Drugs of Abuse, Urine

ORDER CODE: DOA

ORDERING

SPECIMEN

PROCESSING

RESULTS

Test Code

SHC TEST CODE LPCH TEST CODE
LABDOA LAB3782

Specialty

Toxicology, Therapeutic Drug Monitoring

Clinical Utility

The amphetamines are known as the sympathomimetic amines as they mimic the effects of stimulation of the sympathetic nervous system. These small molecules, based on ß-phenylethylamine, structurally resemble the body's own catecholamines. A wide variety have been created via substitutions anywhere on the structure. The amphetamines are potent central nervous stimulants. As such they can increase wakefulness, physical activity, and decrease appetite. The amphetamines have some limited indications and approval for use in ADHD, narcolepsy, and obesity. However, because these CNS stimulants convey a sense of self-confidence, well being, and euphoria, they are highly addictive, widely abused, and consequently controlled substances.​ Abuse can lead to medical, psychological, and social consequences. Adverse health effects include memory loss, aggression, psychotic behavior, heart damage, malnutrition, and severe dental problems.​ Amphetamine may be self-administered either orally or by intravenous injection in amounts of up to 2000 mg daily by tolerant addicts. It is a metabolite of a number of other drugs including methamphetamine. Normally about 30 % is excreted unchanged in the 24 hour urine, but this may change to as much as 74 % in acid urine and may decrease to 1 % in alkaline urine.​ The barbiturates, a class of drugs derived from barbituric acid (malonylurea), are sedative hypnotics with central nervous system (CNS)‑depressant activity.As CNS‑depressants, the barbiturates are classified relative to their duration of action (ultra short‑, short‑, intermediate‑, and long‑acting). They have been used medically as sedatives to reduce emotional tension and induce sleep, and in certain types of epilepsy to reduce seizure frequency by raising the seizure threshold. Excessive dosages may cause impaired motor coordination (slurred speech, loss of balance), perceptual alterations (faulty judgment, inflated perceptions of performance), and disinhibition euphoria. Overdoses can result in stupor, coma, and death. The combined use of the barbiturates with alcohol, opiates, or other CNS‑depressants can result in fatal, additive respiratory depression. Although their utilities as sedative‑hypnotic drugs have largely been replaced by the benzodiazepines, the barbiturates still maintain an important role as anesthetic and anticonvulsant drugs. Oral administration is most common, although the barbiturates may be injected intravenously or intramuscularly. Following ingestion, they are rapidly absorbed from the stomach and enter the circulation. Their resulting distribution and concentration in various tissues is largely dependent on the lipid solubility and protein‑binding characteristics of the different barbiturates; fat deposits and protein‑rich tissues accumulate the highest concentration. Most of the barbiturates are metabolized by the liver via oxidation and conjugation, nitrogen‑dealkylation, nitrogen‑hydroxylation, and/or desulfuration of thiobarbiturates. The extent of liver metabolism is drug‑dependent; secobarbital, for example, is extensively oxidized to a series of pharmacologically inactive metabolites, while a relatively high percentage of phenobarbital and barbital are excreted unchanged in the urine. As a drug class, the barbiturates are excreted as active drug/metabolite mixes whose ratios and concentrations depend on the specific barbiturate in question. The benzodiazepines constitute a class of versatile and widely prescribed central nervous system (CNS) depressant drugs with medically useful anxiolytic, sedative, hypnotic, muscle relaxant, and anticonvulsant activities.​ The absorption rates, distribution, metabolism, and elimination rates differ significantly among the benzodiazepine derivatives. The quantitative differences in their potencies, pharmacodynamic spectra, and pharmacokinetic properties have led to various therapeutic applications. Clinical distinction of short acting versus long-acting benzodiazepines have been observed in their efficacy, side effect, withdrawal, and dependence potential.​ The extensive and efficacious therapeutic use of the benzodiazepines over the last several decades has inadvertently led to their misuse. Benzodiazepine overdoses are frequently associated with co-administration of drugs of other classes.​ Acute or chronic alcohol ingestion and benzodiazepines co-administered may lead to various significant toxicological interactions. Following ingestion, the benzodiazepines of the 1,4-substituted class (including the triazolobenzodiazepine derivatives) are absorbed, metabolized, and excreted in the urine at different rates as a variety of structurally related metabolites. Metabolite diversity reflects the different physiochemical properties and metabolic pathways of the individual drugs. Overall metabolic similarities include removal of substituents from the β ring of the 1,4-substituted benzodiazepines, α-hydroxylation of the triazolobenzodiazepines, demethylation, hydroxylation of the three-position carbon of the β ring, and conjugation of hydroxylated metabolites followed by urinary excretion predominantly as glucuronides.