Saliva Drug Analysis
Steven H. Y. Wong, Iraving Sunshine in Handbook of Analytical Therapeutic Drug Monitoring and Toxicology, 2017
Phencyclidine (PCP; l-[l-phenylcyclohexyl]piperidine) is a dissociative anesthetic with a wide range of pharmacological actions, including CNS stimulant, depressant, hallucinogenic, and analgesic actions.120 It is well absorbed by all routes and is commonly ingested or smoked with marijuana, or after impregnating parsley flakes with PCP in solution. However, it may also be administered orally, intranasally, or by injection. PCP is initially metabolized by hydroxylation, with further oxidative metabolism resulting in the formation of polar inactive metabolites. A relatively small portion (4 to 19%) of the original dose is excreted unchanged in the urine. PCP can be detected in urine by immunoassay and by GC/MS at a cutoff concentration of 25 ng/ml. Detection time in urine is dependent on pattern of usage. Single doses of PCP may be detected for as long as 5 to 8 days, whereas chronic users may remain positive for as long as 30 days.
Psychiatric Emergencies Associated with Drug Overdose
R. Thara, Lakshmi Vijayakumar in Emergencies in Psychiatry in Low- and Middle-Income Countries, 2017
The most common psychiatric symptoms of drug overdose are agitation and psychosis. Psychosis includes delusions, especially paranoid, hallucinations, especially visual, and also catatonia, which may occur in those who have taken a phencyclidine overdose. The most crucial element of the assessment of these symptoms of drug overdose is the differentiation of these symptoms from those of a functional psychotic disorder or a metabolic disturbance. Clarity of sensorium and the predominance of auditory modality hallucinations are a hallmark of functional psychosis. Electrolyte screening and neuroimaging are required to rule out metabolic, focal infectious, and an oncological origin of these symptoms. Adequate sedation with the help of benzodiazepines and antipsychotic support with drugs such as haloperidol are the specific modes of treatment for this category of symptoms (Olson 2004).
Inhalational Durg Abuse
Jacob Loke in Pathophysiology and Treatment of Inhalation Injuries, 2020
Considering that more than 50 million Americans have used marijuana (Nicholi, 1983) and that 20 million Americans use marijuana daily, remarkably few seek medical attention. Even in a large city, emergency room visits related strictly to marijuana smoking are a rarity. Acute fatal toxicity of cannabis is extremely rare (Heyndrickx, 1970). The adverse acute psychological reactions occasionally bring marijuana smokers to the health care system. Patients with anxiety reactions and panic attacks associated with acute intoxication occasionally seek medical attention. These reactions are usually self limited resolving within several hours, and are best treated conservatively with reassurance (Cohen, 1986), a quiet setting, and occasionally a benzodiazepine. Acute toxic reactions with delirium or organic psychosis are comparatively rare. Reactions of this severity may indicate the presence of other abused drugs, particularly phencyclidine in the smoked substance. While these reactions are self-limited, they can require hospitalization and observation. Rarely, symptoms may last for months to years; there is a report of chronic cannabis psychosis lasting for more than 1 year (Tunving, 1985). It may be difficult to attribute the chronic psychosis to marijuana, as opposed to underlying mental disorder and attempts should be made to distinguish the chronic cannabis syndrome from other psychopathology. A trial of abstinence from marijuana use in patients with the chronic cannabis syndrome can lead to an increase in alertness and physical ability (Cohen, 1986) when coupled with psychotherapy.
Resistance is not futile: treatment-refractory schizophrenia – overview, evaluation and treatment
Published in Expert Opinion on Pharmacotherapy, 2019
While the etiology of schizophrenia is unclear, and there are likely many different pathophysiological pathways that lead to the symptoms of schizophrenia, the interaction between dopamine and glutamate may play a role for most patients. It has long been thought that increased dopamine activity in the mesolimbic pathway is responsible for the positive symptoms of schizophrenia. The origins of this may lie in the hypothesis that hypofunction of the N-methyl-D-aspartate (NMDA) glutamate receptor may lead to excess dopamine release in the mesolimbic pathway and in addition, inadequate release of dopamine in prefrontal cortex, causing negative symptoms and cognitive dysfunction [8,9]. This can be seen in clinical practice when observing an otherwise healthy individual that is intoxicated on the NMDA receptor antagonistic phencyclidine (PCP). Symptoms of PCP intoxication can mimic the positive, negative, and cognitive symptoms of schizophrenia.
Novel Sunifiram-carbamate hybrids as potential dual acetylcholinesterase inhibitor and NMDAR co-agonist: simulation-guided analogue design and pharmacological screening
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2022
Khalid A. Agha, Nader E. Abo-Dya, Abdul Rashid Issahaku, Clement Agoni, Mahmoud E. S. Soliman, Eatedal H. Abdel-Aal, Zakaria K. Abdel-Samii, Tarek S. Ibrahim
N-methyl-D-aspartate receptor (NMDAR) is another approach in enhancing cognition,8 it is a glutamate receptor and ion channel protein found in nerve cells as tetrameric complex and is a promising target for cognitive enhancement since it is centrally involved in cognitive processes.9 It was shown that transient activation of NMDAR is the trigger for the induction of long-term potentiation (LTP) at synapses of neurons in the hippocampus which are likely to explain their importance for learning and memory.10 Also, it has the ability to increase acetylcholine release and its inhibition result in decrease in acetylcholine secretion.11,12 Biochemical and molecular studies of NMDA receptor showed that both mRNA and protein levels of NMDARs are reduced in AD brain and AD model, suggesting hypofunction of NMDAR with increasing AD pathologic severity.13 These observations supported by findings that blocking NMDAR by ketamine and phencyclidine can induce schizophrenic like symptoms including cognitive decline in healthy individuals and exacerbate cognitive deficit in schizophrenic individuals.14,15
Pro-psychotic effects of synthetic cannabinoids: interactions with central dopamine, serotonin, and glutamate systems
Published in Drug Metabolism Reviews, 2018
William E. Fantegrossi, Catheryn D. Wilson, Michael D. Berquist
Glutamate (Glu) is the major excitatory neurotransmitter, and it binds to both ionotropic and metabotropic receptors. Metabotropic Glu receptors (mGluR) have at least eight subtypes classified into three groups based on sequence homology, signal transduction, and pharmacology. Maksymetz et al. (2017) have recently reviewed current strategies to target mGluR to treat schizophrenia, but there is scant data on interactions between mGluRs and CB receptors, so further discussion of this is largely outside the scope of this review. However, there are three currently recognized ionotropic Glu receptors (α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA), kainate, and N-methyl-d-aspartate (NMDA) receptors), and the NMDA receptors are most closely associated with neurological disorders, including schizophrenia and psychosis (Maeng and Zarate 2007). Importantly, administration of the non-competitive NMDA antagonist phencyclidine (PCP) to healthy human subjects reliably induces psychosis-like effects (Davies and Beech 1960; Cohen et al. 1962), as does the structurally related arylcyclohexylamine ketamine (Krystal et al. 1994; Malhotra et al. 1996). Accordingly, the remainder of this section will focus on interactions between CB1R and NMDA receptors.
Related Knowledge Centers
- Cannabis
- Hallucination
- Smoking
- Violence
- Recreational Drug Use
- Dissociative
- Anesthetic
- Oral Administration
- Insufflation
- Injection