Drug Dependence and Addiction
Drug Dependence and Addiction
LECTURE 6
Drug Use
Drug users are found in all occupations and
professions, at all income and social class levels,
and in all age groups.
No one is immune to drug use, which often leads
to drug dependence. Thus, drug use is an equal-
opportunity affliction.
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Six Examples of Drug Misuse
DETOXIFICATION
It is one of the process of drug dependence treatment. It involves
administration of abused drug in reduced doses so that slow
withdrawal is possible.
TERMINOLOGIES: ADDICTION
Chronic use of drug leads to drug addiction. Drug addiction is
characterized by the following:
The person aims to consume the drug at any circumstances.
Procurement of the drug becomes a must for the person.
Drug addiction leads to the development of tolerance.
Tolerance development increases the effective dose
requirement production of normal therapeutic effect.
Addicted people must use the drugs regularly to avoid
abstinence (self-restraint) syndrome.
Discontinuation or cessation of the drug leads to relapse.
Examples : The drugs like Amphetamines, Lysergic Acid Diethylamide,
Cocaine, Cannabis and others are liable for addiction. These drugs
produce addiction without physical dependence.
TERMINOLOGIES: HABITUATION
It is a state of mind of a drug abuser characterized
by the following features:
There is no compulsion to consume the drug.
Tolerance, withdrawal symptoms are developed to
a maximum extent.
Habituation is not harmful to society but is
problematic for an individual.
It is closely related to addiction.
DRUG ABUSE
Substance Abuse is the less severe diagnosis.
It includes symptoms like:
The repeated and continued use of a substance despite
negative consequences (within a 12-month period) etc.
Drug addiction is a chronic, relapsing
behavioral disorder
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Development & maintenance
Intended responses
reason for using the drug
Unintended responses
side effects
Nausea or vomiting
Changes in mental alertness
Dependence
Withdrawal
Allergic reactions
Changes in
cardiovascular activity
Potency
the amount of drug necessary to
cause an effect
Toxicity
the capacity of a drug to do damage/cause
adverse effects in the body
Required Doses for Effects
2 ON CARDIOVASCULAR SYSTEM
Nicotine stimulates autonomic ganglia and adrenal medulla
which results in vasoconstriction of peripheral regions and
the ultimate effect is tachycardia, increased cardiac output and
arterial pressure.
3 ON GASTROINTESTINAL TRACT
Salivary secretions are increased by stimulatory effects of nicotine. Other effects
on GIT include nausea, vomiting. Excess stimulation of GIT delays healing of
peptic ulcers, increased motor activity and diarrhoea are noticed.
NICOTINE
PHARMACOKINETICS
Nicotine is absorbed rapidly when it is inhaled in the form of
smoke. Cigarettes possess 0.8g of tobacco and 9-17g nicotine.
Cigar or pipe smoke gets absorbed rapidly from mouth to
pharynx. Absorption of nicotine from cigar occurs at slower
rate and lasts for longer duration.
Consumption of one cigarette increases about 15-30mg/ml of
nicotine concentration in the plasma within 10 minutes. The
obtained concentration reduces to half after another 10
minutes and slowly declines within 1 to 2 hours as it gets
distributed to tissues and blood.
Nicotine is metabolized by liver. Oxidation of nicotine takes
place and the oxidized metabolic product is cotinine, plasma
half-life of metabolic product is for longer duration.
NICOTINE
ADVERSE EFFECTS
1 RESPIRATORY DISORDERS
Chronic smokers have high risk of cancer attack. Occurrence of cancer in
lungs, upper respiratory tract, oesophagus, bronchi, larynx have been
noticed. Cancer is associated with symptoms like dyspnoea, wheezing
cough, chest pain, respiratory tract infections, etc. Risk of cancer is greater
in smokers when compared to non-smokers.
2 ON CARDIOVASCULAR SYSTEM
Thrombosis induced by smoking results in coronary heart
diseases. Hypertension and ischemia may also occur due to
excess release of catecholamine, antidiuretic hormone and fatty
substances in plasma
3 REPRODUCTIVE DISORDERS
Smoking may lead to several complications in pregnant
women such as premature delivery, spontaneous abortion and
placenta praevia. It may also show deleterious effects in the newborns
such as decreased birth weight, physical and mental abnormalities. It may
also lead to tachycardia in infants dependent on mother’s milk.
NICOTINE
DEPENDENCE & TOLERENCE
ALCOHOL
Alcohol beverages are widely
distributed and available globally.
Alcohol is one of the most abused
drugs. People prefer alcohol for
pleasure and euphoria.
The reinforcement of alcohol is high
as a result several people are currently
suffering from alcoholism.
Alcohol primarily acts as a CNS
depressant and gradually initiates
sedation.
