PCP is a white, crystalline powder (contaminants may cause tan to
brown color), or a clear, yellowish liquid.
Synonyms: 1-phenylcyclohexylpiperidine; amp,
angel dust, animal tranquilizer, dips, dust, elephant, embalming fluid,
formaldehyde, fry, hog, ozone, peace pill, rocket fuel, Sernyl, Sernylan,
super kools, TicTac, tranq, water, wet.
Source: Synthetic chemical made in clandestine
laboratories, or diverted from veterinary sources. PCP is currently
a Schedule II controlled substance. In illicit synthesis, piperidine
is reacted with cyanide and cyclohexanone to make piperidinocyclohexanecarbonitrile
(PCC), which is then reacted with phenylmagnesium bromide to make PCP.
PCP can be mixed with dyes and sold in a variety of tablets, capsules
and colored powders. PCP is also sold as a liquid in small shaker bottles.
PCP analogs are also available: cyclohexamine (PCE), phenylcyclohexylpyrrolidine
(PHP), phenylcyclopentylpiperidine (PCPP), and thienylcyclohexylpiperidine
(TCP).
Drug Class: Hallucinogen, dissociative anesthetic,
psychotomimetic, sedative-hypnotic.
Medical and Recreational Uses: Formerly used
as a surgical anesthetic, however, there is no current legitimate medical
use in humans. Used as a veterinary anesthetic or tranquilizer. Recreationally
used as a psychedelic and hallucinogen.
Potency, Purity and Dose: A
light dose typically consists of 3-5 mg; a common dose is 5-10 mg; while
a strong dose is greater than 10 mg. Lighter doses are usually smoked,
intravenously or intranasally administered, while heavier doses are
commonly ingested orally. The liquid can be sprinkled on tobacco or
marijuana then smoked, or the cigarettes or joints themselves can be
dipped in PCP solution; the resulting PCP dose can therefore vary widely.
Due to difficulty of synthesis, street preparations have highly variable
concentrations of PCP and byproducts. PCC, the PCP precursor, is found
in approximately 20% of illicit samples and is more toxic than PCP as
it releases cyanide. Abuse of PCP precursors or analog chemicals leads
to similar or more devastating pharmacological effects than PCP. PCP
is often administered or mixed with other drugs such as crack cocaine
(“beam me up”), cocaine hydrochloride (“lovelies”),
and marijuana (“crystal supergrass”, “donk”, “killer
joints”, “sherms”, “wacky weed”, “wicky
stick”).
Route of Administration: Smoked, intravenous
injection, snorted, added as eye drops, oral ingestion, and transdermal
absorption.
Pharmacodynamics: Dopaminergic, anticholinergic and opiate-like
activities exist. PCP is a non-competitive NMDA-receptor antagonist,
and blocks dopamine reuptake and elevates synaptic dopamine levels.
It has high affinity to sites in the cortex and limbic structures.
Pharmacokinetics: Well absorbed following
all routes of administration, although ~ 50% of PCP in cigarette smoke
is converted to an inactive thermal degradation product. PCP is highly
lipid soluble and is stored in fat and brain tissue. The plasma binding
of PCP is 65% and its half-life ranges from 7-46 hours (average 21 hours).
PCP is extensively metabolized to inactive metabolites by a variety
of metabolic routes.
Molecular Interaction / Receptor Chemistry: The
cytochrome P450 3A isoenzyme plays a major role in PCP biotransformation.
Potential inhibitors of this isoenzyme could decrease the rate of PCP
elimination if administered concurrently, while potential
inducers could increase the rate of elimination. PCP itself may inhibit
2B1 and 2C11 isoforms.
Blood to Plasma Concentration Ratio: 0.94
and 1.0 reported.
Interpretation of Blood Concentrations: There
is no direct correlation between PCP concentration and behavioral or
physical findings. Blood levels peak 1-4 hours after ingestion. Average
peak plasma concentrations of 2.7 and 2.9 ng/mL were achieved after
a 1 mg oral and intravenous dose, respectively. PCP concentrations ranged
from 0.3 to 143 ng/mL in 63 patients presenting at a psychiatric hospital
emergency room and were associated with a wide variety of psychotic
clinical pictures resembling mania, depression or schizophrenia. All
these patients had at least one manifestation of toxic psychosis and/or
acute delirium, in addition to other symptoms. Similarly, plasma PCP
concentrations ranged up to 812 ng/mL in 22 patients with nonfatal PCP
intoxication. The most common physical findings were combativeness-agitation
(64%), depressed level of consciousness (50%), hypertension (43%), miosis
(43%) and tachycardia (43%). Blood PCP concentrations ranged from 12
to 118 ng/mL in 26 individuals arrested for public intoxication.
