Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
19 Cards in this Set
- Front
- Back
|
What effect does alcohol have on adolescent brain development? |
Impairment: remodelling and functional changes in synapse plasticity and neuronal connectivity in different brain regions Compared to adults, adolescents exposed to alcohol are more likely to exhibit cognitive deficits e.g. learning and memory dysfunction |
|
|
Alcohol and cognitive impairment |
Includes spatial skills, planning, learning and memory. Syndrome of cognitive impairment with no fluctuations. |
|
|
Alcohol related brain damage |
Includes: neuropathies e.g. gait ataxia due to peripheral neuropathy Cerebellar degeneration, leading to ataxia and coordination failure Alcohol dementia Wernicke-Korsakoff syndrome/amnestic syndrome |
|
|
Role of neuroinflammation |
Ethanol can trigger activation of astroglial cells, producing a proinflammatory response Upregulation of inflammatory mediators leads to apoptosis |
|
|
Role of dopamine and glutamate |
Changes in dopaminergic and glutamatergic pathways have long term effects on memory and learning Decrease in DR2 and phosphorylation of NMDAR leads to mesocorticolimbic sensitisation |
|
|
Role of hippocampus |
Inhibition of hippocampal neurogenesis Cell cycle is arrested, preventing cell proliferation This prevents neurogenesis of hippocampus |
|
|
What is Wernicke-Korsakoff's syndrome? |
WKS is combined presence of Wernicke's encephalopathy and Korsakoff's syndrome due to thiamine (B1) deficiency |
|
|
What does thiamine do? |
Thiamine helps to break down glucose, acting as an essential enzyme to the TCA cycle and pentose phosphate shunt The body only stores 2-3 weeks of thiamine reserves Thiamine is involved in metabolism of carbs, production of neurotransmitters, lipid metabolism, amino acid modification, neuromodulation |
|
|
What is the primary injury in Wernicke's encephalopathy? |
Threefold: 1. Oxidative damage 2. Mitochondrial injury leading to apoptosis 3. Direct stimulation of pro-apoptotic pathways |
|
|
What is the triad of symptoms seen in Wernicke's? |
Ophthalmoplegia - eye movement abnormalities Ataxia - imbalance, or other cerebellar signs Confusion or other mental changes |
|
|
What characterises Korsakoff's syndrome? |
Memory impairment, confabulation, confusion and personality changes Normal activity and functions impaired, and symptoms present even when not delirious, intoxicated or withdrawing |
|
|
What are common pathological features of Korsakoff's syndrome? |
Atrophy of the thalamus and mamillary bodies, with frontal lobe involvement |
|
|
How should Wernicke's encepathalopathy be treated? |
Medical emergency: prompt administration of thiamine Daily thiamine requirement 1-2mg |
|
|
What characterises alcohol dementia? |
Impaired cognitive function i.e. planning, thinking, judgement Commonly presents with WKS, characterised by short term memory loss and thiamine deficiency |
|
|
Diagnositic criteria of alcohol dementia? |
Must involve a decline from a previous level and memory loss Includes: Agnosia - inability to recognise an object Aphasia - language disturbance Apraxia - inability to carry out motor tasks Loss of executive function: poor planning and organising of simple actions into a more complex sequence of events e.g. dressing |
|
|
Outline Lishman's hypothesis on aetiology of alcohol related brain damage |
Non alcohol forms of WKS due to thiamine depletion alone usually show full recovery with time Alcohol neurotoxicity on its own leads to a slowly reversible form of global cognitive impairment, with cortical and subcortical damage |
|
|
Describe the action of alcohol at the cellular level |
Depressant, although it increases level of neuronal activity - presumably by disinhibition - in some parts of the CNS, notably in the mesocorticolimbic pathway involved in reward |
|
|
Action of ethanol on GABA and glutamate |
Enhances both GABA and glycine mediated inhibition Alcohol binds to GABAa receptors to give short term effects of alcohol: relaxation, sedation, ataxia, increase in appetite, lowering of inhibitions Ethanol also decreases glutamate's ability to bind with NMDA and acts as an NMDA receptor Inhibits some of glutamates excitatory effects, giving some of the depressive effects of alcohol, as well as the memory blanks |
|
|
Chronic effect of alcohol on glutamate |
Upregulation of NMDA receptors as the brain tries to reestablish homeostasis - When a chronic drinker stops for more than 10 hours, apoptosis can occur due to excitotoxicity |
