The Distance Learning Center for Addiction Studies
(DLCAS)
Pharmacology Update
Special Topics
2 hours of educational credit
Approved by such credentialing bodies as:
· National Association of Alcoholism and Drug Abuse Counselors
· National Board of Certified Counselors
· National Association of Social Workers
(All approval bodies are listed at http://www.dlcas.com/states.html)
Welcome to the growing family of coursework participants at the DLCAS – The Premier Source for Addiction Information and Continuing Education on the World Wide Web.
This Distance Learning Course (DLC) was developed for the Distance Learning Center for Addiction Studies (DLCAS) by Kevin R. Scheel, MS, MAC, LADC, LMFT. It provides need-to-know information about special topics in the field of pharmacology.
This manual contains the complete set of course materials, along with the post test that is required to obtain the certificate of completion for the course. For your convenience, we have also enclosed an answer sheet that will allow you to submit your answers by mail or by fax. If you prefer, however, there is always the option of submitting your test results online. This option allows faster response and mailing of your certificate. To take advantage of this option, simply set your browser to the following URL and follow the directions:
http://www.dlcas.com/testcenter.html .
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About the Author:
Kevin R. Scheel is a Masters prepared chemical dependency counselor with more than twenty-three years of experience in the human service field. He has served as the director of programs in the public sector as well as in private care facilities, both in the profit and not-for-profit arenas. He has been involved in the delivery of education services to the field since 1986 as an instructor at McLennan Community College in Waco, Texas, and as a private training consultant with Hazelden. Mr. Scheel is the author of “Alcohol: Chemistry & Culture,” as well as a series of education videotapes on the various drugs of abuse, published and marketed by WRS Group, Inc. He has also created a preparation and review manual that is currently in use by a variety of colleges and universities in Texas, designed to aid students preparing for their Texas chemical dependency credential.
While in Texas, Kevin served as the Texas Coordinator for the federally funded Project for Addiction Counselor Training (PACT) program. For this project Mr. Scheel designed a 270 curriculum for beginning counselors, delivering over 45,000 hours of classroom training to 415 minority students.
Kevin also served in the position as Coordinator for the Texas Addiction Training Center (currently the Texas Addition Technology Transfer Center), a federally funded project from the Center for Substance Abuse Treatment in Washington, D.C. In Texas this project worked with 8 major colleges and universities to increase the level of addiction education to the various disciplines offering counseling services to drug and alcohol affected clients.
Kevin is one of the founders of the Distance Learning Center for Addiction Studies and is currently serves ad the Director of Educational Services.
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Welcome to the Distance Learning Center for Addiction Studies online/distance course “Pharmacology Update – Special Topics.” DLCAS.com offers an annual update course that covers information on such topics as use statistics, current drugs that are causing increased problems in the field, research finding, and new trends in the field of treatment and prevention. This piece, however, is intended to focus on two of the more pressing problems we have in the field right now.
The first is the issue of “club” drugs. This is a broad category of drugs that are being use and abused by young-age populations because of their popularity in the dance and party scene. This covers a broad category of drugs that have been around for some time, but that are showing increased problems and difficulties for the treatment field. They are of particular concern because of the population most at risk for use and abuse – adolescents and young adults. The information provide here will help you know more about these drugs, their effects, and the problems they cause.
The second is probably one of the more hotly debated issues today with regards to treatment approaches – the value and use of pharmacotherapy in recovery programming. I do a significant amount of travel doing live training events. This hot-button issue creates a vast amount of controversy and discussion wherever I’ve gone. It’s an issue that I struggled with myself for many years, but based on new findings and the direction of research today, it’s an issue that all counselors must explore and examine if they are to have the opportunity of offering the best possible care to the clients with which they work.
The following alert was recently issued to the treatment field by Dr. Alan Leshner, Director of NIDA.
Dear Colleague;
A number of our Nation's best monitoring mechanisms are detecting alarming increases in the popularity of some very dangerous substances known collectively as "club drugs." This term refers to drugs being used by young adults at all-night dance parties such as "raves" or "trances," dance clubs, and bars. MDMA (Ecstasy), GHB, Rohypnol, ketamine, methamphetamine, and LSD are some of the club or party drugs gaining popularity. NIDA-supported research has shown that use of club drugs can cause serious health problems and, in some cases, even death. Used in combination with alcohol, these drugs can be even more dangerous. Thus, we are issuing this alert to aid communities in identifying and responding to this threat to the health and safety of their young people.
"Club drug" is a vague term that refers to a wide variety of drugs. Uncertainties about the drug sources, pharmacological agents, chemicals used to manufacture them, and possible contaminants make it difficult to determine toxicity, consequences, and symptoms that might be expected in a particular community. The information in this alert will be useful, whatever the local situation.
No club drug is benign. Chronic abuse of MDMA, for example, appears to produce long-term damage to serotonin-containing neurons in the brain. Given the important role that the neurotransmitter serotonin plays in regulating emotion, memory, sleep, pain, and higher order cognitive processes, it is likely that MDMA use can cause a variety of behavioral and cognitive consequences as well as impairing memory.
Because some club drugs are colorless, tasteless, and odorless, they can be added unobtrusively to beverages by individuals who want to intoxicate or sedate others. In recent years, there has been an increase in reports of club drugs used to commit sexual assaults - yet another reason why NIDA is alerting you to these escalating trends.
What follows is an overview of the scientific data we have on several of the most prevalent club drugs. Because many of these drug-use trends are still emerging, some of the data presented here are preliminary. However, we feel obliged to share what we know now, to provide whatever help we can to you and your community as you anticipate or respond to club drug-related problems. We also will be increasing our research efforts on club drugs to better understand how they act on the brain and how they produce their behavioral effects. And we will facilitate the development of treatment and prevention strategies targeted to the populations that abuse club drugs. As new research emerges, NIDA will continue to disseminate findings to you quickly. Toward this end, we are establishing a web site to provide scientific information about club drugs - www.clubdrugs.org. We hope this information will be helpful as you combat drug use in your own community.
Sincerely,
Alan I. Leshner, Ph.D.
Director
The following information focuses on the more commonly used and available drugs that define this category.
Slang or Street Names: Ecstasy, XTC, X, Adam, Clarity, Lover's Speed
MDMA was developed and patented in the early 1900's as a chemical precursor in the synthesis of other pharmaceuticals. Chemically, MDMA is a synthetic, psychoactive drug with both stimulant (amphetamine-like) and hallucinogenic (LSD-like) properties. Street names for MDMA include Ecstasy, Adam, XTC, hug, beans, and love drug. Its chemical structure (3-4 methylenedioxymeth-amphetamine, "MDMA") is similar to methamphetamine, methylenedioxy-amphetamine (MDA), and mescaline - other synthetic drugs known to cause brain damage.
