DRUG ABUSE AND DRUG DEPENDENCE are major social problems in our culture. The use of mind-altering substances is sanctioned in almost every group in Western society.

Drug abuse as excessive drug use that is inconsistent with acceptable medical practice. Some drug abuse results in tolerance, which is an altered physiologic state caused by continuous use of a drug, resulting in a diminished response to the same dose of the drug over time, so that progressively larger doses are required to produce the same drug effect.

Drug dependence refers to the psychological or physical compulsion to take a drug in order to experience its psychic effects or to avoid the discomfort of its absence. Clinicians often speak of two types of drug dependence: physical dependence in-volves an altered somatic state due to continued drug use that results in physiologic symptoms (withdrawal syndrome) when the drug is discontinued; psychic depend-ence is a less specific used to refer to drug dependence without any apparent physical component. Psychic and physical dependence often occur together, so that treatment must address both somatic and psychological cravings.

What causes people to abuse drugs and alcohol?
Obviously, there is no single factor that accounts for why some people develop these disorders and others do not. The following variables seem to be important in determining patterns of drug abuse:



Availability of drugs.
People who work in situations where drugs are readily ac-cessible are more prone to abuse them (e.g., bartenders).

Onset of action of the drug.
Drugs that act quickly (e.g., alcohol, fast-acting barbi-turates) are more prone to be abused than those that exert their effects more slowly.

Development of tolerance and physical dependence.
Withdrawal symptoms are unpleasant and may be life-threatening. The avoidance of these symptoms is a powerful factor in the continued use of drugs that create physiologic dependence (e.g., alcohol, heroin).

Genetic background.
The child of an alcoholic is at a greater risk of developing alcoholism than the child of a nonalcoholic family. There thus appears to be some genetic predisposition to alcoholism.

Childhood environment.
In addition to the genetic factors mentioned above, alco-holics (particularly men) are more likely than nonalcoholics to have alcoholic par-ents and siblings. In these family drinking habits are allowed.

Culture.
Drug abuse is less likely where drug use is prohibited on religious grounds, or where there are clear guidelines for nonabusive drug use. Thus, rates of alcoholism are very low among Moslem and Mormon communities, where alcohol is prohibited.

Socioeconomic status.
Drug abusers often fail to conform to popular stereotypes. To be sure, there are sociopathic addicts who live on the street and steal to finance a heroin habit. But other "hard-core" addicts and alcoholics include physicians, teachers, housewives, and students—people from all backgrounds and socioeco-nomic groups.

Psychiatric illness.
Many people who abuse drugs and alcohol suffer from mental disorders. It is often difficult to distinguish between psychiatric symptoms that re-sult from substance abuse and those that prompt it. It is clear that many patients begin to abuse drugs to "medicate" pre-existing emotional disorders such as de-pression, anxiety, and psychosis (e.g., the depressed homemaker who becomes ad-dicted to Valium). Disorders that commonly underlie drug abuse include affective disorders, anxiety disorders, somatoform disorders, and personality disorders (e.g., borderline, narcissistic, and antisocial personality disorders). No one personality type has been found among substance abusers. People who become alcoholics have often been stereotyped as passive, dependent, and depressed..



ALCOHOLISM
It is estimated that 5 to 10 percent of the adult population in the United States is suffer from alcoholism. It is more prevalent among men than women, but the inci-dence among women is increasing. A public health problem of major proportions, alcoholism is also significantly underdiagnosed—perhaps as many as half of the alcoholics seen by physicians go entirely undiagnosed. This occurs in part because alcoholics tend to strongly deny that they have a problem,-in many cases, only family and friends can supply accurate information about drinking habits and re-sulting impairment of functioning. The alcoholic is likely to explain job difficulties and interpersonal problems as the causes rather than the results of drinking. Alco-holics commonly do not seek treatment until they are forced to by others. This of-ten involves some sort of confrontation. For example, an spouse may threaten to leave if the alcoholic does not stop drinking. Alcoholics want to hide the severity of their drinking problem from you, from friends and family, and from themselves. They will tend to minimize the extent to which they abuse alcohol, and see their current physical or psychiatric symptoms as unrelated to drinking.



