Prepared by Assist Prof Prepared by Assist Prof Dr Sirwan K AliDr Sirwan K AliCollege of Medicine (2012-2013)College of Medicine (2012-2013)

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A primary, chronic, neurobiological disease, with genetic, psychosocial, and environmental factors influencing its development and

manifestations

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Chronic Compulsive use, not associate with

willpower Control-impaired--unable to limit intake Craving--desire for the drug when it is

absent Continued use despite harm—irrational

pursuit of mood change/high at expense of family, job, emotional well-being, and

health

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DIAGNOSIS AND DSM-IV CRITERIA

Abuse is a pattern of substance use leading to

impairment or distress for at least 1 year with one or more of the following manifestations:

1. Failure to fulfill obligations at work, school, or home

2. Use in dangerous situations (i.e., driving a car)

3. Recurrent substance-related legal problems4. Continued use despite social or interpersonal

problems due to the substance use

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A maladaptive pattern of substance use leading to clinically significant impairment or distress, manifested by 3 or more of the following occurring at any time within the same 12 month period:

Tolerance-need for more to achieve the same effect-decreased effect with same amount

Withdrawal -Characteristic withdrawal syndrome -Using substance to avoid withdrawal Sx

Substance taken in larger amount or for longer time than intended

Persistent unsuccessful attempts to cut down or control use

Great deal of time spent obtaining, using, or recovering from use

Important social, occupational, recreational activities given up or reduced

Use is continued despite knowledge that has persistent or recurrent physical or psychological problems that were caused or exacerbated by use

Reinforcing behaviors / Pleasure Circuit/ reward circuit/ hippocampal and limbic memory circuit

acute increases of levels of neurotransmitters in the brain

Increased Dopamine (DA) in the limbic areas (ventral tegmental DA neurons synapsing on the nucleus accumbens neurons is very rewarding.

Some drugs also increase serotonin and/or norepinephrine.

Reinforcing behaviors / Pleasure Circuit/ reward circuit/ hippocampal and limbic memory circuit

acute increases of levels of neurotransmitters in the brain

Ex. Increased Dopamine (DA) in the limbic areas (ventral tegmental DA neurons synapsing on the nucleus accumbens neurons is very rewarding.

Some drugs also increase serotonin and/or norepinephrine.

Lifetime prevalence of substance abuse or dependence in the United States: Approximately 17%

More common in men than women

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Up to 50% spousal abuse 50% traffic accidents 49% murders 68% manslaughter charges 69% drownings 38% child abuse 52% rapes 62% assaults 20-35% suicides

(Johnson-1997)

100 million annually 40% industrial fatalities 47% workplace injuries 50% of motor vehicle fatalities(2005)

Illegal drugs: $181 billion/year Alcohol: $185 billion/year Tobacco: $158 billion/year

Total: $524 billion/year

Surgeon General’s Report, 2004; ONDCP, 2004; Harwood, 2000.

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Alcohol Amphetamines and

related substances Caffeine Cannabis Cocaine Hallucinogens

Inhalants Nicotine Opioids Phencyclidine and

related substances Sedatives,

hypnotics, or anxiolytics

Categories of DrugsCategories of Drugs

Stimulants - “uppers”

- stimulate the central nervous system

- amphetamines, amyl nitrite, cocaine, crack, ecstasy

Depressants - “downers”

- depress the central nervous system

- alcohol, barbiturates, benzodiazepines

Analgesics - powerful painkillers

- from opium poppy or synthetically produced

Hallucinogens - dramatically alter perception

- LSD, psilocybin, cannabis, ecstasy

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Biological Factors Genetics: apparent hereditary factor, particularly with

alcoholism Biochemical: alcohol may produce morphine-like substances in

the brain that are responsible for alcohol addictionPsychological Factors Developmental influences:

◦ Punitive superego◦ Fixation in the oral stage of psychosexual

development Personality factors: certain personality traits suggested to play a

part in both development and maintenance of alcohol dependence, including◦ Low self-esteem◦ Frequent depression◦ Passivity◦ Inability to relax or defer gratification◦ Inability to communicate effectively

Social learning: children and adolescents more likely to use substances with parents who provide model for substance use

Use of substances may also be promoted within peer group

Conditioning: pleasurable effects from substance use act as a positive reinforcement for continued use of substance

Cultural and ethnic influences: some cultures are more prone to the abuse of substances than others

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Alcohol activates gamma-aminobutyric acid (GABA) and serotonin receptors in the central nervous system (CNS) and inhibits glutamate receptors. GABA receptors are inhibitory, and thus alcohol has a sedating effect.