MDMA is neurotoxic (Neurotoxicity refers to the
capability of inducing adverse effects in the central nervous system,
peripheral nerves or sensory organs. A chemical is considered to be neurotoxic
if it is capable of inducing a consistent pattern of neural dysfunction or
change in the chemistry or structure of the nervous system.). In addition, in
high doses it can cause a sharp increase in body temperature (malignant
hyperthermia) leading to muscle breakdown and kidney and cardiovascular system
failure.
Problems with MDMA include the following:
Brain imaging research in humans indicates that MDMA causes injury to the brain, affecting neurons that use the chemical serotonin to communicate with other neurons. The serotonin system plays a direct role in regulating mood, aggression, sexual activity, sleep, and sensitivity to pain. Many of the risks users face with MDMA use are similar to those found with the use of cocaine and amphetamines:
Research links MDMA use to long-term damage to those parts of the brain critical to thought and memory. One study, in primates, showed that exposure to MDMA for 4 days caused brain damage that was evident 6 to 7 years later.
MDA, the parent drug of MDMA, is an amphetamine-like drug that has also been abused and is similar in chemical structure to MDMA. Research shows that MDA also destroys serotonin-producing neurons in the brain.
MDMA also is related in its structure and effects to methamphetamine, which has been shown to cause degeneration of neurons containing the neurotransmitter dopamine. Damage to these neurons is the underlying cause of the motor disturbances seen in Parkinson's disease. Symptoms of this disease begin with lack of coordination and tremors and can eventually result in a form of paralysis.
Slang or Street Names: Grievous Bodily Harm, G, Liquid Ecstasy, liquid x, Goop, gamma-oh!, Georgia Home Boy
Gamma Hydroxybutyrate (GHB) is a central nervous system depressant abused for its ability to produce euphoric and hallucinatory states and its alleged ability to release a growth hormone and stimulate muscle growth. Although GHB was originally considered a safe and "natural" food supplement and was sold in health food stores, the medical community soon became aware that it caused overdoses and other health problems. GHB can produce drowsiness, dizziness, nausea, unconsciousness, seizures, severe respiratory depression, and coma.
GHB can be produced in clear liquid, white powder, tablet, and capsule forms, and it is often used in combination with alcohol, making it even more dangerous. Abusers include high school and college students and rave party attendees who use GHB for its intoxicating effects. Some body builders also abuse GHB for its alleged anabolic effects. In 1990, the Food and Drug Administration (FDA) issued an advisory declaring GHB unsafe and illicit except under FDA-approved, physician-supervised protocols. In March 2000, GHB was placed in Schedule I of the Controlled Substances Act.
Some basic facts on GHB:
Slang or Street Names: Roofies, Rophies, Roche, Forget-me Pill
Rohypnol® (flunitrazepam) belongs to the class of drugs known as benzodiazepines (such as Valium®, Halcion®, Xanax®, and Versed®). Flunitrazepam is used in the short-term treatment of insomnia and as a sedative hypnotic and preanesthetic medication. It is not approved for prescription use in the United States, although it is approved in Europe and is used in more than 60 countries as a treatment for insomnia, as a sedative, and as a presurgery anesthetic.
Flunitrazepam is ingested orally, frequently in
conjunction with alcohol or other drugs, including heroin. The drug’s effects
begin within 30 minutes, peak within 2 hours, and may persist for up to 8
hours or more, depending upon the dosage. Adverse effects associated with the
use of flunitrazepam include decreased blood pressure, memory impairment,
drowsiness, visual disturbances, dizziness, confusion, gastrointestinal
disturbances, and urinary retention. Paradoxically, although the drug is
classified as a depressant, flunitrazepam can induce excitability or
aggressive behavior in some users.
Flunitrazepam use causes dependence in humans. Once dependence has developed,
abstention induces withdrawal symptoms, including headache, muscle pain,
extreme anxiety, tension, restlessness, confusion, and irritability. Numbness,
tingling of the extremities, loss of identity, hallucinations, delirium,
convulsions, shock, and cardiovascular collapse also may occur. Withdrawal
seizures can occur a week or more after cessation of use. As with other
benzodiazepines, treatment for flunitrazepam dependence must be gradual, with
use tapering off.
Flunitrazepam is touted as an effective “parachute” or remedy for the
depression that follows a stimulant high. Reports indicate that flunitrazepam
is used by drug addicts in Spain and Malaysia to allay withdrawal symptoms and
to gain a state of oblivion. Abuse of the drug in Western Europe and the
Caribbean has been reported over the last 10 years. In Germany, Roche recently
removed the 2-milligram dosage from retail distribution—restricting it to
hospital use only—due to the increasing abuse of flunitrazepam in that
country.
In the United States, flunitrazepam is used widely in Texas where it is
popular among high school students. Flunitrazepam is reported to be readily
available in the Miami area, and epidemiologists from that area have stated
that it is South Florida’s fastest growing drug problem. Additional reports
from Miami indicate that the largest and fastest growing group of
flunitrazepam users is high school students who take the drug with alcohol or
use it after cocaine ingestion. Two common misperceptions about flunitrazepam
may explain the drug’s popularity among young people: first, many erroneously
believe that the drug is unadulterated—and therefore “safe”—because it comes
in presealed bubble packs; second, many mistakenly think its use cannot be
detected by urinalysis testing.
Slang or Street Names: Speed, Ice, Chalk, Meth, Crystal, Crank, Fire, Glass
Methamphetamine is a toxic, addictive stimulant. Like
cocaine, meth is a potent central nervous system stimulant. Meth represents
the fastest growing drug threat in America today.
The drug is often made in clandestine laboratories from relatively inexpensive over-the-counter ingredients. It is being used by diverse groups, including young adults who attend raves, in many regions of the country.
Meth can be smoked, snorted, injected, or taken orally, and its appearance varies depending on how it is used. Typically, it is a white, odorless, bitter-tasting powder that easily dissolves in water. Another common form of the drug is crystal meth, or "ice," named for its appearance (that of clear, large chunky crystals resembling rock candy). Crystal meth is smoked in a manner similar to crack cocaine and about 10 to 15 "hits" can be obtained from a single gram of the substance. Users have referred to smoking ice as a "cool" smoke, while the smoking of crack is a "hot" smoke. The euphoric effect of smoking ice lasts longer than that of smoking crack.