​ Cocaine, a natural product found in the leaves of the coca plant, is a potent central nervous system (CNS) stimulant and a local anesthetic. Its pharmacological effects are identical to those of the amphetamines (also CNS stimulants), though cocaine has a shorter duration of action. Cocaine induces euphoria, confidence and a sense of increased energy in the user; these psychological effects are accompanied by increased heart rate, dilation of pupils, fever, tremors, and sweating. The “crash” following a cocaine “high” is profound, ranging from irritability, lassitude, and the desire for more drug, to anxiety, hallucinations, and paranoia. Users may resort to other drugs at this time to relieve the depressive effects of the “crash”.Cocaine is traditionally administered intranasally or smoked in its purer, free-base form; oral ingestion is ineffective, as cocaine is broken down in the gastrointestinal tract. It is absorbed readily across the mucous membranes of the nose and lungs into the circulation. Its effects are intense but short-lived. Cocaine is rapidly inactivated by hydrolysis of its ester linkages. Blood cholinesterases hydrolyze cocaine to ecgonine methyl ester, while hydrolysis of the parent drug to benzoylecgonine is thought to be non-enzymatic; both of these metabolites may be further hydrolyzed to ecgonine. Unmetabolized cocaine has an affinity for fatty tissue and rapidly enters the brain; cocaine metabolites, however, are more water soluble and are readily excreted in the urine along with some portion of unchanged drug.The prominent benzoylecgonine metabolite is the primary urinary marker for detecting cocaine use.Tolerance has been observed with some chronic, high-dose users. Physical dependence does not appear to occur in abusers, although the development of strong psychological dependence is well known. Cessation of drug use may result in depression, hallucinations, and in extreme cases, psychosis. Methadone is a synthetic diphenylpropylamine used for detoxification and temporary maintenance of narcotic addiction, as well as treatment of acute and chronic pain. Methadone has many of the pharmacologic properties of morphine, and its analgesic potency is similar. Unlike morphine, repeated administration causes marked sedative effects due to drug accumulation in the body. Methadone withdrawal syndrome is qualitatively similar to morphine, yet it differs in that it develops more slowly, is less intense, and is more prolonged.For these reasons, methadone is used in the management of narcotic dependence, hopefully eliminating the need for illicit opiate drugs. Overdoses of methadone are characterized by stupor, respiratory depression, cold and clammy skin, hypotension, coma, and circulatory collapse.Methadone is given intramuscularly for analgesic purposes and orally for methadone maintenance therapy. Following ingestion, the drug is well absorbed from the gastrointestinal tract and is widely distributed to the liver, lung, kidney, spleen, blood, and urine. The fact that methadone is highly bound to tissue protein may explain its cumulative effects.Methadone is metabolized largely by mono- and di-N-demethylation. Spontaneous cyclization of the resulting unstable compounds forms the major metabolites, 2-ethylidene-1,5-dimethyl-3,3-diphenylpyrrolidine (EDDP) and 2-ethyl-5-methyl-3,3-diphenylpyrroline (EMDP). Both are hydrolyzed to some extent, with subsequent glucuronidation.In maintenance patients, excretion of unchanged methadone can account for 5-50 % of the dose. Urinary pH affects the percentage of unchanged drug excreted, as does urinary volume, dose, and individual metabolism. Morphine, a natural product of the opium poppy, is a narcotic analgesic used for centuries as a medicine for the relief of severe pain. Extracted from opium obtained from the poppy’s resin, morphine may, in turn, be further chemically refined to heroin (the more potent, diacetylated analog of the parent drug). These chemically similar “opiates” reduce sensitivity to physical and psychological stimuli, dulling pain, fear and anxiety. Users are usually lethargic and indifferent. Accompanying effects may include constriction of the pupils, itching, constipation, nausea, vomiting, and respiratory depression. Death by overdose, usually resulting from dose miscalculation or dose-strength variability, is caused by respiratory failure.The opiates are usually administered intravenously or subcutaneously, but may also be smoked or sniffed. Upon entering the circulation, they tend to concentrate in the lungs, spleen, kidneys, and liver; lower concentrations are found in the body’s musculature and central nervous system. A variety of pathways are involved in the body’s detoxification of the opiates, including the removal of chemical side groups (dealkylation), addition of hydroxyl groups, hydrolytic breakdown, and conjugation to glucuronic acid (a common body sugar).Morphine is excreted in the urine as morphine-3-glucuronide, unchanged free morphine, and other minor metabolites. Although some opiate metabolites appear in the bile and feces, urinary excretion is the primary route of elimination.The opiates produce strong physical