undergo glucuronidation, and threo- and erythrohydrobupropion are also hydroxylated to threo-4’-hydroxy- and erythro-4’-hydroxy-hydrobupropion (Gufford et al. 2016; Sager et al. 2016a, 2016b, 2017). The metabolic polymorphic pathway of bupropion is considered crucial to explain the interindividual and interspecies variability in dose-response. Indeed, bupropion exerts antidepressant effects in a mouse model (Musso et al. 1993), which metabolizes bupropion mainly to hydroxybupropion, but it is incapable of exerting that effect in rat models (Welch et al. 1987), which metabolizes bupropion mainly by side-chain cleavage. Hydroxybupropion was thought to be the major active metabolite since the early published reports, being thus extensively studied. However, information available about the pharmacological effects of threohydrobupropion and erythrohydrobupropion, the two other active metabolites of bupropion is scarce. Therefore, dosing bupropion and its metabolites and genotyping metabolizing enzymes and pharmacological targets (Swan et al. 2005; Swan et al. 2007; Choi and Shin 2015) might have a role in the future to evaluate the patient’s response to bupropion. Given bupropion instability in biological samples (Laizure and DeVane 1985), toxicological analysis must target both bupropion and its major metabolites. It is also important to be aware of the chiral inversion of bupropion stereoisomers that may confound some in vitro to in vivo extrapolations. However, this artifact proved to have a minor influence in altering in vivo bupropion R/S ratios dependent on the CYP2B6 activity (Sager et al. 2016b). Due to the bioactive enantiomer’s differences, a stereoselective bioanalytical method for bupropion, hydroxybupropion, erythrohydrobupropion, and threohydrobupropion was recently validated (Teitelbaum et al. 2016a, 2016b). Further studies concerning bupropion HBr are also needed to clarify the implication in the bromism, a toxic syndrome characterized by neurologic, psychiatric and dermatologic adverse effects, when high amounts of bromide are ingested (Bowers and Onoroski 1990; Shader 2009).