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Pharmacology 201 > Ethanol > Flashcards

Ethanol Flashcards

1
Q

What is ethanol?

A

Also known as alcohol, it is a class of organic compounds and is a byproduct of fermentation.

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2
Q

How much ethanol is the standard?

A

14 g per unit.

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3
Q

The consumption of alcohol is the ______ in society.

A

most widely consumed drug

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4
Q

What is the correlation with effect to concentration?

A

They are proportional to each other.

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5
Q

What is the legal limit for alcohol?

A

0.05

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6
Q

What is BAC and how do you calculate it?

A

Blood Alcohol Concentration. It is calculated with a formula. Refer to slides.

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7
Q

Why is ethanol hard to classify?

A

It is hard to classify due to its non-specific effects.

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8
Q

What are the effects of ethanol?

A

The effects are dose dependent and occur in different phases. 1) Anxiolytic 2) Sedative/Depressant and 3) Hypnotic.
+ additional miscellaneous effects

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9
Q

What is its Anxiolytic effects? (0.05%)

A

Potential GABA agonist. It provides relief of social reservation or anxiety. There may be mild speech, memory or coordination impairments.

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10
Q

What are the sedative effects? (0.06-0.15%)

A

BAC increases, and it works more as a sedative. Impairs ability to walk or move around.

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11
Q

What are its Hypnotic effects?

A

Sleep inducing agent

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12
Q

What are the miscellaneous effects? (0.31-0.40%)

A

vasodilation of the blood vessels close to the skin, which as a result make you feel warmer. With a high BAC you may have loss of consciousness, threat to alcohol poisoning, and it can impair judgment and decision making.

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13
Q

As BAC increases…….

A

so does impairment.

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14
Q

What parts of the brain are affected by alcohol?

A

This is relevant to BAC levels.
At the lowest it affects the Frontal cortex (highest levels of cognition). Then the limbic system (emotional changes). Then sensory motor cortex (slurred speech, and impaired fine motor skills).
Then, Diencephalon (memory formation).
Then, Cerebellum (balance, and gross motor skills).
Then, Midbrain structures (level of consciousness).
Then, the brain stem (respiration and heart rate).

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15
Q

What are the key points of the monkey study?

A
  • Ethanol can be universally appreciated, even by some animals.
  • it is an acquired taste for the monkeys, most likely due to fermented cane sugars
  • the liking for alcohol may be determined by genes
  • it is parallel for humans and monkeys
  • there are similar rates of non-drinkers in both species (human and monkey)
  • same rate of heavy drinking and dependency
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16
Q

How is ethanol metabolized?

A

The bulk of it is metabolized by non-specific ADH (alcohol dehydrogenase) enzymes. ADH converts alcohol into an aldehyde.
-It should be noted that approx. 10% of alcohol is excreted unchanged through urine and respiration.
20% of alcohol is metabolized by CYP2E1 enzyme.

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17
Q

What are the two random facts from the pervious lessons?

A

Alcohol is an inducer, and that is why an individual can build up tolerance.
-ethanol is an antagonist for dopamine, hence increasing the dopamine in the body.

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18
Q

What does zero oder elimination mean? (linear)

A

ADH enzymes are easily saturated (rate is at its max) at even low concentrations of alcohol, and so is NAD+ the cofactor required for metabolism. This means that only a constant amount of ethanol can be metabolized per unit of time (15g per hour). Essentially, the processing of metabolism is dependent on how fast the enzyme works.

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19
Q

What is first order elimination? (exponential graph)

A

First order elimination is dependent on the half life of that drug. Rate of elimination is proportional to the drug concentration.

20
Q

What is the variability in metabolism with regards to the ADH1 enzyme?

A

ADH1 enzymes are mostly expressed in the liver. ADH1B*2 is an isozyme of that enzyme that is better at breaking down alcohol. As a result of the increased metabolism, it overwhelms the ADH enzymes and too much acetaldehyde is accumulated. Since there are not enough enzymes to break it down, the side effects are mild toxicity (flushing of the skin), tachycardia and nausea.

21
Q

What is the variability in metabolism with regards to the ADH2 enzyme?

A

This enzyme is a change in a single amino acid that inhibits the ALDH (Acetal Aldehyde) metabolism by 95 percent. As a result, you get too much ALDH again and it becomes toxic.

22
Q

Where do these variations happen most often?

A

Asian populations.

23
Q

What positive effects do these mutations offer?

A

Protection against alcoholism, which is a condition based on its unpleasant effects.

24
Q

What are the assumptions made when it comes to Absorption when calculating BAC?

A
  • That it occurs in the stomach and small intestine
  • Did you eat before drinking? Food will be metabolized first, slower gastric emptying, hence the alcohol will have a slower absorption and lower peak BAC.
25
Q

What are the assumptions made when it comes to Distribution when calculating BAC?

