Stimulants
 People use these substances to stay awake, lose weight,
or boost mood or athletic performance.
 Stimulants can be addictive and may induce an
aftermath crash into fatigue, headaches, irritability,
and depression.
Background
 Stimulants (analeptics) produce a variety of different
kinds of effects by enhancing the activity of the central
and peripheral nervous systems.
 Common effects, which vary depending on the
substance in question, may include enhanced
alertness, awareness, wakefulness, heart rate and
blood pressure for food and sleep.
 Many stimulants are also capable of improving mood
and relieving anxiety, and some can even induce
feelings of euphoria.
Background
 Stimulants exert their effects through a number of
different pharmacological mechanisms, the most
prominent of which include facilitation of
norepinephrine (noradrenaline) and/or dopamine
activity (e.g., via monoamine transporter inhibition
or reversal), and nicotinic acetylcholine receptor
agonism.
Therapeutic indications
 Stimulants are used both individually and clinically for




therapeutic purposes in the treatment of a number of
indications, including the following:
To counteract lethargy and fatigue throughout the day
while at work or while doing other activities.
To reduce sleepiness and to keep the person awake when
necessary, as well as to treat narcolepsy.
To decrease appetite and promote weight loss, as well as
to treat obesity.
To improve concentration and focus while at work or
school, especially for those with attentional disorders
such as ADHD.
Caffeine
 Caffeine is a mild stimulant compound that is found
naturally in coffee, tea, and to a lesser degree, in
cocoa or chocolate.
 It is included in many soft drinks, as well as a larger
amount in energy drinks. Caffeine is the world's most
widely used psychoactive drug and by far the most
common stimulant.
 Caffeine is also included in some medications, usually
for the purpose of enhancing the effect of the primary
ingredient, or reducing one of its side effects
(especially drowsiness).
Nicotine
 Nicotine is the active chemical constituent in
tobacco, which is available in many forms, including
cigarettes, cigars, chewing tobacco, and smoking
cessation aids such as nicotine patches and nicotine
gum.
 Nicotine is used widely throughout the world for its
stimulating effects.
Amphetamines
 Amphetamines are a group of phenylethylamine
stimulants such as amphetamine and
methamphetamine.
 Amphetamine increases the levels of norepinephrine
and dopamine in the brain via reuptake inhibition;
however, the more important mechanism by which
amphetamines cause stimulation is through the direct
release of these catecholamines from storage vesicles
in cells.
 Amphetamines are known to cause elevated mood and
euphoria as well as rebound depression and anxiety.
Amphetamines
 Amphetamine
 Dextroamphetamine
 Methamphetamine
 Methylphenidate
 Phenylpropanolamine
 Phentermine
 4- Hydroxyamphetamine
 Phenmetrazine
Mechanism of action of
amphetamines
 At high doses amphetamine increases the
concentration of dopamine in the synaptic cleft in 4
ways:
1- Induction the release of dopamine
2- Interaction with dopamine containing
synaptic vesicles
3- Prevent degradation of dopamine by
binding to MAO
4- Binding to dopamine reuptake transporter
Mechanism of action
Mechanism of action
3,4- Methylenedioxymethamphetamine
(MDMA)
Street names
 ECSTASY
 WHIZZ BOMB
 LOVE DRUG
 MDM
 LOVE HEART
 ESSENCE
 X TABLET
 CALIFORNIA
E
 BUFFALO
 BEAN
 DOUBLE DIAMOND
 XTC
 M&M
 ADAM
 ROLL
 WHIZZ
 DOVE
Pharmaceutical dosage
forms
 Tablet ( Contain 80- 120 mg of MDMA)
 Capsule
 Powder
 Suppository
MDMA Pharmacokinetic
Absorption:
Readily absorbed
Onset - 30 to 60 minutes
Peak effect - approximately 90 minutes with
a peak plasma concentration of 2 to 3
hours following ingestion
Duration - up to 8 hour or more
Tolerance - tolerance to the desired effects
can occur with frequent and repeated use
of MDMA
MDMA Pharmacokinetic
DISTRIBUTION:

A) VOLUME OF DISTRIBUTION

Although it has not been fully established, it is thought to
be large (>5L/kg)

B) PEAK PLASMA LEVEL

MDMA - Following a single oral dose of 50 mg was 0.106
mg/L
MDMA Pharmacokinetic
 Metabolism
 MDMA is metabolized in the liver by Cytochrome P-
450.
