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PHAR 300 > L8: Ethanol > Flashcards

L8: Ethanol Flashcards

1
Q

What are the general effects of ethanol?

A

It is a general depressant of the CNS.

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2
Q

What are the effects of an increased dose of alcohol?

A
  1. Relief from anxiety at lowest dose
  2. Disinhibition (ex: actions that they will not do under normal circumstances)
  3. Sedation
  4. Hypnosis (sleepiness)
  5. General anaesthesia (passing out)
  6. Coma
  7. Death (at highest dose)
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3
Q

What are the 5 concepts of CNS depressants?

A
  1. Additive effects when combined: Should not combine CNS depressants like antidepressants, sedatives, anticonvulsants, anti-anxiety, opioids.
  2. Can’t reverse effects with CNS stimulants
    Ex: drinking coffee after drinking alcohol won’t reverse the effects of drinking alcohol.
  3. General depressants are not totally general: they affect different pathways differently.
  4. Chronic use leads to rebound excitation upon stopping
  5. All CNS depressants results in some degree of tolerance (frequent cross tolerance of CNS depressants).
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4
Q

What are the consequences (noticeable) of alcohol consumption in increasing order of blood alcohol concentration?

A
  1. Emotional changes
  2. Impaired judgement
  3. Impaired voluntary motor skills
  4. Impaired involuntary system (ex: control of heart and respiration)
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5
Q

What is disinhibition?

A

It is the inhibition of inhibitors. Disinhibition depresses inhibitory pathways, leading to brief excitation, which leads to behavioural excitation.

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6
Q

How can you tell when someone is close to the lethal dose of alcohol?

A

When they are passed out and not waking up. “dead drunk”

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7
Q

What kinds of amnesia can you get from consuming ethanol? Explain.

A
  1. Partial amnesia: fragmentary loss of memory. Person later unaware of memory gaps. It’s universal, and dose related.
  2. Total amnesia (blackouts): Total loss of memory for specific amount of time. Person later aware of no memory. Susceptibility varies.
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8
Q

Until what age does your brain continue developing? How does this relate to binge drinking?

A

25 years old. People who binge drank at younger ages have impaired brain activity compared to non-drinkers. Learning and memory are affected.

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9
Q

Where does ethanol act on the brain and what does it do?

A
  1. Cortex: affects judgement
  2. Hippocampus: affects memory
  3. Cerebellum: Coordination
  4. Other: vision, movement, sensation, reward pathway.
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10
Q

What receptor and ion channels does ethanol act on?

A
  1. Sodium, potassium, calcium ion channels
  2. 5HT and acetylcholine receptors
  3. Inhibitory neurons: GABA and Glycine
  4. Excitatory neurons: Glutamate
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11
Q

What is a GABA A receptor and where are they found?

A

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.

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12
Q

What neurotransmitter do GABAminergic neurons release? Where do they act? What is the effect?

A
  1. Neurotransmitter released: GABA
  2. Acts on the post-synaptic GABA receptor.
  3. Leads to an inhibitory potential.
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13
Q

What GABA A receptors can be activated by ethanol and how does ethanol activate them?

A
  1. The synaptic GABA A receptors and extra-synaptic GABA A receptors.
  2. 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).
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14
Q

What happens when ethanol binds a pre-synaptic neuron and stimulates glycine release?

A

Glycine acts on its post-synaptic receptors. This enhances the post synaptic inhibitory response.

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15
Q

What receptor does ethanol block? What is the affect?

A

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.

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16
Q

What neurotransmitters have an inhibited release due to ethanol? What is the affect?

A

Less acetylcholine: cognitive impairment and amnesia.

Less serotonin: Impulsiveness and aggression.

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17
Q

How does ethanol facilitate the release of dopamine (and opiate neuropeptides)?

A

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).

18
Q

What acts on opiate receptors? What is it related to?

A
  1. Endorphins released by ethanol acts on opiate receptors

2. It is linked to dependence.

19
Q

What is the size and solubility of ethanol?

A

Small & lipid soluble.

20
Q

How fast is the absorption of ethanol?

A

Rapid, detected in the blood and brain within 5 min after consumption. Peak occurs 30-90 min after consumption.

21
Q

What are the sites of ethanol absorption?

A

Stomach and small intestine (majority).

22
Q

When is the absorption of alcohol increased and decreased? Explain.

A

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).

23
Q

What enzyme in the stomach breaks down ethanol?

A

Alcohol dehydrogenase in the gastric mucosa.

24
Q

What is the apparent volume of distribution of ethanol equal to?

A

The total body water

25
Q

What affect does total body water have on concentration of alcohol in males vs females?

