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DRUGS OF ABUSE

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					‫سوء إستخدام‬
   ‫العقاقير‬
 ‫‪DRUGS‬‬
    ‫‪OF‬‬
  ‫‪ABUSE‬‬       ‫1‬
COMMON DRUGS OF ABUSE
1-CANNABINOIDS:Marijuana, Hashish 
Oil

2-STIMULANTS:Amphetamine, 
Methamphetamine, Ritalin



3-DEPRESSANTS: Alcohol, Barbiturates, 
Benzodiazepines, GHB,
RohypnolNARCOTIC
                                          2
COMMON DRUGS OF ABUSE
4-ANALGESICS: Opium, Heroine, 
Codeine, Methadone

5-HALLUCINOGENS:LSD, Mescaline, PCP, MDMA 


6- INHALANTS:Nitrous, Glue, 


7- EtherDISSOCIATIVE ANESTHETICS: 
PCP, Ketamine 

                                              3
Definitions
I. Drug abuse.
II. Drug dependence.
A) Psychological dependence.
B) Physiological dependence.
III. Drug addiction.
IV. Drug tolerance.
                               4
  I. Drug abuse
Inappropriate and usually excessive, self-
administration of a drug for non-medical purposes.
Abused drugs exert their effects in the •
CNS.
Compulsive drug-seeking behavior. •
Preoccupation with the procurement •
and use of the drug may be so
demanding as to decrease the users
productivity.
Prolonged abuse may cause chronic •
toxicity.                                            5
 II. Drug dependence
Repetitive use of substances that
produce an optimal state of well
being because of their positive
reinforcing effects in the CNS.

A) Psychological dependence.
B) Physical dependence.
                                    6
 II. Drug dependence
A) Psychological Dependence
Motivational component: great subjective 
need, compulsion, drive to get the drug.
Will take drug periodically. 
Although physical dependence for a drug 
may not occur, “drug-seeking behavior” is
present.
Habituation; Just "like" the drug; Drug 
effects serve as “positive reinforcers”.
No tolerance increase. 
                                             7
 II. Drug dependence
B) Physiological Dependence
The body needs the drug for normal •
physiological function.
Tend to increase dose because of •
tolerance.
Withdrawal Symptoms/Absence •
Syndrome (negative reinforcement).
Predictable group of signs and symptoms    
resulting from abrupt removal of a drug.
Psychological dependence is also present. •
                                               8
 III. Drug addiction
The drug-use and drug-seeking behavior 
of dependent individuals is maintained by
the reinforcing central activity of the
drug despite its negative social,
psychological and physical consequences.
Physiological and psychological 
dependence is present. Physiological
changes have occurred. Symptoms of
withdrawal, will be involved.
High tendency to relapse. 
                                        9
IV. Drug tolerance
                        After chronic use, the 
                        same amount of drug is
   Normal               insufficient to cause the
                        desired effect and thus,
                        more drug is used.
            Tolerance   A compensatory response. 



   Drug Dose


                                                10
 IV. Drug tolerance
A) Innate Tolerance
1. Sensitivity
2. Insensitivity


B) Acquired Tolerance
1. Pharmacokinetic or metabolic
2. Pharmacodynamic or functional
3. Learned or behavioral



                                   11
  IV. Drug tolerance
C) Tachyphylaxis
Rapid development of tolerance to the drug after a few
doses or a single administration.
       Blood Pressure




                        1X           1X            2X




                        activated   desensitized    tolerance


                                    Time
                                                                12
V. Cross-dependence
When a drug is administered to achieve the same 
                outcome as that of another drug.


              i.e. heroin  methadone. 

 In a heroin user, methadone can be
substituted for heroin in preventing
            the withdrawal syndrome.

                                                    13
 VI. Cross-tolerance
When an individual has become tolerant 
to a drug and requires higher than normal
doses of a second drug to have its effects.

Barbiturates  BDZ.  i.e.     •
Amphetamine  cocaine.
BARBs or BDZs 
Anesthetics.

                                              14
  VI. Cross-tolerance
In general there is cross-dependence and 
cross-tolerance between drugs of the
same class, but not between drugs in
different classes.

Exceptions:
Sedative-hypnotics and volatile intoxicants. 
LSD and phenylethylamines, but not with other 
hallucinogens.


