Exam 3 Flashcards

1
Q

What are the severe symptoms of alcohol withdrawal?

A

Hallucinations, seizures, and delirium tremens.

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2
Q

What drug is used or medically controlled alcohol withdrawal?

A

Benzodiazepines

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3
Q

What are the pharmacokinetics of alcohol?

A

Absorbed in GIT through passive diffusion. Small molecule that easily crosses BBB.
Absorption will be slower when taken with food due to competing absorption.
Distributed more in blood than in fatty tissue. Liver can metabolize 1 ounce of alcohol per hour.

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4
Q

How is alcohol metabolized in the liver?

A
  1. Alcohol converted to acetaldehyde by alcohol dehydrogenase. (Acetaldehyde is the toxic part that makes us feel hungover)
  2. Acetaldehyde is converted to acetic acid via acetaldehyde dehydrogenase.
  3. Acetic acid converted to carbon dioxide, water, and energy via an oxidation reaction
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5
Q

What is the drug Disulfiram?

A

This was the first drug created to treat alcohol dependence. This drug inhibits the acetaldehyde dehydrogenase enzyme so that acetaldehyde stays in the blood longer and makes you feel super sick.

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6
Q

What is acute alcohol tolerance?

A

This is when you drink and feel intoxicated but then 3 hours later you feel less intoxicated but your BAC is actually higher than it was 3 hours ago. Behaviorally you think you are less intoxicated because you are intoxicated and not rational.

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7
Q

What is alcohol metabolic tolerance?

A

This type of tolerance is seen in chronic alcohol users. This is when there is an up regulation of alcohol dehydrogenase enzymes in the liver due to their chronic overstimulation. This is the body trying to get back to homeostasis.

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8
Q

What is tolerance based on a change in the number of receptors?

A

Pharmacodynamic tolerance

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9
Q

How does alcohol work on AMPA and NMDA glutamate (excitatory) receptors?

A

Alcohol acts like magnesium in the NMDA receptor and blocks the flow of positive ions into the cell making it hyperpolarize (no action potential formed).

In pharmacodynamic tolerance, after years of heavy drinking, the body will up regulate the amount of these NMDA receptors so they can try to top being inhibited by alcohol. This is why when chronic alcohol consumers stop drinking, they experience a lot of over excitation from glutamate finally being allowed to bind to those receptors. It results in shaking, seizures, tremors, and more.

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10
Q

What are the CNS effects of alcohol at low doses?

A

At low doses, alcohol is stimulating, relaxing, can reduce anxiety, cause fine motor impairments, and act like an analgesic.

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11
Q

What are the CNS effects of alcohol at high doses?

A

Black out can occur, suppression of reflexive respiratory centers in brain stem, liver toxicity. Slurred speech, exaggerated emotions, and more.

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12
Q

How is alcohol rewarding and also a depressant?

A

Alcohol acting on dopamine and opioid receptors is the rewarding pathway.

Alcohol acting on glutamate and GABA receptors is the depressant pathway.

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13
Q

How does alcohol effect glutamate receptors?

A

Alcohol has the greatest effects on NMDA glutamate receptors. Alcohol acts like magnesium in these receptors and blocks the flow of positive ions into the cell therefore hyperpolarizing it. When these receptors are blocked by alcohol, long-term potentiation of memories is not possible.

Acute admin of alcohol just causes decreased activity of NMDA receptors. Chronic admin of alcohol causes up-regulation of NMDA receptors.

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14
Q
A
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