 MDMA is metabolized by N- demethylation to form
MDA.
MDMA Pharmacokinetic
• Excretion
 Urinary excretion of unchanged drug and its
metabolites is complete usually with in 24 hours.
 As much as 75% of a dose of MDMA is excreted
unchanged and 7% is excreted as MDA.
Pharmacodynamic
 Its ability to stimulated both the sympathetic
and central nervous system results from its
structural similarity to the endogenous
catecholamines (Epinephrine & Norepinephrine)
and Dopamine.
 MDMA produce toxicity to serotonergic neurons
in the brain.
 Single doses of MDMA have also been shown to
produce long- lasting serotonin depletion ( 30% of
neurons for up to 2 weeks).
Axonal and cell body damage of serotonin
nerve fiber in the cerebral cortex
Clinical effects
 Desired effects:
 Self Confidence Feeling
 Happiness feeling
 Euphoria
 Libido Increasing
 Empathy
Clinical effects (acute)
 Undesired Effects:
 Acute Effects :
Mild intoxication
Agitation, Hypertension, Tachycardia, Mydriasis, Trismus,
Diaphoresis, Fatigue, Difficulty Concentrating, Headache,
Insomnia, Nasea, Xerostomia
Moderate intoxication:
Anxiety, Confusion, Delirium, Panic attacks, Hallucinations,
Antisocial Behaviors
Clinical effects (acute)
 Severe intoxication:
 Hyperthermia
 Seizure
 Rhabdomyolysis
 Dysrhythmias
 Acute Renal Failure(ARF)
Clinical effects (chronic)
 Paranoia
 Flash Back
 Memory impairment
 Data processing impairment
 Personality disorders
 Suicide Attempt
 Judgment impairment
 Depression
Introduction
 Methamphetamine or methamfetamine,
methylamphetamine, N-methylamphetamine, or
desoxyephedrine, known as “crystal, meth or ice", is
a psychostimulant of the phenethylamine and
amphetamine class of psychoactive drugs.
Chemical structure
 Methamphetamine is chiral, with two isomers,
levorotatory and dextrorotatory.
 The levorotatory form, called levomethamphetamine,
is an OTC drug used in inhalers for nasal
decongestion.
 Levomethamphetamine does not possess any
significant CNS activity or addictive properties.
Street names
 Meth
S
 Crystal
 Speed
 Crystal meth
 Snap
 Glass
 Tina
 Shabu
 Crank
 Shaboo
 Shabs
 Ice
 Shard
 Go fast
 Batu
Street names
 Tik (South Africa)
 Piko (Czech Republic)
 Bato (Philippines)
 ‫( شيشه‬Iran)
 Vint (Russia)
 Ya ice (Thailand)
 Yaa Baa (Thailand)
 P (New Zealand)
 Shabu (Japan, Hong
Kong, Indonesia,
Malaysia)
 Bay (Vietnam)
Methamphetamine (Strawberry)
Methamphetamine (Ice)
Methamphetamine (Crystal)
Methamphetamine forms
Routes of administration
 Studies have shown that the subjective pleasure of
drug use (the reinforcing component of addiction) is
proportional to the rate at which the blood level of the
drug increases.
 IV injection is the fastest route of drug administration,
causing blood concentrations to rise the most quickly,
followed by Suppository (anal or vaginal insertion),
Insufflation (snorting), and Ingestion (swallowing).
Smoking route of administration
Use Meth on foil paper
Pharmacokinetics
 Following oral administration, methamphetamine is
readily absorbed with peak methamphetamine
concentrations occurring in 3 to 6 hours.
 The amphetamine metabolite peaks at 10 to 24 hours.
Methamphetamine is also well absorbed following
inhalation and following intranasal administration.