                                                  15
 VII. Co-abuse
Many of these drugs are used in combination with other 
drugs from one or more categories.
Alcohol and Heroin 
Nicotine and Alcohol 
Speed balls  cocaine + heroin 
Cocaine + BDZs 
Heroin and BARBs 

Be aware of the possibility of combination of drugs when 
treating withdrawal or overdose, each drug will require a
specific treatment.
                                                        16
  VIII. Toxicology
A) Tissue and organ toxicity
Acute use
Respiratory depression --- narcotics, inhalants, 
barbiturates.
Cardiovascular effects and seizures --- cocaine, 
amphetamines.
Arrhythmias --- volatile intoxicants. 
Lack of motor coordination Accidents (car 
accidents, big machinery accidents) death ---
alcohol, narcotics, stimulants, PCP, marihuana,
hallucinogens, CNS depressants.
                                                     17
 VIII. Toxicology
Tissue and organ toxicity. (A
Chronic use
Abnormal neuronal activity --- ALL   
Liver damage --- alcohol. 
Increase incidence of lung, breast, gastrointestinal   
and rectal cancer, and cardiovascular diseases ---
                                     tobacco.
Pregnancy complications and babies born dependent      
                             --- narcotics.
                                                       18
  VIII. Toxicology
B) Psychic toxicity
Acute use
Bad trips, flashbacks --- hallucinogens, CNS stimulants. 
Mood liability --- marihuana, hallucinogens, PCP. 
Panic attacks --- cocaine, amphetamines, marihuana, 
hallucinogens, PCP.



Chronic use
  Reality distortion --- alcohol, hallucinogens, stimulants . 
                                                             19
 VIII. Toxicology
C) Behavioral toxicity

Acute use
Lack of motivation. 
      Lack of judgment. 
Loss of concentration. 
Violence  death. 
CAUSED BY : Alcohol, narcotics, stimulants, PCP,
marihuana, hallucinogens, CNS depressants.


                                                   20
 VIII. Toxicology
C) Behavioral toxicity (con’t)
Chronic use
Amotivational syndrom 
Loss of productivity. 
Decrease hygiene. 
Decrease health. 
CAUSED BY: 
Alcohol, narcotics, stimulants, PCP, marihuana,
hallucinogens, CNS depressants.

                                                  21
 VIII. Toxicology
D) Associated Diseases
Infections
AIDS
Venereal diseases

F) Others:
Tobacco-related fires.
Toxicity due to bad batches of drug can
produce permanent damage such as
Parkinson-like disorders --- heroin (MPTP).
                                              22
A) Drug-self administration
Drugs as reinforcers 
in animals.
High correlation 
with
human dependence
liability.

                              23
24
 OPIOIDS or NARCOTICS
Morphine, Codeine, Meperidine,
Methadone
 I. Morphine, Heroin, Hydromorphone,Oxymorphone.


                            Pharmacology .A

- Heroin  6-mono-acetyl
    morphine  morphine
                                                   25
Heroin




         26
 OPIOIDS or NARCOTICS
B. Acute effects
1. Positive Effects
Desirable
Subjective
2. Negative Effects
Undesirable

                        27
Desirable Effects:
Euphoria                        Drowsiness
Sedation                        Subjective CNS
Relief of anxiety and various   effects:Difficulty
other forms of distress.        concentrating
Analgesia.                      Apathy
Depression of cough reflex*     Decreased physical activity
                                Lethargy
                                Extremities feel heavy and
                                the body feels warm


Undesirable Effects:
Dysphoria          Dizziness          Nausea
Vomiting           Constipation*      Biliary tract spasm
Urinary retention
                                                              28
  OPIOIDS
C. Toxicology
- “Heroin lung” with acute overdose.
- No apparent tissue damage.
- Acute and chronic drive reduction.
- Criminal behavior to obtain drugs.
Unsterile syringes: AIDS, hepatitis,, tetanus, -
localized infections, pulmonary infiltration
of contaminants, Neuropathies.
Violent deaths. -
                                                   29
  OPIOIDS
D. Acute Toxicity/Overdose
1.Disruption of central control of peripheral sympathetic
activity.
 Brainstem  Respiratory depression  DEATH
 Circulatory depression  BP
Pupils constricted (miosis), (may be dilated with
meperidine or severe hypoxia)
Nausea and Vomiting
Pulmonary edema
Reflexes 


