PCP - Phencyclidine Information, Use, Testing and Treatment
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Illegally manufactured in labs and sold as tablets, capsules, or colored powder. It can be snorted, smoked, or eaten. Developed in the 1950s as an IV anesthetic, PCP was never approved for human use because of problems during clinical studies, including intensely negative psychological effects.
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Many PCP users are brought to emergency rooms because of overdose or because of the drug's unpleasant psychological effects. In a hospital or detention setting, people high on PCP often become violent or suicidal.
Statistics and Trends:
In 2006, 187,000 Americans age 12 and older had abused PCP at least once in the year prior to being surveyed. Source: National Survey on Drug Use and Health. The NIDA-funded 2007 Monitoring the Future Study does not measure PCP use among 8th and 10th graders but showed that 0.9% of 12th graders had abused PCP at least once in the year prior to being surveyed. Source: Monitoring the Future.
(phencyclidine) was developed in the 1950s as an intravenous anesthetic. Its use has since been discontinued due to serious adverse effects.
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How Is PCP (phencyclidine) Abused?
is a white crystalline powder that is readily soluble in water or alcohol. It has a distinctive bitter chemical taste. PCP can be mixed easily with dyes and is often sold on the illicit drug market in a variety of tablet, capsule, and colored powder forms that are normally snorted, smoked, or orally ingested. For smoking, PCP is often applied to a leafy material such as mint, parsley, oregano, or marijuana. Depending upon how much and by what route PCP is taken, its effects can last approximately 4–6 hours.
PCP (phencyclidine) Affects On The Brain
The use of PCP as an approved anesthetic in humans was discontinued in 1965 because patients often became agitated, delusional, and irrational while recovering from its anesthetic effects. PCP is a “dissociative drug,” meaning that it distorts perceptions of sight and sound and produces feelings of detachment (dissociation) from the environment and self. First introduced as a street drug in the 1960s, PCP quickly gained a reputation as a drug that could cause bad reactions and was not worth the risk. However, some abusers continue to use PCP due to the feelings of strength, power, and invulnerability as well as a numbing effect on the mind that PCP can induce. Among the adverse psychological effects reported are:
Symptoms that mimic schizophrenia, such as delusions, hallucinations, paranoia, disordered thinking, and a sensation of distance from one’s environment.
Mood disturbances: Approximately 50 percent of individuals brought to emergency rooms because of PCP-induced problems—related to use within the past 48 hours—report significant elevations in anxiety symptoms.
People who have abused PCP for long periods of time have reported memory loss, difficulties with speech and thinking, depression, and weight loss. These symptoms can persist up to one year after stopping PCP abuse.
Addiction: PCP is addictive—its repeated abuse can lead to craving and compulsive PCP-seeking behavior, despite severe adverse consequences.
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Other Adverse Effects of PCP (phencyclidine) on Health
At low to moderate doses, physiological effects of PCP include a slight increase in breathing rate and a pronounced rise in blood pressure and pulse rate. Breathing becomes shallow; flushing and profuse sweating, generalized numbness of the extremities, and loss of muscular coordination may occur.
At high doses, blood pressure, pulse rate, and respiration drop. This may be accompanied by nausea, vomiting, blurred vision, flicking up and down of the eyes, drooling, loss of balance, and dizziness. PCP abusers are often brought to emergency rooms because of overdose or because of the drug’s severe untoward psychological effects. While intoxicated, PCP abusers may become violent or suicidal and are therefore dangerous to themselves also cause seizures, coma, and death (though death more often results from accidental injury or suicide during PCP intoxication). Because PCP can also have sedative effects, interactions with other central nervous system depressants, such as alcohol and benzodiazepines, can also lead to coma.
What Treatment Options Exist?
Treatment for alkaloid hallucinogen (such as psilocybin) intoxication—which is mostly symptomatic—is often sought as a result of bad “trips,” during which a patient may, for example, hurt him- or herself. Treatment is usually supportive: provision of a quiet room with little sensory stimulation. Occasionally, benzodiazepines are used to control extreme agitation or seizures.
There is very little published data on treatment outcomes for PCP intoxication. Doctors should consider that acute adverse reactions may be the result of drug synergy with alcohol. Current research efforts to manage a life-threatening PCP overdose are focused on a passive immunization approach through the development of anti-PCP antibodies. There are no specific treatments for PCP abuse and addiction, but inpatient and/or behavioral treatments can be helpful for patients with a variety of addictions, including that to PCP.
How Widespread Is the Abuse of PCP (phencyclidine)?