Alcohol is the most commonly abused substance in the United States. 7 to 10% of Americans are alcoholics, (also in our community)

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Alcohol Abuse and Dependence Patterns of Use or Abuse Phase I: Pre-alcoholic phase: characterized

by use of alcohol to relieve everyday stress and tensions of life

Phase II: Early alcoholic phase: begins with blackouts: brief periods of amnesia that occur during or immediately following a period of

drinking; alcohol is now required by the person. Phase III: The crucial phase: person has lost

control; physiological dependence clearly evident Phase IV: The chronic phase: characterized by

emotional and physical disintegration; person is usually intoxicated more often than sober

The CAGE questionnaire is used to screen for alcohol abuse. Two or more “yes” answers are considered a positive screen; one “yes” answer should arouse suspicion of abuse:

1. Have you ever wanted to cut down on your drinking?

2. Have you ever felt annoyed by criticism of your drinking?

3. Have you ever felt guilty about drinking?

4. Have you ever taken a drink as an “eye opener” (to prevent the shakes)?

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Maladaptive drinking leading to clinically significant impairment or distress, shown by 3+ of the following in the same 12-month period:

1. Drinking more or longer than intended2. Persistent desire or unsuccessful efforts to cut down or

stop3. A great deal of time spent on drinking or getting over its

effects4. Important activities given up or reduced because of

drinking5. Continued drinking despite knowledge of a serious physical

or psychological problem6. Tolerance7. Withdrawal, or drinking to avoid or relieve drinking

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Not dependent, and maladaptive drinking leading to clinically significant impairment or distress, shown by 1 + of the following:

1. Continued use despite social/interpersonal problems

2. Hazardous use (e.g., driving when impaired by alcohol)

3. Frequent drinking leading to failure to function in major roles

4. Legal problems

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What is the safe level of alcohol?A widely accepted measure is the term of units of alcohol One unit is a 8 grams of ethanol, correspond to half a pint of beer, a wine glass of wine..etcSafe level; Men; up to 21 units per week. Women: up to 14 units per week.Dangerous level; Men: over 50 units per week. Women: over 35 units per week.

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Acute intoxication:◦ euphoria, flushed face, ataxia, slowed reaction

time, impaired motor performance, slurred speech, poor concentration; in higher doses behavioural changes – disinhibition of sexual and aggressive impulses, increased suicidal and homicidal behaviour

Pathological intoxication:◦ sudden change of consciousness with aggressive

behaviour and amnesia Harmful use:

◦ physical complications – hypertension, arteriosclerosis, heart infarction, cardiomyopathy, brain stroke, liver cirrhosis, fatty liver, gastritis, etc.

◦ psychic complications - depression 04/21/23 25

Hypoglycemia, hypoxia, mixed EtOH–drug overdose, ethylene glycol or methanol poisoning, hepatic encephalopathy, psychosis, and psychomotor seizures

DIAGNOSTIC EVALUATIONSerum EtOH level or an expired air

breathalyzer can determine the extent of intoxication.

A computed tomographic (CT) scan of the head may be necessary to rule out subdural hematoma or other brain injury.

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Intoxication (Acute) Ensure adequate airway, breathing, and circulation. Monitor

electrolytes and acid–base status. Obtain finger-stick glucose level to exclude hypoglycemia.

Thiamine (to prevent or treat Wernicke’s encephalopathy), naloxone

(to reverse the effects of any opioids that may have been ingested), and

folate are also administered.

