CLIA Waived 12 Panel Drug Test Cup with Adulterants

Procedure & Results

This 12 Panel CLIA Waived Urine Drug Test Cup will Detect the Following Drugs:

• Cocaine - Cocaine derived from leaves of the coca plant, is a potent central nervous system stimulant and a local anesthetic. Among the psychological effects induced by using cocaine are euphoria, confidence and a sense of increased energy, accompanied by increased heart rate, dilation of the pupils, fever, tremors, and sweating. Cocaine is excreted in the urine primarily as benzoylecgonine in a short period of time.
• Marijuana (THC) - Cannabinoid is a hallucinogenic agent derived from the flowering portion of the hemp plant. The active ingredients in Cannabinoids, THC & Cannabinol can be metabolized and excreted as 11-nor- Δ9-tetrahydrocannabinol-9carboxylic acid with a half-life of 24 hours. It can be detected for 1 to 5 days after use. Smoking is the primary method of the use of Cannabinoids/cannabis. Higher doses used by abusers produce central nervous system effects, altered mood and sensory perceptions, loss of coordination, impaired short-term memory, anxiety, paranoia, depression, confusion, hallucinations, and increased heart rate. A tolerance to the cardiac and psychotropic effects can occur, and withdrawal syndrome produces restlessness, insomnia, anorexia, and nausea.
• Opiates 300 ng/ml - The opiates such as heroin, morphine, and codeine are derived from the resin of opium poppy. The principal metabolites of opiates are morphine, morphine-3-glucuronide normorphine, and codeine with a half-life of about 3 hours. Heroin is quickly metabolized to morphine. Thus, morphine and morphine glucuronide might both be found in the urine of a person who has taken only heroin. The body also changes codeine to morphine. Thus, the presence of morphine (or the metabolite, morphine glucuronide) in the urine indicates heroin, morphine and/or codeine use. The test for Morphine (MOP) of the Multi-Drug Urine Test Panel yields a positive result when the morphine in urine exceeds 300ng/mL.
• Amphetamines - Amphetamine and the structurally related “designer” drugs are sympathomimetic amines whose biological effects include potent central nervous system (CNS) stimulation, anorectic, hyperthermic, and cardiovascular properties. They are usually taken orally, intravenously, or by smoking. Amphetamines are readily absorbed from the gastrointestinal tract and are then either deactivated by the liver or excreted unchanged in the urine with a half-life of about 12 hours. It can be detected in the urine for 1 to 2 days after use. Amphetamine is metabolized to deaminated (hippuric and benzoic acids) and hydroxylated metabolites. Methamphetamine is partially metabolized to amphetamine and its major active metabolite. Amphetamines increase the heart rate and blood pressure and suppress the appetite. Some studies indicate that heavy abuse may result in permanent damage to certain essential nerve structural in the brain.
• Methamphetamine - Methamphetamine is a potent sympathomimetic agent with therapeutic applications. Acute higher doses lead to enhanced stimulation of the central nervous system and induce euphoria, alertness, and a sense of increased energy and power. More acute responses produce anxiety, paranoia, psychotic behavior, and cardiac dysrhythmias. The pattern of psychosis which may appear at half-life of about 15 hours and is excreted in urine as amphetamine and oxidized as deaminated and hydroxylated derivatives. However, 40% of methamphetamine is excreted unchanged. Thus the presence of the parent compound in the urine indicates methamphetamine use.
• Ecstasy (MDMA) - Methylenedioxymethamphetamine (ecstasy) is a designer drug first synthesized in 1914 by a German drug company for the treatment of obesity. Those who take the drug frequently report adverse effects, such as increased muscle tension and sweating. MDMA is not clearly a stimulant, although it has, in common with amphetamine drugs, a capacity to increase blood pressure and heart rate. MDMA does produce some perceptual changes in the form of increased sensitivity to light, difficulty in focusing, and blurred vision in some users. Its mechanism of action is thought to be via release of the neurotransmitter serotonin. MDMA may also release dopamine, although the general opinion is that this is a secondary effect of the drug (Nichols and Oberlender, 1990). The most pervasive effect of MDMA, occurring in virtually all people who took a reasonable dose of the drug, was to produce a clenching of the jaws.