A

If comparing same sized people: Males have a larger total body water compared to females. Therefore, females will have stronger concentrations of alcohol in the body than males when drinking the same amount.

26
Q

Does the blood brain barrier prevent alcohol from entering?

A

No bc it is lipid soluble and small.

27
Q

Why does alcohol trigger vomiting?

A

It stimulates the chemoreceptor trigger zone (CTZ) which has no blood brain barrier. The CTZ sends a signal to the vomiting center in the brain (in the BBB) and you throw up.

28
Q

What order of kinetics is associated with alcohol metabolism?

A

At low doses, metabolism is first order. Elimination proportional to half lives.

At high doses, metabolism is zero order. Elimination is constant at half a drink per hour.

29
Q

What is the 2 step metabolism of ethanol and where does it occur?

A

2 step metabolism occurs in the liver (mostly).
Step 1: Ethanol -> acetaldehyde by alcohol dehydrogenase (higher amount in males) found in the gastric mucosa and liver. There are different polymorphisms of ADH, which changes the metabolizing potential and rate of alcohol.

Step 2: Acetaldehyde -> acetate by acetaldehyde dehydrogenase. This is important bc acetaldehyde is toxic (causes headaches, nausea, vomiting, flushing, hypotension, sweating, etc.). People deficient in acetaldehyde dehydrogenase (50% of asians) tend to not binge drink because of negative affects of acetaldehyde.

30
Q

What are the 3 ezymes that can metabolize ethanol?

A
  1. Alcohol dehydrogenase
  2. CYP450
  3. CYP2E1
31
Q

How does direct elimination of ethanol occur?

A

breath, sweat, and urine.

32
Q

When is the CYP2E1 enzyme activated?

A

When there is chronic exposure to alcohol, it induces the enzyme to metabolize ethanol faster.

33
Q

What is ethanol’s affects on the kineys?

A

Blocks water reabsorption from tubules which increases excretion (diuresis).

34
Q

What is the therapeutic index of alcohol and what does it mean about alcohol safety? (give formula)

A

Therapeutic index = lethal level/recreational level = 4.

This is a very low therapeutic index. Alcohol is NOT a safe drug.

35
Q

What are the most vulnerable organs in the body to alcohol?

A

Liver & Brain. But it affects all systems.

36
Q

What are the 10 toxic affects of alcohol on the body?

A
  1. Chronic consumption leads to cirrhosis (fibrosis of liver)
  2. Long term effects on the nervous system: neurodegeneration, dementia, depression, cerebellar ataxia, psychiatric illness.
  3. Muscle weakness
  4. Brain problems: hallucination, confusion
  5. Liver impairment: damages blood flow
  6. Cardiovascular: arrhythmia, hypertension, stroke, cardiomyopathy.
  7. Sexual function
  8. Damage to pancreas
  9. Irreversible brain damage
  10. Cancer (Ex: esophageal)
37
Q

What can increased acetaldehyde damage?

A

Mitochondria, DNA, other cellular components.

38
Q

What is hepatic encephalopathy?

A

Blood flow to the liver is impaired, therefore the body diverges the blood flow to the brain without detoxifying the alcohol. Causes damage.

39
Q

How does the brain develop an acute tolerance to ethanol?

A

it increases excitation to compensate for the depression of the CNS after one bout of drinking.

40
Q

Why can withdrawal from alcohol kill you?

A

Since chronic tolerance causes an increase in excitation, when you quit drinking, there is a rebound excitation as a consequence of withdrawal. The upregulation of glutamate neurotransmitter as well as NMDA rceptors causes hyperexcitability during withrawal. Excess excitation causes upregulation and hyperexcitability which can cause neuronal death. This can kill you because of the intensive rebound in the opposite direction (Can cause seizures).

41
Q

What affect does tolerance to ethanol have on glutamate receptors (NMDA) and glutamate?

A
  1. Upregulation of NMDA receptors on the postsynaptic neuron in order to allow some glutamate to bind and stimulate release of dopamine.
  2. Upregulation of glutamate production in the pre-synaptic terminal to increase the chance of glutamate binding to NMDA receptors in the post-synaptic terminal.
42
Q

How do professionals treat acute withdrawal to ethanol?

A
  1. With other CNS depressants.
  2. Disulfiram: drug that blocks acetaldehyde dehydrogenase so more acetaldehyde (toxic) accumulates and causes them to experience unpleasant symptoms due to its toxicity. This leads to them not wanting to drink alcohol.
  3. NMDA receptor antagonists & Opioid receptor antagonists: subdue the intensity of withdrawal symptoms.
  4. Alcoholics anonymous: beneficial because alcoholism is largely environmental rather than genetic.

PHAR 300 (20 decks)

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