The liver will eventually metabolize alcohol without any other interventions provided that a reliable airway is maintained;

a severely intoxicated patient may require intubation while he or she is recovering.

Gastrointestinal evacuation (e.g., gastric lavage and charcoal) has no role in the treatment of EtOH overdose but may be used in mixed EtOH–drug overdose.

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1. Alcoholics Anonymous—self-help group2. Disulfiram (Antabuse)—aversive

therapy; inhibits aldehyde dehydrogenase,

causing violent retching when the person drinks3. Psychotherapy and selective serotonin

reuptake inhibitors (SSRIs)4. Naltrexone—though an opioid

antagonist, helps reduce cravings for alcohol.

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The pathophysiology of the alcohol withdrawal syndrome is poorly understood.

Patients experiencing mild withdrawal may be irritable and complain of insomnia. Those in more severe withdrawal may experience fever, disorientation, seizures, or hallucinations.

The signs and symptoms of the alcohol withdrawal syndrome include insomnia , anxiety, tremor, irritability, anorexia, tachycardia, hyper-reflexia, hypertension, fever, seizures, hallucinations, and delirium.

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Delirium tremens (DTs) is the most serious form of EtOH withdrawal and often begins within 72 hours of cessation of drinking.

In addition to delirium, symptoms of DTs

may include visual or tactile hallucinations, gross tremor, autonomic instability, and fluctuating levels of psychomotor activity.

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DIAGNOSTIC EVALUATION Accurate and frequent assessment of vital

signs is essential, as autonomic instability may occur in cases of severe withdrawal and DTs.

Careful attention must be given to the level of consciousness, and the possibility of trauma should be investigated.

Signs of hepatic failure (e.g., ascites, jaundice, coagulopathy) may be present.

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DIFFERENTIAL DIAGNOSISAlcohol-induced hypoglycemia, acute

schizophrenia, drug-induced psychosis, encephalitis, thyrotoxicosis, anticholinergic poisoning, and withdrawal from

other sedative–hypnotic type drugs TREATMENT Tapering doses of benzodiazepines

(chlordiazepoxide, lorazepam) Thiamine, folic acid, and a multivitamin to

treat nutritional deficiencies Magnesium sulfate for post with-drawal

seizures

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Wernicke–Korsakoff syndrome is caused by thiamine (vitamin B1) deficiency resulting from the poor diet of alcoholics. Wernicke’s encephalopathy is acute and can be reversed with thiamine therapy:

1. Ataxia2. Confusion3. Ocular abnormalities (nystagmus, gaze

palsies) If left untreated, Wernicke’s encephalopathy may

progress into Korsakoff’s syndrome, which is chronic and often irreversible.

1. Impaired recent memory2. Anterograde amnesia3. +/− Confabulation

Confabulation: Making up answers when memory has failed04/21/23 33

Discussion

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A profile of the substance◦ Amphetamines◦ Nonamphetamine stimulants◦ Cocaine◦ Caffeine◦ Nicotine

Patterns of use and abuse Effects on the body

◦ CNS effects◦ Cardiovascular effects ◦ Pulmonary effects◦ GI and renal effects◦ Sexual functioning

Cocaine Powder

cocaine

Cracked cocaine

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Cocaine blocks dopamine reuptake from the synaptic cleft, causing a stimulant effect. Dopamine plays a role in behavioral reinforcement (“reward” system of the brain).

Cocaine Intoxication

CLINICAL PRESENTATION Cocaine intoxication often produces euphoria, increased or

decreased blood pressure, tachycardia or bradycardia, nausea, dilated pupils, weight loss, psychomotor agitation or depression, chills, and sweating. It may also cause respiratory depression, seizures, arrhythmias, and hallucinations (especially tactile).

Cocaine’s vasoconstrictive effect may result in myocardial infarction (MI) or cerebrovascular accident (CVA).

