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‫‪1‬‬
‫سوء إستخدام‬
‫العقاقير‬
‫‪DRUGS‬‬
‫‪OF‬‬
‫‪ABUSE‬‬
COMMON DRUGS OF ABUSE
1-CANNABINOIDS:Marijuana, Hashish 
Oil
2-STIMULANTS:Amphetamine, 
Methamphetamine, Ritalin
3-DEPRESSANTS: Alcohol, Barbiturates, 
Benzodiazepines, GHB,
RohypnolNARCOTIC
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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 
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Definitions
I. Drug abuse.
II. Drug dependence.
A) Psychological dependence.
B) Physiological dependence.
III. Drug addiction.
IV. Drug tolerance.
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I. Drug abuse
Inappropriate and usually excessive, selfadministration 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.
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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.
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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. 
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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. •
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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. 
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IV. Drug tolerance
Normal
Tolerance
After chronic use, the 
same amount of drug is
insufficient to cause the
desired effect and thus,
more drug is used.
A compensatory response. 
Drug Dose
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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
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IV. Drug tolerance
Blood Pressure
C) Tachyphylaxis
Rapid development of tolerance to the drug after a few
doses or a single administration.
1X
activated
1X
desensitized
2X
tolerance
Time
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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.
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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.
•
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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.
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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.
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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.
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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.
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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 . 
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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.
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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.
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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).
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A) Drug-self administration
Drugs as reinforcers 
in animals.
High correlation 
with
human dependence
liability.
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OPIOIDS or NARCOTICS
Morphine, Codeine, Meperidine,
Methadone
I. Morphine, Heroin, Hydromorphone,Oxymorphone.
Pharmacology .A
- Heroin  6-mono-acetyl
morphine  morphine
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Heroin
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OPIOIDS or NARCOTICS
B. Acute effects
1. Positive Effects
Desirable
Subjective
2. Negative Effects
Undesirable
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Desirable Effects:
Euphoria
Sedation
Relief of anxiety and various
other forms of distress.
Analgesia.
Depression of cough reflex*
Drowsiness
Subjective CNS
effects:Difficulty
concentrating
Apathy
Decreased physical activity
Lethargy
Extremities feel heavy and
the body feels warm
Undesirable Effects:
Dysphoria
Dizziness
Vomiting
Constipation*
Urinary retention
Nausea
Biliary tract spasm
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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 
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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
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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.
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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.
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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.
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G. Treatment of Dependence
a. Methadone
Heroin


Opiate Antagonists
Naltrexone, Trexan®
Maintenance
w/Methadone
(daily dosage = 6-8mg)
Naltrexone
Heroin
Methadone
Severity of Withdrawal
Detoxification
w/Methadone
titrated to pt.
reduced to
5mg/day => discontinue

TIME
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d. Clonidine, an agonist at 2-AR.
ANS EFFECTS
Clonidine
2-AR
NA
NE
SN
DA
LC
VTA
VTA
Motivational:
Pleasure
Reward
Euphoria
Used to block 
autonomic signs and
symptoms of
withdrawal:
cramps
nausea
vomiting
tachycardia
sweating
hypertension






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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
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Alcohol
Acute Intoxication/Overdose
SHORT TERM EFFECTS 
Loss of inhibition 
Anxiolysis 
Sedation 
Decreased motor coordination 
Treatment : chlordiazepoxide (BDZ).
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Alcohol
C. Toxicity/Overdose
Slowed and slurred speech, ataxia,
nystagmus, drowsiness
==> coma, confusion; reflexes are low,
respiratory depression or apnea, low
blood pressure => death.
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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
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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. 

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Alcohol
ETHANOL (CH3CH2OH)
Alcohol dehydrogenase

ACETALDEHYDE (CH3CHO)
Aldehyde dehydrogenase  ===
=
Disulfiram

ACETYL COENZYME A

÷
citric acid cycle

water
energy
÷
carbon dioxide
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Sedative/Hypnotics
I. Barbiturates
II. Benzodiazepines
III. Methaqualone
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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).

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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.
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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.
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Sedative Hypnotics
Barbiturates: I).
Used clinically as anticonvulsant, antianxiety drugs or preanesthetics.
Phenobarbital (purple hearts) 
Pentobarbital (yellow jackets) 
Secobarbital (red devils) 
Amobarbital (blue angels) 
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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". 
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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.


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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.
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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.
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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.
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CNS Stimulants
Cocaine, Crack (free base or hydrochloride) .I
Amphetamines. .II
Khat:
Cathinone, methcathinone.
. Methylxanthines: caffeine, theophyline, theobromide.
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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.
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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.
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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.
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Cocaine/Amphetamines
“The Runs”
DRUG TAKING
CRAVING
DRUG TAKING
The Blues
FATIGUE
DEPRESSION
HYPERPHAGIA
sleep
CRASH
CRAVING
DRUG TAKING
CRAVING
DRUG TAKING
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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.
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Cocaine
D. Treatment of overdose
Many patients do not require medication
- Beta blockers for autonomic hyperactivity.
1 blockade (Atenolol, metoprolol, esmolol and nonselective : 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.
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Cocaine
D. Treatment of overdose (con’t)
After the acute toxic effects are handled:
Antidepressants 
Haloperidol for psychosis. 
Alprazolam for panic attacks. 
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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 --
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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. 
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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.
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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.
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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.
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Temperature 
Hair loss 
Pallor 
Nail hypertrophy 
Ulcer 
Gangrene 
Dry - non infected black eschar 
Wet - tissue maceration and purulence 
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Acute Thromboembolic Disease
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Sites of Embolization
Bifurcations 
Femoral - 40% 
Aortic - 10-15% 
Iliac - 15% 
Popliteal - 10% 
Upper extremities - 10% 
Cerebral - 10-15% 
Mesenteric/visceral - 5% 
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Buerger’s Disease
Thrombangiitis
Obliterans
Exclusively associated with cigarette smoking 
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 
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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 
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Buerger’s Disease Management
Revascularization options are limited 
Clinical remission with smoking cessation 
Sympathectomy has a limited role in patients with 
ulcerations
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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.
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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
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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. 
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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. 
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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.
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Hallucinogens
D. Withdrawal
These drugs do not cause physical dependence, but they
have tremendous abuse potential (psychological
dependence).
- Use is occasional.
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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
Acute effects
UntowardB.Effects
LOW DOSE
Dreamy, carefree state,
mood elevation,
heightened or altered perception.
Impaired judgment,
Mood swings,
Partial amnesia
MODERATE DOSE
Inebriation, dissociation,
depersonalization, perceptual
distortions, diminished pain
sensitivity
Ataxia, motor impairment,
confusion, disorientation,
preoccupation with
abnormal body sensations,
amnesia, nystagmus,
exaggerated mood swings, PANIC
HIGH DOSE
Catatonia, “blank” stare, delirium,
severe motor impairment, psychotic
behavior, hypertensive crisis,
, amnesia.
101
All of the above and
hallucinations
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
& narcotics
PCP & Ketamine
Depression and mood
disturbances
Antisocial behavior
107