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drugs and behaviors > cns depressants: alcohol > Flashcards

cns depressants: alcohol Flashcards

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1
Q

what is alcohol?

A

a class of chemicals ; not all are safe for consumption

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2
Q

what form of alcohol is used in beverages?

A

ethanol (ethyl alcohol)

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3
Q

what form of alchohol are toxic?

A
  1. isopropyl - liver forms it into acetone (rubbing alcohol)

symptoms: blindness, coma, death

  1. methyl alcohol - liver forms it into formic acid and formaldehyde ; found in antifreeze (wood alcohol)

symptoms: flushing, hypothermia, low BP

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4
Q

what factors help determine alcohol content?

A
  1. percentage alcohol: alcohol per 100mL of sol (ABV)
  2. proof of alcohol: double the alcohol by volume
    ex. beverage that is 50% alcohol by volume = 100 proof
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5
Q

if there is different concentrations of ethanol in our drinks, what is the standard drinks in order to consume 0.6 floz or 14 g of pure ethano;?

A
  • 5oz wine glass
  • 12oz can of beer
  • 1.5oz spirit
  • 12oz wine cooler
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6
Q

what is true about the blood alcohol concentration in all the standard drinks?

A

they raise by the same amount

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7
Q

what is BAC formula?

A

mg alcohol/per 100mL

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8
Q

what are the different types of drinking?

A
  • light: 1 per day
  • moderate: most days but low quantity
  • heavy: most days, high quantity
  • binge: a lot over a short time period
  • extreme: 2 times of binge drinking
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9
Q

what is the route of admin of alcohol?

A
  • oral (most common)
  • rectal
  • inhalation
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10
Q

which method of admin has poor bioavailability?

A
  • in men, enzymes in stomach wall (ADH) breaks down alcohol (men have lower bio than females)
  • first pass metabolism reduces bioavailability
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11
Q

where is ethanol easily absorbed?

A

the GI tract and diffuses throughout the body, readily entering most tissues, including the brain

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12
Q

what are behavioral effects of alcohol based on?

A

your BAC rather than the amount ingested

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13
Q

how is alcohol distributed? what happens when great concentration of alcohol is consumed?

A

by passive diffusion across membranes from higher concentration (in the GI) to lower concentration (the blood).

the greater the concentration, the more rapid the movement

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14
Q

what slows down alcohol absorption?

A

food

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15
Q

what are sex and age differences in absorption and distribution?

A
  1. Lower total body water content in women - less dilution
  2. Reduced first pass metabolism in women
    Alcohol dehydrogenase in gastric fluid is about 60% more active in men than in women.
  3. Older women would have same BAC as younger male
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16
Q

why is prenatal ethanol dangerous?

A

it readily passes through BB and placental barrier because the fetus reached the same BAC as the mother

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17
Q

what is fetal alcohol syndrome? what are features of it?

A
  • due to alcohol exposure as a developing fetus
  • Intellectual disability and other developmental delays
  • Low birthweight; failure to thrive and grow
  • Neurological problems—some infants born with high alcohol levels experience withdrawal after birth
  • Physical abnormalities:
    Craniofacial malformations, cardiac defects, failure of kidney development, undescended testes, and skeletal abnormalities in fingers and toes
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18
Q

how is ethanol is metabolized if taken in moderate doses?

A
  • in liver
  1. enzyme Alcohol dehydrogenase (ADH) converts ethanol into acetaldehyde (toxic!)

2.Enzyme aldehyde dehydrogenase (ALDH) converts acetaldehyde into acetic acid

  1. ADH pathway used
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19
Q

how is ethanol is metabolized if taken in excessive doses?

A
  1. CYP450 enzymes (CYP2E1) converts ethanol into acetaldehyde
  2. 1st order kinetics!
  3. MEOS pathway used
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20
Q

what is the form of excretion of alcohol?

A

urine and sweat, and the remaining 5% is excreted by the lungs

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21
Q

what is the breathalyzer used to measure?

A

what is excreted by the lungs

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22
Q

what is a genetic polymorphism in the ADH gene found in Asians?

A

speeds up the activity of ADH and codes for an inactive form of ALDH

so rapid breakdown of ethanol + poor ALDH function leads to toxic build up of acetaldehyde.

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23
Q

why does drug competition occur?

A

Cytochrome P450 enzymes metabolize many other drugs too.

If alcohol is consumed with other drugs, they must compete for the same enzyme molecules
drug molecules can accumulate to dangerous levels.