                                                            30
  OPIOIDS
D. Acute Toxicity/Overdose
2. CNS depression
Drowsiness  Sedation  Coma


3. CNS abnormal neuronal activity
Convulsions -- with propoxyphene or
meperidine

4. Cardiac toxcicity
Arrythmias -- with propoxyphene

                                      31
  OPIOIDS
E. Treatment of toxicity and overdose:
Methadone. Used in the detoxification
process. It causes a less pronounce euphoria
and less severe withdrawal.
Naloxone. Opioid antagonist, used to block
the actions of opioids in a life-threatening
situation of opioid overdose. Given IV. Short
half-life. It precipitates withdrawal.


                                                32
  OPIOIDS
F. Withdrawal
Most severe withdrawal of all drugs of abuse. 

Onset related to time-effect curve and t½ of narcotic. 

Not life threatening, no convulsions, no delirium, no 
disorientation.




                                                           33
  Opiate Withdrawal
6-8 hr =>drug seeking behavior, restless, anxious.

8-12 hr => Pupils dilated (mydriasis), reactive to light;
increased pulse rate; blood pressure; yawning; chills;
rhinorrhea; lacrimation; piloerection/ gooseflesh;
sweating; restless sleep.

48-72 hrs (peak) => All of the above plus muscular
weakness, aches (cramps) and twitches; nausea,
vomiting and diarrhea;  temperature;  respiratory
rate;  heart rate and blood pressure; dehydration.

                                                            34
G. Treatment of Dependence
a. Methadone




                                                 Naltrexone

                 Severity of Withdrawal
                                                 Heroin
                                                 Methadone




                                          TIME
                                                              35
d. Clonidine, an agonist at 2-AR.
        ANS EFFECTS
Clonidine                                   Used to block 
                                      autonomic signs and
  2-AR                                      symptoms of
            NE                                withdrawal:
                                                cramps    
                             DA
                                                 nausea   

                                               vomiting   

                                            tachycardia   
                                               sweating   
                      Motivational:
                      Pleasure
                                           hypertension   
                      Reward
                      Euphoria

                                                          36
  CNS DEPRESSANTS
 I. Alcohol
II. Sedative/Hypnotics, Anxiolytics

All are very addictive and cause withdrawal 
symptoms (mild anxiety, convulsions, seizures).
All of these drugs create "lethal potentiation" when 
combined.

Alcohol<>Anxiolytics<>Hypnotics<> Anesthetics


                                                     37
  Alcohol
Acute Intoxication/Overdose

SHORT TERM EFFECTS 

Loss of inhibition 
Anxiolysis 
Sedation 
Decreased motor coordination 

Treatment : chlordiazepoxide (BDZ).

                                      38
  Alcohol
C. Toxicity/Overdose
Slowed and slurred speech, ataxia,
nystagmus, drowsiness

==> coma, confusion; reflexes are low,

respiratory depression or apnea, low
blood pressure => death.
                                         39
  Alcohol
D. Withdrawal Syndrome
“Delirium Tremens”:
Insomnia, tremulousness, REM rebound, reflexes are
high, weakness, anorexia, orthostatic hypotension,
sweating, agitation
Delirium, vivid auditory and visual hallucinations;
convulsions and seizures (probably caused by
increase NMDA receptor number and
hyperexcitability),
may generate “status epilepticus”
Disorientation, paranoid delusions, hyperthermia
dehydration, cardiovascular collapse.
Risk of death
                                                      40
   Alcohol
E. Treatment
Disulfiram (antabuse) 
Both of these drugs are acetaldehyde dehydrogenase 
blockers.
Drinking alcohol with these drugs produces increased 
concentration of acetaldehyde and this makes the person sick.
Sometimes tranquilizers and antidepressants are given to relieve   
the anxiety.
DETOX is best in a hospital setting. 




                                                                       41
Alcohol
          ETHANOL (CH3CH2OH)
                       Alcohol dehydrogenase   
        ACETALDEHYDE (CH3CHO)
    Aldehyde dehydrogenase  ===   Disulfiram
                       =
                        
                 ACETYL COENZYME A
                    ÷
  citric acid cycle          energy
                       ÷
       water          carbon dioxide
                                                   42
  Sedative/Hypnotics
I. Barbiturates

II. Benzodiazepines

III. Methaqualone



                       43
   Sedative/Hypnotics
Pharmacology
Well absorbed after oral administration .A

Form active metabolites    .B

Patients experience rebound insomnia or anxiety.        
   
