Drug Dependence and Drug Abuse

DRUG DEPENDENCE
AND DRUG ABUSE
www.revolutionpharmd.com
DEFINITIONS
DRUG DEPENDENCE - state when drug-taking becomes compulsive,
taking precedence over other needs. Syn. substance dependence
DRUG ADDICTION - is not clearly defined but implies a physical
dependence, however, sometimes it is used as a syn. to drug
(substance) dependence
DRUG ABUSE - more general term, includes recurrent use of any
illegal/harmful substance, e.g., in sport
TOLERANCE - the decrease in a pharmacological effect on repeated
administration of the drug
 imply the need to increase the dose to reach the pharmacological effect of the
same intensity on repeated administration of the drug
 often accompanies the state of dependence
WITHDRAWAL (syn. ABSTINENCE) SYNDROME - adverse effects,
both psychological and physical, of stopping taking a drug. Distinguish
commonly observed rebound phenomenon from the true dependence.
REWARDING EFFECT – important and common feature of
psychoactive addictive substances.
Tolerance induction
Two major mechanisms

 Pharmacokinetic (auto-induction of enzymes
responsible for drug metabolism, e.g., in
barbiturates)
 Pharmacodynamic (tissue type)
changes in receptor density (downregulation in
most of drugs in this topic – the agonists)
changes in receptor sensitivity (desensitisation,
adaptation at the level of second messengers)
process of habituation, or adaptation, is coupled with the
direct rewarding effect of the drug when the drug is given
repeatedly or continuously
cessation of the drug leads to the aversive effect (negative
reinforcement) from which the subject will attempt to escape
by self-administration of the drug
Dependence types and conditions

1. psychological dependence – result of positive/negative
reinforcement associated with drug aadministration.
Drug withdrawal  ‘craving’
1. physical dependence (tolerance and withdrawal syndrome)
2. conditioning - significant especially in sustaining
psychological dependence-effect of environment, perception
of stimuli associated with pleasurable experiences
REWARD PATHWAYS
virtually all dependence-inducing drugs so far tested ,
including opioids, nicotine, amphetamine, ethanol and
cocaine, activate the REWARD PATHWAY - mesolimbic
dopaminergic pathway, which runs via the medial forebrain
bundle, from the ventral tegmental area (VTA) of the midbrain
to the nucleus accumbens and limbic region
 positive reinforcing effect
addictive drugs increase the release of dopamine in the
nucleus accumbens even though primary sites of action are
generally elsewhere in the brain
the hedonic effect of dependence-producing drugs results
from activation of this pathway, rather than from a subjective
appreciation of the diverse other effects (e.g. alertness or
stimulation)
Importance for drug-seeking behaviour
Classification of drugs (substances)
of abuse
nicotine (tobacco)
ethanol
cannabis
psychotomimetic drugs (hallucinogens)
psychomotor stimulants
opiates
CNS depressants (sedatives/hypnotics)
solvents
NICOTINE AND TOBACCO
Originally, Nicotiana plant growing, tobacco chewing and
smoking was common only on American subcontinent
It was brought to Europe during 16th century
currently, estimation is that 18% of world population are
smokers, the number rapidly increases in the third-world
countries, while it has been slowly declining in developed
countries
the only pharmacologically active agent in cigarette smoke

is nicotine, apart from the toxic carcinogenic tars and
carbon monooxide
An average cigarette provides about 0.8-1.5 mg of

nicotine
MECHANISM OF ACTION
Nicotine is an agonist on nicotinic acetylcholine
receptor, ligand-gated cation channels type, widely
expressed in brain, in cortex and hippocampus, supposed to
play a role in cognitive function
→ neuronal excitation and enhanced transmitter release
EFFECTS
central: mixture of inhibitory and excitatory effects;
increased alertness, reduction of anxiety and tension,
decreased appetite ( lower average body weight in
smokers  4 kg)
peripheral: NN-receptors in autonomic ganglia: tachycardia,
↑blood pressure, ↑cardiac output, ↑GIT motility,, first dose
vomiting (stimulation of sensory receptors in the stomach);
NM-receptors: tremor, skeletal muscle relaxation
Pharmacokinetic aspects
during smoking cca. 10% of nicotine contained in a cigarette is
absorbed
Absorption rapid from the lungs (when smoking a cigarette) or
more slowly from the mouth and nasopharynx (when smoking a
cigar or a pipe)
following drop in nicotine plasma concentration is due to
distribution from blood to other tissues and later slow decrease
caused by nicotine liver metabolism in to inactive cotinine
nicotine patch applied for 24 hours causes plasma
concentration to rise to 75-150 mmol/l over 6 hours and to
remain mainly constant for about 20 hours
In smokers there is an induction of liver and intestine
CYP450s  decreased effects of some drugs (e.g.,
theophyline)
Tolerance and dependence
very quick tolerance to peripheral (not central) ganglionic