Because meth production and trafficking for a period of time were concentrated primarily in the West and Southwest United States, particularly California, Arizona, Utah, and Texas, availability and abuse were high in those areas. However, the expansion of Mexico-based meth traffickers and the growth of independent U.S.-based laboratories have dramatically increased the availability and abuse of meth in the Pacific Northwest, Midwest, and some portions of the Southeast, particularly Georgia, Tennessee, and the surrounding states. There is also evidence that meth production and availability is beginning to spread to Mid-Atlantic states, such as Virginia, and even as far north as New England. In 1998, meth labs were, for the first time, found in New Jersey, Delaware, and Massachusetts.
Methamphetamine use increases the heart rate, blood
pressure, body temperature, and rate of breathing, and it frequently results
in violent behavior in users. Meth also dilates the pupils and produces
temporary hyperactivity, euphoria, a sense of increased energy, and tremors.
High doses or chronic use have been associated with increased nervousness,
irritability, memory loss, aggression, violence, psychotic behavior, and
potential cardiac and neurological damage. Withdrawal from high doses produces
severe depression.
Chronic abuse produces a psychosis similar to schizophrenia and is characterized by paranoia, picking at the skin, self absorption, and auditory and visual hallucinations. Violent and erratic behavior is frequently seen among chronic, high-dose methamphetamine abusers. The most dangerous stage of the binge cycle is known as "tweaking." Typically, during this stage, the abuser has not slept in three to fifteen days and is irritable and paranoid. The tweaker has an intense craving for more meth; however, no dosage will help recreate the euphoric high. This causes frustration and leads to unpredictability and a potential for violence. Methamphetamine is also neurotoxic. Methamphetamine abusers may have significant reductions in dopamine transporters.
Slang or Street Names: Windowpane, Blotter Acid, Micro-dots, acid, barrels, California sunshine.
Lysergic acid diethylamide (LSD) is the most potent
hallucinogen known to man. It was originally synthesized in 1938 by Dr. Albert
Hoffman, but its hallucinogenic effects were unknown until 1943, when Dr.
Hoffman accidentally consumed some LSD. Because of its structural similarity
to a chemical present in the brain and the similarity of its effects to
certain aspects of psychosis, LSD was used as a research tool to study mental
illness decades ago.
After a decline in its illicit use after its initial
popularity in the 1960s, LSD made a comeback in the 1990s. However, the
current average oral dose consumed by users is 30 to 50 micrograms, a decrease
of nearly 90 percent from the 1960 average dose of 250 to 300 micrograms.
Lower potency doses probably account for the relatively few LSD-related
emergency incidents during the past several years and its present popularity
among young people.
LSD is a clear or white, odorless, water-soluble material synthesized from lysergic acid, a compound derived from a rye fungus. LSD is the most potent mood- and perception-altering drug known: oral doses as small as 30 micrograms can produce effects that last 6 to 12 hours.
LSD is initially produced in crystalline form. The pure crystal can be crushed to powder and mixed with binding agents to produce tablets known as "microdots" or thin squares of gelatin called "window panes"; more commonly, it is dissolved, diluted, and applied to paper or other materials. The most common form of LSD is called "blotter acid" - sheets of paper soaked in LSD and perforated into 1/4-inch square, individual dosage units. Variations in manufacturing and the presence of contaminants can produce LSD in colors ranging from clear or white, in its purest form, to tan or even black. Even uncontaminated LSD begins to degrade and discolor soon after it is manufactured, and drug distributors often apply LSD to colored paper, making it difficult for a buyer to determine the drug's purity or age
The precise mechanism by which LSD alters perceptions is still unclear. Evidence from laboratory studies suggests that LSD, like hallucinogenic plants, acts on certain groups of serotonin receptors designated the 5-HT2 receptors, and that its effects are most prominent in two brain regions: One is the cerebral cortex, an area involved in mood, cognition, and perception; the other is the locus ceruleus, which receives sensory signals from all areas of the body and has been described as the brain's "novelty detector" for important external stimuli.
LSD's effects typically begin within 30 to 90 minutes of ingestion and may last as long as 12 hours. Users refer to LSD and other hallucinogenic experiences as "trips" and to the acute adverse experiences as "bad trips." Although most LSD trips include both pleasant and unpleasant aspects, the drug's effects are unpredictable and may vary with the amount ingested and the user's personality, mood, expectations, and surroundings.
Users of LSD may experience some physiological effects, such as increased blood pressure and heart rate, dizziness, loss of appetite, dry mouth, sweating, nausea, numbness, and tremors; but the drug's major effects are emotional and sensory. The user's emotions may shift rapidly through a range from fear to euphoria, with transitions so rapid that the user may seem to experience several emotions simultaneously.
LSD also has dramatic effects on the senses. Colors, smells, sounds, and other sensations seem highly intensified. In some cases, sensory perceptions may blend in a phenomenon known as synesthesia, in which a person seems to hear or feel colors and see sounds.
Hallucinations distort or transform shapes and movements, and they may give rise to a perception that time is moving very slowly or that the user's body is changing shape. On some trips, users experience sensations that are enjoyable and mentally stimulating and that produce a sense of heightened understanding. Bad trips, however, include terrifying thoughts and nightmarish feelings of anxiety and despair that include fears of insanity, death, or losing control.
LSD users quickly develop a high degree of tolerance for the drug's effects: After repeated use, they need increasingly larger doses to produce similar effects. LSD use also produces tolerance for other hallucinogenic drugs such as psilocybin and mescaline, but not to drugs such as marijuana, amphetamines, and PCP, which do not act directly on the serotonin receptors affected by LSD. Tolerance for LSD is short-lived it is lost if the user stops taking the drug for several days. There is no evidence that LSD produces physical withdrawal symptoms when chronic use is stopped.
Two long-term effects persistent psychosis and hallucinogen persisting perception disorder (HPPD), more commonly referred to as "flashbacks"-have been associated with use of LSD. The causes of these effects, which in some users occur after a single experience with the drug, are not known.
Psychosis. The effects of LSD can be described as drug-induced psychosis-distortion or disorganization of a person's capacity to recognize reality, think rationally, or communicate with others. Some LSD users experience devastating psychological effects that persist after the trip has ended, producing a long-lasting psychotic-like state. LSD-induced persistent psychosis may include dramatic mood swings from mania to profound depression, vivid visual disturbances, and hallucinations. These effects may last for years and can affect people who have no history or other symptoms of psychological disorder.
Hallucinogen Persisting Perception Disorder. Some former LSD users report experiences known colloquially as "flashbacks" and called "HPPD" by physicians. These episodes are spontaneous, repeated, sometimes continuous recurrences of some of the sensory distortions originally produced by LSD. The experience may include hallucinations, but it most commonly consists of visual disturbances such as seeing false motion on the edges of the field of vision, bright or colored flashes, and halos or trails attached to moving objects. This condition is typically persistent and in some cases remains unchanged for years after an individual has stopped using the drug.
