Recreational drugs 10/11/2014. Drugs of abuse: Recreational drugs. Tobacco. Absorption of Nicotine (pharmacokinetics)
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1 Drugs of abuse: Recreational drugs Dr B.Vahabi Recreational drugs Are alleged to enhance sociability and liberate inhibition Diagnosis and treatment of toxic effects can be very challenging Recent trends: Ketamine GHB (Gamma-hydroxybutyrate) Rohypnol Tobacco Cigarettes account for 98% of tobacco consumption 27% of UK s population are cigarette smokers Causes 130,000 deaths each year in the UK Over 300 chemical compounds are present in tobacco smoke key adverse effects are mainly due to tar and carbon monoxide Tar: heavy organic chemicals which form the visible smoke Carbon monoxide reduces the oxygen-carrying capacity of the blood Absorption of Nicotine (pharmacokinetics) On average cigarette contains: 0.8g tobacco 9-17mg nicotine Only 10% of nicotine is absorbed Smoke inhalation is a rapid and efficient route for drug delivery Bulk absorption from lungs (ionized), small amounts from mouth (unionized form) An average cigarette, smoked over 10mins, increases blood nicotine levels to nM Metabolism in the liver results in production of cotinine Absorption of Nicotine (pharmacokinetics) 1
2 Mechanism of action of nicotine Nicotine binds to nicotinic acetylcholine ionotropic receptors (nachr) mainly of the α 4 β 2 subtype (the main subtypes in the brain: α 4 β 2, α 3 β 4, a 7 ) Causes neuronal excitation nachrs are widely distributed in the brain (cortex/ hippocampus and ventral tegmental area) and the peripheral nervous system nachrs are found pre-synaptically and post-synaptically Effect of nicotine on the mesolimbic reward pathway Nicotinic receptors are abundantly expressed in the VTA and NAc Administration of nicotine promotes dopamine release in NAc and VTA In VTA, nachrs are found on dopaminergic, GABAergic cell bodies and terminals as well as glutamatergic terminals In NAc are found on dopaminergic terminals as well as GABAergic and glutamatergic terminals Stimulation of nicotinic receptors in the VTA is the primary mechanism underlying nicotine-induced increases in accumbal dopamine, whereas stimulation of nicotinic receptors in NAc modulates the amplitude of this response Activation pre-synaptically results in release of many other neurotransmitters e.g. dopamine, serotonin, etc. Release of norepinephrine, ACh, serotonin, GABA, glutamate and endorphins mediate various behaviours of nicotine Nicotine + + Glutamate inputs Pharmacological effects of Nicotine I Central Nervous System effects CNS effects are extremely complex Multitude of different subtypes, different agonistbinding affinities and different electrophysiological responses diversity of effects Initial effects activation of neurons In continued presence desensitization Chronic use increases number of receptors Overall effect a balance between activation (neuronal excitation) and desensitization (synaptic block) Pharmacological effects of Nicotine II Peripheral Nervous System effects Smaller doses of nicotine can stimulate autonomic ganglia and peripheral sensory receptors in heart and lungs This can elicit various autonomic reflex responses causing: tachycardia, increased cardiac output Increase arterial pressure Reduction of GI motility Sweating In regular smokers resting heart rate is increased by 1 30 beats per min Psychoactive effects of nicotine Nicotine induces stimulation and pleasure and reduces stress and anxiety Smoking may improve concentration, reaction time and performance of certain tasks. Tests of motor and sensory performance (reaction time measurement or vigilance tests) in humans generally show improvement after smoking. Withdrawal syndrome increased irritability, depressed mood, restlessness, anxiety, impaired performance of psychomotor tasks and sleep disturbances 2
3 Tolerance and dependence Effects of nicotine associated with peripheral ganglia stimulation show rapid tolerance Tolerance to the central effects of nicotine is much less than periphery The addictiveness of smoking is due solely to nicotine Nicotine cause excitation of the mesolimbic reward pathway + increased dopamine release in nucleus accumbens Conditioned behaviour plays an important role in nicotine addiction Harmful effects of smoking Life expectancy of smokers is shorter In 1990 smoking was responsible for 10% of deaths worldwide By 2030 expected increase to 17% Harmful effects on numerous organ systems: Respiratory effects Cardiovascular effects Psychological effects Miscellaneous Respiratory effects of smoking Decrease in oxygen-carrying capacity of the blood Increased mucus secretion with reduction of activity in bronchial cilia Progressive destruction of supporting tissue in bronchioles emphysema Increased risk of lung cancer (10-fold) Cardiovascular effects of smoking Stimulation of autonomic nervous system and sensory receptors in heart increased heart rate, blood pressure and cardiac output Oxygen deficiency increased risk of coronary artery disease heart attacks Arteriosclerosis in lower limbs peripheral vascular disease tissue death and gangrene limb amputation Other effects of smoking Cancer of the mouth, pancreas and bladder Harmful effects during pregnancy Peptic ulceration Treatment of nicotine addiction Combination of psychological and pharmacological treatments success rate of 25% Nicotine replacement therapy and bupropion main pharmacological treatments Ecstasy (MDMA) Popular street name for a substance identified chemically as N-methyl-3,4-methylenedioxymethamphetamine ( MDMA) Is a psychotomimetic (hallucinogenic) /psychostimulant drug Is an amphetamine derivative with properties of hallucinogen mescaline Widely used as a party drug induces euphoria/loss of inhibition and energy surge 13% of British university students have taken it 2 nd popular drug in USA after cannabis 3