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DIFFERENTIAL DIAGNOSISAmphetamine or phencyclidine (PCP) intoxication, sedative

withdrawal

DIAGNOSTIC EVALUATIONUrine drug screen (positive for 3 days, longer in heavy

users)

TREATMENTIntoxication1. For mild-to-moderate agitation: Benzodiazepines2. For severe agitation or psychosis: Haloperidol3. Symptomatic support (i.e., control hypertension,

arrhythmias) Dependence1. Psychotherapy, group therapy2. Tricyclic antidepressants (TCAs)3. Dopamine agonists (amantadine, bromocriptine)

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Abrupt abstinence is not life threatening but produces a dysphoric “crash”:

malaise, fatigue, depression, hunger, constricted pupils, vivid dreams, psychomotor agitation or retardation

TREATMENT:Usually supportive—let patient sleep off

crash.

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Methamphetamine

shabu

I C E

S p e e dS p e e d

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Classic amphetamines: Dextroamphetamine (Dexedrine), methylphenidate(Ritalin), methamphetamine (Desoxyn, ice, speed, “crystal meth,” “crack”)

Substituted (“designer”) amphetamines: MDMA (ecstasy), MDEA (eve)

Classic amphetamines release dopamine from nerve endings, causing a stimulant effect. They are used medically in the treatment of narcolepsy, attention deficit hyperactivity disorder (ADHD), and depressive disorders.

Designer amphetamines release dopamine and serotonin from nerve endings and have both stimulant and hallucinogenic properties.

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CLINICAL PRESENTATIONAmphetamine intoxication causes symptoms similar to

those of cocaine. DIFFERENTIAL DIAGNOSISCocaine or PCP intoxication. schizophrenia. DIAGNOSTIC EVALUATIONUrine drug screen (positive for 1 to 2 days). A negative

routine drug screen does not rule out amphetamine use, since most assays are not of adequate sensitivity.

A negative drug screen can never completely rule out substance abuse or dependence.

TREATMENTSimilar to cocaine Amphetamine WithdrawalSimilar to cocaine withdrawal

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- Is the most commonly used psychoactive Is the most commonly used psychoactive substance usually in the form of coffee or substance usually in the form of coffee or tea.tea.

- Caffeine acts as an adenosine antagonist , Caffeine acts as an adenosine antagonist , causing increased cyclic adenosine causing increased cyclic adenosine monophosphate (cAMP) and a stimulant monophosphate (cAMP) and a stimulant effect via the dopaminergic system.effect via the dopaminergic system.

- One cup of coffee One cup of coffee :100 to 150 mg caffeine.:100 to 150 mg caffeine.- One cup of tea One cup of tea : 40 to 60 mg caffeine.: 40 to 60 mg caffeine.

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- May occur with consumption of over 250 mg of caffeine.May occur with consumption of over 250 mg of caffeine.

- Signs and symptoms include anxiety, insomnia, twitching, Signs and symptoms include anxiety, insomnia, twitching,

rambling speech, flushed face, GI disturbance and rambling speech, flushed face, GI disturbance and

restlessness.restlessness.

- Consumption of more than 1 g of caffeine may cause Consumption of more than 1 g of caffeine may cause

tinnitus , sever agitation and cardiac arrhythmias.tinnitus , sever agitation and cardiac arrhythmias.

- In excess of 10g death may occur secondary to seizures and In excess of 10g death may occur secondary to seizures and

respiratory failure.respiratory failure.

- Treatment: supportive and symptomatic.Treatment: supportive and symptomatic.

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Caffeine withdrawalCaffeine withdrawal::

-resolve within 1 week and include headache, -resolve within 1 week and include headache,

nausea/vomiting, drowsiness, anxiety or nausea/vomiting, drowsiness, anxiety or

depression.depression.

Treatment : taper consumption of coffee containing Treatment : taper consumption of coffee containing

products , use analgesia to tx headache , rarely products , use analgesia to tx headache , rarely

short course of benzadiazepines may be indicated short course of benzadiazepines may be indicated

to control anxiety.to control anxiety.

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- - is derived from the tobacco plant and is derived from the tobacco plant and

stimulate nicotinic receptors in autonomic stimulate nicotinic receptors in autonomic

ganglia of the sympathetic and ganglia of the sympathetic and

parasympathetic nervous systems.parasympathetic nervous systems.