Monitoring the Future Survey:
In 2008, 1.8 percent of high school seniors reported lifetime use of PCP; past-year use was reported by 1.1 percent of seniors; and past-month use was reported by 0.6 percent. Data on PCP use by 8th- and 10th-graders are not available.
National Survey on Drug Use and Health:
In 2007, 6.1 million persons aged 12 or older reported that they had used PCP in their lifetime (2.5 percent), although only 137,000 persons in the same age group reported use in the past year—this represents a decrease from 187,000 persons in 2006.
PCP (phencyclidine) Biochemistry and pharmacology
The N-methyl-D-Aspartate (NMDA) receptor, a type of ionotropic receptor, is found on the dendrites of neurons and receives signals in the form of neurotransmitters. It is a major excitatory receptor in the brain. Normal physiological function requires that the activated receptor fluxes positive through the channel part of the receptor. PCP enters the ion channel from the outside of the neuron and binds, reversibly, to a site in the channel pore, blocking the flux of positive ions into the cell. PCP therefore inhibits depolarization of neurons and interferes with cognitive and other functions of the nervous system.
In a similar manner, PCP and analogues also inhibit nicotinic acetylcholine receptor channels (nAChR). Some analogues have greater potency at nAChR than at NMDAR. In some brain regions, these effects act synergistically to inhibit excitatory activity.
PCP is retained in fatty tissue and is broken down by the human metabolism into PCHP, PPC and PCAA.
The most troubling clinical effects are likely produced by the indirect action of phencyclidine on the presynaptic dopamine receptor (DA-2). This has been suggested to account for most of the psychotic features. The relative immunity to pain is likely produced by indirect interaction with the endogenous endorphin and enkephalin system in rats.
More than 30 different analogues of PCP were reported as being used on the street during the 1970s and 1980s, mainly in the USA. The best known of these are PCPy (rolicyclidine, 1-(1-phenylcyclohexyl)pyrrolidine); PCE (eticyclidine, N-ethyl-1-phenylcyclohexylamine); and TCP (tenocyclidine, 1-(1-(2-Thienyl)cyclohexyl)piperidine). These compounds were never widely-used and did not seem to be as well-accepted by users as PCP itself, however they were all added onto Schedule I of the Controlled Substance Act because of their putative similar effects.
The generalized structural motif required for PCP-like activity is derived from structure-activity relationship studies of PCP analogues, and summarized below. All of these analogues would have somewhat similar effects to PCP itself, although, with a range of potencies and varying mixtures of anesthetic, dissociative and stimulant effects depending on the particular substituents used. In some countries such as the USA, Australia, and New Zealand, all of these compounds would be considered controlled substance analogues of PCP, and are hence illegal drugs, even though many of them have never been made or tested.
Like other NMDA receptor antagonists, it is postulated that phencyclidine can cause a certain kind of brain damage called Olney's lesions. Studies conducted on rats showed that high doses of the NMDA receptor antagonist MK-801 caused irreversible vacuoles to form in certain regions of the rats' brains, and experts say that it is possible that similar brain damage can occur in humans. All studies of Olney's Lesions have only been performed on animals and may not apply to humans. The research into the relationship between rat brain metabolism and the creation of Olney's Lesions has been discredited and may not apply to humans, as has been shown with ketamine.
Phencyclidine has also been shown to cause schizophrenia-like changes in the rat brain, which are detectable both in living rats and upon necropsy examination of brain tissue. It also induces symptoms in humans that are virtually indistinguishable from schizophrenia.
History and medicinal use
PCP was first synthesized in 1926, and later tested after World War II as a surgical anesthetic. Because of its adverse side effects, such as hallucinations, mania, delirium, and disorientation, it was shelved until the 1950s. In 1953, it was patented by Parke-Davis and named Sernyl (referring to serenity), but was withdrawn from the market two years later because of side-effects. It was renamed Sernylan in 1967, and marketed as a veterinary anesthetic, but again discontinued. Its side effects and long half-life in the human body made it unsuitable for medical applications.
When smoked, some of it is broken down by heat into 1-phenyl-1-cyclohexene (PC) and piperidine.
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PCP comes in both powder and liquid forms (PCP base is dissolved most often in ether), but typically it is sprayed onto leafy material such as marijuana, mint, oregano, parsley, or ginger leaves, then smoked.
PCP is a Schedule II substance in the United States, a List II drug of the Opium Law in the Netherlands and a Class A substance in the United Kingdom.