Gross binges of intoxication that last several days.    

 Others ingest large quantities on a daily basis and    
remain chronically intoxicated.
They are teratogenic if used during pregnancy       
(malformations of the limbs, facial features, CNS,
heart, skeleton).
                                                            44
   Sedative/Hypnotics
Pharmacology (con’t) .A
Concurrent or substitute use
May be lethal with other depressants. -
Co-abused with alcohol, amphetamines, cocaine.       -
Not likely to abuse narcotics, but not vice-versa. -

Tolerance
- Pharmacodynamic tolerance exists to most CNS
depressants.
- Tolerance of modest degree to the sedative effects but not to
the respiratory depressant effects.
- Cross-tolerance with alcohol, anesthetics and volatile
intoxicants.
                                                                  45
   Sedative/Hypnotics
B. Acute effects
Euphoria, impaired judgement, loss of self-control 
and anterograde amnesic effects.
Physiological consequences resemble those of alcohol 
intoxication. Slowed and slurred speech. Drowsiness 
coma. Fatal with Barbiturates or mixtures of CNS
depressants. Death unlikely with pure benzodiazepines.

The person may feel a remarkable capability for coping 
with stress and anxiety, a general feeling of well being,
may feel euphoric and stimulated. These effects
(euphoria and stimulation) may be due to inhibition of
inhibitory pathways, in other words, desinhibition.

                                                            46
  Sedative Hypnotics
Barbiturates: I).
Used clinically as anticonvulsant, anti-
anxiety drugs or preanesthetics.
Phenobarbital (purple hearts) 
Pentobarbital (yellow jackets) 
Secobarbital (red devils) 
Amobarbital (blue angels) 

                                           47
  Sedative Hypnotics
II.) Benzodiazepines:
Used as anxiolytics and hypnotics.
Flurazepam => sleeping pills. •
Flunitrazepam => “date rape drug”. •
Diazepam (Valium) => tranquilizer. •
Chlordiazepoxide (Librium) => •
tranquilizer.
Clonazepam => anticonvulsant. •
They all cause sedation and muscle relaxation. 
Induce sleep (hypnosis). 
Abuse may cause "BDZ-induced aggression". 
                                                   48
   Sedative/Hypnotics
Rapid acting barbiturates such as secobarbital or 
pentobarbital are more widely abused than depressants
with a slower onset such as phenobarbital or the
benzodiazepines.

Drugs with half-lives of 8 to 24 hrs produce a rapid   
evolving, severe withdrawal syndrome.
Drugs with half-lives of 48 to 96 hrs produce a slow   
evolving, less severe but longer withdrawal.




                                                           49
Sedative/Hypnotics
 D. Withdrawal:
 Minor: tremors; insomnia (REM rebound); high fever; 
  clonic blink. Anxiety and dysphoria. Sleep disturbances.
 12-16hrs: minor symptoms plus abdominal cramps; 
 nausea and vomiting, o. hypotension;  deep tendon
                                    reflexes, hyperreflexia.
 24hrs: pronounced weakness, course tremors (“the 
 shakes”), hyperactive reflexes, early illusions and
                             hallucinations. Hyperpyrexia.
 48-72hrs: convulsive seizures (“rum fits”); vivid auditory 
 and visual hallucinations (“the horrors”), formication,
  agitation, disorientation, delirium, paranoid delusions.

                                                           50
Sedative/ Hypnotics
 D. Withdrawal (con’t)
 Hyperthermia, dehydration, 
 electrolyte imbalance, exhaustion, cardiovascular collapse
 => Threat to life.
 Time of onset and symptoms experienced vary with CNS 
 depressant use, similar to alcohol withdrawal.
 Additive effect of sedative/hypnotics. 

 Treatment:
 Stabilization: diazepam, chlordiazepoxide, 
 phenobarbital (cross-dependence).
 Drug tapered off slowly => prevention of onset 
 (reversible only early in course).
 Propranolol or clonidine for nausea, vomiting, 
 tremors and twitching.
                                                              51
Sedative Hypnotics
E. Acute toxicity/Overdose
Acute Intoxication
Pupils are normal; BP and respiration are
depressed; nystagmus on lateral gaze; tendon
reflexes depressed; ataxia; slurred speech;
confusion; coma; shock => Risk of Death,
particularly with BARBs.