4 Routes of administration and pharmacokinetics of Ecstasy Almost always taken by mouth as single-dose tablets Typical dosage range for recreational use varies from mg Readily absorbed by the intestinal tract. Reaches peak plasma concentration about 2hrs after administration Is broken down metabolically mainly in the liver Elimination of drug from the body is moderately slow (half life being order of 8hrs) 5 half-lives are needed for 95% of drug to be cleared completely long after effects Mechanism of action of Ecstasy Acts by increasing the net release of monoamine neurotransmitters (serotonin, noradrenaline and to smaller extent dopamine) Its main effect is an indirect 5-HT(hydroxytryptamine, or serotonin) agonist binds to the serotonin transporter blocks reuptake Net effect increase in 5-HT in certain brain regions followed by depletion MDMA Actions of Ecstasy 5-HT is involved in various psychological functions: happiness, sadness, sleeping, sex, etc. Acute effects of Ecstasy Desired effects produced by low doses or single occasions (acute effects): Reported effects of MDMA vary according to dose and frequency of use a single exposure releases up to 80% of stored 5-HT into synaptic cleft Effects on the individual can be divided into: Acute effects Chronic effects Fatal effects Increased wakefulness Endurance Sense of energy Sexual arousal Euphoria Greater sociability Heightened sense of closeness to people Undesired effect Powerful sympathomimemtic effect maintenance of physical exertion for prolonged periods Impairs temperature control of the body serotonergic neurotoxicity and hyponatremia Increased arousal hyperactivity insomnia Hallucinations Psychological problems few days after administration during the period of serotonergic depletion: lethargy Depression Irritability Nausea Headache Chronic effects of Ecstasy: Psychiatric problems Long term effects arise from neurotoxic actions of MDMA Repeated use reduces serotonin levels of brain Destruction of serotonin nerve axons in cerebral cortex reduced serotonin activity in the higher brain regions Regular users experience: Impairment of memory Impairment of decision making/ information processing Panic attacks Lack of self control Recurrent paranoia Severe depression Hypothalamus and suprachiasmatic nucleus are also affected deregulation of temperature, feeding behaviour and biological rhythms 4
5 Chronic effects of Ecstasy: Physical problems Hepatic toxicity Jaundice Enlarged liver Repeated attacks of hepatitis Liver failure Cardiovascular toxicity Noradrenaline release is responsible for adverse cardiovascular effects Hypertension Tachycardia Intracranial haemorrhage Retinal haemorrhage Damage to blood vessel walls Fatal effects of Ecstasy Ecstasy induced depression and suicide Risk taking activities Motor vehicle accidents Ecstasy addiction Some addiction has been reported Decrease in pleasurable effects after frequent use Increase in unpleasant effects in chronic users Cannabis Extracts of the hemp plant, Cannabis sativa Marijuana is the name given to the dried leaves and flower heads prepared as a smoking mixture Hashish is the extracted resin Cannabis has been used for thousands of years as a treatment for various medical conditions Most popular recreational drug in the 20 th century Gateway drug 11% of 11-15yr olds and 28% 15-16yr olds have used cannabis in UK Chemical aspects of cannabis Cannabis extract contains numerous related compounds cannabinoids Most abundant cannabinoids are D 9 -tetrahydrocannabinol (THC) THC most active and abundant substance constituting 1-10% by weight of marijuana and hashish THC metabolite, 11-hydroxy-THC is more active than THC pharmacological effect Pharmacokinetics of cannabis Cannabis is usually smoked in a joint Deep inhalation of smoke Can be eaten Intravenous injection Smoking rapid effects THC enters circulation immediately, reaching peak concentration within 10min The onset of psychoactive effects 30-60mins to develop fully The effect lasts for 2-3hrs Mechanism of action of cannabis THC acts on the cannabinoid CB1-receptors which are widely distributed in the brain CB1 receptors are found in cerebral cortex, hippocampus, mesolimbic system, cerebellum and hypothalamus CB1-receptors-G-protein coupled receptors Activation reduction of camp concentration/ inhibition of Ca 2+ channels and activation of K + channels membrane hyperpolarization 5
6 Effect of cannabis on the mesolimbic reward pathway Cannabinoid Cannabinoid - Glutamate inputs Cannabinoid - GABAergic input Pharmacological effects of cannabis The main subjective effects in humans: Feeling of relaxation and well-being Feeling of sharpened sensory awareness Euphoria Panic reactions Hallucination Pharmacological effects can be divided: Central effects Peripheral effects Central effects Impairment of short-term memory and simple learning tasks Impairment of motor coordination (driving performance) Catalepsy-the retention of fixed unnatural postures Analgesia Increased appetite Peripheral effects Tachycardia Vasodilatation Reduced intraocular pressure Bronchiodilation Smoke tars could predispose users to heart disease/ lung cancer Adverse effects Overdose produces drowsiness and confusion not life threatening Risk of road accidents is high In animal studies, tertogenic and mutagenic effects have been recorded Endocrine effects reduced testostrone and sperm count Cannabis increases the likelihood of schizophrenia more than six fold 6
7 Tolerance and dependence Minor physical tolerance and dependence Withdrawal symptoms: Nausea Irritability Agitation Confusion Psychological dependence occurs to some extent Can produce chronic tolerance but controversial Key references Parrott, A et al (2007) Drugs and behaviour. John Wiley & Sons Ltd. Rang, H.P., Dale, M.M. (2007) Pharmacology. 6 th ed. Churchill Livingstone. Benowitz, N,L (2008) Neurobiology of nicotine addiction: Implications for smoking cessation treatment. Am J Med. 121:S3-S10 Kalant, H (2001) The pharmacology and toxicology of ecstasy (MDMA) and related drugs? CMAJ. 165: Lupica et al (2004) Marijunana and cannabinoid regulation of brain reward circuits. Br J Pharmaol 143:
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