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Mortality from acute dosage
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Long-term impact of alcohol
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Alcohol
Uni of Notts, Addiction & The Brain, first year
| Term | Definition |
|---|---|
| Mortality from acute dosage | Very difficult to die as a direct result of alcohol on the body as individuals will likely pass out or throw up first, although these may also lead to complications |
| Long-term impact of alcohol | Cancer, liver problems, social neglect, healthcare costs, dangerous behaviour, accidents, suffocation from vomit, losing consciousness in dangerous situations. Increased fluidity of neuronal membranes |
| Is alcohol the most dangerous drug? (i.e., more than crack-cocaine or heroin) | If measured by morbidity per amount taken then no but if weighted by both total morbidity & harms to society then yes |
| Quote about psychological effects of alcohol compared to other drugs | "If recreational drugs are tools, alcohol would be a sledgehammer. Few cognitive functions are unaffected" |
| Dirty pharmaceuticals | Compounds which have pharmaceutical effects on many general regions of the brain & body whereas other synthesised compounds would have very specific drug targets |
| Immediate effects of alcohol on the brain | Enhancing the function of receptors with inhibitory effects (NMDA, GABA-A, glycine, 5-HT3 etc.) to reduce neuronal action potentials & cause general inhibition |
| Legal Blood Alcohol Content (BAC) limit | BAC increase correlates with a deterioration in behaviour. At .08-.1% BAC, alcohol enters the spine & inhibits motor & sensory neurones which causes motor impairment & makes driving dangerous so it's illegal to drive at this BAC |
| Effects on anxiety | Due to GABAergic properties, alcohol inhibits anxiety causing sufferers to self-medicate with alcohol making alcohol abuse a statistically significant comorbidity with anxiety disorders |
| Effects of alcohol on rats in different anxious conditions (2) | Cat odour - more likely to venture into these areas & stick their heads up elevated plus maze - significantly more likely to enter the open arm of the maze More anxious rats steeply increased their consumption of alcohol compared to non-anxious rats |
| Alcohol induced memory loss (amnesia) | Disrupts hippocampal LTPs encoding declarative memory by allosterically agonising inhibitory receptors & reducing action potentials which interferes with anterograde recollections leading to lapses & blackouts |
| Goodwin et al. state dependent memory study | Compared 4 experimental conditions of alcohol/sober at learning or recall. Participants formed 10 association words to stimulus words & at recall were asked to remember those words based off original words |
| Biological experimentation of alcohol effect on memory | Stimulated the perforant pathway to tetanus with an electrode in the dendate gyrus. In baseline tetanus remained high after stimulation demonstrating hippocampal plasticity but in alcoholic conditions it decreased |
| Alcohol's effect on reward systems | Acting allosterically on GABA-A inhibitory interneurons of the VTA, it disinhibits dopamine release in the nucleus accumbens which stimulates D2 receptors in the mesolimbic pathway |
| Intracerebral microdialysis | Probe inserted into region of interest, flooded with perfusate (artificial CSF) through a semi-permeable membrane. Liquid is then taken & analysed to measure extracellular concentrations of neurotransmitter |
| Substance abuse (4 criteria) | Impairs environmental mastery Causes legal issues from consumption & effect Could be used dangerously Continued use despite, legal, social, or medical problems |
| Substance dependence (4 criteria) | Tolerance to positive effects Physical or psychological withdrawal Regular desire & effort to reduce consumption (inability to quit) Daily routine dictated by procurement, consumption, & side effects of the drug |
| Mechanisms of withdrawal, tolerance, & comedown | Neuropharmacological adaptations to chronic use raise baseline excitability meaning a depressant is needed to regulate neural function. These changes directly mirror acute effects of alcohol |
| How the brain adapts to chronic alcohol use | GABA-A receptors (& other inhibitory receptors) are downregulated while glutamate (& other) receptors are upregulated |
| Chronic alcohol morbidity mechanisms | Withdrawal can lead to extreme excitement & potentially excitotoxicity of vital neurones, tremors, & seizures. Alcohol can inhibit brainstem neurones to the point of cardiac & respiratory depression but this is very rare |
| Dopamine transmission of alcoholic rats | Alcoholic rats decrease dopamine transmission more quickly after an initial rise due to alcohol compared to non-alcoholic control groups |
| Wernick-Korsakoff syndrome | Combination of Wernick encephalopathy & Korsakoff amnesia. Caused by severe thiamine deficiency due to alcoholic obtaining all calories from alcohol & not consuming a source of thiamine |
| Wernicke encephalopathy: 1 Korsakoff amnesia: 2 | 1. paralysis of eye muscles, confusion, ataxia. Can be treated with thiamine supplements 2. Permanent brain shrinkage & degradation of mamillary bodies causing global impairment forming new memories |
| Neurological deficits in "uncomplicated alcoholics" | Small, but statistically significant reduction in grey & white matter volume in users taking only 1-2 units of alcohol daily |
Created by:
Beech47
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