50% usage, 3% associated with drug problem
80% usage, 8% drug problem, 20% community problem.
88% associated with drug problems.
1.1 Costs of Drug Abuse
Difficult to quantify due to presence of health costs, crime and violence, social disruption.
Taxes also raise money for the government.
Drug induced deaths such as heroin overdose and opiods.
Cancer and tobacco.
i.e 50% Indigeneous Australians are smokers and 20% had high long term risks from alcohol.
2 Reward Pleasure and Addiction
More than just tolerance and dependance, compulsive drug-taking and use, even in the face of negative health and social consequence.
A lifelong brain disease
It is a vicious/viscous? cycle.
Acute to chronic
Reward to tolerance and dependence
Activation of mesolimbic DA pathway to adaptive changes in receptors
Acute abstinence to chronic abstinence
Withdrawal syndrome to craving.
2.2 Central reward/Pleasure centres
Certain parts of the brain elicit pleasure when stimulated.
Commonly, the Mesolimbic Dopaminergic pathway (reward parthway)
All drugs activate this pathway maybe other pathways are involved but this is the main pathway.
Sites of interaction differs but all will result in release of dopamine.
2.3 Actions of Drugs
Alcohol and sedative/hypnotics
Acts on aminergic neurotransmission.
Increased euphoria and energy and alertness, sympathomimetic, stereotypical behaviour with appetite suppression.
Caffeine: Inhibits phosphodiesterase to increase adrenaline and noradrenaline
(adenosine receptor antagonist)
Cocaine: Blocks Dopamine reuptake and increase noradrenaline and seratonin, block voltage dependent Na+ channels
Amphetamine: Increase DA release, blocks DA reuptake, increase noradrenaline and 5-HT.
Ecstasy: Blocks seratonin uptake, incrase DA and Nor.
Confusion and depression
Impairment of memory and attention
Nausea, chills, sweating
Overdose: LOC and seizures
Opioid Agonist (morphine, codeine, heroin)
Natural/Endogenous (endorphins, enkephalins, dynorphins)
Opioid antagonist (naloxone,naltrexone)
Treatment of choice for moderate-severe pain
Diacetyl morphine, metabolized to morphine.
Further metabolized in liver and excreted in urine
Cause: Intense rush followed by dreamy state, side effect includes nausea and constipation, overdose and addiction.
Withdrawal symptoms begins 10 hours and last maybe indefinitely.
Treatment includes, antagonist, partial agonists, agonist
Can be quantified using Blood alcohol concentration and clinical effects.
Impaired motor functiom, slurred speech, ataxia (lack of order/concentration)
Respiratory depression and death
It inhinits neurotransmission at GABA and glycinergic synapses
Decreased activity of voltage dependent Calcium channels to reduce neuronal excitability
Inhibits glutamate mediated excitatory neurotransmission.
Rapidly absorbed and distributed into brain and activate central nicotinic acetylcholine receptors.
Treatment includes abstinence and replacement therapy, verenicline or bupropione drug is also recommended
From cannabis sativa, active ingredient THC (tetrahydrocannabinol)
Specific receptor, endogenous ligands and transport systems
Rapidly absorbed, slow removal
Possible medical use as anti-emetic and appetite stimulator, antihypertensive, analgesic and movement disorders.
7TM and G-protein coupled recpetors, CB1 and CB2
CB1: mostly in the brain, mediates euphoric and most therapeutic effects, decreases neuronal activity by lowering cAMP decreasing calcium channels and increasing potassium channels
CB2: 50% homology (immune cells, long temrm case memory effects, hence increased risk of lung cancer.
Interact with Serotonin neurotransmitter (5-HT2 receptor activation)