drug info...

Amphetamine and methamphetamine are Schedule II drugs included in a group of chemicals called sympathomimetic amines, which contain a phenethylamine chemical nucleus. Sympathomimetic amines mimic the effects of the endogenous neurotransmitters such as epinephrine (adrenaline), norepi-nephrine (noradrenaline) and dopamine. Also included in this group are various over-the-counter drugs such as phenylpropanolamine, pseudoephedrine, ephedrine as well as the Schedule I drug methylenedioxymethamphetamine (MDMA or Ecstasy). The amphetamines are powerful central nervous system stimulants and can be taken orally, intravenously, snorted or smoked. Methamphetamine is one of the most commonly abused drugs in the Western United States. It is readily synthesized, with ephedrine being used as the primary precursor.

Amphetamines are rapidly absorbed from the gastrointestinal tract and are either deactivated by the liver or excreted unchanged into the urine. Methamphetamine is excreted primarily unchanged (44%) and some of the drug (6%) is metabolized and excreted as amphetamine. Amphetamine is also excreted largely unchanged (30%) with 20-25% being metabolized to deaminated (hippuric and benzoic acids) and hydroxylated metabolites. The elimination rate of amphetamines varies with the pH of the urine, as at low pH the excretion of unchanged drug increases, while at high pH the excretion of unchanged drug decreases. Within a few hours after any type of administration, amphetamines appear in the urine and can typically be detected for up to 72-96 hours.

Amphetamines, particularly methamphetamine, are among the most popular drugs of abuse. Common street names include speed, crank, crystal, meth, and ice. Ice and crystal meth are crystals of methamphetamine HCL. Snot and glue are oils formed from methamphetamine free base and baking soda. Methamphetamine is frequently smoked in a glass pipe as it is easily volatilized into a gas that is inhaled. Although the ice form is primarily found in Hawaii, it has gained the most notoriety mainly due to the fact that it is 98-100% pure methamphetamine HCL and its effects are rapid, intense, and of longer duration than other forms of metham-phetamine. The signs and symptoms associated with the abuse of methamphet-amine depend upon the amount used and the duration of use. With infrequent or low dose use, a person may experience euphoria, lowered anxiety, talkativeness, decreased appetite, increased sexual arousal, increased alertness, and decreased fatigue. Physiologically there can be increased heart rate and blood pressure. With increased dose or prolonged abuse (either binge or chronic), an individual may experience a set of secondary effects that can include increased anxiety, irritabil-ity, aggressiveness, paranoia and hypersexuality. Physiological effects can include dilated pupils, dry mouth, hippus, increased body temperature and tachycardia. In overdose situations, a person may experience hallucinations, coma or death. Crash symptoms typically follow binge abuse of methamphetamine. This phase is marked by extreme fatigue, depression, mental exhaustion and prolonged periods of sleep.

Barbiturates are a class of drugs capable of producing CNS depression and depending upon the drug and dosage may produce varying states of sedation or hypnosis and are thus classi?ed as sedative/hypnotics. They are further categorized according to the duration of their effects ranging from ultra-short acting, short acting, intermediate acting, and long acting. Duration of effects lasts anywhere from 15 minutes for the ultra-short acting barbiturates to a day or more for the long acting drugs. Short and intermediate acting barbiturates include amobarbital, butalbital, pentobarbital, and secobarbital, while the long acting barbiturates include phenobarbital. Other common therapeutic indications for use are as anticonvulsants and for migraine headaches.

Barbiturates are distributed throughout the body with highest concentrations oc-curring in the brain, liver and kidneys. In general, duration of action is dependent upon lipid solubility and extent of protein binding with the short acting barbiturates showing the most lipid solubility and percentage of protein binding. The short and intermediate acting barbiturates are nearly entirely metabolized by the liver and excreted in the urine, while 25-50% of a dose of a long acting barbiturate is excreted as unchanged drug. The half-life is variable with short acting barbiturates being detectable in urine for 24 hours and the long acting drugs detectable for 2-3 weeks following ingestion.