stimulation, perhaps due to desensitization of receptors
addictiveness of smoking is solely caused by nicotine
withdrawal syndrome: craving ! increased irritability,
anxiety, impaired performance of psychomotor tasks,
aggressiveness and sleep disturbances, headache
increased appetite lasts for 2-3 weeks
highly addictive with the very strong psychological
component (‘craving’ most commonly hampers efforts to
give up)
Harmful effects of smoking
smoking - greatest preventable cause of death; it is responsible
for 10% adult deaths worldwide (estimation is 17% in 2030)
CANCER - lung (the upper respiratory tract, oesophagus…)
 20 cigarettes/day is estimated to increase the risk about 10fold; 90% of
lung cancer is due to smoking; tar is responsible !
 “ Low tar cigarettes“ – smokers puff harder
CORONARY HEART DISEASE AND OTHER FORMS OF

PERIPHERAL VASCULAR DISEASE – nicotine and carbon
monoxide
CHRONIC BRONCHITIS - smoking remains the main cause of
this disease in developed countries
HARMFUL EFFECTS IN PREGNANCY -significant reduction in
birth weight, increased perinatal mortality, retardation in mental
and physical development
Acute Intoxication after swallowing cigarettes/butts – risk in
children (1-2 peaces)  salivation, vomiting, arrhythmias and/or
convulsions (fatality is mostly reduced by vomiting)
Treatment of nicotine dependence
Most smokers would like to quite but few succeed
Combination of psychological and pharmacological treatment
achieve success rate about 25% (after 1 year)
Nicotine replacement therapy
 Nicotine in patches (controlled release), chewing gums, nasal sprays
several times daily (short effect)
Adjunct therapy
 Bupropion (NDRI, even in non-depressed patients! Mechanism: an
increase in dopamine activity in nucleus accumebens?)
 Clonidine – rarely used due to the side-effects (hypotension,
drowsiness…)
Are there any „positives“ of nicotine and smoking?

Decreased incidence of both Parkinson´s and Alzheimer´s
disease?
ETHANOL
most commonly taken substance leading to physical

dependence (it is legal for adults!)
content in beverages varies from 3.5% (weak beer) to
40-50% (spirits)
single drink usually contains 8-12g of ethanol
intake expressed in units (1 unit = 8g)
→ current official recommendation is a maximum of 3
drinks/day for MEN, 2 drinks/day for WOMEN
alcohol dependence (‘alcoholism’) occurs in 4-5% of
European population
Pharmacokinetics of ethanol
- rapid absorption after oral administration (measurable concentration after
5 min), immediately from the stomach
- Wide distribution to the whole body fluids
- More than 90% of ethanol is metabolised , less than 5-10% excreted
unchanged in expired air and in urine (but this fraction is not significant from
PK point of view, however, it is used for plasma conc. estimation )
- Saturation character of metabolism  linear fall of plasma concentration
- Significant first pass effect (drinking on empty stomach  higher effects)
Main metabolism via 2 subsequent oxidations:
a) cytoplasmic alcoholdehydrogenase (→acetaldehyde)
b) aldehydedehydrogenase (→acetic acid)
this enzyme can be inhibited by various substances →‘ disulfiram effect’
(disulfiram but also chlorpropamide, nitrofurantoin etc.)
Symptoms: nauzea, flushing, tachycardia, hyperventilation, panic ….
Alternative metabolic pathway MEOS - microsomal ethanol oxidizing
system - minor alcohol → acetaldehyde pathway, inducible in alcoholics.
Limiting factor for ethanol metabolism
is a NAD+ availability
Genetic factors in ethanol metabolism
50% Asians have the inactive isoform of

aldehydedehydrogenase experiencing disulfiram-like
reaction after alcohol intake
Another group of Asian population has an isoform of
alcoholdehydrogenase with lower activity – increased
effects and excessive drinking behaviour
American indians?
Pharmacological effects of ethanol
1. CNS EFFECTS
- mainly depressant action at the cellular level
- three main theories:
 enhancement of GABA-mediated inhibition, similar to that of
benzodiazepines (different binding site)
 inhibition of Ca2+ entry through voltage-gated calcium channels
 inhibition of NMDA-receptor function
relationship btw plasma concentration / effect is highly variable
symptoms of acute intake:

- slurred speech, euphoria, motor incoordination, increased self-
confidence, decreased concentration and learning ability.
- higher plasma levels lead to mood lability, later ataxia, stupor and coma,
death from respiratory failure
- Rather excitatory effects in low doses are attributed to neuronal
desinhibition
Ethanol plasma concentrations vs.
CNS effects
Ethanol plasma concentration Effect

(permill)
0.2 Feeling of relaxation
0.3 Slight euphoria

0.5 Slight motor incoordination
1 ataxia
3 stupor
>4 Coma, death due to the
respiratory failure
!!!! alcohol potentiate the effects of other drugs with central depressant
effects – barbiturates, benzodiazepines, H1-anithistamines….
Pharmacological effects of ethanol
2. effect on peripheral systems

- cutaneous vasodilatation ‘warm feeling’, sweating 
heat loss
- ↑diuresis (due to ↓ADH secretion)
- heart rate; ↑blood pressure
- ↑salivatory and gastric secretion
- ↑concentrations of hydrocortisone
-  oxytocin secretion (delay in parturition at the term)
Tolerance and dependence
The major component is tissue tolerance – it develops over
1-3 weeks of continuing administration = 2-fold decrease in
alcohol potency. There is a cross-tolerance with many
anaesthetics (e.g. halothan, problems with alcoholics)
Mechanism: not well explained, changes in CNS neurons –
down-regulation of GABAA-receptors, up-regulation of
voltage-gated Ca channels and NMDA receptors?
Minor tolerance component - increased metabolism
Physical abstinence syndrome develops, in severe forms,
after cca 8 h (culminating in 24-36h): tremor, nausea,
sweating, fever, occasionally hallucinations and epilepsy-
like seizures!
‘delirium tremens’ over few following days: confusion,
agitation, aggression, unpleasant hallucinations
Anorexia, tremor, nausea, vomiting and anxiety might be
present even 2 weekswww.revolutionpharmd.com
later
Harmful effects of chronic alcohol abuse
Behavioural defects: loss of self-control, reliability and productivity,
disrupted social and family network
Neurological disorders: CNS damage associated with dementia,
peripheral neuropathies (thiamine deficiency).
GIT disturbances: gastritis, peptic ulcers and GIT bleeding, hematemesis.
Liver damage: fatty liver, progression to hepatitis and eventually to
irreversible hepatic necrosis and fibrosis
 Mechanisms (rather complex):
Cummulation of NAD+ dependent substrates: lactate,
hydroxybutarate, α-glycerofosfate   gluconeogenesis →
hypoglycaemia → ↑ triglyceride synthesis
↑ release of fatty acids from adipose tissue
impaired fatty acid oxidation due to metabolic load of ethanol itself
 Diverted portal blood flow  oesophageal varices and bleeding
 Biochemistry: Gamma glutamoyl traspeptidase (ALT, AST, bilirubin….)
Pancreatitis: ↑secretin production, ↑pancreatic enzyme, Oddi sphincter
oedema  partial pancreas www.revolutionpharmd.com
autodigestion (other factors like ROS…)
Ethanol & fetal development
FAS (fetal alcohol syndrome)

