Sedative, hypnotic, and anxiolytic withdrawal The severity of withdrawal varies with dose and duration; however, it can occur with short-term, relatively low dose use of BZDs. Withdrawal symptoms include: ● Autonomic hyperactivity (diaphoresis, tachycardia). ● Hand tremors. ● Insomnia. ● Nausea/vomiting. ● Transient visual, tactile, or auditory hallucinations. ● Psychomotor agitation. ● Anxiety. ● Grand mal seizures. Sedative use disorder treatment No standard exists for determination of the appropriateness of inpatient versus outpatient settings for the management of patients who are suffering withdrawal symptoms or who are attempting to manage their long-term sedative use. Tapering doses of benzodiazepines can be managed effectively in the outpatient setting in stable healthy patients using the strategies discussed earlier. Substitution of a long-acting benzodiazepine such as Clonazepam for
Deprescribing BZDs is an important clinical skill, and the first goal of treatment in detoxification. Certain individuals may not require long-term BZDs. When deprescribing BZDs, consider duration of treatment, dose, and half-life of the BZD. Consider a taper over several weeks or months. Often switching to a long- acting BZD is an effective method in an individual who has serious abuse problems. Tapering is effective in cases of long-acting benzodiazepines but is not as effective in short-acting benzodiazepines. For example, an individual who has been taking a BZD for 12 weeks should be monitored closely while implementing a reduction of 10-25% of the dose per week. 40 a short-acting drug such as Valium would eliminate the associated euphoria and illicit market value of the medication and may assist in detoxification and inappropriate use. Acute withdrawal that may be associated with delirium, abnormal vital signs, seizures, or patients with multiple comorbidities that may be at risk from labile vital signs during the withdrawal period would be more appropriately managed in a supervised inpatient setting. 145
STIMULANT-RELATED DISORDERS
Stimulant use disorders include a range of issues related to illicit cocaine, methamphetamine, and ecstasy, as well as prescription stimulants that include methylphenidate and amphetamine. The general mechanism of stimulants revolves around increased catecholamine levels and increased agonistic activity at adrenergic receptors. Acute adverse effects can cause acute conditions including tachycardia, vasoconstriction, and bronchodilation, as well as hyperthermia. Psychological and neurological effects include panic attacks, hostility, paranoia, psychosis, and even violent behavior. 41 Stimulant- involved overdoses have risen in the last decade. The psychostimulant-involved death rate increased by over 300%. 42 Stimulant use and disorders are associated with a range of physical, psychological, and societal harms. The highs and lows from these drugs create a binge and crash pattern. Chronic stimulant use can alter brain structures with decreased attention span, confusion, impaired memory, inhibited impulse, and reduced motor skills. Common stimulants of abuse Cocaine is a naturally occurring alkaloid obtained from the Erythroxylon coca shrub. It was first used by ancient Peruvians; psychologists such as Freud later proposed cocaine as a treatment for depression, asthma, and cachexia in the early 20th century. Today, cocaine has limited medical use as a treatment for epistaxis but is widely used as an illicit drug through inhalation (snorting), smoking, and other routes, including parenteral use. When snorted, the onset of action is within 5 minutes and typically peaks within 30 minutes. The half-life of cocaine is 30-90 minutes, and it can be absorbed
Table 4: Stimulant Drugs by Schedules 43 Schedule I
Aminorex; methyl-aminorex; methcathinone, animal imal use only; 3,4-Methylenedioxy- methamphetamine, commonly known as MDMA Amphetamines, dextroamphetamine; methamphetamine, methylphenidate; cocaine Clortermine, not currently in use; phendimetrazine, weight loss; benzphetamine, weight loss Diethylpropion, weight loss; Modafinil; Phentermine
Schedule II
Schedule III
Schedule IV
Schedule V
Pyrovalerone
across any mucosal surface including respiratory, gastrointestinal, and genitourinary tracts. 44 Cocaine has a local anesthetic affect by blocking presynaptic reuptake of the neurotransmitters norepinephrine and dopamine. Cocaine also increases the quantity of neurotransmitters at the postsynaptic receptor sites. The resultant activation of the sympathetic nervous system produces an acute rise in arterial pressure, tachycardia, and a predisposition to ventricular arrhythmias and seizures. Sympathetic activation also may result in mydriasis, hyperglycemia, and hyperthermia along with tremors and restlessness.
Book Code: MDCO1025
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