F. Treatment of overdose
Treatment of overdose w/BDZs: flumazenil (BDZ
receptor blocker).
No treatment for Barbiturates.
                                                52
   CNS Stimulants
Cocaine, Crack (free base or hydrochloride) .I

Amphetamines. .II



Khat:             Cathinone, methcathinone.


. Methylxanthines: caffeine, theophyline, theobromide.
                                                         53
54
55
  Cocaine
A. Pharmacology
Cocaine and the amphetamines have very similar 
effects on mood, patterns of abuse, the type of
dependence produced, and their toxic effects.

Differences are mainly in the pharmacokinetics (t½ 
of cocaine is shorter (50-90min) vs longer (5-10hrs)
t½ for amphetamines).

. Cocaine free base (“crack”, “rock”) is smoked => 
delivered directly to pulmonary circulation, left
heart and brain.
                                                       56
57
  Cocaine
B. Acute effects
Causes an initial but temporary euphoria, “rush”.
Causes craving within 30 minutes of taking the drug.
Increase alertness, feeling of elation and well being,
increased energy, feelings of competence, increased
sexuality.
The user becomes more talkative, restless and often
more irritable. Consciousness is clear, but delusions
may occur as well as visual, tactile (formication) and
auditory hallucinations.
These drugs are sympathomimetic, thus, they cause
HR, BP, skeletal muscle tension, but musculature
of the bronchi and intestines relax.
                                                         58
  Cocaine
Given unlimited access to the drugs, animals will self- 
administer these drug until they die.
C. Toxicity/Overdose
“Runs” – Uninterrupted sequences of stimulant abuse 
to maintain a continuous state of intoxication, to
extend the pleasurable feeling, and to postpone the
postintoxication “crash” than ensues as the drug
effects subside.
Acute tolerance may occur in such people,
particularly in those taking the drug I.V., resulting in
the need of increasingly larger doses. This spiral of
tolerance and dose increases continues until the drug
is depleted or the person collapses from exhaustion.
Drug taking and drug seeking take a compulsive
character.
                                                            59
  Cocaine/Amphetamines
                                “The Runs”
  DRUG TAKING   CRAVING
                          DRUG TAKING
The Blues
                                CRAVING
FATIGUE
DEPRESSION
HYPERPHAGIA                     DRUG TAKING


   sleep                        CRAVING


       CRASH                DRUG TAKING
                                          60
  Cocaine
Stimulant overdose results in excessive activation of the
sympathetic nervous system. The resulting tachycardia
and hypertension may result in myocardial infarction and
cerebrovascular hemorrhage in susceptible individuals.

Cocaine can cause coronary vasospasms and cardiac
dysrhythmias.

CNS symptoms include anxiety feelings of paranoia and
impending doom, and restlessness.
Users exhibit unprediactable behavior and may become
violent.


                                                            61
   Cocaine
D. Treatment of overdose
Many patients do not require medication
- Beta blockers for autonomic hyperactivity.
1 blockade (Atenolol, metoprolol, esmolol and non-
selective : labetolol).
This treatment is controversial: Problems with using non-selective   
 blockers may lead to unopposed  effects => BP
- Nitroglycerine or other nitrites/nitrates for angina.
- Calcium channel blockers (verapamil, diltiazem) for
hypertension.
- Ice baths for high fever.
- Acifdify urine to hasten excretion.

                                                                         62
  Cocaine
D. Treatment of overdose (con’t)

After the acute toxic effects are handled:

Antidepressants 

Haloperidol for psychosis. 

Alprazolam for panic attacks. 
                                             63
  Amphetamines
d, l-Amphetamine,
Methylphenidate (Ritalin®, use to treat attention deficit and
hyperactivity disorders in children),
Phenmetrazine (used to treat obesity),
Methamphetamine (“crystal”, “speed”, “ICE”).
methylendioxyamphetamine, (MDA).
methylenedioxymetamphetamine, (MDMA, ecstasy, XTC).

A. Pharmacology:
Used as nasal decongestants (benzedrine, 
replaced by propylhexedrine).
Used as antidepressants and to treat obesity         
(anorectic) => can cause dependence.
Used to stay awake. 