Diagnosis
Ask every patient about the amount and frequency of alcohol use. Assume alcohol use and begin with such questions as "How much do you drink? In what situations? How often do you take a drink?"
"Do you have several drinks each day?" When you suspect a problem, the follow-ing questions may help you clarify the situation.
Are you irritated when your family or friends comment on your drinking? Have you ever argued with someone close to you about your drinking?
When drinking with others, do you try to have a few extra drinks when others will not know it? Did you ever wake up "the morning after" and discover that you could not remember part of the evening before, even your friends tell you that you did not pass out? Can you control your drinking? Do you try to avoid family or close friends when you are drinking?
Are you having more financial or work problems lately? Do you eat little or irregu-larly when you are drinking?
Have you ever been in a car accident after you have been drinking, or have you ever been arrested for drunk driving?
Do you sometimes have "the shakes" in the morning and find that it helps to have a little drink?
Do you sometimes drink for several days at a time?
After periods of drinking, do you sometimes see or hear things that aren't really there?
Positive answers to any of the questions at the beginning of this list should make you think seriously about alcoholism and explore the matter further. If you suspect that your patient is denying the seriousness of the problem, ask to speak with fam-ily members, and do so with the patient in the room. This should help you assess the extent to which alcohol has impaired work, home life, or health. In particular, be alert to a history of withdrawal symptoms ("the shakes," delirium tremens) or "blackouts" (memory loss while intoxicated), for these are clear signals that the problem is significant and may result in serious withdrawal reactions in the future.

Treatment
Once you have diagnosed alcohol abuse, you must decide what forms of treatment are indicated and assess your patient's motivation for treatment Obviously, emer-gency situations must be treated first Anyone presenting with severe intoxication that threatens to compromise respiratory functioning, or with severe withdrawal symptoms like delirium tremens or seizures, should be admitted immediately to a medical ward or intensive care unit For information on the management of these situations, consult a general medical textbook.
Patients who present for psychiatric evaluation are generally those for whom there is no medical emergency, but they may require careful medical and psychiatric treatment in order to avert consequences of alcohol abuse or withdrawal.

Detoxification.
Detoxification is the first step in the treatment of those who are addicted to alcohol and have experienced significant withdrawal symptoms when they have stopped drinking in the past. Detoxification is generally carried out on a medical or psychiatric inpatient unit, in order to allow careful monitoring of the pa-tient's physical status and to prevent potentially lethal withdrawal reactions. Inpa-tient treatment also allows the patient to begin other types of therapy, which can be continued on an outpatient basis.
Physiologic withdrawal from alcohol usually begins 6 to 24 hours after the patient has stopped a period of heavy drinking, and may begin as late as 36 hours after the patient's last drink.



EARLY MANIFESTATIONS OF ALCOHOL WITHDRAWAL.

Signs
Tachycardia (increasing pulse rate)
Elevation of systolic blood pressure
Sweating
Fever
Hyperventilation
Hyperreflexia

Symptoms
Irritability
Agitation
Difficulty concentrating
Insomnia
Abdominal pain
Nausea, vomiting
Diarrhea
Tremulousness ("shakes")
Self-limiting
agitation, delirium, and hallucinations

Acute alcoholic hallucinosis
Most common in the first 24-48 hours after the last drink. It involve auditory hallu-cinations. Consciousness is kept.

Delirium tremens
Usually occur 50-100 hours after the last drink,- may last up to 1 week
Hallucinations, delusions
Hypermetabolic state: hyperpyrexia, dehydration, electrolyte imbalance
Mortality as high as 15 percent
Major withdrawal syndromes can usually be prevented by treating earlier manifes-tations before they become severe.