dependence; withdrawal symptoms can begin to appear within a few hours of the last dose and may continue for 5-10 days. The addict may pursue continued opiate use as much to avoid the discomfort of withdrawal as to achieve the desired insensate euphoria. Oxycodone is a semi‑synthetic opioid prescribed for pain management in patients with moderate to severe pain. It is similar to codeine and morphine in its analgesic properties but it is more potent than morphine and has higher dependence potential. The drug oxycodone is supplied as OxyContin (Oxycodone HCl) or in combination with aspirin (Percodan) or acetaminophen (Percocet).Drug abusers crush the pills into powder and snort them for faster effect which may result in a potentially fatal outcome. According to Drug Abuse Warning Network (DAWN), there has been a dramatic increase in oxycodone related deaths. Oxymorphone, noroxycodone and noroxymorphone are the only known metabolites of oxycodone. The metabolite, oxymorphone, is a potent narcotic analgesic, while the other two metabolites are relatively inactive. From 33‑61 % of a single dose of oxycodone is excreted in urine within 24 hours as unconjugated oxycodone (13‑19 %), conjugated oxycodone (7‑29 %), and conjugated oxymorphone (13‑14 %). Phencyclidine (PCP) is an arylcyclohexylamine with potent analgesic and anesthetic properties.Originally developed as an intravenous anesthetic, the occurrence of emergence psychosis side effects negated its potential clinical utility. PCP was never approved for human use because of the post-anesthetic confusion and delirium that arose during clinical studies. Illegally sold on the street, PCP is known by various names such as “angel dust”; whereas, names such as “supergrass” refer to PCP combined with marijuana. PCP possesses hallucinogenic, central nervous system (CNS)-stimulant, and CNS-depressant properties, the expression of which is dose- and species-dependent. PCP and its structural analog, ketamine, are NMDA (N-methyl-D-aspartate) receptor antagonists.Known as dissociative anesthetics, they produce mind-altering feelings of dissociation from the environment and self. Dextromethorphan, a cough suppressant, can produce similar effects when taken in high doses.The water-soluble powder of PCP can be ingested, snorted, injected intravenously, or smoked. Typical street doses (1-10 mg) can cause tachycardia, hypertension, hallucinations, stupor, lethargy, sensory isolation, and loss of coordination. Excitation and agitation may also occur, leading to unpredictably violent behavior not usually encountered with other hallucinogens. Repeated use of PCP can result in addiction and higher doses can cause symptoms that mimic schizophrenia and can culminate in convulsions and prolonged or fatal coma. PCP is metabolized via ring-hydroxylation and oxidation by the cytochrome P450 enzymes. An amino acid metabolite of PCP exists in human urine in significant quantities.Significant variations in the PCP elimination half-life have been found in humans; however, phase II metabolism of PCP sulfation and glucuronidation could also contribute to the variation in PCP half-life. The principal psychoactive component of the hemp plant, Cannabis sativa, is generally accepted to be delta-9 tetrahydrocannabinol (delta-9 THC), although other cannabinoids may contribute to the psychological and physiological actions of marijuana. The acute effects of marijuana use, concomitant with the desired “high”, are memory impairment, time confusion, interference with learning, impaired motor skills and depersonalization. These effects are also manifested in chronic users in addition to cardiovascular, pulmonary, and reproductive effects. Marijuana is usually smoked, but may be ingested, either incorporated into food or as a liquid extract (tea). It is rapidly absorbed from the lungs into the blood with rapid onset of effects; the onset is slower but prolonged when ingested. The natural cannabinoids and their metabolic products are fat soluble and are stored in the body’s fatty tissues, including brain tissue, for prolonged periods after use. Cannabinoid metabolites are found in blood, bile, feces, and urine and may be detected in urine within hours of exposure. Because of their fat solubility, they also remain in the body’s fatty tissues with slow release and subsequent urinary excretion for days, weeks, and even months after the last exposure, depending on the intensity and frequency of use. The prominent delta-9 THC metabolite, 11-nor-delta-9 THC-9-carboxylic acid (delta-9 COOH-THC), is the primary urinary marker for detecting marijuana use. References: 1. Elecsys Acetamenophines Package Insert, V 9.0, Roche Diagnostics, 2015 2. Elecsys Barbituates Package Insert, V 10.0, Roche Diagnostics, 2013 3. Elecsys Benzodiazepines Package Insert, V 10.0, Roche Diagnostics, 2016 4. Elecsys Phencyclidine Package Insert, V 11.0, Roche Diagnostics, 2014 5. Elecsys Cocaine Package Insert, V 7.0, Roche Diagnostics, 2014 6. Elecsys Methadone Package Insert, V 9.0, Roche Diagnostics, 2014 7. Elecsys Opiates Package Insert, V 11.0, Roche Diagnostics, 2017 8. Elecsys Oxycodone Package Insert, V 7.0, Roche Diagnostics, 2014 9. Elecsys Cannabinoids Package Insert, V 9.0, Roche Diagnostics, 2014