Because HPPD symptoms may be mistaken for those of other neurological disorders such as stroke or brain tumors, sufferers may consult a variety of clinicians before the disorder is accurately diagnosed. There is no established treatment for HPPD, although some antidepressant drugs may reduce the symptoms. Psychotherapy may help patients adjust to the confusion associated with visual distraction and to minimize the fear, expressed by some, that they are suffering brain damage or psychiatric disorder.
Slang or Street Names: Angel Dust, Supergrass, Killer Weed, embalming fluid, and rocket fuel
In the 1950s, phencyclidine, more commonly known as PCP,
was investigated as an anesthetic but, due to the side effects of confusion
and delirium, its development for human medical use was discontinued. It
became commercially available for use as a veterinary anesthetic in the 1960s
under the trade name of Sernylan and was placed in Schedule III of the
Controlled Substances Act (CSA). In 1978, due to considerable abuse of PCP, it
was transferred to Schedule II of the CSA, and commercial manufacturing of
Sernylan was discontinued. Today, all of the PCP encountered on the illicit
market in the United States is produced in clandestine laboratories.
PCP is illicitly marketed under a number of other names
including angel dust, supergrass, killer weed,
embalming fluid, and rocket fuel that reflect the range of its
bizarre and volatile effects. In its pure form, it is a white crystalline
powder that readily dissolves in water. 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.
The chemicals needed to manufacture PCP are readily available and inexpensive, and the production process requires little formal chemical knowledge or laboratory equipment. The drug is sold primarily in urban neighborhoods in a limited number of U.S. cities. The liquid form of PCP is actually PCP base dissolved most often in ether, a highly flammable solvent. PCP typically is sprayed onto leafy material such as marijuana, mint, oregano, or parsley, and smoked.
The drug's effects are as varied as its appearance. A moderate amount of PCP often causes users to feel detached, distant, and estranged from their surroundings. Numbness, slurred speech, and loss of coordination may be accompanied by a sense of strength and invulnerability. A blank stare, rapid and involuntary eye movements, and an exaggerated gait are among the more observable effects. Auditory hallucinations, image distortion, severe mood disorders, and amnesia may also occur. In some users, PCP may cause acute anxiety and a feeling of impending doom; in others, paranoia and violent hostility; and in some, it may produce a psychoses indistinguishable from schizophrenia. Many believe PCP to be one of the most dangerous drugs of abuse. Modification of the manufacturing process may yield chemically related analogues capable of producing psychotic effects similar to PCP.
Slang or Street Names: Special K, K, Vitamin K, Cat Valiums
Ketamine is a dissociative anesthetic developed in 1963 to replace PCP and currently used in human anesthesia and veterinary medicine. Much of the ketamine sold on the street has been diverted from veterinarians' offices. Although it is manufactured as an injectable liquid, in illicit use ketamine is generally evaporated to form a powder that is snorted or compressed into pills or smoked with marijuana or tobacco products. In some cities (Boston, New Orleans, and Minneapolis/St. Paul, for example), ketamine is reportedly being injected intramuscularly.
Ketamine gained popularity for abuse in the 1980s, when it was realized that large doses cause reactions similar to those associated with use of phencyclidine (PCP), such as dream-like states and hallucinations.
Ketamine's chemical structure and mechanism of action are similar to those of PCP, and its effects are similar, but ketamine is much less potent than PCP with effects of much shorter duration. Low-dose intoxication from ketamine results in impaired attention, learning ability, and memory. Users report sensations ranging from a pleasant feeling of floating to being separated from their bodies.
At higher doses, ketamine can cause delirium, amnesia, impaired motor function, high blood pressure, depression, and potentially fatal respiratory problems.
Some ketamine experiences involve a terrifying feeling of almost complete sensory detachment that is likened to a near-death experience. These experiences, similar to a "bad trip" on LSD, are called the "K-hole."
Ketamine is odorless and tasteless, so it can be added to beverages without being detected, and it induces amnesia. Because of these properties, the drug is sometimes given to unsuspecting victims and used in the commission of sexual assaults referred to as "drug rape."
Slang or Street Names: DXM, DM, Robo, Velvet, Rojo
Dextromethorphan is a cough-suppressing ingredient in a variety of over-the-counter cold and cough medications. The abuse of DXM by teenagers and young adults is currently on the rise and seems to be related to its over-the-counter availability, as well as the sale of the powdered form over the Internet.
Like PCP and ketamine, dextromethorphan acts as an NMDA receptor antagonist. The most common source of abused dextromethorphan is "extra-strength" cough syrup, which typically contains 3 milligrams of the drug per milliliter of syrup. At the doses recommended for treating coughs (1/6 to 1/3 ounce of medication, containing 15 mg to 30 mg dextromethorphan), the drug is safe and effective. At much higher doses (4 or more ounces), dextromethorphan produces dissociative effects similar to those of PCP and ketamine. The following is a list of some common over-the-counter products that contain dextromethorphan:
· Benylin Adult Formula Cough Syrup
· Benylin Pediatric Cough Suppressant
· Cough-X
· Creo-Terpin
· Delsym Cough Formula
· Diabe-TUSS DM Syrup
· Hold DM
· Pertussin CS Children's Strength
· Pertussin DM Extra Strength
· Robitussin Maximum Strength Cough Suppressant
· Robitussin Pediatric Cough Suppressant
· Sucrets 4 Hour Cough Suppressant
· Trocal
· Vicks 44 Cough Relief
The effects vary with dose, and dextromethorphan users describe a set of distinct dose-dependent "plateaus" ranging from a mild stimulant effect with distorted visual perceptions at low (approximately 2-ounce) doses to a sense of complete dissociation from one's body at doses of 10 ounces or more. The effects typically last for 6 hours. Over-the-counter medications that contain dextromethorphan often contain antihistamine and decongestant ingredients as well, and high doses of these mixtures can seriously increase risks of dextromethorphan abuse.
Four ounces of Robitussin contains either 360 or 240 mg of DXM, depending on the formulation, and either quantity is sufficient to cause intoxication. Case reports identify abuse patterns from 4 ounces (1/2 bottle) up to 3 to 4 bottles a day. Internet sites inform the young users to drink the syrup expeditiously in order to absorb enough DXM from the drink prior to the impending incidence of vomiting which will occur as a result of the ingestion of the large volume of syrup required for intoxication.
Most abusers report a heightened sense of perceptual
awareness, altered time perception, and visual hallucinations. The typical
clinical presentation of DXM intoxication involves hyperexcitability,
lethargy, ataxia, slurred speech, sweating, hypertension, and/or nystagmus (a
condition where the eyes don’t track together when moving from side-to-side).