                                                                64
 Amphetamines
Present clinical therapeutic use, only in narcolepsy. 
Amphetamine and methamphetamine -HCl 
(speed),
Amphetamine or methamphetamine => I.V. 
D-methamphetamine (“ice”) => smoked like has a 
much longer duration of action.

Psychological Dependence
Similar to Cocaine -
May cause hallucinations --   -

                                                          65
  Nicotine
A. Pharmacology
One of the most widely used licit drugs. 
Drug found exclusively in the tobacco plant 
(Nicotiana tabacum, serves as a natural
insecticide), which is harvested, cured, and
manufactured into snuff, chewing tobacco, pipe
tobacco, cigars and cigarettes. Nicotine is
absorbed best by the lungs and it is distributed
rapidly throughout the body.
It has a half-life of about 30 min. 
Highly lipophylic: Crosses BBB and placenta. 
                                                   66
  Nicotine
B. Dependence
Drug seeking behavior. 


C. Withdrawal
Withdrawal symptoms include nervousness, 
anxiety, drowsiness, lightheadedness, insomnia,
dizziness, tremor, sleep disturbances, decrease
inability to concentrate, irritability and an intense
craving for tobacco. Other physical symptoms
include nausea, headache, constipation and an
increase in appetite and increase body weight.
                                                        67
  Nicotine
D. Acute Effects
-  Fibrinolytic activity
-  Free fatty acids
-  Epinephrine and NE release from adrenal gland.
-  Sympathetic and Parasympathetic activity.
-  ACTH release from pituitary.
- depolarization of thermo, mechano, and nociceptors.
- depolarization of carotid body and other ganglia.
- depolarization of baroreceptors.
- depolarization of chemoreceptors in area posterma =>
Stimulation of emetic centers.



                                                         68
   Nicotine
E. Acute Intoxication
Respiratory arrest due to blockade of respiratory centers and
neuromuscular junctions controlling breathing.
F. Long term effects
Associated diseases: Heart disease, lung disease, cancer,
babies with small birth weight, asthma in children, others.

     G. Detoxification treatment
Smoking therapy => substitution, tapering off: nicotine gum
(Nicorette), nicotine patches, nicotine nasal spray.




                                                                69
70
                           Temperature      
                               Hair loss    
                                 Pallor     
                       Nail hypertrophy     
                                   Ulcer    
                              Gangrene      
        Dry - non infected black eschar 
Wet - tissue maceration and purulence 




                                                71
Acute Thromboembolic Disease




                               72
Sites of Embolization
                            Bifurcations 
                        Femoral - 40% 
                        Aortic - 10-15% 
                            Iliac - 15% 
                         Popliteal - 10%    
                Upper extremities - 10%     
                      Cerebral - 10-15%     
                Mesenteric/visceral - 5%    


                                                73
74
Buerger’s Disease
Thrombangiitis Obliteranssmoking 
       Exclusively associated with cigarette

     More prevalent in Middle East 
                          and Asia
        Occlusive lesions seen in muscular arteries, with a 
                              predilection for tibial vessels
         Presentation - rest pain, gangrene and ulceration 




                                                                75
Buerger’s Disease
   Recurrent superficial thrombophlebitis (“phlebitis 
                                           migrans”)
Young adults, heavy smokers, no other atherosclerotic 
                                          risk factors
   Angiography - diffuse occlusion of distal extremity 
                                                vessels
                      Progression - distal to proximal 



                                                       76
Buerger’s Disease -
Management
              Revascularization options are limited 
         Clinical remission with smoking cessation 
  Sympathectomy has a limited role in patients with 
                                        ulcerations




                                                    77
Drugs causing hallucinations, delusions or
delusions.
Psychedelics and hallucinogens.   .I

1- Indolamines: Lysergic acid
diethylamide (LSD), morning glory seed (LSM),
psilocybin, psilocin, ibogaine,
dimethyltryptamine (DMT).
Phenyethylamines: mescaline, bufotenin,
dimethoxymethyl-amphetamine (DOM).