Interpretation of Urine Test Results: Elimination
of PCP in 72 hours urine ranges from 4 to 19% for unchanged drug and
25 to 30% for conjugated metabolites. Approximately 97% of a dose is
excreted in 10 days, and PCP use can be detected in urine by immunoassay
up to a week following a high dose. Urine PCP concentrations ranged
from 0.4-340 mg/L in 19 intoxicated patients.
Effects:
Psychological: Effects are usually dose dependent, and include
euphoria, calmness, feelings of strength and invulnerability, lethargy,
disorientation, loss of coordination, distinct changes in body awareness,
distorted sensory perceptions, impaired concentration, disordered thinking,
illusions and hallucinations, agitation, combativeness or violence,
memory loss, bizarre behavior, sedation, and stupor.
Physiological: Rise in blood pressure and heart rate, flushing,
profuse sweating, generalized numbness of extremities, blurred vision,
grimacing facial expression, speech difficulties, ataxia, muscular incoordination,
marked analgesia, nystagmus, and anesthesia. In the anesthetized state,
the patient remains conscious with a staring gaze and rigid muscles.
Side Effect Profile: Excessive salivation,
nausea, vomiting, amnesia, combativeness, severe anxiety, paranoia,
flashbacks, seizures, coma, and death. PCP can simulate schizophrenic-like
symptomatology such as flattened affect, dissociative thought disorder,
depersonalization and catatonic states. Long periods of use may lead
to memory loss, difficulties with speech and thinking, depression, weight
loss, liver function abnormalities, and rhabdomyolysis.
Duration of Effects: Onset of effects is
very rapid when smoked or injected
(1-5 minutes) and are delayed when snorted or orally ingested (30 minutes),
with a gradual decline of major effects over 4-6 hours. A return to ‘normal’ may
take up to 24 hours. Consciousness is regained within 10-60 minutes
following intravenous administration, with a prolonged recovery period
of 3-18 hours. Long-term psychological effects are possible and PCP
may precipitate a psychotic reaction lasting a month or more that clinically
appears like schizophrenia.
Tolerance, Dependence and Withdrawal Effects: Most
PCP users administer the drug intermittently, although daily use has
been reported and tolerance may develop. There is evidence of tolerance
to behavioral effects of PCP in animals. PCP can be addicting and use
can lead to psychological dependence, craving and drug seeking behavior.
There has been no demonstration of physical dependency in humans. Upon
abrupt discontinuation, physical distress, lack of energy, and depression
are reported. Long periods of use may lead to memory loss, difficulties
with speech and thinking, depression, and weight loss. These can last
up to a year after cessation of use.
Drug Interactions: Benzodiazepines can decrease
hypertensive effects and reverse seizure activity of PCP. Chlorpromazine
and PCP use can cause severe hypotension. PCP may enhance effects of
other CNS depressants like barbiturates and alcohol.
Performance Effects: Laboratory studies have
shown that PCP causes disorientation, drowsiness, dizziness, ataxia,
double or blurred vision, body image changes, disorganization of thoughts,
combativeness, impairment of eye-hand coordination, memory impairment,
paresthesia, slowed reaction time, distorted perceptions of space. Effects
generally occur within 1 hour post dose. Subjective sensation of intoxication
has been reported up to 8 hours and slowed reaction time up to 14 hours.
Effects on Driving: Fifty-six (56) subjects
were arrested for erratic driving and were evaluated by a drug recognition
examiner. All subjects were judged to be driving under the influence
of PCP, and blood PCP concentrations ranged from 12 to 188 ng/mL (mean
51 ng/mL). Similarly,blood PCP concentrations ranged
from 10 to 180 ng/mL (mean
73 ng/mL) in 50 subjects arrested for driving under the influence of
PCP.
DEC Category: Phencyclidine.
DEC Profile: Horizontal gaze nystagmus present;
vertical gaze nystagmus present; lack of convergence present; pupil
size normal; reaction to light normal; pulse rate elevated; blood pressure
elevated; body temperature elevated. Other characteristic indicators
may include rigid muscles, cyclic behavior, sudden turn to violence,
lack of response to painful stimuli, trance-like state or blank stare,
sweating, incomplete or delayed verbal responses.