• Oxycodone - Oxycodone is known as Oxycontin and Roxicodone. It is an ingredient of Percodan, Percocet, Roxicet, and Tylox. Oxycodone is a semi-synthetic opiate derived from opium. Like other opiates, Oxycodone is characterized by its analgesic properties, and the tendency for users to form a physical dependency and develop tolerance with extended use. Oxycodone is usually administered in combination with non-opiate analgesics such as acetaminophen and salicylates for the relief of moderate to severe pain. Oxycodone is a central nervous system depressant that may cause drowsiness, dizziness, lethargy, weakness, and confusion. Toxicity in an overdose of Oxycodone can lead to stupor, coma, muscle flaccidity, severe respiratory depression, hypotension, and cardiac arrest. Oxycodone is metabolized by N- and O-demethylation. One of the metabolites, oxymorphone, is a potent narcotic analgesic, while the other, nor oxycodone, is relatively inactive. Between 33 to 61% of a single dose of Oxycodone is excreted in a 24-hour urine collection and consists of 13-19% free Oxycodone, 7-29% glucuronide conjugated Oxycodone, 13-14% glucuronide conjugated oxymorphone and an unknown amount of nor oxycodone. The detection time window of Oxycodone is 1-3 days following use.
• Benzodiazepines - Benzodiazepines are medications that are frequently prescribed for the symptomatic treatment of anxiety and sleep disorders. They produce their effects via specific receptors involving a neurochemical called gamma-aminobutyric acid (GABA). Because they are safer and more effective, Benzodiazepines have replaced barbiturates in the treatment of both anxiety and insomnia. Benzodiazepines are also used as sedatives before some surgical and medical procedures, and for the treatment of seizure disorders and alcohol withdrawal.
• Barbiturates - Barbiturates are a class of central nervous system depressions. They have a wide range of half-life of 2 to 40 hours and can be detected in the urine for 1 to 4 days after use. Phenobarbital is a long-acting barbiturate derivative that has been used as a daytime sedative and very extensively as an anticonvulsant. Pentobarbital and secobarbital are two examples of a short-acting barbiturate sedative. Abuse of barbiturates can lead not only to impaired motor coordination and mental disorder but also to respiratory collapse, coma, and even death. Barbiturates are taken orally, rectally, or by intravenous and intramuscular injections. Short-acting barbiturates will generally be excreted in urine as metabolites, while the long-acting barbiturates will primarily appear unchanged.
• Methadone - Methadone is a synthetic analgesic drug that is originally used in the treatment of narcotic addicts. Among the psychological effects induced by using methadone are analgesia, sedation, and respiratory depression. Overdose of methadone may cause coma or even death. It is administered orally or intravenously and is metabolized in the liver and excreted in urine as methadone, EDDP, EMDA, and methanol. The kinneys are a major route of methadone excretion. Methadone has a biological half-life of 15 to 60 hours.
• Phencyclidine (PCP) - Phencyclidine is an arylcyclohexylamine that was originally used as an anesthetic agent and a veterinary tranquilzer. Phencyclidine can produce hallucinations, lethargy, disorientation, loss of coordination, trance-like ecstatic states, a sense of euphoria and visual distortions. It has many street names, such as “angel dust” and “crystal cyclone,” etc. phencyclidine can be administered orally, by nasal ingestion, smoking, or by intravenous injection. It is metabolized in the liver and excreted through the kidneys in urine in unchanged form and oxidized metabolites with a half life of about 12 hours. Suction and urinary acidification in the treatment of overdose typically reduces its half-life from three days to one day.
• Buprenorhine - Buprenorphine is a semi-synthetic opioid derived from thebaine, an alkaloid of the poppy Papaver somniferum. Buprenorphine is an opioid partial agonist. This means that, although Buprenorphine is an opioid, and thus can produce typical opioid effects and side effects such as euphoria and respiratory depression, its maximal effects are less than those of full agonists like heroin and methadone. At low doses Buprenorphine produces sufficient agonist effect to enable opioid-addicted individuals to discontinue the misuse of opioids without experiencing withdrawal symptoms. The agonist effects of Buprenorphine increase linearly with increasing doses of the drug until it reaches a plateau and no longer continues to increase with further increases in dosage. This is called the "ceiling effect." Thus, Buprenorphine carries a lower risk of abuse, addiction, and side effects compared to full opioid agonists. In fact, Buprenorphine can actually block the effects of full opioid agonists and can precipitate withdrawal symptoms if administered to an opioid-addicted individual while a full agonist is in the bloodstream. This is the result of the high affinity Buprenorphine has to the opioid receptors. The affinity refers to the strength of attraction and likelihood of a substance to bind with the opioid receptors.