CPT Code

80306, 80358

LOINC Code

19261-7, 19270-8, 14316-4, 14314-9, 19550-3, 19644-4, 14310-7
Preferred Specimen Type
Urine, Random
Container Type
Sterile Container
Container Image 1

Volume

REQUESTED VOLUME MINIMUM VOLUME(PEDIATRIC)
10 mL 1 mL

Specimen Stability

Special Handling
Refrigerate. Specimens are stable for 5 days at 2 to 8°C.

Department

Chemistry

Standard Run Time(s)

24 hours/7 days a week

Turnaround Time

ROUTINE STAT
1 hour 1 hour

Methodology

Kinetic Interaction of Microparticles in Solution (KIMS)

Components

COMPONENT
Amphetamine
Barbiturates
Benzodiazepines
Cocaine Metabolites
Methadone
Opiates
Oxycodone
PCP
Tricyclics
THC

Test Code

SHC TEST CODE LPCH TEST CODE
LABDOA LAB3782

Specialty

Toxicology, Therapeutic Drug Monitoring

Clinical Utility

The amphetamines are known as the sympathomimetic amines as they mimic the effects of stimulation of the sympathetic nervous system. These small molecules, based on ß-phenylethylamine, structurally resemble the body's own catecholamines. A wide variety have been created via substitutions anywhere on the structure. The amphetamines are potent central nervous stimulants. As such they can increase wakefulness, physical activity, and decrease appetite. The amphetamines have some limited indications and approval for use in ADHD, narcolepsy, and obesity. However, because these CNS stimulants convey a sense of self-confidence, well being, and euphoria, they are highly addictive, widely abused, and consequently controlled substances.​ Abuse can lead to medical, psychological, and social consequences. Adverse health effects include memory loss, aggression, psychotic behavior, heart damage, malnutrition, and severe dental problems.​ Amphetamine may be self-administered either orally or by intravenous injection in amounts of up to 2000 mg daily by tolerant addicts. It is a metabolite of a number of other drugs including methamphetamine. Normally about 30 % is excreted unchanged in the 24 hour urine, but this may change to as much as 74 % in acid urine and may decrease to 1 % in alkaline urine.​ The barbiturates, a class of drugs derived from barbituric acid (malonylurea), are sedative hypnotics with central nervous system (CNS)‑depressant activity.As CNS‑depressants, the barbiturates are classified relative to their duration of action (ultra short‑, short‑, intermediate‑, and long‑acting). They have been used medically as sedatives to reduce emotional tension and induce sleep, and in certain types of epilepsy to reduce seizure frequency by raising the seizure threshold. Excessive dosages may cause impaired motor coordination (slurred speech, loss of balance), perceptual alterations (faulty judgment, inflated perceptions of performance), and disinhibition euphoria. Overdoses can result in stupor, coma, and death. The combined use of the barbiturates with alcohol, opiates, or other CNS‑depressants can result in fatal, additive respiratory depression. Although their utilities as sedative‑hypnotic drugs have largely been replaced by the benzodiazepines, the barbiturates still maintain an important role as anesthetic and anticonvulsant drugs. Oral administration is most common, although the barbiturates may be injected intravenously or intramuscularly. Following ingestion, they are rapidly absorbed from the stomach and enter the circulation. Their resulting distribution and concentration in various tissues is largely dependent on the lipid solubility and protein‑binding characteristics of the different barbiturates; fat deposits and protein‑rich tissues accumulate the highest concentration. Most of the barbiturates are metabolized by the liver via oxidation and conjugation, nitrogen‑dealkylation, nitrogen‑hydroxylation, and/or desulfuration of thiobarbiturates. The extent of liver metabolism is drug‑dependent; secobarbital, for example, is extensively oxidized to a series of pharmacologically inactive metabolites, while a relatively high percentage of phenobarbital and barbital are excreted unchanged in the urine. As a drug class, the barbiturates are excreted as active drug/metabolite mixes whose ratios and concentrations depend on the specific barbiturate in question. The benzodiazepines constitute a class of versatile and widely prescribed central nervous system (CNS) depressant drugs with medically useful anxiolytic, sedative, hypnotic, muscle relaxant, and anticonvulsant activities.