typical of anatomical, mental and behavioural abnormalities:
- facial development, reduced cranium size
- retarded growth
- mental retardation and behavioural abnormalities
ARND (alcohol-related neurodevelopmental
disorder):
- less serious than FAS (3x more common),
- behavioural, cognitive and motor deficits
Treatment of alcoholism
Disulfiram – blockade of aldehydedehydrogenase 
cummulation of acetaldehyde - nausea, flushing,
tachycardia, hyperventilation, panic…
Aim: to make alcohol consumption unpleasant and
intolerable
Naloxone – reduces alcohol-induced reward (unclear
mechanism)
Acamprosate – anti-craving effects (also naltrexon)
The drugs used to alleviate the acute abstinence syndrome:
benzodiazepines, clonidine (inhibits exaggerated
neurotransmitter release) and propranolol (blocks
excessive sympathetic activity).
CANNABIS and Cannabinoids
extracts of the hemp plant (Cannabis sativa,Canabis indica)
originally from Himalaya and Kashmir
Marijuana - dried leaves and flower heads
Hashish - extracted resin
active substances: cannabinoids (lipophilic non-alkaloid
natural compounds)
THC (Δ9-tetrahydrocannabinol) most abundant and active
cannabinoid
THC constitutes 0.5-10% of marijuana and hashish
preparations
routes of administration: mainly inhaled in cigarette
smoke (‘joint’) or orally as an ingredient in various meals or
beverages
Pharmacological effects
On CNS: combination of psychotomimetic, depressant and
centrally mediated peripheral effects
central effects:
 a feeling of relaxation, well-being and euphoria - without
accompanying aggression
 Uncontrolled laughing without reason
 a feeling sharpened sensory awareness, with tastes, sounds
and sights more intense and fantastic
 impairment of motor coordination (driving), short-term memory
and judgement. Feeling of time passing slowly,
depersonalisation; increased appetite and
 Analgesia, antiemetic action
 In high doses: hallucination, paranoia, anxiety
peripheral effects:
 vasodilatation (obvious on conjunctive vessels)
 tachycardia
 Bronchodilation (but opposite may appear during smoking)
 reduction of intraocular pressure
Mechanism of action
Through cannabinoid receptors (GPCR type)
 CB1- brain – highly abundant in: hippocampus (memory),
cerebellum (loss of coordination), and substantia nigra (motor
disturbances), hypothalamus (appetite) and mesolimbic
dopaminergic pathway (reward) and cortex.
 Mostly localised presynaptically – their activation inhibits
neurotransmitter release
Their paucity in the brain stem  lack of serious respiratory and
cardiovascular toxicity.
Endogenous agonist: anandamide
 CB2- periphery - immune system (immunosuppressive effects?!)
Pharmacokinetics
- lipophilic compound - well absorbed, highly bound to
plasma proteins, widely distributed and partially
sequestrated in body fat → excretion lasts for days (can
still be detected in urine)
- liver metabolism to mostly inactive metabolites
Tolerance and drug dependence
Tolerance and physical dependence occur only to a
minor degree in heavy users
Withdrawal syndrome: weak and usually mild
irritability, restlessness, confusion, sweating tremor and
sleep disturbances
Harmful effects
- Relatively safe from the viewpoint of acute drug overdose
- Problems are rather with chronic use:
Somatic effects: decreased testosterone and sperm count
Long-term psychological changes: apathy, impaired memory
and decision ability, may promote schizophrenia in pre-disposed
patients
- „Gateway drug“??? www.revolutionpharmd.com
Therapeutic use of cannabinoids?
Synthetic analogues
 Nabilone and dronabilone
Potential indications
 Antiemetic therapy in cancer chemotherapy
 Analgesia
 Glaucoma
 Multiple sclerosis
Therapeutic values and utility?

Legal limitations
Psychotomimetic drugs
(hallucinogens, psychedelics)
affect thought, perception and mood without causing
psychomotor stimulation or depression
Effects: thoughts and perceptions tend to become distorted
and dream-like, colours and sounds are more sharp. Induction
of euphoria and happiness.
Different kind of hallucination (visual, auditory, tactile and
olfactory appear). Thought process tend to be illogical and
disconnected but subject mostly retain insight that these
effects are drug-induced. Increased sense of empathy.
Major groups/drugs (different classification in literature)
 LSD and related compounds (psilocybin, mescaline)
 MDMA and related compounds
 Phencyclidine and ketamine
LSD (Lysergic acid diethylamide, LSD-25)
 Originally produced as a drug candidate in Sandoz Labs in 1938
by Albert Hoffman – today no medical use!
 It is among the most potent drugs known so far (dose =1 g/kg)
 Abused in the form of „papers“- „trips“ (low amounts of LSD)!
 „Good trips“ vs „bad trips“
 „flash backs“ may appear even months later

Mechanism of action: acting on different 5-HT receptors in CNS
mainly as agonist on 5-HT2A autoreceptors in CNS   firing of 5-HT
neurons in Raphe nuclei (even in spiders – bizarre/erratic webs)
 Somatic effects: sympathomimetic (↑blood pressurere and HR)
neurological (tremor, ataxia)
Mescaline (from Mexican cactus Lophophora)
Psilocybin (from fungus Psilocybe – e.g. Bohemica)
Tolerance: develops quickly (on CNS effects)
Adverse effects and dangers: persistent mental disorder,
schizophrenia, injury due to violent behaviour
Other hallucinogens
MDMA (MethylenDioxyMethAmphetaminem, ecstasy)
 Dance-floor drug
 Stimulant and hallucinogenic effects (related to
amphetamines)
 Danger in acute overdose: exhaustions, dehydratation,
hyperpyrexia, arrhythmias
Phencycline („angel dust“, PCP)