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24
Q

symptoms of alcohol and other drugs

A
  1. tylenol - toxic hepatitis (liver damage)
  2. benzodiazepines, barbiturates, opiates, marijuana - greater effects
  3. antibiotics, anticoagulants, mao inhibitors - decreases the effects of these
  4. oral contraceptives - increased the effect of alcohol
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25
what happens when people use alcohol chronically?
metabolic tolerance: increases CYP450 enzymes that metabolize alcohol and increases rate of alcohol metabolism
26
what is the caveat of alchohol use?
Prolonged use of alcohol causes liver damage that impairs metabolism for alcohol and many other drugs
27
by what kinetics is alcohol broken down?
- zero order - 0.015% every hour - rate limited activity of ADH but high doses activated MEOS metabolism too which then works via 1st order
28
why is alcohol a dirty drug?
- it makes membranes fluid - it disrupts the blood brain barrier proteins and lipids
29
what does alcohol have on neurotransmission of glutamate?
NMDA receptor antagonist (glutamate receptors) & may reduce presynaptic glutamate release Receptor location dictates behavioral effects Hippocampus - affects memory, which is why you don't remember
30
what does alcohol have on neurotransmission of GABA?
pos allosteric modulator for GABAa receptor
31
what do the location of GABA receptors tell about the effects?
- amygdala: Reduction in anxiety, increased motor impairment and increased sedation - Cerebral cortex, hippocampus, and thalamus: depressant effects on cognition -Nucleus accumbens and ventral tegmental area: increased dopamine associated with reward
32
what does alcohol have on neurotransmission of opiods/endorphins?
- contribute to reinforcing effects of alcohol - increases endogenous plasma endorphin levels (acute ingestion) - administration reduces natural endorphin levels (chronic ingestion) - contributes to dysphoria during withdrawal
33
what does alcohol have on neurotransmission of dopamine?
1. Alcohol indirectly (via endorphins) increases dopamine in the nucleus accumbens - contributes to reinforcement associated with alcohol use 2. withdrawal after chronic use reduces the firing rate of mesolimbic neurons & decreases DA release in the nucleus accumbens.
34
know table 10.3 on slide 22
35
what are physiological symptoms of acute alcohol use?
Vasopressin inhibition: ↑ urine output when blood alcohol concentration (BAC) is rising. Peripheral dilator: skin feels warm/ turns red despite actual ↓ in core body temperature Reduced satiety hormones like leptin Disrupts REM sleep Impairs memory Hang-over
36
what is the BAC relationship on behavioral effects?
the higher the BAC gets, the more your functioning gets lower and the euphoric part disappears
37
when do hangover symptoms begin?
when blood alcohol drops significantly and is at or near zero
38
what happens when alcohol is consumed rapidly?
lethal blood levels may be reached before the individual passes out
39
what are the tolerances we see with alcohol?
Acute tolerance: within single exposure to alcohol Metabolic tolerance: increase in P450 liver microsomal enzymes that metabolize the alcohol - enzyme induction Pharmacodynamic tolerance: neurons increase NMDA receptors and decrease GABAa receptors - MOST DANGEROUS TOLERANCE Behavioral tolerance: Compensate for behavioral effects of alcohol Cross tolerance: with other drugs in the sedative–hypnotic class, including barbiturates and benzodiazepines know picture on slide 30
40
what can happen with heavy alcohol use?
- cardiovascular problems - liver disease : stage 1 - liver fibrosis (scarring on liver): stage 2 - liver cirrhosis: stage 3
41
what are symptoms of liver cirrhosis?
Swelling in the legs and abdomen Infections Malnutrition hepatic encephalopathy (looks like dementia) Confusion, difficulty concentrating, overtime, coma Jaundice Bone disease Increased risk of liver cancer
42
what is a deficiency seen in people with chronic alcoholism?
thiamine (vitamin B1)
43
what does the lack of thiamine cause?
1. Wernicke encephalopathy Confusion, ophthalmoplegia, ataxia *Thiamine replacement may resolve symptoms 2. Korsakoff’s syndrome Amnesia, confabulation (making up info because u forgot), distorted memory Damage to hippocampus, mammillary bodies, frontal cortex *Often irreversible 3. Wernicke-Korsakoff’s syndrome Overlapping disorder 75% of patients have permanent brain damage ~20% die
44
what does intensity of withdrawal depend on?
duration and degree of physical dependence
45
what are the general symptoms of withdrawal?
agitation, anxiety, increased heart rate, BP, nausea, vomiting, paranoia, seizures
46
what is alcohol withdrawal we see after 8-10 hrs, 1-3 days, and 1 week?
8-10 hrs: anxiety, insomnia, nausea, abdominal pain 1-3 days: high blood pressure, increased body temp 1 week: seizures & DTs
47
what are DTs?
delirium tremens usually starts 2-5 days after the last drink, and can be fatal. Shaking, confusion, high blood pressure, fever, seizures, agitation, and hallucinations 
48
what is kindling in alcohol withdrawal?
the increased tendency for seizure during alcohol withdrawal that is due to the increase in glutamate receptors causing excessive calcium influx that kills cells and decrease in GABA receptors. Frequent withdrawal episodes may be responsible for irreversible brain damage in AUD due to constant seizures
49
what drugs are taken to prevent alchohol withdrawal symptoms during detox?
Benzodiazepine drugs such as chlordiazepoxide (Librium) or diazepam (Valium) -- increase GABA function
50
what is alchohol use disorder?
complex phenomenon with psychological, neurobiological, genetic, and sociocultural factors, making it difficult to define and treat
51
what gender do we see AUD?
more in men than women
52
what is true about young individuals who begin drinking before the age of 13?
the greater the probability they will develop AUD
53
what is the difference between alchol abuse vs dependence?
abuse: drinking too much, too often dependence: inability to quit key difference: compulsion to drink!
54
what are the ways to characterize AUD?
Mild (2-3 symptoms) Moderate (4-5 symptoms) Severe (6+ symptoms)
55
what are the causes of AUD?
No specific cause of AUD has been identified; a variety of factors contribute to the vulnerability of an individual. but people who are diagnosed with anxiety disorder are most likely to have an AUD
56
what is a significant environmental risk for alcohol abuse in adult?
stress early in life
57
what does alcohol relieve at low levels? why is this contradicitve?
stress and tension alcohol itself = additional stressor that may lead to further alcohol use because it increases brain and endocrine stress system activity
58
what are the 2 strategies for pharmacotherapeutic treatment?
- make drinking unpleasant - reduce alchohol's reinforcing qualities
59
how do we make drinking unpleasant?
give disulfiram - inhibits ALDH which normally breaks down acetaldehyde to acetic acid - this causes toxic build up which feels gross
60
how do we reduce alchohol's reinforcing qualities?
give naltrexone - opioid receptor antagonist - it reduces alcohol consumption and craving and improves abstinence rates. - Reduces the positive feelings and subjective “high” by blocking the effects of alcohol-induced endorphin release.

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