Research is showing that drug addiction therapy that combines different approaches is often more effective than therapy that uses only one approach. According to NIDA Director Dr. Alan I. Leshner. "When all is said and done, the ultimate treatment for drug addiction will probably involve a combination of biological and behavioral treatments and social services." Yet this is probably the biggest dilemma facing the treatment field today.
If you’re like me, my basic training and background early on stressed the need for abstinence to be the model for recovery. “You can never truly recover unless your totally drug free” was a statement I heard time and again during my early days in the field. I know it is a statement I’ve repeated to numerous clients in the course of care.
Yet pharmacotherapy is the focus of a great deal of research being undertaken by many of the federal agencies in our field. Recent advances have show great promise in the use of a variety of drugs for not only safe detoxification from many of the psychoactive drugs, but for both early and long-term recovery processes as well. Investigations are underway on “antabuse-like” drugs to treat cocaine addiction, drugs to counter the effects of marijuana in the bloodstream, and even a vaccination for nicotine.
We won’t go in to the areas of detoxification, but if you are interested in obtaining more training, and looking for credits, you can obtain a course from the DLCAS. Simply return to the DLCAS Homepage for more information. What I’d like to focus on instead is an overview of pharmacotherapeutic modalities, followed by information on the recently approved approach to alcohol treatment using the drug Naltrexone. Also, I’d like to make you aware of the research underway to develop a vaccination for nicotine addiction that is ready to undergo clinical trials.
Substance abuse, by definition, is a chronic disease in which the use of psychoactive substances may result in both physical and psychological addiction. Thus, one treatment approach that has shown favorable outcomes is pharmacotherapy—the use of approved medications with medical supervision. The goals of pharmacotherapy include:
- reduction in the use of illicit drugs or alcohol;
- reduction in criminal behavior; and
- improvement of social behavior and psychological well being.
A further goal is the urgent imperative to control and prevent the spread of substance abuse‑related infectious diseases, such as HIV/AIDS and tuberculosis. For those already infected, treatment for alcohol and other drug addiction may stabilize their physical condition, boost the immune system, and delay or prevent the onset of serious illness.
More research has been conducted on drug therapies for opiate drugs and alcohol than on other categories of abused substances, thought a major thrust of the research efforts being funded by NIDA are centered on the search for drug therapies for each of the major drugs of abuse. Researchers are currently seeking pharmacotherapeutic approaches for the treatment of such drugs as cocaine, amphetamines, marijuana, and nicotine.
There are four categories of pharmacological treatment for substance abuse. Each will be defined, followed by some examples of the more common pharmacotherapeutic agents.
These drugs can be substituted for the drug of abuse to provide a more controllable form of addiction. The properties and actions of these drugs are similar to those of particular abused drugs. Using them alleviates many of the withdrawal symptoms often experienced by persons addicted to various psychoactive substances. Examples of drugs in this category include methadone, clonidine, and LAAM.
Methadone, a synthetic narcotic analgesic compound, is the most commonly used form of pharmacotherapy for opiate drugs. It is medically safe and has few side effects. It produces a stable drug level and is not behaviorally or subjectively intoxicating. It blocks the cravings for opiate drugs and does not produce euphoria, as heroin and other drugs do. The characteristics of methadone patients have changed considerably over the past decade because of increased rates of HIV infection among intravenous drug abusers, concomitant use of cocaine and crack, and homelessness. These changes have resulted in methadone programs' needs for enlarged and more sophisticated physical facilities, better trained staff, and more funding.
Among the various pharmacotherapies, methadone maintenance has been studied most thoroughly. Methadone maintenance is generally successful in meeting treatment goals. When appropriate doses of methadone are administered, heroin use decreases markedly. However, in some cases other drugs, such as cocaine and alcohol, continue to be used. A substantial reduction in criminal behavior has been documented by several studies, and this reduction increases with length of time in methadone treatment. Socially productive behavior, such as employment, education, or homemaking, has also been shown to improve with the length of time in treatment .
Clonidine can partially suppress many withdrawal symptoms of opiates, alcohol, and tobacco. It is most effective for persons who are motivated and involved in their treatment program. It is not as useful in maintaining abstinence after withdrawal from opiate drugs has been achieved.
LAAM (levo-alpha-acetyl-methadol) is a synthetic opioid agonist
medication for use in the treatment of opiate addiction. It was approved
by the Food and Drug Administration (FDA) in July 1993 and became
commercially available in August 1993. Like methadone, LAAM creates a pharmacologic cross-tolerance to other opioids and therefore blocks the euphoric effects of those drugs while also controlling opiate craving.
Methadone suppresses opiate withdrawal symptoms for 24 hours or longer, whereas LAAM achieves this effect for 48 to 72 hours or longer. Under FDA regulations, LAAM must be dispensed by approved opioid substitution therapy programs. Each program must receive approval from their single State agency (SSA) to dispense LAAM and must ensure that program staff receive training in its use.
Because of LAAM's long duration of action, after a patient's tolerance
to LAAM has been established, it can be administered no more frequently than every other day. In humans, LAAM is metabolized into two active metabolites, nor-LAAM and dinor-LAAM. Both are metabolized more slowly than the parent drug. It is believed that this slow metabolism is the basis for LAAM's long duration of action. Like methadone, LAAM is similar in action to morphine. Its effects include analgesia, sedation, and respiratory depression. Tolerance to these effects develops with prolonged use, and an abstinence syndrome similar to that observed with morphine and other opiates occur with cessation of regular use. However, with LAAM, the syndrome has a slower onset and lasts longer, with less acute symptoms. (Check out the same NIDA website above for the TIP on LAAM)
These drugs occupy the same receptor sites in the brain as specific drugs of abuse. However, they do not produce the same effects as the abused drugs, and they are non‑addicting. Thus, when they are present, the effects of the abused drug are blocked because they cannot act on the brain in the usual way. Therefore, they do not produce the expected mood‑altering experiences. Antagonists may be used for persons who do not want to be maintained on drug substitutes (i.e., agonists, like methadone); they also are used, at times, for persons leaving other drug‑free treatment programs and reentering the community, to diminish their risk of relapse.
Naltrexone is an opiate antagonist, but recently this drug has been approved for use in the treatment of alcoholism. More information will follow.
Buprenorphine is a mixed agonist‑antagonist agent. It is long‑acting and blocks the effects of other opiate drugs. It produces less physical dependence than methadone, but some withdrawal symptoms do occur with its use.