The most common detected barbiturates are butalbital and phenobarbital. Butalbital is routinely prescribed for migraine and muscle relaxation while phenobarbital is primarily prescribed for seizure disorders. Trade and street names of some common barbiturates are: Amobarbital-Amytal-Yellow Jackets; Butalbital-Fiorinal-Blue Devils; Secobarbital-Seconal-Reds; Phenobarbital-Luminal-Downers, Goofballs. Chronic abuse leads to tolerance, and abrupt discontinuance of use can induce a life-threatening withdrawal syndrome that can result in seizures.

The benzodiazepines are a class of drugs primarily classi?ed as antianxiety, sedatives, or hypnotics. All contain a benzene ring fused to a 7-membered diazepine ring, hence the term benzo-diazepine. Various modi?cations and substitutions of the ring structure yield compounds of similar activities. The clinical effects of these drugs result from actions on the central nervous system and these effects include sedation, hypnosis, muscle relaxation, and anticonvulsant activity.

The benzodiazepines are well absorbed after oral administration and are rapidly distributed throughout the body. They are extensively metabolized by the liver, and in general, slowly excreted in the urine as pharmacologically inactive conjugated metabolites. Some metabolites may possess some pharmacological activity of their own, thus displaying the “next day” effects of some benzodiazepines. Oxazepam is a common urinary metabolite of several benzodiazepines such as diazepam and temazepam. Duration of detectability in urine is varied. Ingestion of therapeutic dosages may be detectable for 1-3 days while extended usage over a period of months or years can extend excretion times up to 4-6 weeks after cessation of use.

The benzodiazepines are considered one of the most widely prescribed drugs in the United States, thus leading to its widespread abuse. Diazepam (Valium®) and alprazolam (Xanax®) are two of the most widely abused of the benzodia-zepines. Many abusers will attempt to accentuate the effects of benzodiazepines by the concomitant use of alcohol or other CNS depressant drugs. As a result, benzodiazepines are involved in approximately one third of all drug self induced poisonings. Other commonly abused benzodiazepines are chlordiazepoxide, ?urazepam, clonazepam, and lorazepam. Prolonged high doses of benzodia-zepines can cause dependency and a withdrawal syndrome may occur following abrupt cessation of use.

Cocaine (benzoylmethylecgonine) is a cen-tral nervous system stimulant derived from the leaves of the coca plant. Cocaine has two major pharmacological actions; one is a local anesthetic, and the other is an indirect acting sympathomimetic having many of the properties of an amphet-amine. The drug is either in the salt/ powder form (cocaine HCL) which can be administered by snorting, or intravenous injection or in the free base “crack” form which is smoked.

After smoking, cocaine is rapidly absorbed with peak plasma concentrations occurring at about 5 minutes, versus 30-40 minutes following intranasal ingestion. Cocaine is extensively metabolized by the liver and blood enzymes with approxi-mately one percent of the dose excreted in the urine unchanged. The major metabolite found in the urine is benzoylecgonine (25-40% of the dose), followed by ecgonine methyl ester (18-22%). Depending upon the dosage ingested, frequency of use, and metabolic variation, benzoylecgonine can remain detectable in the urine for as long as 48-96 hours post ingestion.

Cocaine produces a short-lived, intense high which is extremely addictive. The signs and symptoms associated with the abuse of cocaine depend upon the amount used and the duration of use. With infrequent or low dose use a person may experience euphoria, lowered anxiety, talkativeness, decreased appetite, increased sexual arousal, increased alertness, and decreased fatigue. Physiologically there can be increased heart rate and blood pressure. With increased dose or prolonged abuse (either binge or chronic) an individual may experience a set of secondary effects that can include increased anxiety, irritability, aggressiveness, paranoia and hypersexuality. Physiological effects can include dilated pupils, dry mouth, hippus, increased body temperature and tachycardia. In overdose situations, a person my experience hallucinations, coma or death. Crash symptoms typically follow binge abuse of cocaine. This phase is marked by extreme fatigue, depression, mental exhaustion and prolonged periods of sleep.