​ The absorption rates, distribution, metabolism, and elimination rates differ significantly among the benzodiazepine derivatives. The quantitative differences in their potencies, pharmacodynamic spectra, and pharmacokinetic properties have led to various therapeutic applications. Clinical distinction of short acting versus long-acting benzodiazepines have been observed in their efficacy, side effect, withdrawal, and dependence potential.​ The extensive and efficacious therapeutic use of the benzodiazepines over the last several decades has inadvertently led to their misuse. Benzodiazepine overdoses are frequently associated with co-administration of drugs of other classes.​ Acute or chronic alcohol ingestion and benzodiazepines co-administered may lead to various significant toxicological interactions. Following ingestion, the benzodiazepines of the 1,4-substituted class (including the triazolobenzodiazepine derivatives) are absorbed, metabolized, and excreted in the urine at different rates as a variety of structurally related metabolites. Metabolite diversity reflects the different physiochemical properties and metabolic pathways of the individual drugs. Overall metabolic similarities include removal of substituents from the β ring of the 1,4-substituted benzodiazepines, α-hydroxylation of the triazolobenzodiazepines, demethylation, hydroxylation of the three-position carbon of the β ring, and conjugation of hydroxylated metabolites followed by urinary excretion predominantly as glucuronides.​ Cocaine, a natural product found in the leaves of the coca plant, is a potent central nervous system (CNS) stimulant and a local anesthetic. Its pharmacological effects are identical to those of the amphetamines (also CNS stimulants), though cocaine has a shorter duration of action. Cocaine induces euphoria, confidence and a sense of increased energy in the user; these psychological effects are accompanied by increased heart rate, dilation of pupils, fever, tremors, and sweating. The “crash” following a cocaine “high” is profound, ranging from irritability, lassitude, and the desire for more drug, to anxiety, hallucinations, and paranoia. Users may resort to other drugs at this time to relieve the depressive effects of the “crash”.Cocaine is traditionally administered intranasally or smoked in its purer, free-base form; oral ingestion is ineffective, as cocaine is broken down in the gastrointestinal tract. It is absorbed readily across the mucous membranes of the nose and lungs into the circulation. Its effects are intense but short-lived. Cocaine is rapidly inactivated by hydrolysis of its ester linkages. Blood cholinesterases hydrolyze cocaine to ecgonine methyl ester, while hydrolysis of the parent drug to benzoylecgonine is thought to be non-enzymatic; both of these metabolites may be further hydrolyzed to ecgonine. Unmetabolized cocaine has an affinity for fatty tissue and rapidly enters the brain; cocaine metabolites, however, are more water soluble and are readily excreted in the urine along with some portion of unchanged drug.The prominent benzoylecgonine metabolite is the primary urinary marker for detecting cocaine use.Tolerance has been observed with some chronic, high-dose users. Physical dependence does not appear to occur in abusers, although the development of strong psychological dependence is well known. Cessation of drug use may result in depression, hallucinations, and in extreme cases, psychosis. Methadone is a synthetic diphenylpropylamine used for detoxification and temporary maintenance of narcotic addiction, as well as treatment of acute and chronic pain. Methadone has many of the pharmacologic properties of morphine, and its analgesic potency is similar. Unlike morphine, repeated administration causes marked sedative effects due to drug accumulation in the body. Methadone withdrawal syndrome is qualitatively similar to morphine, yet it differs in that it develops more slowly, is less intense, and is more prolonged.For these reasons, methadone is used in the management of narcotic dependence, hopefully eliminating the need for illicit opiate drugs. Overdoses