These drugs create adverse physical reactions when the person consumes the substance of abuse. These drugs are used to develop an aversion to the abused drug.
Antabuse (disulfiram) interferes with the metabolism of alcohol, causing unpleasant side effects when alcohol is ingested. Facial flushing, heart palpitations and a rapid heart rate, difficulty in breathing, nausea, vomiting, and possibly a serious drop in blood pressure are the major effects produced by the combination of alcohol and Antabuse. Paired with other treatment approaches, Antabuse has been successful in preventing relapse.
These control various symptoms associated with drug use and withdrawal. Antianxiety drugs, antipsychotics, antidepressants (for major depressions), and lithium have been tested. However, further research is needed on the effectiveness of these agents, as current research has produced conflicting results in some cases or has been inconclusive.
Researchers conceptualize two categories of therapeutic medications. Those that help patients stop abusing drugs include medications that reduce acute drug withdrawal symptoms, medically maintain patients, decrease drug craving, and block the drugs' reinforcing effects. Methadone, clonidine, buprenorphine, LAAM, desipramine, bromocriptine, and naltrexone are included in this category. Medications that help prevent relapse are able to reduce prolonged withdrawal syndromes, decrease drug craving, alter the drug's reinforcing effects, treat underlying psychopathology, and treat drug‑induced psychopathology. Included in this category are antidepressants, desipramine, bromocriptine, naltrexone, and disulfiram.
Most research and development of medications used in the treatment of addictive diseases has been fostered by the federal government. In treating most diseases, clinical trials of new medications usually are undertaken by pharmaceutical companies. However, these companies have been reluctant to associate their organizations and medications with drug addiction. This is, in part, due to the negative stereotypes of drug abusers. The number of persons who could benefit from a particular pharmacological treatment for addiction is also comparatively small. Thus, if involved in developing medications for addictive disorders, the pharmaceutical industry would not realize the degree of profit or recover its investment for research and development to the extent desired. There is also concern that medications will be diverted for street use or will be used in combination with other illegal drugs. Pharmaceutical companies worry that the drugs or their companies will gain a bad reputation if this occurs.
In 1994, the FDA granted quick approval to the use of the narcotic antagonist Naltrexone for use in the treatment of alcoholism. A psychiatrist at the University of Pennsylvania Medical Center, Joseph R. Volpicelli, M.D., PhD., discovered that the use of the drug could reduce craving for alcohol. The FDA’s quick approval was based on a significant amount of information that researchers were able to produce showing great benefit with minimal risk. Below is an article from Penn Health Magazine which details some of the finding. Also, a significant amount of information can be found at the following website:
http://www.med.upenn.edu/~recovery/pros/reco2000.html
CURBING THE CRAVING
By Jennifer Baldino
From Penn Health Magazine, July/August 1995. Reprinted with permission.
For the first time in 50 years, the federal government has approved a new drug treatment for alcoholism. The treatment is based on the research of a psychiatrist at the University of Pennsylvania Medical Center. For more than a decade, Joseph R. Volpicelli, M.D., PhD., worked to show the medical community that naltrexone, a drug used since the 1980s to treat heroin addiction, can also curb the craving for alcohol. Last December, the U.S. Food and Drug Administration approved the use of naltrexone specifically to treat alcohol addiction. The drug, manufactured by DuPont Pharma and formerly sold under the name Trexan as a heroin-addiction treatment, will now be sold as ReVia.
Volpicelli first recognized naltrexone's potential to treat alcoholism 15 years ago as a graduate student in Penn's Department of Psychology. What prompted his study of naltrexone was his suspicion that the drug might work in alcoholics the same was it did in heroin addicts. He discovered that rats had a higher preference for alcohol following stressful events, what Volpicelli calls the "weekends-were-made-for-Michelob" effect. He also found that the rats taking naltrexone didn't increase their intake of alcohol. In 1981, he began publishing his findings on the drug.
But the research was met with skepticism. As Volpicelli told Penn Health: "Everybody--academics, the drug company--thought it was a pretty wild idea."
The exception was Charles P. O'Brien, M.D., PhD. A professor and vice chair of psychiatry at Penn and chief of psychiatry at Philadelphia's Veterans Administration Center, he says he was won over by Volpicelli's naltrexone research on rats. Volpicelli in turn credits O'Brien with giving him the financial and moral support and time to continue his research on naltrexone.
"We did it without any outside funding," says O'Brien. "We got it started against pretty great odds." According to O'Brien, the researchers even had difficulty recruiting subjects for their studies in the 1980s because treating alcoholism with medication was not common.
Volpicelli, O'Brien, and their colleagues Arthur I. Alterman, PhD., and Motoi Hayashida, D.Sc., started a naltrexone study using volunteers at the Veterans Administration Hospital in 1985. They tracked 70 men for 12 weeks following their outpatient detoxification program. Half received naltrexone, half a placebo. The researchers found that while 23 percent of the volunteers who took naltrexone experienced a drinking relapse, 54 percent of those who received a placebo reverted to drinking. During the study period, half the participants in both groups took at least one drink each (an act known among alcoholics as "slipping"). But when those who took naltrexone slipped, they were able to stop drinking after a few drinks, avoiding a total relapse.
"Ordinarily in alcoholics even one or two drinks stimulates the body's craving for more," Volpicelli told The New York Times. But with naltrexone, "the cycle of craving was broken. This made it easier for them to stop drinking again and continue their treatment."
In 1991, researchers at Yale University School of Medicine tested the effects of naltrexone in conjunction with psychological therapy in 104 alcohol-dependent men and women. The Yale study found that patients who took naltrexone were nearly twice as successful in their clinical outcomes, including abstinence and avoiding a relapse, as those who took a placebo.
The corroborating results gave Volpicelli's research the credibility it needed in the eyes of those in academe and the pharmaceutical industry. As Volpicelli puts it, they realized that "the findings were real, not just an accident." The Penn and Yale studies were published in the Archives of General Psychiatry in November of 1992. DuPont Pharma showed interest in manufacturing the drug. (DuPont Pharma, a partnership between DuPont and Merck & Co., Inc., is a research-based pharmaceutical company. DuPont Pharma receives the profits from the sale of ReVia and has provided Volpicelli with funding for educational programs.)
Last summer, the drug was presented to the FDA for approval. Controversial because of its lengthy approval process, the FDA surprised the researchers by authorizing naltrexone's use in alcoholism treatment in just six months. According to Volpicelli, the FDA was "pretty confident" that the drug was safe: It had been under research for 20 years and on the market for 10 as a treatment for heroin addiction.
"It's very rewarding for us to see that the research we've been doing for the past decade or so has found a niche," says Volpicelli.
