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PSYC383 - Psychopharmacology > Alcohol - CH10 > Flashcards

Alcohol - CH10 Flashcards

1
Q

what type of drug is alcohol

A

depressant

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2
Q

what is the typical route of admin for alcohol

A

oral (first pass)

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3
Q

what is the duration of the effect of alcohol

A

moderate

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4
Q

what NT are affected by alc

A

GABA, glutamate, dopamine and opioids

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5
Q

what is the tolerance of alcohol

A

moderate

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6
Q

what is the physical dependence of alcohol vs psychological dependance

A

intense vs moderate

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7
Q

withdrawal symptoms of alc

A

cramps, delirium, vomiting, sweating, hallucinations, seizures and delirium tremens

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8
Q

what is the schedule of alc

A

legal

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9
Q

how was alc used in ancient times?

A

used as medicine: stress relief, relaxation, antiseptic properties and anesthetic

  • comboed with natural botanicals
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10
Q

how was alc used in the middle ages

A

used as medicine: wine could “Preserve the stomach, strengthen the natural heat, help
digestion, defend the body from corruption”
- in moderation, otherwise it will cause great harm and ill affect the brain

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11
Q

what was the first distilled drink

A

in middle ages (12th century) of Italy: wine to brandy

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12
Q

what % alc do we reach with fermentation

A

up to 15%: beer, wine, cider

*naturally fermented beverages cannot exceed this amount since yeast cannot survive then

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13
Q

in which century did concern about alcohol begin

A

18th century
- 1725: Royal College of Physicians express concerns about “growing use of spirituous liquors”

  • Benjamin Rush (USA) introduced the concept of addiction as disease, describing the uncontrollable desire for alcohol
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14
Q

when did temperance movements start and what was their goal

A

1830s
- calling for complete abstinence
- call alc the source of evil and stereotyped it as a thing for the lower class

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15
Q

when did prohibition of alc begin/end

A

1900, lasted until 1920
- provincial bans in early 20th century
- PEI first @ 1901
- Quebec last @ 1919
- most provinces repealed the ban in 1920s

** national prohibition enforced from 1918 to 1920 as a temporary wartime measure

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16
Q

what is the avg age of initiation into alc in canada: CADUMS 2012

A

18.3

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17
Q

what % canadians have used alc in their life?: CADUMS 2012

A

91

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18
Q

what % canadians have used alc in the past year?: CADUMS 2012

A

78

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19
Q

how is brain atrophy indicated in brain structure?

A

increased sulci, and ventricle size

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20
Q

define fermentation

A

a process that occurs naturally whenever microscopic yeast cells in the air fall on a product containing sugar, such as honey, fruit, sugar cane, or grains like rye, corn

(Yeast converts each sugar molecule into two molecules of alcohol and two molecules of carbon dioxide)

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21
Q

what determines the type of alcoholic beverage

A

the material that provides the sugar

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22
Q

3 ways to increase alc concentration

A
  • heating the fermented mixture
  • add additional alcohol
  • fractional freezing
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23
Q

how does heating a fermented mixture increase alcohol

A

alcohol boils off in steam leaving some of the water behind
- The alcohol vapor passes through a series of cooling tubes (called a still) and condenses to be collected as “hard liquor,” or distilled spirits

**alc concentration then varies from 40%-50%

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24
Q

fractional freezing

A

the fermented mixture is cooled until partially frozen, and the ice crystals are removed, resulting in the removal of water while the unfrozen alcohol remains in the mixture

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25
Q

what determines absorption of alc

A
  • presence of food
  • ulcer medication
  • sex differences
  • hydration levels
  • aspirin
  • carbonation
  • stress/anxiety/fear
  • illness
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26
Q

2 ways alc is metabolized

A
  1. alcohol dehydrogenase
  2. enzymes from cytochrome 450 family
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27
Q

4 types of tolerance

A

pharmacodynamic, acute, metabolic, behavioral

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28
Q

symptoms of withdrawal from chronic alc use

A
  • can last up to weeks:
    sleep disturbance
    intense anxiety
    fast HR
    tremors

high BP
excessive sweating
rapid breathing
nausea/vomiting

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29
Q

more severe symptoms of alc withdrawal

A

convulsions, delirium, hallucinations, total disorientation

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30
Q

effect of alc on CNS: judgement (low dose, social vs quiet)

A

in low doses: relaxed and less anxious

Social setting = more friendly, confident, talkative (judgement is imapired)
**Risk taking behavior = unprotected sex, more sex

Quiet setting = sleepy

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31
Q

effect of alc on CNS: memory (low dose vs high dose)

A

Low dose = memory defects are based on expectation rather than the amount of alc consumed
- Under high stress = enhance performance by minimizing the damaging effects of anxiety

High dose = results in total amnesia for events that occur during intoxication, despite the fact that the individual is behaving quite normally (blackout)

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32
Q

effect of alc on CNS: motor skills

A

Reduced coordination lead to slurred speech and impaired fine motor skills and delayed RT

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33
Q

effect of alc on CNS depression

A

Increasing doses: mild sedation and sleepiness

Suppresses REM episodes
- Withdrawal produces a rebound in REM sleep that interferes with normal sleep patterns and causes headaches

High doses: unconsciousness and death

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34
Q

signs of alcohol poisoning

A

Unconciousness, vomiting, slow and irregular breathing, cold/clammy/pale skin

Eventual death from acute alc ingestion is caused by depression of the respiratory control center in the brainstem

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35
Q

what leads to brain damage from alc

A

high levels of alcohol, elevated acetaldehyde, liver deficiency, and inadequate nutrition.