 It is distributed to most parts of the body.
Methamphetamine has a high lipophilicity and is
distributed across the BBB and crosses the placenta.
Pharmacokinetics
 Methamphetamine is metabolized in the liver with the
main metabolites being amphetamine (active) and 4hydroxymethamphetamine.
 Other minor metabolites include:
4-hydroxyamphetamine
Norephedrine
4-hydroxynorephedrine
Pharmacokinetics
 It is excreted by the kidneys, with the rate of excretion
into the urine heavily influenced by urinary pH.
 Between 30-54% of an oral dose is excreted in urine
as unchanged methamphetamine and 10-23% as
unchanged amphetamine.
 The half-life of methamphetamine is variable with a
mean value of between 9 and 12 hours.
Pharmacology
 Methamphetamine is a potent CNS stimulant that
affects neurochemical mechanisms responsible
for regulating heart rate, body temperature, blood
pressure, appetite, attention, mood and
emotional responses associated with alertness or
alarming conditions.
 The acute physical effects of the drug closely
resemble the physiological and psychological
effects of an epinephrine-provoked fight-or-flight
response, including increased heart rate and
blood pressure, vasoconstriction,
bronchodilation, and hyperglycemia.
 Methamphetamine is a potent neurotoxin,
shown to cause dopaminergic degeneration.
 It has been proposed that dopamine plays a
role in methamphetamine-induced
neurotoxicity, because experiments that
reduce dopamine production or block the
release of dopamine decrease the toxic effects
of methamphetamine administration.
 When dopamine breaks down, it produces
ROS such as hydrogen peroxide.
Physical Effects (Acute)
 Physical effects can include:
Anorexia, hyperactivity, dilated pupils, flushing,
restlessness, dry mouth, headache, tachycardia,
bradycardia, tachypnea, hypertension, hypotension,
hyperthermia, diaphoresis, diarrhea, constipation,
blurred vision, dizziness, twitching, insomnia,
numbness, palpitations, arrhythmias, tremors, dry
and/or itchy skin, acne, convulsions, heart attack,
stroke, and death.
Long-term effects
 Depression, suicide Ideations, serious heart disease,




Psychosis, Anxiety, Violent behaviors.
Methamphetamine also has a very high addiction risk.
Methamphetamine is neurotoxic and is associated with an
increased risk of Parkinson's disease.
Methamphetamine abuse can cause neurotoxicity which is
believed to be responsible for causing persisting cognitive
deficits, such as memory, impaired attention and executive
function.
Over 20 % of people addicted to methamphetamine develop a
long-lasting psychosis resembling schizophrenia after stopping
methamphetamine which persists for longer than 6 months and
is often treatment resistant.
Meth Mouth
Meth mouth
 Methamphetamine users and addicts may lose
their teeth abnormally quickly, a condition
informally known as meth mouth.
 It is probably caused by a combination of drug-
induced psychological and physiological changes
resulting in xerostomia , extended periods of
poor oral hygiene, frequent consumption of highcalorie, carbonated beverages and bruxism .
 Some reports have also speculated that the
caustic nature of the drug is a contributing factor.
Crank Bugs
 All Meth users suffer from what they call "Crank
Bugs".
 Meth is manufactured with chemicals that are toxic to
the human body, and once the drug is taken the
chemicals remain.
 The body's natural reaction is to try and eliminate the
toxins.
 Users itch and scratch which causes the open sores.
Crank Bugs
Methadone
‫قرص و شربت متادون‬
Methadone dosage forms
 Each tablet contains 5 mg or 10 mg methadone
hydrochloride.
Pharmacology: The Mode of Action
 Methadone acts by binding to the µ-opioid receptor for the
effects of analgesia and respiratory depression.
 Methadone also binds to the glutamatergic NMDA (N-methyl-D-
aspartate) receptor .
 Glutamate is the primary excitatory neurotransmitter in the
CNS.
 Acting as an NMDA antagonist may be one mechanism by which
methadone decreases craving for opioids and tolerance.