Only one other medication, Antabuse, known generically as disulfiram, has been widely used to treat alcoholism. The drug is designed to cause vomiting and severe nausea when mixed with alcohol but it does little to stop the alcoholic's craving.
Volpicelli reports that his patients who take naltrexone have been happy with the results. They've told him that "they went to a bar, had a drink, and didn't get anything from it. They didn't get that buzz." And several did something they had never done before: "They left half their drink on the bar."
In speaking to the media about the effects of naltrexone, however, Volpicelli and O'Brien warned that the drug is not a "magic bullet." Naltrexone does not cure the addiction; it eliminates the pleasurable "high" of drinking alcohol and reduces the craving for more.
Volpicelli calls naltrexone an "anti-psychoactive drug" because it works by blocking the effects of drugs like heroin or alcohol on the mind and behavior. While people may turn to such drugs as alcohol to "escape," naltrexone blocks their psychoactive effects so people can learn to cope with life without drugs.
Naltrexone actually works in the brain, blocking the pleasurable effects of alcohol on nerve cells known as opioid receptors, which help dull emotional and physical pain and lead to feeling high.
Naltrexone's critics argue that is was not very effective when used to treat heroin abuse; some have called taking a pill to curb alcoholism a "quick fix"; others have wondered if naltrexone can help people who abuse more than one substance or if naltrexone fits into the "drug-free" philosophy of many addiction treatment centers.
Volpicelli uses two words--they are quite a mouthful--to respond to their criticisms: Biopsychosocial support. To recover fully from addiction to alcohol or any drug, he explains, most people need what he calls a "tripod" of support: medication, counseling, and support from family, friends, or other addicts. In Volpicelli's view, a pill alone won't help an addict. But without medication, he says, neither will psychotherapy nor social support. "If you have two legs of the tripod," he says, "you're going to tip over. If you have three legs, you have a good foundation."
Volpicelli feels so strongly that naltrexone works well only in combination with psychosocial treatment that, with the support of the national alcohol research community, he successfully urged the FDA to approve naltrexone only as an adjunct to conventional treatments.
"Our results show that naltrexone, when used with a 12-step or other recovery program, may be effective--particularly in the early stages of treatment," says Volpicelli. "But it is essential that recovering alcoholics also undergo a comprehensive treatment program which helps them cope with the social, legal, family, physical, and psychological problems that occur as a result of their drinking behavior."
Naltrexone is taken orally once a day. Its most common side effects, reported in approximately 10 percent of patients, are nausea, difficulty in sleeping, anxiety, nervousness, abdominal pain or cramps, vomiting, low energy, joint and muscle pain, and headaches. The National Institute on Alcohol Abuse and Alcoholism, which funded the Penn and Yale studies, is supporting nine clinical trials to determine the patient type, dose, therapy combinations, and treatment duration with which naltrexone works best.
At Penn's Treatment Research Center in September, Volpicelli will begin clinical trials on whether a three- or nine-month course of treatment with naltrexone works better. He is also studying the effects of giving naltrexone to people at risk for alcoholism because of their family history. In other research, Volpicelli and his team are studying a comprehensive treatment program or, as the psychiatrist puts it, "one-stop shopping," for women addicted to cocaine.
According to the Department of Health and Human Services, alcohol abuse and dependence affect about 15.3 million adult Americans and approximately 38 percent of adult Americans have experienced alcoholism or alcohol abuse in their families. An article in Alcohol, Health, and Research World includes the estimate that alcoholism and alcohol abuse cost $98.6 billion in 1990; some 70 percent of that total is attributed to lost earnings and decreased productivity because of alcohol-related illness and early death. The immediate physical effects of alcohol include decreased motor coordination and respiratory capacity. Long-term alcohol abuse can cause the liver and other organs to degenerate, a point Volpicelli underscores in presentations with a slide of Promethues Bound, a painting by Peter Paul Rubens depicting a mythical titan doomed to have his liver plucked out again and again.
According to Volpicelli, the recent findings on naltrexone reinforce the little-appreciated theory that alcoholism is biochemically based addiction and not a personal flaw; studies have proven that alcoholism runs in families and that alcohol triggers the release of natural opioids in the body. The proof of biochemical motivation for alcohol dependence, says Volpicelli, may help alcoholics "overcome their shame, come out of hiding, and get treatment."
Volpicelli also sees approval of naltrexone as another step in educating the public and the medical community about alcoholism. He says patients unable to control their drinking through conventional programs have told him they'd been blaming themselves and asking, "What's the matter with me?" Now, he says, there is proof that their drinking has a physiological base. Naltrexone, says Volpicelli, "has given them hope."
By Barbara Shine, NIDA NOTES Staff Writer
A new vaccine that prevents nicotine from reaching the brains of rats may offer hope for smokers trying to break their addiction. The compound, called NicVAX, may even prove useful as an inoculation against nicotine addiction, much like those that protect children from tetanus, measles, and polio.
"Some form of vaccination against nicotine would be highly useful because vaccinated individuals would not be able to get a 'kick' from the nicotine in tobacco smoke or chewing tobacco," says NIDA Director Dr. Alan I. Leshner. "If people found tobacco less rewarding, they would be less likely to continue using it. Ultimately, however, our best treatment for nicotine addiction is prevention."
NicVAX is manufactured by Nabi, a Florida-based pharmaceutical company that has NIDA grant support to conduct preclinical studies to determine whether the vaccine is toxic to animals and, then, if the compound is proven safe, clinical trials to evaluate its safety and efficacy in humans. The 4-year project begins this fall, and clinical trials are planned for 2002. Primary coinvestigators include Dr. Ali Fattom and other Nabi scientists in Rockville, Maryland, as well as the Minnesota- and Texas-based researchers who conducted the early animal studies.
Dr. Paul Pentel and his colleagues at the Minneapolis Research Foundation and Hennepin County Research Center in Minneapolis and Dr. David Malin at the University of Houston at Clear Lake tested NicVAX with rats. Injection of NicVAX stimulated antibodies to neutralize nicotine in the blood, reducing by 65 percent the amount of nicotine that reached the animals' brains. The nicotine-specific antibodies produced by NicVAX also reduced the effects of nicotine on blood pressure and the heart.
Now NicVAX is proposed as a therapy that can enhance current treatments for nicotine addiction by helping quitting smokers resist the urge to light up. The hypothesis is that the vaccine may inhibit nicotine's "priming effect"-the phenomenon in which a formerly addicted individual experiences an increased desire to use a drug after a single exposure, which contributes to relapse. A treatment program built around NicVAX might also include supportive counseling and a medication such as bupropion (Zyban) to reduce withdrawal symptoms.