of methadone are characterized by stupor, respiratory depression, cold and clammy skin, hypotension, coma, and circulatory collapse.Methadone is given intramuscularly for analgesic purposes and orally for methadone maintenance therapy. Following ingestion, the drug is well absorbed from the gastrointestinal tract and is widely distributed to the liver, lung, kidney, spleen, blood, and urine. The fact that methadone is highly bound to tissue protein may explain its cumulative effects.Methadone is metabolized largely by mono- and di-N-demethylation. Spontaneous cyclization of the resulting unstable compounds forms the major metabolites, 2-ethylidene-1,5-dimethyl-3,3-diphenylpyrrolidine (EDDP) and 2-ethyl-5-methyl-3,3-diphenylpyrroline (EMDP). Both are hydrolyzed to some extent, with subsequent glucuronidation.In maintenance patients, excretion of unchanged methadone can account for 5-50 % of the dose. Urinary pH affects the percentage of unchanged drug excreted, as does urinary volume, dose, and individual metabolism. Morphine, a natural product of the opium poppy, is a narcotic analgesic used for centuries as a medicine for the relief of severe pain. Extracted from opium obtained from the poppy’s resin, morphine may, in turn, be further chemically refined to heroin (the more potent, diacetylated analog of the parent drug). These chemically similar “opiates” reduce sensitivity to physical and psychological stimuli, dulling pain, fear and anxiety. Users are usually lethargic and indifferent. Accompanying effects may include constriction of the pupils, itching, constipation, nausea, vomiting, and respiratory depression. Death by overdose, usually resulting from dose miscalculation or dose-strength variability, is caused by respiratory failure.The opiates are usually administered intravenously or subcutaneously, but may also be smoked or sniffed. Upon entering the circulation, they tend to concentrate in the lungs, spleen, kidneys, and liver; lower concentrations are found in the body’s musculature and central nervous system. A variety of pathways are involved in the body’s detoxification of the opiates, including the removal of chemical side groups (dealkylation), addition of hydroxyl groups, hydrolytic breakdown, and conjugation to glucuronic acid (a common body sugar).Morphine is excreted in the urine as morphine-3-glucuronide, unchanged free morphine, and other minor metabolites. Although some opiate metabolites appear in the bile and feces, urinary excretion is the primary route of elimination.The opiates produce strong physical dependence; withdrawal symptoms can begin to appear within a few hours of the last dose and may continue for 5-10 days. The addict may pursue continued opiate use as much to avoid the discomfort of withdrawal as to achieve the desired insensate euphoria. Oxycodone is a semi‑synthetic opioid prescribed for pain management in patients with moderate to severe pain. It is similar to codeine and morphine in its analgesic properties but it is more potent than morphine and has higher dependence potential. The drug oxycodone is supplied as OxyContin (Oxycodone HCl) or in combination with aspirin (Percodan) or acetaminophen (Percocet).Drug abusers crush the pills into powder and snort them for faster effect which may result in a potentially fatal outcome. According to Drug Abuse Warning Network (DAWN), there has been a dramatic increase in oxycodone related deaths. Oxymorphone, noroxycodone and noroxymorphone are the only known metabolites of oxycodone. The metabolite, oxymorphone, is a potent narcotic analgesic, while the other two metabolites are relatively inactive. From 33‑61 % of a single dose of oxycodone is excreted in urine within 24 hours as unconjugated oxycodone (13‑19 %), conjugated oxycodone (7‑29 %), and conjugated oxymorphone (13‑14 %). Phencyclidine (PCP) is an arylcyclohexylamine with potent analgesic and anesthetic properties.Originally developed as an intravenous anesthetic, the occurrence of emergence psychosis side effects negated its potential clinical utility. PCP was never approved for human use because of the post-anesthetic confusion and delirium that arose during clinical studies. Illegally sold on the street, PCP is known by various names such as “angel dust”; whereas, names