Treatment of early signs of alcohol withdrawal.
Chlordiazepoxide (Librium) is an effective pharmacologic substitute for alcohol that has a wide margin of safety, little respiratory depression, low addiction potential, anticonvulsant effects, and a long half-life (24-30 hours).
Treatment should be begun as soon as patients show any of the early signs of with-drawal evaluated pulse rate (over 110 beats per minute), elevated systolic blood pressure, sweating, or elevated temperature. These signs are more reliable indica-tors than subjective symptoms like anxiety and agitation, which may be present for many reasons other than withdrawal.
1. Give 50-100 mg of chlordiazepoxide orally at the first signs of withdrawal (the dose will depend on the patient's physical size and extent of recent alcohol abuse). For persistent symptoms, the dose may be repeated in an hour.
2. Patients experiencing withdrawal can then be put on an ongoing regimen of 25-100 mg of chlordiazepoxide orally every 4 hours as needed to keep vital signs sta-ble during the first day. The average patient will require 300-400 mg/day on the first day. The total daily dosage should not exceed 600 mg.
3. Further doses should be given as needed for agitation, hypertension, or tachy-cardia. A useful guideline is to medicate so as to keep the pulse rate below 110, provided the patient is alert.
4. After the first 24 hours, if symptoms are controlled, the dosage of chlordi-azepoxide may be cut in half each day until it is tapered off within four to five days.
5. If more than 400 mg/day of chlordazepoxide is required to control symptoms in the first day of withdrawal, 50 mg of chlorpromazine (Thorazine) can be added orally to each 100-mg dose of chlordiazepoxide, but this may complicate the treatment, since chlorpromazine lowers the patient's seizure threshold.
Once withdrawal symptoms have been controlled, other forms of treatment may be initiated.
You may be surprised by the onset of alcohol withdrawal among patients you have admitted to the hospital for seemingly unrelated medical or psychiatric reasons but who have a history of recent heavy drinking. These people may only admit to the full extent of their alcohol abuse when, in a setting where alcohol is suddenly un-available, withdrawal symptoms set in. You must therefore consider the possibility of alcohol withdrawal whenever you hospitalize a patient who has a history of al-cohol abuse.

Korsakoff's syndrome.
The medical consequences of alcohol addiction, such as hepatic cirrhosis and polyneuropathy, are well outlined in general medical texts. One neuropsychiatric syndrome deserves special mention here because it is charac-terized by dramatic psychological symptoms. Chronic alcoholics develop the syn-drome, presumably because of a prolonged inadequate diet that results in thiamine deficiency. Korsakoffs syndrome is a chronic condition. It may also occur after one or more episodes of delirium tremens. The most prominent feature of Korsa-koff's syndrome is recent memory impairment, although peripheral neuropathy, ataxia, and oculomotor difficulties may also be present. Classically, these patients have been described as using confabulation— i.e., fabricating answers to questions in an attempt to fill in details they do not recall. However, confabulation is actually infrequent and is not necessary to establish the diagnosis. The most common mem-ory impairment involves difficulty in learning new information (e.g., your name). Korsakoff's syndrome improves in about 75 percent of patients who stop alcohol abuse and are maintained on an adequate diet for six months to two years, but only about 25 percent of those with this syndrome achieve full recovery. The only pre-vention against Wernicke-Korsakoff syndrome is an adequate diet, and, after emergency treatment with thiamine, diet is the only necessary treatment for those recovering from the syndrome.

