Monday, October 7, 2013

What is PCP?


History of Use

Phencyclidine (PCP) was originally synthesized in 1926 as 1-(1-phenylcyclohexyl)piperidine. It was intended for use as an intravenous surgical anesthetic during World War II because it caused decreased sensitivity to pain (analgesia) without decreasing heart and lung function or muscle tone. Its use was discontinued for this purpose after patients had adverse psychological side effects that included increased agitation and psychosis.




PCP was patented 1963 as the anesthetic Sernyl by Parke-Davis Pharmaceutical but was taken off the market two years later because of the drug’s negative psychological effects and long half-life. PCP reappeared for veterinary use in 1967 as an animal tranquilizer.


PCP gained popularity as a recreational substance in the late 1960s because of the psychological effects. In 1969, however, PCP was made an illegal substance to possess, sell, or manufacture. In the early 1970s, the drug was categorized as a schedule III controlled substance. It was moved from schedule III to schedule II in 1978.


Since the 1970s, PCP’s popularity has substantially decreased, but the drug remains readily available. Initial data from the peak of PCP use in 1979 revealed that 7 percent of high school students had used the drug. Data in 2009 from the National Survey on Drug Use and Health showed that only 122,000 Americans had used PCP within the previous calendar year; 1 percent of these persons were high school students.


Many persons are exposed to PCP without their knowledge. One study found that almost 25 percent of marijuana also contained trace levels of PCP. Additionally, PCP and other recreational drugs are gaining popularity as alternative drugs for treating chronic pain.




Effects and Potential Risks

PCP acts as an N-methyl d-aspartate (NMDA) receptor antagonist by blocking NMDA receptor activity. It also inhibits the nicotinic acetylcholine receptor channels. By both of these mechanisms, PCP interferes with the brain’s natural neurotransmitter responses. The actions of PCP on the brain are complex, causing both stimulation and depression of the central nervous system. This explains why some users may have a calming response to PCP exposure, while others may have an agitated or aggressive reaction.


The timing of drug effects depends on the mode of administration. Inhalation of PCP is the most common route because the drug works quite rapidly if inhaled; symptoms can be observed within about five minutes. With oral ingestion, symptoms can take up to one hour to be realized. The first effects of PCP last for approximately four to seven hours, but the long-lasting consequences continue for several days or even one week.


Initial effects of low doses (3 to 5 milligrams [mg]) resemble those of alcohol intoxication, including slurred speech and an unsteady gait (ataxia), and a numbing of the arms and legs. There is a significant increase in blood pressure (hypertension), pulse rate (tachycardia), and analgesia.


At increased doses (of more than 5 mg), PCP causes a decrease in respiratory rate, an irregular heart beat (arrhythmia), increased muscle tone (hypertonia), and seizures. In addition to the physiological effects, PCP also produces significant alterations in mental status at high doses. The psychological effects include hallucinations, delusions, an “out-of body” experience, amnesia, paranoia, a catatonic state, and disorganized thinking. Depression and psychosis may persist for an extended time after withdrawal.


The risk of permanent schizophrenic-like symptoms exists with PCP abuse rather than with occasional recreational use. PCP is unpredictable in how mood and mental status will be changed, and some users have negative experiences that lead to an increased tendency for suicidal thoughts or committing violent acts. Hospitalization may be required to closely monitor symptoms while recovering.


Coma and deaths have been reported from cardiac arrest, strokes from hypertension, increased body temperature (hyperthermia), breakdown of muscle (rhabdomyolysis), and increased potassium levels (hyperkalemia). Suicides and accidents secondary to violent behavior also are commonly reported. Deaths also occur because of the consumption of an unknown dosage, the presence of contaminated materials in substances that have been illegally manufactured and distributed, underlying medical issues, and the use of other drugs simultaneously.




Bibliography


Bey, Tareg, and Anar Patel. “Phencyclidine Intoxication and Adverse Effects: A Clinical and Pharmacological Review of an Illicit Drug.” California Journal of Emergency Medicine 8.1 (2007): 9–14. Print.



Deroux, Stephen, Anthony Sgarlato, and Elizabeth Marker. “Phencyclidine: A 5-Year Retrospective Review from the New York City Medical Examiner’s Office.” Journal of Forensic Sciences 56.3 (2011): 656–59. Print.



“Hallucinogens: LSD, Peyote, Psilocybin, and PCP.” National Institute on Drug Abuse. National Inst. of Health, Dec. 2014. Web. 28 Oct. 2015.



Liu, F., et al. “Changes in Gene Expression after Phencyclidine Administration in Developing Rats: A Potential Animal Model for Schizophrenia.” International Journal of Developmental Neuroscience 29.3 (2011): 351–58. Print.



“Substance Use - Phencyclidine (PCP).” MedlinePlus. US Natl. Lib. of Medicine, 21 May 2014. Web. 28 Oct. 2015.

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