L8: Ethanol Flashcards
(42 cards)
What are the general effects of ethanol?
It is a general depressant of the CNS.
What are the effects of an increased dose of alcohol?
- Relief from anxiety at lowest dose
- Disinhibition (ex: actions that they will not do under normal circumstances)
- Sedation
- Hypnosis (sleepiness)
- General anaesthesia (passing out)
- Coma
- Death (at highest dose)
What are the 5 concepts of CNS depressants?
- Additive effects when combined: Should not combine CNS depressants like antidepressants, sedatives, anticonvulsants, anti-anxiety, opioids.
- Can’t reverse effects with CNS stimulants
Ex: drinking coffee after drinking alcohol won’t reverse the effects of drinking alcohol. - General depressants are not totally general: they affect different pathways differently.
- Chronic use leads to rebound excitation upon stopping
- All CNS depressants results in some degree of tolerance (frequent cross tolerance of CNS depressants).
What are the consequences (noticeable) of alcohol consumption in increasing order of blood alcohol concentration?
- Emotional changes
- Impaired judgement
- Impaired voluntary motor skills
- Impaired involuntary system (ex: control of heart and respiration)
What is disinhibition?
It is the inhibition of inhibitors. Disinhibition depresses inhibitory pathways, leading to brief excitation, which leads to behavioural excitation.
How can you tell when someone is close to the lethal dose of alcohol?
When they are passed out and not waking up. “dead drunk”
What kinds of amnesia can you get from consuming ethanol? Explain.
- Partial amnesia: fragmentary loss of memory. Person later unaware of memory gaps. It’s universal, and dose related.
- Total amnesia (blackouts): Total loss of memory for specific amount of time. Person later aware of no memory. Susceptibility varies.
Until what age does your brain continue developing? How does this relate to binge drinking?
25 years old. People who binge drank at younger ages have impaired brain activity compared to non-drinkers. Learning and memory are affected.
Where does ethanol act on the brain and what does it do?
- Cortex: affects judgement
- Hippocampus: affects memory
- Cerebellum: Coordination
- Other: vision, movement, sensation, reward pathway.
What receptor and ion channels does ethanol act on?
- Sodium, potassium, calcium ion channels
- 5HT and acetylcholine receptors
- Inhibitory neurons: GABA and Glycine
- Excitatory neurons: Glutamate
What is a GABA A receptor and where are they found?
It’s an inhibtory chloride ion channel made up of 5 subunits. It is the main inhibitory receptor in the brain and found abundantly throughout the CNS.
What neurotransmitter do GABAminergic neurons release? Where do they act? What is the effect?
- Neurotransmitter released: GABA
- Acts on the post-synaptic GABA receptor.
- Leads to an inhibitory potential.
What GABA A receptors can be activated by ethanol and how does ethanol activate them?
- The synaptic GABA A receptors and extra-synaptic GABA A receptors.
- Ethanol has 3 binding sites on alpha subunits (GABA A has 2). Pre-synaptic effect: Ethanol binding to presynaptic receptors (not necessarily GABAA receptors) lead to an increase in calcium which increases the release of GABA which facilitates GABAminergic inhibition of the post-synaptic neuron (because when GABA binds the post-synaptic GABAA receptor it lets Cl- in to hyperpolarize the cell). Post-synaptic effect: ethanol acts on both extrasynaptic and synaptic receptors to potentiate GABA A receptors, to further allow chloride influx and hyperpolarization (stops action potentials).
What happens when ethanol binds a pre-synaptic neuron and stimulates glycine release?
Glycine acts on its post-synaptic receptors. This enhances the post synaptic inhibitory response.
What receptor does ethanol block? What is the affect?
NMDA receptors, which are glutamate receptors.
This leads to decreased excitation and also leads to an upregulation of glutamate receptors to counteract the affect of blocked NMDA receptors.
What neurotransmitters have an inhibited release due to ethanol? What is the affect?
Less acetylcholine: cognitive impairment and amnesia.
Less serotonin: Impulsiveness and aggression.
How does ethanol facilitate the release of dopamine (and opiate neuropeptides)?
It facilitates the release of dopamine and opiate neuropeptides because There is an inhibitory GABAminergic neuron that synapses onto a dopaminergic neuron in the VTA. The GABAminergic neuron has GABA A receptors on its pre-synaptic terminal. When bound by ethanol, GABA release is inhibited, which allows for more dopamine to be released (inhibition of inhibitor).
What acts on opiate receptors? What is it related to?
- Endorphins released by ethanol acts on opiate receptors
2. It is linked to dependence.
What is the size and solubility of ethanol?
Small & lipid soluble.
How fast is the absorption of ethanol?
Rapid, detected in the blood and brain within 5 min after consumption. Peak occurs 30-90 min after consumption.
What are the sites of ethanol absorption?
Stomach and small intestine (majority).
When is the absorption of alcohol increased and decreased? Explain.
Increased: on an empty stomach (20% absorbed in stomach). Presence of carbonation since it increases gastric emptying.
Decreased: On a full stomach. On a full stomach, ethanol is less in contact with the stomach wall. Also, high fat in the food causes a slower gastric emptying (takes longer to get to intestine and for majority of ethanol to be absorbed).
What enzyme in the stomach breaks down ethanol?
Alcohol dehydrogenase in the gastric mucosa.
What is the apparent volume of distribution of ethanol equal to?
The total body water