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36
Q

wernickes encephalopathy: cause

A

lack of thiamine
- thiamine is critical for brain glucose metabolism, its deficit causes cell death.

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37
Q

wernickes encephalopathy: characterization

A

confusion and disorientation, as well as poor coordination, tremors, weakness, and ataxia

  • oculomotor dysfunction such as abnormal eye movements or double vision
38
Q

wernickes encephalopathy: results from

A

lesions in the periaqueductal gray, medial thalamus, and mammillary bodies of the hypothalamus

39
Q

wernickes encephalopathy: if treated early/without treatment

A

the symptoms are readily reversible with massive vitamin supplementation that reverses the biochemical damage

Without treatment the brain damage is permanent and leads to death in approximately 20% of cases

40
Q

what is WE associated with?

A

excessive alcohol use but can be caused by malnutrition, weight loss surgery, HIV/AIDS, anorexia nervosa, and other conditions that may cause vitamin B1 deficiency

41
Q

what happens if someone survives WE

A

develop korsakoff syndrome
- potentially irreversible memory loss, anterograde amnesia (inability to form new memories), decreased spontaneity, confabulation, hallucinations and personality changes

42
Q

what causes korsakoff syndrome

A

result of permanent damage to thalamic nuclei and brain regions involved with memory subsequent to lack of thiamine

43
Q

examples of cell loss, unrelated to diet

A
  • tissue shrinkage
  • frontal lobe affect
  • cerebellar cell loss
44
Q

cell loss: tissue shrinkage (DEF AND PROOF)

A

occurs in medial temporal lobe structures, including the hippocampus and cholinergic cells in the basal forebrain, contributes to memory disturbances

  • caused by enlarged ventricles in the brain of people with AUD
45
Q

cell loss: frontal lobes

A

most affected by cell loss, and may be responsible for the personality changes, including apathy, disinhibition, and diminished executive functioning

46
Q

cell loss: cerebellar cell loss

A

correlated with ataxia and incoordination, particularly of the lower limbs.

47
Q

what plays a central role in brain changes due to cell loss

A

glutamate-induced hyperexcitability of neurons during abstinence

48
Q

effect of alc on cardiovascular system

A

Dilation of peripheral blood vessels: brings them closer to skin surface and makes the person feel warm and looked flushed

49
Q

what does superficial vasodilation tell us

A

superficial vasodilation means that heat is actually being lost from the body rather than being retained

50
Q

vasodilation within the brain

A

vasodilation may improve cognitive function in older adults

51
Q

how much alc can reduce the risk of heart disease and why

A

low to moderate dose
- it increases the amount of “good” cholesterol in the blood while reducing the “bad”

-Reduces blood clots and stroke

52
Q

effect of alc on renal-urinary system

A

produces larger volumes of urine that is far more dilute than normal
- The loss of fluids is caused by reduced secretion of antidiuretic hormone
- People who need to maintain fluids should not ingest alc

53
Q

effect of alc on reproductive system

A

Believed to enhance sexual arousal and lower inhibitions (expectations play a role on sexual response)

54
Q

alc effect on male reproductive system

A

low doses of alcohol enhanced arousal to a small extent, but higher blood levels reduced the sexual response

55
Q

what happens to males reproductive system if alc use is heavy and chronic

A

males may become impotent and may show atrophy of the testicles, reduced sperm production, and shrinkage of the prostate and seminal vesicles

56
Q

alc effect on female reproductive system

A

Physiological measures of sexual arousal decreased with increasing alcohol levels; however, reported subjective arousal was increased

57
Q

what happens to the female reproductive system when women misuse alc

A

experience disrupted ovarian function and show a higher-than-normal incidence of menstrual disorders

58
Q

effect of alc on GI system

A

increases salivation and secretion of gastric juices, which may explain its ability to increase appetite and aid digestion

59
Q

how does higher conc of alc affect the GI system

A

irritates the stomach lining

60
Q

how does chronic vs heavy use of alc affect the GI system

A

chronic use produces inflammation of the stomach (gastritis) and esophagus

Heavy alcohol use causes diarrhea, inhibits utilization of proteins, and reduces absorption and metabolism of vitamins and minerals