Wernicke's encepbalopatby
is an acute, life-threatening condition characterized by clouding of consciousness, ophthalmoplegia (weakness of the muscles controlling movement of the eyes), and ataxia (a wide-based gait, falling, or inability to walk or stand).
.
Long-term treatment of alcoholism.
Most clinicians consider alcoholism a dis-ease rather than a moral failing. This viewpoint is useful in helping to alleviate the heavy burden of guilt carried by many alcoholic patients. However, the disease concept does not absolve alcoholics from responsibility for their drinking, nor does it imply that other people can bail them out of their difficulties. The treatment of alcoholism is long and difficult for patients, families, and treaters alike. Alcoholics are asked to give up forever a substance they truly (if ambivalently) love.
Effective treatment involves giving patients a nonchemical substitute for the lost addiction, reminding them continuously that even one drink can lead to relapse, re-pairing the social and medical damage that has occurred, and restoring their self-esteem. A variety of treatment modalities have been employed to achieve these goals, the most effective of which are listed below.
Alocholics Anonymous (AA). This is the most effective treatment known for al-coholics. It provides continuously available group support by individuals who have themselves suffered from alcoholism. Meetings are held in many cities at every hour of the day and night, so that support is available as frequently as the alcoholic wishes it. These meetings involve peer support and gentle confrontation of the ways in which alcoholics deny their illness. AA techniques also help the alcoholic understand the conditioned and impulsive aspects of drinking. AA replaces drink-ing companions with a new group of peers with whom the alcoholic can identify. It allows members not only to receive help from other alcoholics, but also to give help to others, thereby enhancing self-esteem.
Many alcoholics are initially reluctant to participate in AA. In recommending this treatment, you should be consistently supportive and, if possible, find a way for other AA members to personally introduce the patient to these meetings. Because alcoholism often takes a devastating toll on the families of alcoholics, you may want to refer them to Al-Anon, a self-help group that helps spouses deal with their own emotional difficulties, as well as teaching them about alcoholism and how to avoid interfering with the alcoholic's recovery. Alateen is a similar organization that offers support to adolescents who are coping with alcoholic parents.
Psychotherapy. This is not the primary treatment of choice of alcoholism, for it cannot provide the continuous support that is often required. However, when used adjunctively with other modalities like AA, it can be extremely useful—e.g., in helping to uncover family problems that perpetuate the patient's drinking, and in helping the patient to see ways in which drinking provides him or her with certain benefits (secondary gains). In most cases, psychotherapy cannot be effective until the patient stops drinking, for only then can the therapy address the uncomfortable feelings and symptoms the alcoholic habitually "medicates" away with ethanol.
Disulfiram (Antabuse). This medication blocks the normal oxidation of alcohol so that acetaldehyde accumulates in the bloodstream and causes unpleasant symp-toms, such as tachycardia and vomiting. Obviously, the use of this medication is voluntary (usually in oral doses of 125 or 250 mg/day) and patients must be made aware of its adverse interactions with alcohol. Although Antabuse provides a deter-rent to drinking, it does not help with such factors as low self-esteem and the loss of the addicting substance. By itself, therefore, it is of limited use in the treatment of alcoholism. However, many clinicians use it in conjunction with AA or psycho-therapy.
Behavior modification. Hypnosis, desensitization, relaxation training, and aver-sion therapy (coupling alcohol use with noxious stimuli like shocks or emesis) have been somewhat successful in treating alcoholism. In particular, aversion ther-apy that couples alcoholism with emesis has shown some promise.
Adjunctive services. Halfway houses, vocational rehabilitation programs, and other social institutions that give alcoholics support and help them recover lost skills have been useful as part of a treatment plan that includes other modalities like AA.

OPIATES
Opium is an ancient drag around which entire cultures and economies have re-volved. Today, many opium-related compounds are used illegally in this country. In addition to the natural alkaloids of opium— morphine and codeine—there are important synthetic derivatives— such as heroin, dihydromorphinone (Dilaudid), and oxymorphone (Numorphan)—as well as purely synthetic opioids, such as meperidine (Demerol), methadone (Dolophine), phenazocine (Prinadol), pentazo-cine (Talwin), and dextropropoxyphene (Darvon).
All of these drags are sedating,- more importantly, they are the strongest pain-killers known. Thus, they are highly useful for medical purposes. However, they have strong potential for the development of tolerance, as well as psychological and physiological dependence. Although the majority of narcotics addicts live in the slums of large cities and obtain drugs on the street, addiction cuts across all class and social lines. Some health care professionals who have ready access to narcotics become addicted to them. Men outnumber women by almost four to one among narcotics addicts.
Many addicts seek treatment for their addiction in outpatient settings, but you may also encounter them in emergency rooms when they are experiencing acute symp-toms of overdose or withdrawal.
Overdose
The signs of acute overdose are the following: constricted pupils, diminished pulse rate, diminished respiratory rate, pulmonary edema, and stupor or coma. Acute overdose requires emergency treatment. First, support the patient's vital functions, and administer glucose intravenously. Then use an opioid antagonist. Although there are several drugs that block the action of opiates, naloxone (Narcan) is the drug of choice, since it is pharmacologically inert in the absence of opiates. The usual initial adult dose is 0.4 mg intravenously, although up to 1.2 mg may be re-quired to reverse coma and respiratory depression. Comatose patients should be put into physical restraints before Narcan is given, since they may be combative as they emerge rapidly from coma. Narcan will reverse the signs of acute overdose within minutes, but its effect may wear off within 30 to 120 minutes, at which time the narcotic will again produce symptoms of overdose. Thus, patients who emerge from coma must not be allowed to leave the hospital but must be monitored care-fully for up to 48 hours, repeating the administration of Narcan as needed.
Withdrawal
Withdrawal from opiates has been given much publicity in films and on televi-sion, and the abstinence syndrome associated with narcotics is very unpleasant. However, abrupt withdrawal is not life-threatening in otherwise healthy patients, as it may be from severe alcohol or barbiturate addiction. In fact, in terms of discom-fort and medical danger, opiate withdrawal has been compared to a one-week bout with influenza.