2- Cannabis. Marihuana, delta-9-THC. .II
3- Phencyclidine (PCP). .III
4- Anticholinergics., atropine, scopolamine.
                                                78
79
  Hallucinogens
A. Pharmacology
These four classes of drugs are usually considered
together because of their prominent feature of
intoxication

(hallucinations,
DELUSION
  False believe brought about without apropriate external
inconsistent with the individual’s own knowledge and
experience stimulation

ILLUSION
Inaccurate perception a misinterpretation of senosry
impression without external stimulus,
They occur naturally in plants, mushroom                    80
  Hallucinogens
B. Acute Effects
At low doses:
Euphoria; Changes in affect (mood): anxiety, tension, labile 
mood; Thought and feeling disorders: perceptual changes
(distortion), depersonalization, illusions visual
hallucinations, time and visual distortions, synesthesias;
nausea, pupils are dilated, HR, BP, temperature,
reflexes, tremors.
Panic, paranoia. 




                                                                 81
  Hallucinogens
At high doses:
Dangerous behavior may cause accidents. 

For the amphetamines:
Visual hallucinations => convulsions, coma. 



Cross-tolerance between LSD and mescaline. 
Usually polydrug users. 



                                                82
 Hallucinogens
C. Toxicity/Overdose
Depends on the individual drug .
Tissue toxicity. Some are neurotoxic. .1
Psychic toxicity. Acute transient .2
psychosis. Flash backs.
Behavioral toxicity. Distorted behavior, .3
aggressive, violent.


                                              83
 Hallucinogens
D. Withdrawal
These drugs do not cause physical dependence, but they
have tremendous abuse potential (psychological
dependence).

- Use is occasional.




                                                         84
 Hallucinogens
E. Mechanism of Action
LSM (from morning glory seeds), LSD 
(synthetic), mescaline (from the peyote
cactus) and psilocybin (from mushrooms)
have chemical resemblances to 5-HT, NE
and DA.
Scopolamine is a cholinergic antagonist. 
    They all cause hyperarousal of the CNS. 

                                                85
 Hallucinogens
Systems Affected:
5-HT. Presynaptic agonists. decrease 5- 
HT transmission. “Cocktail party effect"
all sensory information goes in. temporal
lobe. Postsynaptic agonists to 5-HT1A and
5-HT1C receptors.
NE. Postsynaptic agonists. increase NE 
activity in temporal lobe. Produce a lot of
“bad trips”. Anxiety and hyperactivity.
ACh. Produce delirium. Anticholinergic 
effects. Not addictive.
                                              86
 Hallucinogens
F. Treatment

None




                 87
 Marihuana (Cannabis)
A. Pharmacology
From the Indian hemp plant, or Cannabis sativa. 

Delta-9-tetrahydrocannabinol (THC) is the active 
ingredient. 



Marihuana, marijuana, hashish ,red oil. 



                                                     88
 Cannabis
- They have been known to influence levels of NE, DA and
                                                 GABA.
                                                       -



THC concentrates in the limbic system, particularly in
hippocampus and amygdala and sensory centers for
                                            hearing.




                                                           89
    Solvents/Inhalants

Anesthetics, Volatile Intoxicants

They can be easily and inexpensively obtained legally. 
One big problem is that they are most likely to be abused
by the youngest members of the drug-abusing
community.

Boys as young as 7 and 10 years of age, as well as young 
teenagers are those most frequently found sniffing glue of
gasoline.

Few studies of these abused substances. 
                                                             90
   Solvents/Inhalants

Anesthetics, Volatile Intoxicants

Low-income communities and isolated communities 




Solvents such as toluene may cause permanent 
neurological damage.


                                                    91
  Solvents/Inhalants
Four major groups of inhalants:
1. Volatile Solvents:
“Glue sniffing”: model cement (airplane glue),   
lighter fluids, cleaning solutions, lacquer
thinners, industrial solvents, esters ketones,
gasoline and other petroleum distillates,
propane and butane fuel, toluene chlorinated
hydrocarbons, etc.
Toxic solvents such as benzene and carbon 
tetrachloride have been remove from most
products.
                                                     92
   Solvents/Inhalants

2. Aerosols:
Fluorocarbons and other aerosol propellants. spray paint 
(containing alcohols), -- particularly dangerous are the
products containing chlorofluorocarbons, ketones,
organic metals and n-hexane, they cause cardiotoxicity,
axonopathies or hepathotoxicity.




                                                             93
   Solvents/Inhalants
3. Anesthetic agents:
Ethyl ether, chloroform, methylchloride,   
trichloroethylene and nitrous oxide.

Some are contained in oil and grease   
dissolvers.