61
Q

what is the most damaging effect of heavy chronic alc consumption

A

liver dysfunction

62
Q

what 3 disorders does liver dysfunction lead to

A

fatty liver
alc induced hepatitis
alc induced cirrhosis

63
Q

fatty liver

A

involves the accumulation of triglycerides inside liver cells

64
Q

alc induced hepatitis

A

death of liver cells

65
Q

alc induced cirrhosis

A

further progression of hepatitis, includes inflammation of the liver, fever, jaundice, pain, and scar tissue

66
Q

what is the most effective treatment for sever liver damage

A

liver transplant surgery

67
Q

fetal alcohol syndrome

A

a condition in a child that results from alcohol exposure during the mother’s pregnancy

68
Q

fetal alcohol spectrum disorders

A

a group of conditions that can occur in a person who was exposed to alcohol before birth

69
Q

symptoms of FAS

A

Intellectual disability and other developmental delays

Low birthweight (below 10th percentile)

Neurological problems

Distinctive craniofacial malformations

Other physical abnormalities
- cardiac, testes and kidney

70
Q

why are correlational epidemiological studies with humans are much more difficult to conduct because

A

women may inaccurately recall the quantity, timing, frequency, and pattern of alcohol use, all of which are critical factors determining fetal outcome

some may underreport their consumption because of social pressure against drinking during pregnancy

71
Q

prevalence of alc use: what % of americans drink how much

A

10% - 60% of alc
10% - 20% of alc
30% - no alc
50% - 20%

72
Q

what happens in regards to diffusion of ethanol when there is a greater conc of alc consumed

A

absorption movement is faster from GI to blood

73
Q

is alc less distributed in fatty acids

A

yes
BAC is lower in females who have higher fat/lower blood volume

74
Q

how does alc cross in the body vs BBB vs placenta

A

freely, in all cases

*fetal BAC is the same as the drinking mother

75
Q

induction

A

= type of metabolic tolerance
= when alcohol is consumed on a regular basis, these liver enzymes increase in number, which increases the rate of metabolism of alcohol as well as any other drugs normally metabolized by these enzymes

76
Q

when does BAC peak and decline

A

peak: 1hr after consumption
decline: for the following 4 hours, in a linear manner
- 0 order kinetics = declines at a constant rate (10mL ethanol/hour)

77
Q

how much alc is eliminated by breaking down into metabolites

A

90%

the rest 2-10% is excreted in breath, sweat or urine

78
Q

factors that do not affect metabolism/elimination

A

caffeine, cold showers, exercise, sleep

79
Q

BAC effect on behavior: 0.02-0.03 VS 0.05-0.06

A

0.02-0.03: SOCIALABLE EFFECTS
- minimal effects, slight relaxation and mild mood elevation

0.05-0.06: COGNITIVE EFFECTS
- decreased alertness, relaxed inhibitions, mildly impaired judgment

80
Q

BAC effect on behavior: 0.08-0.10 VS 0.14-0.16

A

0.08-0.10
- loss of motor coordination, slower RT, less caution

0.14-0.16
- major impairment of mental/physical control, slurred speech, exaggerated emotions, blurred visions, serious loss of judgement, large gap in RT

**chronic users may not exhibit symptoms till this point^

81
Q

BAC effect on behavior: 0.15-0.18

A

this is when ones body would vomit in response the bad feeling

82
Q

BAC effect on behavior: 0.20-0.25 VS 0.30

A

0.20-0.25
- staggering, inability to walk/dress without help, tears/rage with little provocation, mental confusion, double vision

0.3
- being conscious but in a stupor, unawareness of surroundings

83
Q

BAC effect on behavior: 0.45

A

this is the LD50
- coma, death for 50% of the population

84
Q

what does the intensity/duration of withdrawal signs depend on?

A

the amount and duration of drug taking
(this is true with any drug)

85
Q

alcohol withdrawal timeline (5 phases)

A

6 hrs: anxiety, insomnia, possible seizures

12-24 hrs: auditory and visual hallucinations

24-48 hrs: withdrawal symptoms, shaking, heavy sweating

48-72 hrs: DT, very high HR, high body temp, seizures

72 hrs: illusions, racing HR, high BP, more sweating, high fever

86
Q

why is ethanol a dirty drug

A

it can interact on many body parts and has many effects (specific and nonspecific)

87
Q

specific vs nonspecific effects

A

specific
- acts as NT at binding sites
- modifies gating mechanism inside channel
- stimulates Gs which is linked to adenylyl cyclase
- interacts directly with channel protein

nonspecific
- disturbs relationship of membrane protein
- interacts with polar heads of phospholipids
- alters lipid composition

88
Q

cognitive control circuit

A

prefrontal cortex - anterior cingulate coretex

89
Q

reward prediction and pleasure circuit

A

ventral pallidum - nucleus accumbens

90
Q

motivations, drive and salience eval circuit

A

orbitofrontal cortex

91
Q

learning and memory circuit

A

amygdala - hippocampus

PSYC383 - Psychopharmacology (3 decks)

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