- Cigarette smoking leads to many health Cigarette smoking leads to many health

risks and nicotine is rapidly addictive risks and nicotine is rapidly addictive

through its effect on the dopaminergic through its effect on the dopaminergic

system.system.

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- Act as a CNS stimulant and may cause restlessness, Act as a CNS stimulant and may cause restlessness,

insomnia, anxiety, and increased GI motility .insomnia, anxiety, and increased GI motility .

- Tobacco users report improved attention, improved mood Tobacco users report improved attention, improved mood

and decreased tension.and decreased tension.

- Treatment: cessation.Treatment: cessation.

Nicotine withdrawalNicotine withdrawal::

- Withdrawal causes intense craving, dysphoria, anxiety, Withdrawal causes intense craving, dysphoria, anxiety,

increased appetite, irritability and insomnia.increased appetite, irritability and insomnia.

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TreatmentTreatment::

smoking cessation with the aid of :smoking cessation with the aid of :

1.1. Behavioral counseling.Behavioral counseling.

2.2. Nicotine replacement therapy (gum, patch).Nicotine replacement therapy (gum, patch).

3.3. Clonidine.Clonidine.

4.4. antidepressant that help reduce cravings.antidepressant that help reduce cravings.

relapse after abstinence is common!!relapse after abstinence is common!!

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-these drugs are highly abused since they are more -these drugs are highly abused since they are more readily available than other drugs such as cocaine or readily available than other drugs such as cocaine or opioids.opioids.

-benzodiazepines are commonly used in the treatment -benzodiazepines are commonly used in the treatment of anxiety disorders and are therefore obtained easily of anxiety disorders and are therefore obtained easily via prescription.via prescription.

-they potentiate the effects of GABA by increasing the -they potentiate the effects of GABA by increasing the frequency of chloride channel opening.frequency of chloride channel opening.

*Barbiturates are used in the tx of epilepsy and as *Barbiturates are used in the tx of epilepsy and as anesthetics , and they potentiate the effects of GABA anesthetics , and they potentiate the effects of GABA by increasing the duration of chloride channel by increasing the duration of chloride channel opening .opening .

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-barbiturates at high doses they act as direct -barbiturates at high doses they act as direct GABA agonists and have a lower margin of GABA agonists and have a lower margin of safety relative to benzodiazepines.safety relative to benzodiazepines.

-in combination BDZs and barbiturates are -in combination BDZs and barbiturates are synergistic due to their complementary effect synergistic due to their complementary effect on GABA channle opening .on GABA channle opening .

-respiratory depression can occur as -respiratory depression can occur as complication.complication.

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- Intoxication with sedatives produces Intoxication with sedatives produces drowsiness , slurred speech , incoordination , drowsiness , slurred speech , incoordination , ataxia , mood lability , impaired judgment , ataxia , mood lability , impaired judgment , nystagmus , respiratory depression and coma nystagmus , respiratory depression and coma or death in overdose (especially barbiturates).or death in overdose (especially barbiturates).

- Symptoms augmented when combined with Symptoms augmented when combined with EtOH.EtOH.

- Long term sedative use cause dependence.Long term sedative use cause dependence.

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Alcohol intoxication , generalized cerebral dysfunction (i.e delirium ) .Alcohol intoxication , generalized cerebral dysfunction (i.e delirium ) .

Diagnostic evaluation Diagnostic evaluation ::

Urine or serum drug screen (positive for 1 week) , electrolytes , ECG.Urine or serum drug screen (positive for 1 week) , electrolytes , ECG.

TreatmentTreatment : :

Maintain airway , breathing and circulation.Maintain airway , breathing and circulation.

Activated charcoal to prevent further GI absorption.Activated charcoal to prevent further GI absorption.

For barbiturate only :alkaline urine with sodium bicarbonate to For barbiturate only :alkaline urine with sodium bicarbonate to

promote renal excretion.promote renal excretion.

for BDZs only : flumazenil in overdose.for BDZs only : flumazenil in overdose.

