Drugs of Addiction

Daniel Elandix G
Mind Map by Daniel Elandix G, updated more than 1 year ago
Daniel Elandix G
Created by Daniel Elandix G over 6 years ago
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Introductory Pharmacology Mind Map on Drugs of Addiction, created by Daniel Elandix G on 09/24/2013.
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Drugs of Addiction
1 Patterns of Drug Use

Annotations:

  • Tobacco: 50% usage, 3% associated with drug problem Alcohol: 80% usage, 8% drug problem, 20% community problem. Illegal/illicit Drugs: 38% used 88% associated with drug problems.
1.1 Costs of Drug Abuse

Annotations:

  • 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.
1.2 Patterns

Annotations:

  • i.e 50% Indigeneous Australians are smokers and 20% had high long term risks from alcohol.
2 Reward Pleasure and Addiction
2.1 Addiction

Annotations:

  • 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. Drug taking Acute to chronic Reward to tolerance and dependence Activation of mesolimbic DA pathway to adaptive changes in receptors Drug withdrawal: Acute abstinence to chronic abstinence Withdrawal syndrome to craving.
2.2 Central reward/Pleasure centres

Annotations:

  • 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

Annotations:

  • Different class: Opioid analgesics Alcohol and sedative/hypnotics Stimulants Cannabis Hallucinogens Nicotine
2.3.1 Stimulants

Annotations:

  • 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.
2.3.1.1 Esctasy

Annotations:

  • Confusion and depression Impairment of memory and attention Nausea, chills, sweating Jaw Clenching hyperthermia Overdose: LOC and seizures MDMA
2.3.2 Opioids

Annotations:

  • Types: Opioid Agonist (morphine, codeine, heroin) Natural/Endogenous (endorphins, enkephalins, dynorphins) Opioid antagonist (naloxone,naltrexone) Treatment of choice for moderate-severe pain
2.3.2.1 Heroin

Annotations:

  • 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
2.3.3 Ethanol

Annotations:

  • Can be quantified using Blood alcohol concentration and clinical effects. Sedation, High Impaired motor functiom, slurred speech, ataxia (lack of order/concentration) Emesis, stupor Coma 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.
2.3.4 Nicotine

Annotations:

  • 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
2.3.5 Marijuana

Annotations:

  • 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.
2.3.6 Hallucinogen

Annotations:

  • Interact with Serotonin neurotransmitter (5-HT2 receptor activation)
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