 Chemically related to ketamine (anaesthetic drug) and
originally also developed as a drug with this indication
 Not so frequent among abusers, unpleasant vegetative
effects
 Some delusions and/or hallucination may turned into the
violent behaviour
PSYCHOMOTOR STIMULANTS
1)AMPHETAMINES AND RELATED DRUGS
2)COCAINE
3)METHYLXANTINES (CAFFEINE & CO.)
Amphetamines and related
compounds
substances: amphetamine (speed), methamphetamine
(pervitine) and other drugs like ephedrine, phentermine,
methylphenidate and MDMA.
Routes of administration: oral, nasal, inhalation and
parenteral
Mechanism of action: indirect CNS „sympathomimetic“ effect
– release of monoamines (noradrenaline, dopamine, or 5-HT)
from nerve terminals in the brain
Main effects on CNS: locomotor stimulation,
euphoria and excitement, increased self-confidence,
stereotyped behaviour, resistance to fatigue, decreased
appetite, anorexia
Peripheral effects: tachycardia and palpitations, ↑blood
pressure, ↓GIT motility
„Morning after“ intoxication: fatigue, depressions, anxiety…
Amphetamines and related
stimulants
Tolerance develops rapidly to the peripheral
sympathomimetic and anorexic effects, but more slowly to
the central effects
no clear-cut physical withdrawal syndrome → dependence
seems to be a consequence of the unpleasant after-effects
(i.e. fatigue, lethargy, anxiety, depression, hunger) and the
effort to avoid them
full-blown dependence occurs in 5% of users –
characterized by strong craving, increased doses, and
common uncontrolled ‘runs’)
Amphetamine psychosis – closely resembles the
Schizophrenic attack – incoherent thought, hallucinations,
paranoia, aggression.
Therapeutic use: minimal e.g., narcolepsia,
phentermine (rather obsolete use in the
treatment obesity)
COCAINE
alkaloid of South American shrub Erythroxylon coca
the most expensive drug illegally sold
Routes of administration: salt - nasal or i.v. (rush effect), free
base: smoking-inhalation (crack, flush effect)
MECHANISM OF ACTION:
inhibition of catecholamine Re-uptake  increase
noradrenaline and dopamine transmission
indirect „sympathomimetic“ agent
Pharmacological effects: very similar to those of
amphetamines yet less prone to cause stereotyped behaviour,
paranoia, delusions
Duration of effect is much more shorter (30 min, i.v.) than in
amphetamines, rapid metabolism – liver and plasma esterase
(hair deposit of metabolites).
no clear-cut physical dependence syndrome but
depression, tiredness and dysphoria coupled with very
intensive craving for the drug (strong psychological
dependence) www.revolutionpharmd.com
Cocaine
Tolerance: in most abusers is on rush/euphoria
Intoxication (overdose): tremor, hypertension,
tachycardia, arhythmias, cardiac pain, hyperpyrexia,
convulsions and shock even with fatal consequences
Long term abuse
Characteristic behavioural changes: paranoia, anxiety,
aggression, loss of social contacts
Increased risk of coronary and cerebral thrombosis
slowly developing damage to myocardium leading to heart
failure may appear
Cocaine used in pregnancy impairs fetal development and
produces fetal malformations
Therapeutic use: rarely as a local anaesthetic drug in
ophthalmology (event. nose/throat surgery)
METHYLXANTHINES
natural alkaloids occurring in various beverages, namely tea,
coffee, cocoa and cola-flavored drinks
substances: caffeine, theophylline, theobromine
a cup of coffee or strong tea contains 50-100 mg of caffeine
Pharmacological effects:
CNS stimulation
diuresis (vasodilatation of the afferent glomerular arteriole)
stimulation of cardiac muscle
relaxation of smooth muscle, especially bronchial.
MECHANISMS:
1) inhibition of phosphodiesterase, responsible for
intracellular metabolism of cAMP
2) antagonism on both A1 and A2 adenosine receptors
tolerance and habituation develop to a small extent and
withdrawal effects arewww.revolutionpharmd.com
very slight (headache, fatigue)
OPIOIDS
Abused drugs: heroin, morphine, codeine but also other drugs
from this group (historically also opium, occasionally today)
Psychotropic effects are route of administration dependent
 i.v. - “rush“ and „flush“ effect („orgasm“ and warm feeling)
 Oral – euphoria and happiness, well-being
 Other routes: nasal, inhalation (smoking) other parenteral (s.c.)
Mechanism
 Opioid receptors – for abuse & dependence mainly
 -receptor subtype!
Tolerance
 On most effects develops quite quickly (including euphoria and
toxicity – respiratory depression, chronic abusers tolerate doses which