SYMPTOMS OF OPIATE WITHDRAWAL.
Early (12-36 hours after last dose)
Yawning
Sweating
Gooseflesh (piloerection)
Insomnia
Dilated pupils
Anorexia
Muscle cramps
Tremor
Late (48-72 hours after last dose)
Abdominal cramps
Diarrhea
Vomiting
Elevated blood pressure
Increased respiratory rate
Increased heart rate
Fever

Treatment of Opiate Withdrawal
Methadone substitution. Methadone is a synthetic opiate that has proved to be ef-fective in treating withdrawal from narcotics because it is long-acting and produces little euphoria (even so, it is commonly abused by recovering addicts). It is used for withdrawal primarily on an inpatient basis and in certain specialized outpatient clinics. It is given orally, beginning with 10 mg every 4-6 hours as needed for signs of withdrawal, and generally no more than 40 mg in a 24-hour period. The dose is adjusted to the minimum level that will suppress symptoms, and is then decreased by 5 mg (or 20 percent) every day until it is discontinued. It is important to use ob-jective signs (blood pressure, temperature, heart rate) to assess the patient's condi-tion, rather than relying on subjective complaints.
Clonidine. Recent studies have demonstrated that clonidine is very effective in al-leviating the signs and symptoms of withdrawal from opiates, presumably by sup-pressing the noradrenergic hyperactivity that appears to mediate the withdrawal process. Clonidine is nonaddicting and produces no euphoria, so it is not likely to be abused. New research suggests that it may be the most effective treatment avail-able for withdrawal from methadone, heroin, and other opiates.
Outpatient methadone maintenance. This is a controversial treatment designed to provide addicts with methadone as a long-term substitute for street drugs, in or-der to reduce the craving for these drugs. Methadone is given in doses of up to 120 mg orally per day, and addicts are monitored carefully with urinalyses and other control measures. However, abuse of methadone and its illicit sale on the street have been complications of such programs. Methadone maintenance must be car-ried out in conjunction with other support services that address the social aspects of addiction.
Long-acting opioid antagonists. These agents, such as naltrexone, prevent addicts from experiencing the effects of narcotics, and thus are thought to act as deterrents to drug abuse. The long-term use of opioid antagonists is still an experimental form of treatment, but some clinicians have achieved promising results with low rates of relapse.

Alcohol damaging stages in liver

Effects of over driniking


CENTRAL NERVOUS SYSTEM DEPRESSANTS
Sedatives, hypnotics, and antianxiety agents all depress the central nervous system (CNS). They are often referred to as downers. Most are prescription drugs that are either obtained illegally or obtained legally from physicians but misused. The pharmacologic properties of these drugs are described in Chapter 15. Downers are commonly abused along with alcohol and opiates, and both abuse and overdose frequently involve combinations of drugs. Individuals who use barbiturates and other sedative-hypnotics are very prone to develop psychological dependence, fol-lowed by increasing tolerance and physical dependence.