Panel’s Assessment of Driving Risks: The
use of PCP is not compatible with skills required for safe driving.
Severe impairment of mental and physical abilities can occur following
single doses.
References and Recommended Reading:
Adams B, Moghaddam B. Corticolimbic dopamine neurotransmission is temporally
dissociated from the cognitive and locomotor effects of phencyclidine. J
Neurosc 1998;18(14):5545-54.
Bailey DN. Phencyclidine abuse. Clinical findings and concentrations
in biological fluids after nonfatal intoxication. Am J Clin Path 1979;72(5):795-9.
Barton CH, Sterling ML, Vaziri ND. Phencyclidine intoxication: Clinical
experience in 27 cases confirmed by urine assay. Ann Emerg Med 1981;10(5):243-6.
Baselt RC. Drug effects on psychomotor performance. Biomedical
Publications, Foster City, CA; pp 330-1; 2001.
Cho AK, Hiramatsu M, Pechnick RN, Di Stefano E. Pharmacokinetic and
pharmacodynamic evaluation of phencyclidine and its decadeutero variant. J
Pharmacol Exp Ther 1989;250(1):210-5.
Cook CE. Pyrolytic characteristics, pharmacokinetics, and bioavailability
of smoked heroin, cocaine, phencyclidine and methamphetamine. NIDA Res
Mon 115 (pp. 6-23);1991.
Cook CE, Brine DR, Jeffcoat AR, Hill JM, Wall ME, Perez-Reyes M, Di
Guiseppi SR. Phencyclidine disposition after intravenous and oral doses. Clin
Pharmac Ther 1982;31(5):625-34.
Ellison G, Keys A, Noguchi K. (1999) Long-term changes in brain following
continuous phencyclidine administration. An autoradiographic study using
flunitrazepam, ketanserin, mazindol, quinuclidinyl benzilate, piperidyl-3,4-3H(N)-TCP,
and AMPA receptor ligands. Pharm Tox 1999;84(1):9-17.
Gao X-M, Shirakawa O, Du F, Tamminga CA. Delayed regional metabolic
actions of phencyclidine. Eur J Pharmacol 1993;241(1):7-15.
Hess JM, Covi L, Kreiter NA. Cognitive functioning of PCP and cocaine
abusers seeking treatment. NIDA Res Mon 132;1993.
Kesner RP, Dakis M, Bolland BL. Phencyclidine disrupts long- but not
short-term memory within a spatial learning task. Psychopharmacology 1993;111(1):85-90.
Kunsman GW, Levine B, Costantino A, Smith ML. Phencyclidine blood concentrations
in DRE cases. J Anal Tox 1997;21(6):498-502.
Laurenzana EM, Owens SM. Metabolism of phencyclidine by human liver
microsomes. Drug Met Dispos 1997;25(5):557-63.
Malizia E, Borgo S, Andreucci G. Behavioral symptomatology indicative
of cannabinoids or phencyclidine intoxication in man. Riv Toss Sperim
Clin 1984;14(1-2):87-95.
McCarron MM, Schulze BW, Thompson GA. Acute phencyclidine intoxication:
Incidence of clinical findings in 1,000 cases. Ann Em Med 1981;10(5):237-42, & 10(6):290-7.
Nakamura GR, Noguchi TT. PCP: A drug of violence and death. J Pol
Sci Admin 1979;7(4):459-66.
Poklis A, Graham M, Maginn D, Branch CA, Ganter GE. Phencyclidine and
violent deaths in St. Louis, Missouri: A survey of medical examiner’s
cases from 1977 through 1986. Am J Drug Alc Abuse 1990;16(3-4):265-74.
Rappolt RT, Gay GR, Farris RD. Phencyclidine (PCP) intoxication: Diagnosis
in stages and algorithms of treatment. Clin Tox 1980;16(4):509-29.
Rawson RA, Tennant FS Jr., McCann MA. Characteristics of 68 chronic
phencyclidine abusers who sought treatment. Drug Alc Depend 1981;8(3):223-7.
Yago KB, Pitts FN Jr., Burgoyne RW. The urban epidemic of phencyclidine
(PCP) use: Clinical and laboratory evidence from a public psychiatric
hospital emergency service. J Clin Psych 1981;42(5):193-6.
|