Method of absorption
The term "embalming fluid" is often used to refer to the liquid PCP in which a cigarette or joint is dipped, to be ingested through smoking, commonly known as "boat" or "water." Smoking PCP is known as "getting wet." A tobacco cigarette or cannabis joint dipped in PCP is called by the street names "sherm stick," "sherm," "fry stick," "amp," "toe tag", "dippa", "happy stick," and "wet stick." There is much confusion over the practice of dipping cigarettes in "embalming fluid" leading some to think that
real embalming fluid may actually be used. Smoking actual formaldehyde will cause intoxication, but may cause serious health consequences beyond those of consuming PCP, due to the toxicity of formaldehyde and other embalming chemicals. The slang term "embalming fluid" likely originated from PCP's somatic "numbing" effect and the feeling of physical dissociation from the body. This is one of the fastest growing means of using PCP, especially in the western United States where its is sold for about $10 to $25 per joint or cigarette.
In its pure (base) form, PCP is a yellow oil (usually dissolved in petroleum or diethyl ether or tetrahydrofuran). Upon treatment with hydrogen chloride gas, or HCL saturated isopropyl alcohol, this oil precipitates into white - tan crystals or powder (PCP hydrochloride) In this form, PCP can be insufflated, depending upon the purity. However, most PCP on the illicit market contains a number of contaminants as a result of makeshift manufacturing, causing the color to range from tan to brown, and the consistency to range from powder to a gummy mass. These contaminants can range from unreacted piperidine and other precursors, to carcinogens like benzene and cyanide - like compounds such as PCC (piperidinocyclohexyl carbonitrile).
Behavioural effects can vary by dosage. Small doses produce a numbness in the extremities and intoxication, characterized by staggering, unsteady gait, slurred speech, bloodshot eyes, and loss of balance. Moderate doses (5-10mg intranasal, or 0.01-0.02mg/kg intramuscular or intravenous) will produce analgesia and anesthesia. High doses may lead to convulsions.
Psychological effects include severe changes in body image, loss of ego boundaries, and depersonalization. Hallucinations and euphoria are reported infrequently.
The drug has been known to alter mood states in an unpredictable fashion, causing some individuals to become detached, and others to become animated. Intoxicated individuals may act in an unpredictable fashion, driven by their delusions and hallucinations.
Included in the portfolio of behavioral disturbances are acts of self-injury including suicide, and attacks on others or destruction of property. The analgesic properties of the drug can cause users to feel less pain, and persist in violent or injurious acts as a result. Recreational doses of the drug can also induce a psychotic state that resembles schizophrenic episodes which can last for months at a time with toxic doses. Users generally report an "out-of-body" experience where they feel detached from reality, or one's consciousness seems somewhat disconnected from consensus reality.
Symptoms are summarized by the mnemonic device RED DANES: rage, erythema (redness of skin), dilated pupils, delusions, amnesia, nystagmus (oscillation of the eyeball when moving laterally), excitation, and skin dryness.
The American rapper Big Lurch murdered an acquaintance and ate her lungs while on PCP. In The Man Who Mistook His Wife for a Hat, a similarly gruesome murder is described. In April 2009, a man in Bakersfield bit out his 4-year-old son's eye, and severely damaged the other, before attempting to chop off his own legs with an axe while under the influence of PCP.
In 1977, actor David Lochary died by bleeding to death in his New York apartment after falling on a piece of glass while on PCP.
Management of intoxication
Management of phencyclidine intoxication mostly consists of supportive care—controlling breathing, circulation, and body temperature—and, in the early stages, treating psychiatric symptoms. Benzodiazepines, such as lorazepam, are the drugs of choice to control agitation and seizures (when present). Typical antipsychotics such as phenothiazines and haloperidol have been used to control psychotic symptoms, but may produce many undesirable side effects—such as dystonia—and their use is therefore no longer preferred; phenothiazines are particularly risky, as they may lower the seizure threshold, worsen hyperthermia, and boost the anticholinergic effects of PCP. If an antipsychotic is given, intramuscular haloperidol has been recommended.
Forced acid diuresis (with ammonium chloride or, more safely, ascorbic acid) may increase clearance of PCP from the body, and was somewhat controversially recommended in the past as a decontamination measure. However, it is now known that only around 10% of a dose of PCP is removed by the kidneys, which would make increased urinary clearance of little consequence; furthermore, urinary acidification is dangerous, as it may induce acidosis and worsen rhabdomyolysis (muscle breakdown), which is not an unusual manifestation of PCP toxicity.
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