Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.16.2 (PCP)
3,761 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The history, symptoms, diagnosis and treatment of phencyclidine hydrochloride (PCP) intoxication and the pharmacology of PCP are reviewed. Intoxication with low to moderate doses of PCP (5-20 mg) resembles an acute, confusional state generally lasting four to six hours. High doses (greater than 20 mg) may cause serious neurologic and cardiovascular complications and the patient is often comatose for several days. Treatment involves supportive psychological and medical measures. Evacuation of the stomach with activated charcoal and a saline cathartic may be indicated and succinylcholine chloride may ease intubation. Diazepam and chlorpromazine may be used to control the combative patient and the "PCP psychosis" patient, respectively. Antihypertensive agents are not usually needed, but diazoxide and hydralazine hydrochloride have been used to treat hypertensive crises. Diazepam and phenytoin have been used to treat seizures. Ion-trapping by continuous gastric suctioning and by urine acidification with ammonium chloride may increase clearance of PCP. Forced diuresis with furosemide in conjunction with acidification may further increase PCP clearance. Use of physostigmine is based on conjecture.
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PMID:Phencyclidine intoxication: a literature review. 36 Aug 32

To characterize the relation between clinical and hemodynamic state in acute myocardial infarction, 200 patients with acute infarction were evaluated with clinical and hemodynamic criteria. Patients were classified clinically on the basis of peripheral hypoperfusion (hypotension, tachycardia, confusion, cyanosis, oliguria) and pulmonary congestion (rales, abnormal chest roentgenogram). Four clinical subsets were defined that correlated with cardiac index (Cl, liters/min per m2) and pulmonary capillary pressure (PCP, mm Hg): (see article). Parallel hemodynamic subsets were developed independently on the basis of depressed cardiac index (2.2 liters/min per m2 or less) and elevated pulmonary capillary pressure (greater than 18 mm Hg). The rate of accuracy of clinical examination in predicting hemodynamic abnormalities was 83 percent. Mortality rates were similar in the clinical and hemodynamic subset calssifications, averaging 2.2 percent in subset I, 10.1 percent in subset II, 22.4 percent in subset III and 55.5 percent in subset IV. Drug interventions in the course of hospitalization resulted in a 38 percent increase in depressed cardiac index and 34 percent decrease in elevated pulmonary capillary pressure. Resolution of clinical abnormalities paralleled this hemodynamic improvement in 70 percent of patients. These data suggest that clinical performance and both clinical and hemodynamic subsets are directly relevant to establishing prognosis and the selection of therapy in patients with acute myocardial infarction.
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PMID:Correlative classification of clinical and hemodynamic function after acute myocardial infarction. 83 73

Phencyclidine (PCP) is a major drug of abuse as well as a 'drug of choice' among substance abusers in the U. S. A. Unfortunately, PCP use may result in the development of psychotic behavior. PCP-induced psychosis is characterized by confusion, excitation, aggression, paranoia, hallucinations and delusions of grandeur and may evoke violent or suicidal behavior. Therefore, many patients suffering from PCP-induced psychosis have been diagnosed initially as schizophrenic. However, PCP-related research has not kept pace with the rise in abuse and PCP-induced psychosis. The neurochemical effects of PCP are not well defined at present, but both behavioral and biochemical studies suggest that it may interact with dopaminergic, cholinergic, noradrenergic, serotonergic, GABAergic and enkephalinergic systems. In addition, the specific reversible, saturable, high affinity 3H-PCP binding site is discovered recently in rat brain. On the other hand, there is now a large body of evidence to suggest that opiate receptors may be subdivided into mu, sigma, kappa and delta receptors. On the basis of behavioral and binding studies, it is proposed that the sigma receptor and the PCP binding site are one and the same. This receptor interacts with PCP and psychotomimetic opioids to produce their psychotomimetic effects. In connection with this receptor, a trial to isolate an endogenous ligand produces psychotomimetic effects, "angeldustin" is progressing. This review has served to illustrate the paucity of information currently available on the central effects of PCP. However, our current notions of the mechanisms of action of PCP are very complicate. Such a review inevitably raises more question than it answers but it is hoped that these may stimulate further investigation in this field.
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PMID:[Phencyclidine, a drug which induces psychosis: its neuropharmacological actions]. 639 56

Snowball sampling techniques were used to generate a sample of 200 phencyclidine users from an area with a 10-year history of extensive PCP use. Three types of users were studied: heavy chronic, light chronic, and recreational users. The extent of PCP use varied from less than twice a month for a period of 6 months to daily use for several consecutive years. Each subject participated in a structured interview which lasted an average of 11/2 h. Subjects were asked about the acute effects of PCP, and about their moods before, during, and after using PCP. Scales based on previous research were used to measure the acute effects and moods. Results showed that heavy chronic users were more likely than recreational users to feel energized by PCP, and to experience negative ideations (thoughts about suicide and death). When age was controlled for, heavy chronic users were also more likely to experience violent effects. Analysis of moods over time showed some similar patterns between heavy chronic and recreational users, as well as some striking differences. Overall, heavy chronic users reported greater mood elevations while high on PCP, and a more dramatic drop in mood after the high wore off, than recreational users. Analysis of the results by user types clarified some of the confusion about contradictory descriptions of the effects of PCP, and point to the need to continue distinguishing between user types.
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PMID:Acute effects of phencyclidine (PCP) on chronic and recreational users. 730 11