Pharmacology: Metabolism
 Methadone has a slow metabolism and very high fat solubility,
making it longer lasting than morphine-based drugs.
 Methadone has a typical elimination half-life of 15 to 60
hours.
 However, metabolism rates vary greatly between individuals.
 Methadone metabolism is largely a function of liver enzyme
activity involving cytochrome P450 isoform.
Pharmacology: Metabolism
 Methadone is stored extensively in the liver and
secondarily in other body tissues.
 The major urinary excretion products are methadone itself,
and metabolites EDDP and EMDP.
 Metabolism rates vary greatly between individuals.
 A single day’s maintenance dose in a tolerant dult can cause
life-threatening respiratory depression in an adult who is
not tolerant, and as little as 10 mg can be fatal in a child.
Methadone abuse
 Most methadone bought from the black market is
thought to be bought by already opioid-dependent
persons attempting to circumvent the substance abuse
treatment system and detoxify themselves with the
methadone or simply by people wishing to use the
drug recreationally, just as other opiates are used.
Methadone abuse
 Although, in general, methadone is not a drug of
choice for opioid addicts due to its long-acting
nature and relatively little euphoria associated with
its use, especially when compared to other drugs of
abuse such as heroin and Oxycodone, it is used by
addicts to relieve withdrawal symptoms when their
opiate of choice cannot be obtained.
Tramadol
‫ترامادول‬
 Tramadol is used similarly to treat moderate to severe
pain.
Tramadol pharmaceutical dosage
forms
 capsules (regular and extended release)
 tablets (regular, extended release, chewable, low-residue and/or







uncoated tablets that can be taken by the sublingual and buccal routes)
suppositories
effervescent tablets and powders
ampules of sterile solution for SC, IM, and IV injection
preservative-free solutions for injection by the various spinal routes
(epidural, intrathecal, caudal, and others)
powders for compounding
liquids both with and without alcohol for oral and sub-lingual
administration, available in regular and bottles, dropper bottles, bottles
with a pump similar to those used with liquid soap and phials with
droppers built into the cap
tablets and capsules containing (acetaminophen), aspirin and other
agents.
Tramadol mechanism
 ULTRAM® (tramadol hcl) contains tramadol, a
centrally acting synthetic opioid analgesic.
 At least two complementary mechanisms appear
applicable:
⚝ Binding of parent and M1 metabolite to μopioid receptors
⚝ Weak inhibition of reuptake of
norepinephrine and serotonin.
Tramadol pharmacokinetic
Tramadol absorption
 The mean absolute bioavailability of a 100 mg oral
dose is approximately 75%.
 Food effect: Oral administration of ULTRAM®
(tramadol hcl) with food does not significantly affect
its rate or extent of absorption, therefore, ULTRAM®
(tramadol hcl) can be administered without regard to
food.
Tramadol metabolism
 Tramadol is extensively metabolized after oral
administration by a number of pathways, including
CYP enzymes, as well as by conjugation of parent and
metabolites.
 Approximately 30% of the dose is excreted in the urine
as unchanged drug, whereas 60% of the dose is
excreted as metabolites.
 The major metabolic pathways appear to be N- and Odemethylation and glucuronidation or sulfation in the
liver.
Tramadol elimination
 Tramadol is eliminated primarily through metabolism
by the liver and the metabolites are eliminated
primarily by the kidneys.
Tramadol abuse
 Tramadol is a widely prescribed drug. Abuse of
tramadol as well as tramadol-related deaths have been
increasingly reported in Iran.
 Tramadol-related deaths in 2008 were 32.5 times more
than in 2005 in Iran.
 Tramadol-related fatalities are growing in Iran
especially in substance abusers.