The animal studies suggest the vaccine's potential for preventing addiction in new tobacco users as well. When rats were injected simultaneously with a nicotine solution and the vaccine, the antibodies that reduced nicotine levels in the rat brains also reduced nicotine dependence. When the nicotine dosing was stopped, the control group, rats injected with nicotine and a placebo solution, showed significantly greater levels of dependence-measured by abstinence signs such as teeth chattering and tremors-than did the rats treated with NicVAX. Rats were exposed to nicotine at levels comparable to 10 packs of cigarettes daily for a week.
Continuing doses of nicotine do not interfere with the vaccine's ability to induce antibodies in the rats. Animals immunized with NicVAX while they were being injected with nicotine still produced nicotine-specific antibodies. Thus it may be possible to vaccinate a smoker while he or she is still using tobacco so that adequate antibodies will be in place at smoking cessation. The vaccine will continue to work during any relapse, inhibiting the pleasurable response that nicotine would otherwise cause. Further, the vaccine never enters the brain and is therefore unlikely to produce neurological side effects.
Sources
Pentel, P.R.; Malin, D.H.; Ennifar, S.; et al. A nicotine conjugate vaccine reduces nicotine distribution to brain and attenuates its behavioral and cardiovascular effects in rats. Pharmacology Biochemistry and Behavior 65(1): 191-198, 1999.
Hieda, Y.; Keyler, D.E.; VanDeVoort, J.T.; et al. Immunization of rats reduces nicotine distribution to brain. Psychopharmacology 143: 150-157.
The knowledge that drug and alcohol counselors have with regards to drugs of abuse is what typically sets us apart from others in the helping profession. Not only are we required to have a majority of our basic training hours in the subject area of alcohol and other drugs, but we tend to continue to advance our knowledge on drugs of abuse in our continuing education endeavors. Keeping abreast of trends and popularity of the various drugs that individuals are using and abusing is critical to the delivery of quality care. But equally important is a continual reexamination of hallmark issues like “abstinence in recovery.”
With the constant advancements of scientific research, and the exploration of the neurobiology of addiction, it is only a matter of time till we are faced with the dilemma of how to further incorporate pharmacotherapy into the recovery process. Already such drugs as antabuse, Naltrexone, nicotine patches, and even the use of anti-depressants create conflict and unease in the field. Because of past abuses of pharmacological approaches to care (e.g. sleeping pills in recovery, liberal use of tranquilizers to deal with anxiety), we are naturally skeptical. Instead of ignoring new approaches, however, it will be our responsibility to keep abreast of developments and findings, and to ask the tough questions as to how to make such advances a part of quality care, rather than simply dismissing such findings out of hand.
Keeping abreast of the knowledge means reading the
journals, taking continuing education coursework, and using the Internet to
our advantage. If you are not already hooked-in or “Internet savvy,” then I
encourage you to start. DLCAS.com has a comprehensive listing of websites
that you will find useful – visit their homepage at
http://www.dlcas.com and look for the “Linkage” bookmark.
Appendix A: Post Test for the Pharmacology Update – Special Topics DLC
Directions: In order to receive credits for this DLC, you are required to take a posttest and receive a passing score. We have set a minimum standard of 80% as the passing score in order to insure the highest standard of knowledge retention and understanding. The test is comprised of multiple choice and/or true/false questions that will investigate your knowledge and understanding of the materials found in this DLC.
After you have completed your reading and review of this material, you will need to answer each of the following questions. Then, submit your test to us for processing. This can be done in any of the following manners:
Kevin Scheel, DLCAS
P.O. Box 240663
Apple Valley, MN 55124-0663.
Once we receive your sheets, we will grade your test and notify you of the results. If successful, your certificate will be mailed to you. If you do not obtain the required 80% score, we will provide you with feedback and instructions on retesting.
http://www.dlcas.com/tests/pharm050.html .
Once there, fill out the requested information at the top of the form. Then, answer your questions by scrolling through the questions and clicking on the selection button for the corresponding answer for your choice of "a" through "e." For true/false questions, select either "a" for true, or "b" for false.
Once you are done, simply click on the submit button at the bottom of the page. Your answers will be graded and you'll receive your results immediately. A copy will also be forwarded to the DLCAS for posting and for the processing of your course certificate. If your score is at least 80% or greater, you'll be provided the link to the course evaluation, which is the final step in the process. Once this is submitted, your certificate of completion will then be processed and mailed to you within 48 business hours of receipt.
If, however, you do not achieve a passing score you will need to review this course manual and return to the Test Center site to resubmit your answers.
If you have any difficulty with this process, or need
assistance, please e-mail us at coordinator@dlcas.com and ask for help.
Answer the following questions by selecting the most appropriate response.
1. The term "club drugs" refers to drugs being used by young adults at all-night dance parties such as "raves" or "trances," dance clubs, and bars.
2. One of the growing concerns related to the use of “club drugs” is the impact such drugs have on neurotransmitters like serotonin. Serotonin is necessary for the regulation of:
3. MDMA is chemically similar to:
4. Many of the “club drugs” are neurotoxic. A chemical is considered to be neurotoxic if it is capable of inducing a consistent pattern of neural dysfunction or change in the chemistry or structure of the nervous system.
5. Aside for its popularity for its ability to produce euphoric and hallucinatory states, GHB is a central nervous system depressant abused for its alleged ability to release a growth hormone and stimulate bone growth and density.
6. Forget-me Pill is a slang or street name for the drug:
7. Though it has physiological effects similar to diazepam, flunitrazepam is approximately 100 times more potent.
8. On the street, Rohypnol is touted as an effective “parachute” or remedy for the depression that follows a stimulant high.
9. Methamphetamines can be used in all of the following ways except:
10. "Tweaking" is:
11. "Window pane" LSD is;
12. Phencyclidine (PCP) is the most potent hallucinogen known to man.
13. Hallucinogens like LSD create a phenomenon known as synesthesia. Synesthesia is:
14. Hallucinogen Persisting Perception Disorder (HPPD) is the medical term for the phenomenon known as:
15. Phencyclidine, more commonly known as PCP, was originally brought on to the market as an anesthetic agent.
a. True
b. False
16. Ketamine is a dissociative anesthetic which was developed to replace which other pharmaceutical agent?
17. Dextromethorphan’s action on receptor sites of the brain is that of an:
18. Typically, the goals of pharmacotherapy include all of the following except:
19. These drugs occupy the same receptor sites in the brain as specific drugs of abuse. However, they do not produce the same effects as the abused drugs, and they are non‑addicting.
20. These drugs create adverse physical reactions when the person consumes the substance of abuse. They are used to develop an aversion to the abused drug.