Overdose
The symptoms of intoxication and overdose resemble those of drunkenness—drowsiness (coma in severe overdoses), slurred speech, lack of coordination, mem-ory impairment, confusion, nystagmus, tremor, decreased muscle tone, agitation, paranoia, and inappropriate affect
Management of overdose. If the patient is awake, induce vomiting or perform gastric lavage to clear the stomach of any unabsorbed substance. Send blood and urine samples and gastric contents for toxicologic analysis. Monitor and support respiratory and cardiac functions for at least 24 hours.
If the patient is comatose or semicomatose, attempt gastric lavage if the drug was taken less than 12 hours before. Alkalinize the urine to increase excretion. Support basic Life functions through intubation, administration of oxygen, plasma expand-ers, and vasopressors.
Obviously, severe overdose with CNS depressants requires immediate medical at-tention and necessitates admission to a facility where intensive care can be pro-vided.

Withdrawal
Withdrawal from CNS depressants can be quite dangerous if it occurs abruptly. In particular, withdrawal can result in seizures and cardiovascular collapse, and it car-ries a significant risk of death. The possibility of withdrawal must be considered for every patient who presents with a history of abuse of or dependence on CNS depressants.

SYMPTOMS OF WITHDRAWAL FROM CNS DEPRESSANTS.
Agitation
Anxiety
Anorexia
Vomiting
Increased heart rate
Postural hypotension
Hyperreflexia
Tremor
Severe Seizures
Delirium
Hypothermia
Cardiovascular collapse

Treatment of withdrawal
Treatment is conducted on an inpatient basis and relies on substitution of pento-barbital for the abused CNS depressant Pentobarbital is a shorts acting barbiturate that is used to alleviate withdrawal symptoms and subsequently tapered over many days. Treatment begins with a pentobarbital tolerance test on day 1, to determine how much pentobarbital must be given initially to prevent severe withdrawal.

Pentobarbital tolerance test. First, a 200-mg test dose of pentobarbital is given orally. If intoxication results (with nystagmus and/or ataxia), then tolerance is not presumed to be great, and the patient is maintained on 150-200 mg of pentobarbital orally every six hours for the first day of treatment.
If no intoxication results from the 200-mg test dose, the patient is given 100 mg orally every 2 hours until intoxication develops. The total dose required to produce intoxication is then given every six hours for the first 24 hours of treatment. That is, if intoxication develops after 400 mg has been given, the dose for day 1 is 400 mg orally every six hours.
After the first 24 hours, the dose of pentobarbital is reduced by 10 percent each day and withdrawn gradually over a period of about three weeks. Patients are moni-tored carefully for signs of intoxication or withdrawal, with subsequent adjust-ments in dosage.
Some clinicians use phenobarbital instead of pentobarbital in the treatment of withdrawal, because there is less fluctuation in blood levels of phenobarbital and because it has antiseizure activity. In this procedure, substitute 30 mg of phenobar-bital for each 100 mg of pentobarbital, in three divided doses, and decrease the dose by 30 mg/day.
If a patient is dependent on both opiates and barbiturates, barbiturate withdrawal is carried out first.

CENTRAL NERVOUS SYSTEM STIMULANTS
Amphetamines
Amphetamines are prone to abuse by a wide variety of people, including students who want to be able to stay up for many hours preparing for examinations or writ-ing papers. However, amphetamine use in large doses can produce acute delirium and psychosis. Overdose is potentially lethal. The symptoms of amphetamine in-toxication and overdose are listed in Table 11-5.
Treatment of acute intoxication involves decreasing CNS irritability and control-ling psychotic symptoms. Toward this end, support and reassurance in a quiet set-ting may suffice hi mild intoxication. In more severe cases, 25-50 mg of chlorpro-mazine (Thorazrne) administered orally every six hours will ease agitation and di-minish psychosis.
Amphetamine psychosis occurs in a more chronic form after prolonged use of the drug. The psychotic symptoms can be difficult to distinguish from schizophrenia. Symptoms include talkativeness, hyperactivity, stereotyped or repetitious behavior, bruxism (grinding the teeth), picking movements, suspiciousness, and (in more se-vere cases) persecutory delusions, hallucinations, ideas of reference, and hypersex-uality. Management of amphetamine psychosis is also carried out with antipsy-chotic medication (e.g., chlorpromazine in the doses noted above) to decrease agi-tation and diminish psychotic symptoms.