Supportive care –improve respiratory status, control Supportive care –improve respiratory status, control

hypotension.hypotension.

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- Abrupt abstinence after chronic use can be life Abrupt abstinence after chronic use can be life

threatening while physiological dependence is more likely threatening while physiological dependence is more likely

with short acting agents , longer acting agents can also with short acting agents , longer acting agents can also

cause withdrawal symptoms .cause withdrawal symptoms .

Clinical presentationClinical presentation::

Symptoms of autonomic hyperactivity Symptoms of autonomic hyperactivity

(tachycardia ,sweating, etc..) insomnia, anxiety, tremor, (tachycardia ,sweating, etc..) insomnia, anxiety, tremor,

nausea/vomiting, delirium and hallucinations, seizures nausea/vomiting, delirium and hallucinations, seizures

may occur and can be life threatening.may occur and can be life threatening.

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Treatment:Treatment:

- Administration of long acting BDZs such as diazepam or Administration of long acting BDZs such as diazepam or

chlorodiazepoxide , with tapering of the dose .chlorodiazepoxide , with tapering of the dose .

- Tegretol or valproic acid may be used for seizure control.Tegretol or valproic acid may be used for seizure control.

In general withdrawal from drugs that are In general withdrawal from drugs that are

sedating is life threatening while withdrawal sedating is life threatening while withdrawal

from stimulants and hallucinogens is not.from stimulants and hallucinogens is not.

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- Examples : heroin, codeine, dextromethorphan Examples : heroin, codeine, dextromethorphan , morphine, methadone, meperidine , morphine, methadone, meperidine (demerol ).(demerol ).

- These compounds stimulate opiate receptors These compounds stimulate opiate receptors ((mu, kappa , and deltamu, kappa , and delta ) which are normally ) which are normally stimulated by endogenous opiates and are stimulated by endogenous opiates and are involved in analgesia ,sedation, and involved in analgesia ,sedation, and dependence.dependence.

- Opiates also have effects on the dopaminergic Opiates also have effects on the dopaminergic system , which mediates their addictive and system , which mediates their addictive and rewarding properties. rewarding properties.

- Endorphins and enkephalins are endogenous Endorphins and enkephalins are endogenous opiates.opiates.

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Ketamine - special

Ketamine

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Methadone

Morphine

Morphine in various forms

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Heroin in plastic

Heroin in off white powder form

Heroin in various formswith balloons

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- Opiate intoxication causes drowsiness , Opiate intoxication causes drowsiness , nausea/vomiting , constipation , slurred nausea/vomiting , constipation , slurred speech , speech , constricted pupilsconstricted pupils , seizures and , seizures and respiratory depressionrespiratory depression which may progress which may progress to coma or death in overdose.to coma or death in overdose.

- Meperidine and monoamine oxidase inhibitors Meperidine and monoamine oxidase inhibitors taken in combination may cause taken in combination may cause the serotonin the serotonin syndrome syndrome : hyperthermia , confusion , hyper- or : hyperthermia , confusion , hyper- or hypotension and muscular rigidity.hypotension and muscular rigidity.

Differential diagnosis Differential diagnosis ::Sedative hypnotic intoxication , sever EtOH Sedative hypnotic intoxication , sever EtOH

intoxication.intoxication.

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Diagnostic evaluationDiagnostic evaluation::

Rapid recovery of consciousness following the Rapid recovery of consciousness following the

administration of IV naloxone (opiate antagonist) is administration of IV naloxone (opiate antagonist) is

consistent with opiate overdose.consistent with opiate overdose.

Urine and blood test remain positive for 12 to 36 Urine and blood test remain positive for 12 to 36

hours .hours .

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TreatmentTreatment::

- Intoxication: ensure adequate airway ,breathing and - Intoxication: ensure adequate airway ,breathing and

circulation.circulation.

- Overdose: administration of naloxone or naltrexone - Overdose: administration of naloxone or naltrexone

(opiate antagonist ) will improve respiratory depression (opiate antagonist ) will improve respiratory depression

but may cause severe withdrawal in an opiate but may cause severe withdrawal in an opiate

dependant patient ventilator support may be required.dependant patient ventilator support may be required.