ALCOHOL
MECHANISM OF ACTION
Chronic alcohol consumption produces various adaptive
neuronal changes in order to counter attack the acute
cellular effects produced by alcohol.
The density of GABAA receptors decreases up-regulation
of NMDA (N-methyl-D-aspartate) receptors and
propagation (proliferation) of Ca2+ Channels takes place.
Alcohol enhances the neurotransmitters of reward
pathway. It elevates dopamine, 5-HT, acetylcholine,
norepinephrine and other opioid receptors with a similar
mechanism as that of opioids i.e., enhances the drug
dependence activity since it produces pleasant feelings.
ALCOHOL ADVERSE EFFECTS
1 CNS MANIFESTATIONS
Initial effects include impairment of cognitive functions like ability to
learn, attention, contraction, slurred (inaudible) speech, euphoria, highly
excited nature, self confidence, sedation, ataxia (lack of coordination while
performing voluntary movements, appearing clumsy, inaccurate, or instable). Excess
alcohol results in melancholy, aggressive nature, mood disorders, impaired
sensory parameters, etc.
2 CARDIOVASCULAR MANIFESTATIONS
These include peripheral vasodilation, sweating, excessive
sweating, increased heart rate, flushing (sudden rush of feelings).
3 GASTROINTESTINAL MANIFESTATIONS
Alcohol enhances gastric acid secretions and results in
impairment of normal functioning of GIT.
4 RENAL MANIFESTATIONS
Diuresis due to inhibition of anti-diuretic hormone.
Hyperuricaemia (excess uric acid in blood) due to abnormal
excretion of uric acid.
ALCOHOL
CHRONIC TOXIC EFFECTS
Chronic alcohol consumption leads to
various neurological disorders such as –
a. Wernicke’s Encephalopathy (condition affecting brain)
b. Polyneuropathy (any of the several diseases involving several
peripheral nerves).
c. Karsakoff’s Neuropathy
d. Retrobulbar Neuropathy
e. Marchiafava Bignami Syndrome
f. Hepatic Encephalopathy
ALCOHOL
DEPENDENCE & TOLERENCE
Tolerance and dependence are also major problems.
They are a result of prolonged consumption of alcohol
which desensitizes and decreases GABAA receptors,
increases NMDA subtype glutamate receptors.
These changes play a vital role in development of
tolerance.
Cells and tissues function abnormally due to tolerance
development.
Elimination of alcohol at a faster rate is also one of the
reasons for tolerance development.
ALCOHOL WITHDRAWAL SYMPTOMS
The withdrawal symptoms include seizures, sweating,
hyperthermia, delirium, hallucination, hyper-excitation and
neuro-toxicity. These are due to the effect of sudden
withdrawal of alcohol on Ca2+ ions. Increased Ca2+ ions cause
this.
1 CARDIOVASCULAR SYSTEM
Cardiomyopathy (muscular dysfunction not because of nerve disorder), cardiac
arrhythmias (irregular heart beat), abnormal metabolism, increase of
catecholamine, hypertension are some of the withdrawal
effects of alcohol.
2 GASTROINTESTINAL TRACT
Some effects of alcohol withdrawal on GIT are esophageal
reflux, Barrett’s esophagus, gastric pain, Mallory-Weiss
syndrome and oesophagal cancer. Excess alcohol consumption
affects gastric mucosa and causes gastric bleeding.
ALCOHOL
TREATMENT
OPIOIDS
An opioid is any psychoactive chemical
that resembles morphine in its
pharmacological effects. Opioids work by
binding to opioid receptors, which are
found principally in the central and
peripheral nervous system and the
gastrointestinal tract.
Commonly abused opioids are morphine,
heroin, codeine, oxycodeine and
meperidine.
OPIOIDS
MECHANISM OF ACTION
Opioids act on G-protein coupled receptors μ, κ, δ which are
known to inhibit adenyl cyclase, cAMP, protein kinase A,
voltage gated CA2+ channels.
The inhibitory action of opioids leads to depression upon
mild exposure.
Prolonged exposure of opioids exert an opposite effect on the
G-protein coupled receptors resulting an increase in the
compensatory response element binding [(cAMP, adenyl
cyclase, protein kinase A) CREB].
The rise in CREB exert excitatory actions due to enhanced
Na+ channel functions and cAMP upregulation.
All these cellular effects not only decrease the inhibitory
actions of opioids but also lead to the development of
tolerance, dependence and withdrawal symptoms.
OPIOIDS
DEPENDENCE
Physical and psychological dependence develop in opioid
drug abusers.
Physical dependence develops to a greater extent that
compared to psychological dependence. Sudden withdrawal
of opioids may lead to death of individuals.
The symptoms of physical dependence include dysphoria, GI upset,
mydriasis, cough, hyperventilation, ocular discharge, diarrhea, yawning,
hyperthermia, piloerection, aggressiveness and emesis.
MECHANISM OF ACTION