SYMPTOMS OF AMPHETAMINE INTOXICATION AND OVERDOSE.
Restlessness
Irritability
Weakness
Confusion
Talkativeness
Anxiety
Tremor
Hyperreflexia
Insomnia
Euphoria, with lability of mood
Delirium
Hallucinations
Paranoia166

Although physical addiction to amphetamines does not develop, a sudden with-drawal of the stimulant after prolonged use or administration of high doses results in a marked decrease in CNS activity known as "crashing," which is characterized by somnolence, fatigue, apathy, and severe depression that may lead to suicidal ideation. Patients need sleep, as well as physical and emotional support, until CNS activity returns to normal.

Cocaine
Cocaine use has increased dramatically in the United States in recent years. It en-joys a special status as the recreational drug of the affluent Its use results in an ini-tial stimulation of the CNS like that seen in amphetamine use, followed by CNS depression. The drug is commonly absorbed via the nasal mucosa after "snorting," but smoking and intravenous use are also common and are more likely to be the routes in severe overdoses. Overdose may result in psychosis and even cardiac ar-rest
Antipsychotic drugs help to diminish psychosis in cases of cocaine overdose, and propranolol is used to decrease cardiac excitation. Although cocaine does not cre-ate physical dependence, it can create a psychological dependence resulting in chronic use.

HALLUCINOGENS
Hallucinogens include a wide variety of substances grouped together somewhat ar-bitrarily based on their ability to induce altered states of awareness that resemble those of natural psychoses. Some hallucinogens, like psilocybin (mushroom) and mescaline (peyote cactus), come from natural sources, while drags like D-lysergic acid diethylamide (LSD) and dimethyltryptamine (DMT) are synthetic.
Signs and symptoms of hallucinogen intoxication include alter ation of mood (of-ten euphoria), vividness of real or fantasied sensory illusions and hallucinations, synesthesia ("overflow" from one sensory modality to another), and confusion. Many other psychological manifestations may be present, including a sense of time slowing, a loss of body boundaries, and feelings of grandiosity or omnipotence.
Although each hallucinogen has slightly different characteristics and produces somewhat different signs and symptoms, they all produce adverse reactions in some people. These reactions include acute panic attacks, psychosis, flashbacks, and precipitation of underlying psychosis (e.g., in people with latent schizophre-nia). Whether a person has an adverse reaction to a hallucinogen (a "bad trip") de-pends on such factors as the dose of the drug, the setting in which it is used, and the personality characteristics of the user. LSD intoxication is particularly com-mon, and is manifested by such physical signs as pupillary dilation, hyperreflexia, muscle weakness, increased blood pressure, increased heart rate, and fever.

Treatment of hallucinogen intoxication generally involves support, reassurance, and diminishing stimulation around the patient until the drug wears off. hi many cases, putting the patient in a quiet, dimly lit room and talking to help him or her distinguish psychotic symptoms from reality will suffice to weather the crisis. However, severe panic may be treated effectively with oral or parenteral diazepam (Valium). Unless psychosis is unusually severe and prolonged, it is best to avoid using antipsychotic medication because of possible adverse anticholinergic reac-tions.
Phencyclidine (PCP) is unique in action compared with other psychedelic drugs, and it is not a true hallucinogen. A synthetic drag initially developed as a possible anesthetic agent for humans, it is now licensed only for use as an immobilizing agent for nonhuman primates. Often called "angel dust," it is a common drug of abuse. Its psychological effects include changes in body image (e.g., "My head is growing larger"), depersonalization, anxiety, disorganization of thought, depres-sion, and hostility. PCP abusers sometimes behave with great violence under the influence of the drag. Physical signs of intoxication include elevated blood pres-sure, rapid respiration, and neurological signs such as nystagmus, muscle spasm and rigidity, and ataxia. PCP intoxication can result in coma and death.
Treatment of mild to moderate intoxication is different from that for hallucinogens in that "talking patients down" is not usually helpful and may even increase the pa-tient's anxiety. Instead, placing the patient in a quiet, dimly lit room with a mini-mum of stimulation is successful in most cases. Diazepam (Valium) is used intra-venously if severe myoclonus or seizures result Antipsychotics are not generally helpful. Most cases of intoxication resolve after several hours of reduced stimula-tion (e.g., in a secluded room in an emergency ward), but some result in prolonged and severe behavioral disturbances, exaggeration pre-existing thought disorders, and serious medical complications that require hospital admission.