- Dependence: oral methadone once daily , tapered over - Dependence: oral methadone once daily , tapered over

months to years, psychotherapy , support groups . months to years, psychotherapy , support groups .

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Clinical presentationClinical presentation::- While not life threatening , abstinence in the While not life threatening , abstinence in the

opiate dependent individual leads to an opiate dependent individual leads to an unpleasant withdrawal syndrome characterized unpleasant withdrawal syndrome characterized by dysphoria , insomnia , lacrimation , by dysphoria , insomnia , lacrimation , rhinorrhea , yawning , weakness , sweating , rhinorrhea , yawning , weakness , sweating , nausea/vomiting , fever, dilated pupils , and nausea/vomiting , fever, dilated pupils , and muscle ache.muscle ache.

Treatment:Treatment:Moderate symptoms : clonidine and/or Moderate symptoms : clonidine and/or

buprenorphine .buprenorphine .Sever symptoms : detoxification with methadone Sever symptoms : detoxification with methadone

tapered over 7 days. tapered over 7 days.

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LSD in forms

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- Examples : psilocybin (mushrooms) , mescaline , Examples : psilocybin (mushrooms) , mescaline ,

lysergic acid diethylamide (LSD).lysergic acid diethylamide (LSD).

- Pharmacological effects vary , but LSD is known to Pharmacological effects vary , but LSD is known to

act on the serotonergic system.act on the serotonergic system.

- Tolerance to hallucinogens do not cause physical Tolerance to hallucinogens do not cause physical

dependence or withdrawal .dependence or withdrawal .

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Hallucinogen intoxication:Hallucinogen intoxication:

Cause perceptual changes , pupillary dilation , Cause perceptual changes , pupillary dilation ,

tachycardia , tremors , incoordination , sweating tachycardia , tremors , incoordination , sweating

and palpitations.and palpitations.

Tx: guidance and reassurance are enough in sever Tx: guidance and reassurance are enough in sever

cases antipsychotics or benzodiazepines may be cases antipsychotics or benzodiazepines may be

used.used.

Hallucinogen withdrawal:Hallucinogen withdrawal:

no!!! Only flashbacks.no!!! Only flashbacks.

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Marijuana leaves

In blockIn plastic bag

In joint rolling

seeds

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- The main active component in marijuana or The main active component in marijuana or

cannabis is THC (tetrahydrocannabinol).cannabis is THC (tetrahydrocannabinol).

- Cannabinoid receptors in the brain inhibit adenylate Cannabinoid receptors in the brain inhibit adenylate

cyclase.cyclase.

- Effect are increased when used with EtOH .Effect are increased when used with EtOH .

- Marijuana has been shown to successfully tx nausea Marijuana has been shown to successfully tx nausea

in CA patient and to increase appetite in AIDS pt.in CA patient and to increase appetite in AIDS pt.

- No dependence or withdrawal syndromes has been No dependence or withdrawal syndromes has been

shown. shown.

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- Marijuana causes euophoria, impaired Marijuana causes euophoria, impaired

coordination, mild tachycardia, conjunctival coordination, mild tachycardia, conjunctival

injection, dry mouth and increase appetite.injection, dry mouth and increase appetite.

- Marijuana can be smoked or eaten.Marijuana can be smoked or eaten.

Treatment: supportive and symptomatic.Treatment: supportive and symptomatic.

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Diagnostic evaluationDiagnostic evaluation::

Urine drug screen is positive for up to 4 weeks in Urine drug screen is positive for up to 4 weeks in

heavy users (released from adipose stores ).heavy users (released from adipose stores ).

Marijuana withdrawalMarijuana withdrawal::

-no withdrawal syndrome but mild irritability, -no withdrawal syndrome but mild irritability,

insomnia, nausea and decrease appetite may insomnia, nausea and decrease appetite may

occur in heavy users occur in heavy users

Treatment: supportive and symptomatic.Treatment: supportive and symptomatic.