such as “supergrass” refer to PCP combined with marijuana. PCP possesses hallucinogenic, central nervous system (CNS)-stimulant, and CNS-depressant properties, the expression of which is dose- and species-dependent. PCP and its structural analog, ketamine, are NMDA (N-methyl-D-aspartate) receptor antagonists.Known as dissociative anesthetics, they produce mind-altering feelings of dissociation from the environment and self. Dextromethorphan, a cough suppressant, can produce similar effects when taken in high doses.The water-soluble powder of PCP can be ingested, snorted, injected intravenously, or smoked. Typical street doses (1-10 mg) can cause tachycardia, hypertension, hallucinations, stupor, lethargy, sensory isolation, and loss of coordination. Excitation and agitation may also occur, leading to unpredictably violent behavior not usually encountered with other hallucinogens. Repeated use of PCP can result in addiction and higher doses can cause symptoms that mimic schizophrenia and can culminate in convulsions and prolonged or fatal coma. PCP is metabolized via ring-hydroxylation and oxidation by the cytochrome P450 enzymes. An amino acid metabolite of PCP exists in human urine in significant quantities.Significant variations in the PCP elimination half-life have been found in humans; however, phase II metabolism of PCP sulfation and glucuronidation could also contribute to the variation in PCP half-life. The principal psychoactive component of the hemp plant, Cannabis sativa, is generally accepted to be delta-9 tetrahydrocannabinol (delta-9 THC), although other cannabinoids may contribute to the psychological and physiological actions of marijuana. The acute effects of marijuana use, concomitant with the desired “high”, are memory impairment, time confusion, interference with learning, impaired motor skills and depersonalization. These effects are also manifested in chronic users in addition to cardiovascular, pulmonary, and reproductive effects. Marijuana is usually smoked, but may be ingested, either incorporated into food or as a liquid extract (tea). It is rapidly absorbed from the lungs into the blood with rapid onset of effects; the onset is slower but prolonged when ingested. The natural cannabinoids and their metabolic products are fat soluble and are stored in the body’s fatty tissues, including brain tissue, for prolonged periods after use. Cannabinoid metabolites are found in blood, bile, feces, and urine and may be detected in urine within hours of exposure. Because of their fat solubility, they also remain in the body’s fatty tissues with slow release and subsequent urinary excretion for days, weeks, and even months after the last exposure, depending on the intensity and frequency of use. The prominent delta-9 THC metabolite, 11-nor-delta-9 THC-9-carboxylic acid (delta-9 COOH-THC), is the primary urinary marker for detecting marijuana use. References: 1. Elecsys Acetamenophines Package Insert, V 9.0, Roche Diagnostics, 2015 2. Elecsys Barbituates Package Insert, V 10.0, Roche Diagnostics, 2013 3. Elecsys Benzodiazepines Package Insert, V 10.0, Roche Diagnostics, 2016 4. Elecsys Phencyclidine Package Insert, V 11.0, Roche Diagnostics, 2014 5. Elecsys Cocaine Package Insert, V 7.0, Roche Diagnostics, 2014 6. Elecsys Methadone Package Insert, V 9.0, Roche Diagnostics, 2014 7. Elecsys Opiates Package Insert, V 11.0, Roche Diagnostics, 2017 8. Elecsys Oxycodone Package Insert, V 7.0, Roche Diagnostics, 2014 9. Elecsys Cannabinoids Package Insert, V 9.0, Roche Diagnostics, 2014

CPT Code

80306, 80358

LOINC Code

19261-7, 19270-8, 14316-4, 14314-9, 19550-3, 19644-4, 14310-7

close ORDERING
Preferred Specimen Type
Urine, Random
Container Type
Sterile Container
Container Image 1

Volume

REQUESTED VOLUME MINIMUM VOLUME(PEDIATRIC)
10 mL 1 mL

Specimen Stability

Special Handling
Refrigerate. Specimens are stable for 5 days at 2 to 8°C.

close SPECIMEN

Department

Chemistry

Standard Run Time(s)

24 hours/7 days a week

Turnaround Time

ROUTINE STAT
1 hour 1 hour

close PROCESSING

Methodology

Kinetic Interaction of Microparticles in Solution (KIMS)

Components

COMPONENT
Amphetamine
Barbiturates
Benzodiazepines
Cocaine Metabolites
Methadone
Opiates
Oxycodone
PCP
Tricyclics
THC

close RESULTS