CANNABINOIDS
Cannabinoids, such as marijuana and hashish, are mild euphoriants with some sedative effects. Many people use these drags as others use alcohol socially. It is estimated that as many as 30 million Americans have had some experience with marijuana, but only a fraction of that number use the drug heavily on a continuous basis. Signs and symptoms of acute intoxication include disconnected speech, re-cent memory impairment, emotional lability, depersonalization, and confusion, as well as increased heart rate, conjunctival injection, and decreased body tempera-ture. While adverse reactions such as panic, psychosis, and depression do occur as a result of cannabis intoxication, these reactions are rare.
The effects of chronic use of cannabinoids are the subject of some debate. Chronic psychotic states secondary to cannabis use have been reported in Eastern cultures where doses are presumably much higher, but such reactions have been rare in the West. Some clinicians have identified amotivational syndrome of low drive, poor judgment, introversion, loss of insight, poor communication skills, and depersonal-ization. This syndrome occurs in people who use marijuana heavily on a regular basis for many months or years. At this time, however, it is not clear whether heavy cannabis use causes or results from this condition of low motivation, and adverse effects of intermittent cannabis use have not been clearly identified.

TREATMENT OF POLYDRUG ABUSE
Your first task in dealing with people who abuse drags is to avoid stereotyping them. As was noted above, polydrag abusers come from all backgrounds—including highly educated professionals and "sweet little old ladies." If you only look for people who come in covered with tattoos and needle marks, you will fail to notice the many cases in which substance abuse is a major problem.
Your second task is to take a nonjudgmental approach to the evaluation and treat-ment of drag abusers. Clinicians often see addicts as hopeless cases. Your first im-pulse in dealing with such people may be to try to usher them out of your office as quickly as possible. Every drug abuser you see deserves a thorough medical and psychiatric evaluation, with particular attention to possible underlying psychiatric illness (e.g., affective illness, anxiety disorders, personality disorders). You should either do the evaluation yourself with supervision, or you should refer the patient to a psychiatrist who is experienced in the treatment of drag abuse, or to a drag treatment center.
Treatment of drag abuse is difficult. Detoxification and crisis management are only the beginning of a long and difficult course to recovery. Like alcoholism, polydrag abuse involves substituting a substance for human contact. Many addicts' lives re-volve around the process of obtaining drags, and this provides a daily structure and a set of personal contacts that must be replaced even after physical addiction is eliminated. Also, polydrag abusers often "medicate" unpleasant feelings (anxiety, depression) that are likely to persist or worsen when the drag is taken away.
Reformed drag abusers who come from lower socioeconomic groups often find lit-tle support among peers who are likely to be antisocial and to encourage drag abuse. Thus, an important part of treatment for many patients consists of helping them to establish new support systems. This may take the form of self help groups like Narcotics Anonymous or Pills Anonymous (similar to Alcoholics Anonymous), vocational rehabilitation programs, day care centers, or drag-free residential com-munities (e.g., Synanon).
Psychotherapy
cannot, in and of itself, provide the continuous support and peer group encouragement many recovering substance abusers require. However, as an adjunct to other treatment programs, psychotherapy can help some drag abusers to cope more effectively with feelings and problems that may have promoted drag use in the first place. Family therapy can also be useful in pointing out the family's pathological patterns of coping with stress. Group therapy can be especially useful in providing support, as well as in confronting drug abusers with the consequences of their self-destructive and antisocial behaviors, especially when other group members are themselves recovering or recovered drug abusers. No one treatment modality is as useful as a combination that provides the patient with support, daily structure, and vocational skills that help to increase self-esteem.

TO KILL YOURSELF DRINK ALCOHOL!!!!!!