Chloral hydrate. 
as sleeping medication, used in drinks. 
Produces similar effects as the barbiturates.

                                                94
  Solvents/Inhalants
4. Amyl, butyl, and isobutyl nitrite:

Amyl nitrite was used since 1867 as a 
vasodilator to relieve angina pectoris.




                                          95
   Solvents/Inhalants
A. Pharmacology
The onset of action of most solvents is rapid and their 
duration is short, with the exception of acetone that has
a slower onset and longer duration of action.
1. Psychological Dependence
2. Physical Dependence.
No physiological dependence. -
Alcohol potentiates their effect. 
They seem to disrupt membrane function. 



                                                            96
  Solvents/Inhalants
B. Acute Effects
At low doses these substances generally cause 
marked euphoria and dizziness (resulting from the
hypotension and hypoxia secondary to peripheral
venous pooling); slurred speech, ataxia, impaired
judgement and feelings of giddiness and
drunkenness. Some may experience perceptual
distortions.
At high doses they have a generalized depressant 
effects upon the CNS.
Amyl nitrite -- reputed to act as a sexual enhancer 
(penile vasodilation).
                                                        97
   Solvents/Inhalants
C. Toxicology/Overdose
Photophobia, irritation of the eyes, diplopia, rhinitis, 
sneezing, coughing, nausea, diarrhea, chest pain, and
 vague muscle and joint pains.
Overdose can cause respiratory depression. 
Usually die of asphyxia. 


   Halogenated hydrocarbons in some aerosol propellants
   and cleaning solutions cause cardiac arrest.

                                                             98
  Solvents/Inhalants
D. Mechanism of Action
- Disruption of membranes, disruption of
electrical impulses, disruption of membrane
      components.
- Stimulate Cl- uptake through GABA channels,
inhibit neuronal activity in CNS.




                                                99
 PCP
Phencyclidine, Angel Dust
A. Pharmacology
It is a synthetic phenylcyclohexylamine derivative. 
Initially introduced in 1957 as a “dissociative anesthetic”, 
which caused no loss of consciousness. It was removed from
the market for use in humans, but it was used in veterinary
practice.
It is the most commonly used hallucinogenic agent. 
It may be snorted, taken orally, smoked with tobacco, or 
injected IV.
Usually gives bad trips. 
Behavior under the influence of the drug may be 
unpredictable, bizarre and violent.
                                                                 100
  PCP
                                       UntowardB. Acute effects
                                                Effects
LOW DOSE
                                    Impaired judgment,
Dreamy, carefree state,
                                    Mood swings,
mood elevation,                     Partial amnesia
heightened or altered perception.
MODERATE DOSE                       Ataxia, motor impairment,
Inebriation, dissociation,          confusion, disorientation,
                                    preoccupation with
depersonalization, perceptual       abnormal body sensations,
distortions, diminished pain        amnesia, nystagmus,
sensitivity                         exaggerated mood swings, PANIC
                                    Catatonia, “blank” stare, delirium,
HIGH DOSE                           severe motor impairment, psychotic
All of the above and                behavior, hypertensive crisis,
hallucinations                      , amnesia.                        101
 PCP
C. Acute toxicity /Overdose
Intoxication may last 4 to 6 hrs. 
Usually not lethal. 

D. Treatment of Intoxication/Overdose
No treatment 

Physical dependence is not clear. 


                                        102
 PCP
E. Mechanism of Action
Receptors for PCP have been identified and •
are closely related (if not identical) to
opioid sigma receptors.

PCP acts as an antagonist of NMDA •
glutamate receptors.
May block DA reuptake. •

                                               103
Designer Drugs
.
Ecstasy 
Leads to Parkinsonian 
symptoms, trembling, shaking
with movement
High body temperatures up to 110   
degrees resulting in death
May lead to chronic depression 
Strong psychological addiction 
occurs
                                       104
105
106
    Drug                                 Disorder
Cocaine and Methamphetamine Schizophrenia, paranoia,
                            anhedonia, compulsive
                            behavior

Stimulants                       Anxiety, panic attacks,
                                  mania and sleep disorders

LSD, Ecstasy & psychedelics      Delusions and hallucination

 Alcohol, sedatives, sleepaids    Depression and mood
  & narcotics                      disturbances

 PCP & Ketamine                  Antisocial behavior
                                                        107

				
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