Marijuana is a preparation derived from the leaves and ?owering tops of cannabis plants (Cannabis sativa) that is capable of producing psychoactive effects when ingested. One of the primary classes of compounds found in marijuana is called cannabinoids. There are up to 60 can-nabinoids in marijuana with delta-9-tetra-hydrocannabinol (THC) being the primary psychoactive constituent.

When marijuana is smoked, THC is rapidly absorbed through the lungs and enters the bloodstream in minutes. Following oral ingestion, THC does not reach the blood-stream for approximately 1.5-3 hours. Once in the blood, THC is bound to blood proteins and carried throughout the body where it is either absorbed into body tissues (including the brain, heart, and fat) or transformed by the liver into the water soluble metabolites 11-hydroxy-THC and carboxy-THC. These water soluble metabo-lites, are readily excreted into the urine, with the inactive metabolite carboxy-THC being the predominant metabolite detected. Initially, THC is quickly absorbed into the body tissues and then is slowly released back into the blood stream where it is carried to the liver and metabolized. Because THC tends to be stored in fatty tissues, it accumulates faster than it can be eliminated in chronic repetitive smokers. This leads to extended retention of THC which is then eliminated from the body at a relatively constant rate with the elimination half-life being estimated at 18-30 hours. Urinary concentrations of THC are very dif?cult to interpret due to variables such as dosage of THC ingested, frequency of use, timing of urine collection relative to last exposure to marijuana, rate of release of stored cannabinoids in adipose tissue, and an individual’s hydration state. Therefore, the detection of THC metabolites in the urine is only an indication of past marijuana use and is not related to the degree of intoxication or impairment.

The psychological effects of THC include an increased sense of well being or euphoria, relaxation, slowed psycho-motor response, an altered sense of time, short term memory impairment and impairment of multi-tasking performance.

Methadone is a narcotic analgesic which is approximately equipotent to that of mor-phine. Methadone has been utilized to treat opioid dependency and prescribed as a heroin substitute in methadone maintenance programs since the 1960’s Typically, daily oral dosing with doses up to 180 mg/day, is prescribed with ef?ccy measured by the absence of withdrawl symptons. Dosing is then gradually decreased until opiate dependancy is eliminated.

Methadone is metabolized primarily to two pharmacologically inactive metabolites, EDDP and EMDP. Monitoring for the presence of EDDP (methadone metabolite) is a means to determine compliance to methadone treatment. The elimination half-life of methadone is approximately 15-55 hours with about 5-50% of a dose eliminated as methadone and 3-25% as EDDP. Large indivitual variations in elimination do occur due to urine pH, urine volume, dose, rate of metabolism, drug interation, etc.

The term “opioid” refers to all drugs, natural or synthetic, with morphine-like properties. Both morphine and codeine are naturally occurring alkaloids derived from the seed pod of the opium poppy. Semi-synthetic opiates include heroin, a diacetyl derivative of morphine; hydro-morphone, hydrocodone, and oxycodone derived by a simple modi?cation of the morphine molecule. Synthetic opiates such as methadone and meperidine, mimic opiate effects but are not prepared from the poppy. The drugs may be administered by snorting, subcutaneous or intravenous injection, or smoking. Opioid compounds have analgesic and antitussive properties.