There is widespread agreement that estimates of adolescent drug use prevalence from the National Household Survey of Drug Abuse (NHSDA) and Monitoring the Future (MTF) are subject to considerable measurement error. Nevertheless, some have suggested that trends over time in these prevalence estimates probably reflect true trends in drug use, since underreporting may be assumed to be constant over time. A recent National Research Council report criticizes this assumption on logical grounds. The present study examines adolescent drug use responses on the NHSDA and MTF for evidence of "drug omission," "jargon confusion" and "conceptual confusion," three types of misreporting expected to vary in magnitude with changes in drug use practices and changes in survey items. Results demonstrate that adolescent drug users are significantly more likely than adults to report use of drugs not listed in the NHSDA. Among adolescents who wrote in the "other" drugs they used, 66% and 86% of hallucinogen and inhalant responses showed confusion over the meaning of the pharmacological terms used in the NHSDA. Almost 20% of MTF respondents who report lifetime use of Rohypnol or ecstasy, when specifically queried about these drugs, deny lifetime use of any substances in the drug classes intended to assess use of Rohypnol and ecstasy. MTF respondents reporting lifetime use of PCP underreport use of hallucinogens at rates that vary substantially over time, from a high of 45% (in 1986), to a low of just 8% (in 1998). The implications of these findings for adolescent drug use prevalence estimation and survey design are discussed.
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PMID:Measurement of adolescent drug use. 1462 Nov 28

Pneumocystis was discovered nearly a century ago. It causes fatal pneumonia in immunocompromised individuals, especially in AIDS patients. Knowledge of the different species remained rudimentary until the mid-eighties when DNA analysis revealed its extensive diversity. In fact, it is no longer considered as a zoonosis. Pneumocystis organisms derived from different hosts have very different DNA sequences, indicating multiple species. Due to the genetic and functional disparities, the organism that causes human PCP is now named Pneumocystis jirovecii/Frenkel, 1999. We continue to call Pneumocystis carinii the species found in rats. This will allow for a single international language and avoid confusion. Changing the organism's name does not preclude the use of the well-known acronym PCP because it can also be read "PneumoCystis Pneumonia." The DNA sequences and genotypage have shown that variations exist among samples of P. jiroveci. Molecular biology is helpful in the study of the mechanisms of transmission, which can only occur in the same host and the different resistances as well as providing a better understanding of the relationship between host and pathogen. P. jirovecii pneumonia in immunosuppressed patients was previously thought to result from the reactivation of a latent infection acquired in early childhood. However, today, it is believed to result from a new infection from an exogenous source.
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PMID:[Pneumocystis jirovecii: what does this mean?]. 2116 41

Introduction. Wernicke's encephalopathy is a well-described syndrome characterized by the classic triad of confusion, ataxia, and ophthalmoplegia. Wernicke's encephalopathy results from thiamine (vitamin B1) deficiency. Common causes include alcoholism and gastric disorders. Wernicke's has been described in patients with acquired immune deficiency syndrome (AIDS); however, given these patients' immunosuppressed state, the diagnosis of Wernicke's encephalopathy is not apparent. Case Presentation. A 31-year-old previously healthy male presented to the ER complaining of progressive dyspnea. Workup revealed HIV/AIDS and PCP pneumonia. He was treated and improved. On day 14 he became confused and developed nystagmus and ataxia. Considering his immunocompromised state, infectious and neoplastic etiologies topped the differential diagnosis. CT head was negative. Lumbar puncture was unremarkable. Brain MRI revealed increased T2 signal in the medial thalamus bilaterally. Intravenous thiamine was administered resulting in resolution of symptoms. Discussion. The classic triad of Wernicke's encephalopathy occurs in 10% of cases. When immunosuppressed patients develop acute neurologic symptoms infectious or neoplastic etiologies must be excluded. However, given the relative safety of thiamine supplementation, there should be a low threshold for initiating therapy in order to reverse the symptoms and prevent progression to Korsakoff dementia, which is permanent.
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PMID:Wernicke's Encephalopathy: An Unusual Consequence of the Acquired Immune Deficiency Syndrome-Case Report and Literature Review. 2393 38

There has been growing clinical, public, and media awareness and concern about the availability and potential harmfulness of so-called 'legal highs', which are more appropriately called new or novel psychoactive substances (NPS). A cat-and-mouse process has emerged wherein unknown chemists and laboratories are producing new, and as yet nonproscribed, compounds for human consumption; and as soon as they are banned, which they inevitably are, slightly modified analogues are produced to circumvent new laws. This rapidly changing environment, 81 new substances were identified in 2013 alone, has led to confusion for clinicians, psychopharmacologists, and the public at large. Our difficulties in keeping up with the process has had a two-fold negative effect: the danger of ignoring what is confusing; and the problem that some of the newer synthesized compounds appear ever more potent. This review aims to circumscribe a quick moving and growing field, and to categorize NPS into five major groups based upon their 'parent' compounds: stimulants similar to cocaine, amphetamines and ecstasy; cannabinoids; benzodiazepine based drugs; dissociatives similar to ketamine and phencyclidine (PCP); and those modelled after classic hallucinogens such as LSD and psilocybin. Pharmacodynamic actions, subjective and physical effects, harmfulness, risk of dependency and, where appropriate, putative clinical potentials are described for each class. Clinicians might encounter NPS in various ways: anecdotal reportage; acute intoxication; as part of a substance misuse profile; and as a precipitant or perpetuating factor for longer-term physical and psychological ill health. Current data are overall limited, and much of our knowledge and treatment strategies are based upon those of the 'parent' compound. There is a critical need for more research in this field, and for professionals to make themselves more aware of this growing issue and how it might affect those we see clinically and try to help: a brave new world of so-called 'psychonauts' consuming NPS will also need informed 'psychotherapeutonauts'. The paper should serve as a primer for clinicians and interested readers, as well as provide a framework into which to place the new substances that will inevitably be synthesized in the future.
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PMID:Legal highs: staying on top of the flood of novel psychoactive substances. 2624 Jul 49