Tramadol abuse
Tramadol related deaths
‫قواننی مربوط به داروهای حتت کنرتل‬
‫آئني انمه توليد فرآورده هاي دارويي حتت كنرتل (خمدر و روانگردان)‬
‫‪ ‬داروی تحت کنترل به فراورده دارويی اطالق می شود که از سوی وزارت بهداشت‪ ،‬درمان و‬
‫آموزش پزشکی در زمره داروهايی طبقه بندی شده است که توليد‪ ،‬توزيع‪ ،‬عرضه و تجارت‬
‫(خريد‪ ،‬فروش‪ ،‬واردات و صادرات) آن ها فقط در چارچوب مقررات معين و تحت نظارت‬
‫ويژه امکان پذير است‪.‬‬
‫‪ ‬اين تعريف کليه داروهايی را که با نام شيميايی يا نام غير اختصاصی بين المللی در فهرست‬
‫جاری هيئت بين المللی نظارت بر مواد مخدر مربوط به داروهای مخدر (کنوانسيون ‪ 1961‬و‬
‫اصالحی ‪ )1972‬و داروهای روانگردان در بر می گيرد‪.‬‬
‫توضيح فهرست مواد و داروهاي حتتكنرتل‬
‫‪ ‬اين فهرستها شامل فهرست‌هاي‌سه‌گانه‌مواد‌تحت‌‌مراقبت‌هيأت‌بين‌المللي‌كنترل‌مواد‌مخدر‌‬
‫)‪(INCB‬است كه طبق معاهدات بينالمللي مورد پذيرش جمهوري اسالمي ايران‬
‫(كنوانسيونهاي ‪ 1971 ،1961‬و ‪ 1988‬سازمان ملل متحد) تحت مراقبت بيـنالمللي ميباشند‪.‬‬
‫‪ ‬انجام كليه امور مربوط به واردات و صادرات اين اقالم از جمله مراحل ثبت سفارش‪ ،‬ورود و‬
‫ترخيص از گمركات كشور مستلزم كسب موافقت قبلي از وزارت بهداشت‪ ،‬درمان و آموزش‬
‫پزشكي (ادارهكل نظارت بر امور دارو و مواد مخدر) است‪.‬‬
‫‪ ‬اين‌مواد‌در‌سه‌گروه‌مجزا‌طبقه‌بندي‌مي‌شوند‌كه‌عبارتنــد‌از‌‪:‬‬
‫‪ -1 ‬مواد‌مخدر‌(موضوع كنوانسيون‪ )1961‬در فهرست‌‌زرد‌)‪(Yellow List‬‬
‫‪ -2 ‬مواد‌روانگردان‌(موضوع كنوانسيون‪ )1971‬در‌فهرست‌‌سبز‌)‪(Green List‬‬
‫‪ -3 ‬مواد‌شيميايي‌و‌پيش‌سازهاي‌مخدر‌و‌روانگردان‌(موضوع كنوانسيون‪ )1988‬در‌فهرست‌‌قرمز‌‬
‫)‪(Red List‬‬
‫‪ ‬صدور اقالم تحتكنترل به ديگر كشورها منوط به اخذ مجوز صادرات از وزارت بهداشت‪ ،‬درمان و‬
‫آموزش پزشكي( ادارهكل نظارت بر امور دارو و مواد مخدر) است كه بر اساس كنوانسيونهاي ‪،1961‬‬
‫‪ 1971‬و ‪ 1988‬سازمان ملل متحد فقط با ارائه مجوز از مرجع ملي نظارتي مربوط به كنوانسيونهاي‬
‫فوقالذكر در كشور مقصد صادر ميشود‪.‬‬
‫‪ ‬صدور اقالم تحتكنترل بدون اخذ مجوزهاي الزم موجب توقيف محموله در كشور مقصد خواهد شد‪.‬‬
‫‪ ‬اقالم تحتكنترل كه بدون كسب مجوز قبلي وارد كشور شوند‪ ،‬توقيف خواهند شد‪.‬‬
‫‪ ‬هر گونه جابجايي و تجارت (واردات و صادرات) موادي مانند هروئين‪ ،‬ترياك‪ ،‬كوكائين‪ ،‬حشيش و موارد‬
‫مشابه كه مورد مصرف مجاز پزشكي ندارند ممنوع است‪.‬‬
‫‪‬‬
‫ورود ترامادول به فهرست داروهای حتت کنرتل‬
‫‪ ‬شواهد موجود حاكي از افزايش وقوع عوارض و گسترش سوءمصرف داروي ترامادول در‬
‫سطح جامعه بهويژه بين برخي نوجوانان و جوانان ميباشد به طوري كه اثر بر گيرندههاي‬
‫اپيوئيدي و قابليت سوءمصرف‪ ،‬بخشي از بازار قابلمالحظه آن را به مصارف غيردرماني‬
‫اختصاص داده است‪.‬‬
‫‪ ‬در سوءمصرف اين دارو‪ ،‬پيامدهاي نامطلوبي چون دپرسيون تنفسي و ايجاد وابستگي فيزيكي‬