Morphine is rapidly absorbed. Plasma peak levels following an oral dose occur after 15-60 minutes, and following IV injection occur after 15 minutes. Extensively metabolized by the liver, only 2-12% is excreted as unchanged drug, while 60-80% is excreted as morphine-3-glucuronide. The half-life of morphine is 1.7-4.5 hours. Heroin is rapidly metabolized (plasma half-life is 3 minutes), ?rst to 6-monoacetyl-morphine (6-MAM) and further to morphine. The urinary excretion pro?le is similar to morphine, in that 7% is excreted as unchanged morphine and 50-60% as gluc-uronides. Trace amounts of 6-MAM, a speci?c metabolite of heroin, is also excreted for approximately 6-8 hours following heroin use. Following an oral dose, codeine is also rapidly absorbed and metabolized, principally to codeine-6-glucuronide, with 10-15% metabolized to morphine and norcodeine. Opiates may be detected in urine for 2-4 days following ingestion. The interpretation of results for urines positive for opiates merit special consider-ation. Since codeine is metabolized to morphine, both substances may appear in the urine following codeine ingestion. However, the codeine concentration is gener-ally greater than that of morphine. Street heroin also contains acetylcodeine, which metabolizes to codeine, therefore, both codeine and morphine may be present in the urine of some heroin users, although morphine generally predominates. In cases of low morphine and codeine concentrations in urine, it is not possible to determine whether codeine, morphine, or heroin was ingested. The presence of morphine alone would generally indicate either clinical morphine use or illicit morphine or heroin use. A speci?c metabolite of heroin, 6-monoacetylmorphine, is also at times detected and would de?nitely con?rm illicit drug (heroin) use. Poppy seeds, which have not been effectively washed, contain trace amounts of codeine and morphine. When consumed in suf?cient amounts, poppy seeds may produce urines which test positive for opiates.

Opioid compounds have effects on the CNS and usually on the bowel. They pro-duce analgesia, respiratory depression, euphoria, mood changes, confusion, and constipation. Tolerance and dependence develop with repeated use, with overdose being characterized by coma, respiratory depression, and pinpoint pupils. Discon-tinuing the drug in a dependent individual will precipitate a withdrawal syndrome. Heroin and morphine are the most commonly abused opioid compounds; how-ever codeine, propoxyphene, oxycodone, hydrocodone, etc. are also extensively abused, as they are more readily available. Most heroin and morphine abusers in-ject or “mainline” the drugs intravenously, as this produces the most immediate and intense effects. The heroin or morphine “rush” is the most desired sensation which is characterized by an intense orgasmic sensation centered in the abdomen.

Phencyclidine (l-phencyclohexylpiperidine, PCP) is prepared from l-piperidinocyclo-hexane-carbonitrile in a Grignard reaction, as ?rst performed in 1956 for use as an intravenous anesthetic. Pharmacologically PCP is classi?ed as a dissociative anesthet-ic. PCP is currently a popular drug of abuse and was once used as a veterinary tranquil-izer. A structural analog, ketamine, is cur-rently used as a veterinary tranquilizer. PCP is self-administered either by smoking (drug-laced tobacco, marijuana, or parsley), by nasal insuf?ation and intravenous injection, or by oral ingestion.

PCP is a lipophilic drug with a large volume of distribution. It undergoes extensive hepatic oxidative metabolism with about 10-15% of a dose excreted unchanged in urine, and about 65% excreted as hydroxylated metabolites and other polar metabolites. Renal excretion of PCP (pKa 8.5) is enhanced when urine is acidic, and it is reduced when urine is alkaline. Frequent or chronic PCP users may excrete PCP for 2-10+ days following last use. Urine concentrations may range from <0.1 mcg/mL to 340 mcg/mL.

Phencyclidine’s pharmacological actions are complex, since it interacts with several neurotransmitter systems (i.e.., GABAergic, dopaminergic, cholinergic, and adren-ergic). As a result, PCP has stimulant, depressant, hallucinogenic, and analgesic properties. Adverse effects are unpredictable and include agitation, delusions of grandeur, anxiety, hostility, stupor, paranoia, and coma. Death has been known to result following the ingestion of 120 mg of PCP (toxic dose 10-20 mg).