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- Examples : solvents glue , paint thinners , Examples : solvents glue , paint thinners , fuels , isobutyl nitrates.fuels , isobutyl nitrates.

- Inhalants generally act as CNS depressant , Inhalants generally act as CNS depressant , user is typically an adolescent male.user is typically an adolescent male.

Inhalant intoxication:Inhalant intoxication:- May cause impaired judgment, impulsivity, May cause impaired judgment, impulsivity,

perceptual disturbances, ataxia, slurred perceptual disturbances, ataxia, slurred speech, euophoria, stupor, or coma.speech, euophoria, stupor, or coma.

- Overdose may be fatal secondary to Overdose may be fatal secondary to respiratory depression or arrhythmias.respiratory depression or arrhythmias.

- Long term use may cause permanent Long term use may cause permanent damage to CNS , peripheral nervous damage to CNS , peripheral nervous system , liver , kidney and muscle.system , liver , kidney and muscle.

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Treatment:Treatment:- Monitor airway , breathing , and circulation.Monitor airway , breathing , and circulation.- Symptomatic treatment as needed.Symptomatic treatment as needed.- Psychotherapy and counseling for dependent Psychotherapy and counseling for dependent

patients.patients.Diagnostic evaluationDiagnostic evaluation::Serum drug screen (positive for 4 to 10 hours).Serum drug screen (positive for 4 to 10 hours).Inhalant withdrawal:Inhalant withdrawal:Does not usually occur but symptoms may include Does not usually occur but symptoms may include

irritability, nausea , vomiting, tachycardia and irritability, nausea , vomiting, tachycardia and occasionally hallucinations.occasionally hallucinations.

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Complications

(a) . physical complications: malnutrition neurological disorder gastrointestinal hepatic problem cardiovascular HIV/AIDS by parental substance use

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(b) . Psychiatric complications:

Depression Anxiety disorder Obsessive compulsive neurosis Panic disorder Sexual dysfunction Somatoform disorder Psychosis

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(C) . Social complications :

Absenteeism from work Unemployment Marital tension Child abuse Financial difficulties Problem with law

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Drug Abuse is apreventable behavior

and

Drug Addiction isa treatable disease

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We Need to Keep Our Eye onWe Need to Keep Our Eye on the Real Targetthe Real Target

Abstinence

Functionality in

Family, Work

and Community

In Treating Addiction…In Treating Addiction…

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Address the Behavior (motivational interviewing)

Explore desire to stop drinking/using vs perceived benefits of ongoing use

Gentle confrontation with education (risks to health) / therapeutic alliance

Involve family and friends for support Educate pt regarding substance & need for

rehabilitation plan

2. Treat the Medical Complications-Detoxification- oupatient, "social

detoxification" program, inpatient with close medical care

-Address associated medical complications: dehydration, malnutrition, DT's, seizures, pneumonia, cardiomyopathy, etc

Hospitalization- -Due to drug OD, risk of severe withdrawal,

medical comorbidities, requires restricted access to drugs, psychiatric illness with suicidal ideation

Residential treatment unit-Do not require intensive medical /

psychiatric monitoring-Require a restricted environment-Partial hospitalization-Step down unit

Oupt Program -No risk of med/ psych morbidity/ highly motivated pt

3. Address Comorbid Psychiatric Conditions 50% pf people with SRD have another

mental disorder4. Address Internal & External Reinforcers

Group, individual, family therapy/ educations counseling, AA

5. Treatment in the Ambulatory Setting & Relapse PreventionModify persistent/ habitual behaviorsIntensity of therapy is importantCognitive Behavioral TherapyRelapse prevention model- education and dev. of skills Motivation enhancement therapy"Client centered"- focus on benefits of stopping vs benefits of ongoing use

Group therapyGain support from others with similar

difficultiesImprove communication skills

Family therapyFamily support/ address "enabling

behaviors" Self Help Groups

12 step approach/AA/ Rational recovery

Questions…..Comments….. (welcome)

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Thank you…

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