‫قابل انتظار و حتي در مصارف درماني نيز وقوع عوارض جدي نظير تشنج محتمل است‪.‬‬
‫ورود ترامادول به فهرست داروهای حتت کنرتل‬
‫‪ ‬داروي ترامادول طبق رأي جلسه مورخه ‪1386/2/26‬كميسيون حمرتم تشخيص صالحيت ساخت و ورود در زمره‬
‫داروهاي حتتكنرتل حمسوب و مقررات مربوط به فرآوردههاي دارويي خمدر و روانگردان در مورد توليد‪ ،‬واردات‪،‬‬
‫صادرات‪ ،‬توزيع و عرضه كليه اشكال دارويي آن اعمال ميشود‪.‬‬
‫مقررات مربوط به توزيع ترامادول‬
‫‪ ‬توزيـع كليه اشكال دارويي ترامادول از اين تاريخ فقط از طريق عاملين‌مجـاز‌توزيع‌داروهاي‌‬
‫مخدرمجــاز خواهد بود‪.‬‬
‫‪ ‬توزيع و مصرف شكل دارويي آمپول ترامادول طبق بخشنامه ادارهكل نظارت بر امور دارو و مواد مخدر‬
‫همچنان محدود به بيمارستانها و مراكز درماني مجهز به بخش اورژانس است‪.‬‬
‫‪ ‬اين دارو تنها با نسخه معتبر پزشك (هر‌نسخه‌فقط‌يكبار) قابل عرضه است‪ ،‬در صورت ادامه نياز بيمار‪،‬‬
‫دريافت دوباره آن مستلزم تجويز مجدد پزشك و صدور نسخه جديد خواهد بود‪.‬‬
Social problems correlated to drug
abuse
1. Accidental Poisonings
2. Drug Abuse Cases
3. Drug Facilitated Crime
Suicidal Poisonings
Homicidal Poisonings
Incapacitate victims of kidnapping, robbery, or sexual
assaults
Common Street Names of
Cocaine
Toot
Snow
Blow
Flake
White lady
Snowbirds
Paradise
Cocaine potentiates the synaptic actions of
dopamine, norepinephrine, and serotonin by
blocking their reuptake.
Cocaine Pharmacokinetics





Absorption
snorted thru mucous membranes (cocaine HCL)
injected (cocaine HCL)
smoked (crack cocaine)
can be taken orally (coca leaf chewing, cocaine HCL)
Oral
Intranasal
Intravenous
(Cocaine HCL)
(Cocaine HCL)
Inhalation
(crack)
(Cocaine HCL)
Onset
10min-30min
2min -3min
30-45sec
8-10sec
High
15-30min
30-45min*
10-20min
5-10min
Average
dose
100-200mg
5 X 30mg
25-50mg
250-1000
Pharmacokinetics
 Absorbed from all application sites.
 Penetrates brain rapidly (brain concentrations
exceed blood plasma), then it is rapidly
redistributed to other tissues.
 Rapidly and almost completely metabolized by
enzymes located both in plasma and in the liver.
 Urine is the commonest rout of excretion.
Psychological Effects
Low Doses
 Immediate euphoria*
 Giddiness
 Enhanced selfconsciousness
 Forceful boastfulness
High Doses
Psychological effects
intensified, but followed
by:





Depression
Dysphoria
Anxiety
Somnolence
Drug craving
Side Effects and Toxicity
 Hypertensive crises
 Heart attacks/ failure
 Hemorrhage
 Edema
 Infection
 Anxiety, hyper vigilance, paranoia, persecutory
fears, toxic paranoid psychosis.