might induce respiratory failure in a normal subject)
 Exceptions: miosis and constipation
 Mechanism: unclear, it seems to be neither of PK origin nor due
to the receptor down-regulation
Opioids
Dependence – strong both physical and
psychological
Clear-cut withdrawal syndrome:
- early symptoms (8-12 after last dose of heroin):
profuse nasal and ocular secretion, sweating and yawning, piloerection
„cold turkey“ (influenza-like symptoms)
- later symptoms (maximum in 2-3 days, disappear in 7-10
days):
mydriasis, tremor, hyperalgesia, nausea, diarrhoea, insomnia and typical
abdominal cramps and „colic“ pain
Some residual symptoms and physiological abnormalities persist for
several weeks
- can be suddenly induced by the administration of antagonist
(naloxone, = possible complication in treatment of the acute
overdose)
Psychological dependence: intensive craving
Treatment
• Methadone - similar to morphine
• duration of action is considerably longer (t0.5 >24 h)
• the physical abstinence syndrome is less acute than with
morphine
• main use is treatment of morphine and heroin addiction
• in a patient taking methadone, the injection of morphine does
not cause expected euphoria
AIM: to get the addicts away from morphine and heroin by
treating them with regular oral dose of methadone
• best treated by specialized addiction clinics and centres
• Heroin lung – case report!!!!

Sedative/hypnotic drugs
Barbituretes and benzodiazepines
Mechanism of action: barbiturate and benzodiazepine
receptors on GABA-A receptor complex (coupled with chloride
channels) – increase response to the endogenous ligand -GABA
Tolerance (among major drawbacks)
 In both groups - but in barbiturates it is more pronounced
(PK type)
 In barbiturates - lack of tolerance on toxicity! Danger!
Both groups may induce psychological and physical type of

dependence (markedly more likely, sever and earlier onset in
barbiturates!!!) Do not suddenly stop chronic treatment (t1/2)!
Withdrawal syndrome: nervousness, restlessness, tremor,
anxiety, confusion, dizziness, delirium, convulsions! See the
case report!!!!
Risk of acute intoxication and respiratory depression is much
greater with barbiturates! BZD are safer but severe cases often
appear when they are combined with alcohol!!!
Solvents
Different lipophilic organic solvents act as unspecific
narcotics (e.g., toulene, acetone)
Route of administration: inhalations (plastic bags)
Lower doses – desinhibition and euphoria,
pseudohallucinations, pleasant dreams
High doses profound CNS depressant effect, coma and
respiratory failure
Extremely dangerous and highly likely acute overdose with
potentially fatal consequences
Chronic abuse – neurodegenaration + behavioural and
mental disturbances
Other toxicities according to the specific chemical - e.g.,
hepatotoxicity, pulmonary hypertension
Thank you 

Drug Dependence and Drug Abuse

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Drug Dependence and Drug Abuse

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DRUG DEPENDENCE

AND DRUG ABUSE

Two major mechanisms

Dependence types and conditions

the only pharmacologically active agent in cigarette smoke

An average cigarette provides about 0.8-1.5 mg of

very quick tolerance to peripheral (not central) ganglionic

CORONARY HEART DISEASE AND OTHER FORMS OF

most commonly taken substance leading to physical

50% Asians have the inactive isoform of

symptoms of acute intake:

Ethanol plasma concentration Effect

0.3 Slight euphoria

2. effect on peripheral systems

FAS (fetal alcohol syndrome)

Therapeutic values and utility?

 MDMA and related compounds

 Phencyclidine and ketamine

Phencycline („angel dust“, PCP)

3)METHYLXANTINES (CAFFEINE & CO.)

 Oral – euphoria and happiness, well-being

 Other routes: nasal, inhalation (smoking) other parenteral (s.c.)

toxicity – respiratory depression, chronic abusers tolerate doses which

AIM: to get the addicts away from morphine and heroin by

treating them with regular oral dose of methadone

• best treated by specialized addiction clinics and centres

• Heroin lung – case report!!!!

Both groups may induce psychological and physical type of

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