A

We assume that it distributes to the total body water.

-But this depends on body type (fat content), gender, age and hydration state.

26
Q

What are the assumptions made when it comes to Metabolism when calculating BAC?

A
  • occurs through dehydrogenase enzymes
  • level of familiarity with substance
  • polymorphisms
  • predominately through the liver (so hepatic function, liver damage can occur with chronic alcohol use)
  • gastric enzyme effect (metabolizes alcohol before absorption) (Males> females)
27
Q

What are the assumptions made when it comes to Excretion when calculating BAC?

A

-we assume that renal function is working efficiently

28
Q

When does a hangover occur?

A

it can arrive prior to complete ethanol elimination.

29
Q

What are the most common hangover symptoms?

A 
FISHNET
F(atigue)
I(mpaired attention)
S(sweating)
H(eadache)
N(ausea) 
E(emotional state negative decline)
T(no word)
30
Q

What are the contributing causes to a hangover?

A

Dehydration
Sleep disruption
Congeners
Genetics

31
Q

How does dehydration contribute to a hangover?

A

Alcohol inhibits the anti-diuretic hormone (ADH/Vasopressin). As a result, there is more urination, and less water in the blood plasma.
Vodka produces this effect more than light beers.

32
Q

What are the side effects of dehydration?

A

Hypoglycaemia, and altered electrolyte concentrations such as potassium, sodium etc.

33
Q

How does sleep disruption contribute to a hangover?

A

First half of the night has reduced “sleep onset latency” and you wake up less while sleeping. You receive a more consolidated sleep because of reduced REM.
Second half of the night:
Sleep is more disruptive.

34
Q

Why are individuals more restless in the second half of the evening?

A

This is because alcohol is a glutamine enzyme inhibitor. Glutamine is an amino acid that is a natural stimulant. When the alcohol is depleted from your body, glutamine levels are down. As a result, your body tries to compensate by increasing the amount of glutamine to produce homeostasis. Your body is now stimulated by working hard to fix the deficiency.

35
Q

How does congeners contribute to a hangover?

A

Other chemicals/substances in a drink like methanol/amines can compete with ethanol for metabolism and produce toxic metabolites.
Studies correlate that darker alcoholic drinks produce worsened hangovers

36
Q

How does genetics contribute to a hangover?

A

Some individuals are hangover resistant.

37
Q

What are the long term effects of ethanol consumption?

A
  • Lethal dose does not change significantly

- Tolerance build up due to metabolizing enzymes and increased tissue tolerance

38
Q

What are the withdrawal effects?

A
  • hangover
  • if you have chronic use, the symptoms can be more severe. For example, tremors nausea, sweating, fever and possible seizures.
  • Delirium tremens: agitation, agression, hallucinations. BZDS are used for treatment
39
Q

Alcohol and Pregnancy

A

Impaired development of cells forming the nerves system and cranial structure

  • induction of cell apoptosis (cell death)
  • altered gene expression
  • altered mitochondrial function
40
Q

What are the symptoms of fetal alcohol spectrum disorder?

A
  • low birth weight
  • facial dysmorphism (wide set eyes, small cheek bones, thin upper lip and reduced cranial circumference)
  • delayed growth/development
  • CNS abnormalities (seizures, impaired coordination, intelligence, hyperactivity, and issues with social integration).
  • Cardiac anomalies
41
Q

Alcoholism

A

Largest detriment to recreational ethanol use

- can decrease life expectancy up to 15 years

42
Q

What are the health effects of Alcoholism?

A
  • nutritional effects: alcoholics take in their calories through drinking rather than with food
  • Liver damage
  • dementia, amnesia
  • increased fatty acid release which builds up and causes hepatitis-> necrosis->cirrhosis
43
Q

What is the first line treatment for Alcoholism?

A

Naltrexone: an antagonist of opioid receptors which blocks the reward cycle when consuming alcohol. This reduces the urge to drink.
Acamprosate: The specific mechanism is not fully understood. Multiple receptors are affected. it may be a NMDA receptor antagonist, and activates GABA.

44
Q

What is Disulfiram?

A

A treatment used to reduce alcohol consumption. It works by inhibiting the ALD2 enzyme and mimicking the ALDH2 enzyme polymorphism effect. As a result, individuals who take this drug get the same side effects as those who have this polymorphism. For example: Flushing, Nausea, Panic and Tachycardia. This will make people not want to drink.

45
Q

Why is this not a first line treatment?

A

Compliance. Most individuals won’t take the drug if they know they will feel such unpleasant effects.

46
Q

What are the clinical uses for ethanol?

A

It works as a disinfectant, and during methanol or ethylene glycol poisoning. When those substances are metabolized they produce damage to organs. Ethanol can outcompete with methanol and ethylene for enzymes and allow the methanol to be excreted without being metabolized.

Pharmacology 201 (20 decks)

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