 Sleep deprivation
 Sudden death
Khat
 Khat is a natural stimulant from Catha Edulis, a small
tree or large shrub.
 Fresh leaves and shoot tips of this plant have been
chewed or brewed as a tea to produce stimulating
properties
Khat alkaloids
 Khat contains cathinone and cathine, which
resemble amphetamine.
 Khat consumption induces mild euphoria and
excitement, reduces appetite, increases heart rate
and blood pressure.
Cathinone
 Main psychoactive alkaloid in khat Produces
amphetamine-like action - a naturally occurring
amphetamine
 Cathinone effects are not distinguishable from
amphetamines.
 Functions by releasing catecholamines (dopamine)
from presynaptic storage sites in CNS.
Khat
Pharmacology
 Main Constituents: Cathinone and Cathine.
Varies from 77.7 to 342.8 mg/100g
Mechanism of Action
Central
 Increases the levels of Dopaminergic and
Noradrenergic transmission in the brain
 Serotonin levels are increased in response to
Cathinone administration
Peripheral
 Indirect sympathomimetic actions
Methods of Khat Administration
 Methods of administration
- Fresh leaves and tops are chewed less
frequently dried and consumed as tea.
Mephedrone
Street names
 Mephedrone is the most popular derivative of the
cathinone .
 ‘Legal high’,‘plant food’, ‘meow meow’, ‘miaow’,
‘drone’, ‘meph’, ‘bubbles’, ‘spice E’, ‘charge’, ‘M-Cat’,
‘rush’, ‘Ronzio’, ‘Fiskrens’ and ‘MMC hammer
Definition
 Mephedrone is a psychoactive research chemical that
elicits stimulant and effects similar to amphetamines,
cocaine, metamphetamine, and MDMA.
Amphetamines and cathinones
pharmacology
 Both amphetamines and cathinones bind to
noradrenalin, dopamine and serotonin transporters,
each of them differing from each other by its relative
binding potency.
Mephedrone vs. amphetamines
 Cathinones’ (mephedrone) potencies are mostly
lower than those of amphetamines as beta-keto
amphetamines show a reduced ability to cross the
blood–brain barrier due to the presence of the beta
group.
Mephedrone commercial
appearance
 Mephedrone occurs as a white, or slightly yellowish,
powder or fine crystals.
 Less frequently, it is marketed as capsules or tablets
of various colours, shape and thickness, with or
without a logo.
 Although mainly sold in powder and crystal forms,
mephedrone may be commercially available in tablets
and included within vegetable-based capsules.
Mephedrone
Mephedrone
Routes of administration
 The most common routes for recreational use
include insufflation (snorting) and oral ingestion.
 Because of its solubility in water, mephedrone is
reportedly used by rectal administration (dissolved
in an enema or within gelatine capsules) as well or
injected intravenously.
 Insufflation is likely to be the most common route.
Peak time to get high
 When snorted, mephedrone elicits its effects within a
few minutes, with the peak being reached in <30 min
followed by a rapid comedown.
Pan Parag
 Pan parag is a combination of Betel Nuts, Cardamom,
Lime, Catechu and Natural perfumes.
 Betel chewing has been claimed to produce a sense of
well-being, euphoria, heightened alertness, sweating,
salivation, a hot sensation in the body and increased
capacity to work.
 Betel chewing also leads to habituation, addiction
and withdrawal.
Pan Parag chewing gum
Betel nut
 The Areca nut is the seed of the Areca palm (Areca
catechu), which grows in much of the tropical Pacific,
Asia, and parts of east Africa.
 It is commonly referred to as "betel nut" as it is
often chewed wrapped in betel leaves.
Areca Nut
 An areca nut bunch hanging from the palm.
 Areca nuts wrapped in Betel leaves, appearing as
they are commonly prepared and sold in Taiwan
 Areca nut vendor with red mouth from areca
consumption preparing betel leaves and lime