Alcohol - CH10 Flashcards
(91 cards)
1
Q
what type of drug is alcohol
A
depressant
2
Q
what is the typical route of admin for alcohol
A
oral (first pass)
3
Q
what is the duration of the effect of alcohol
A
moderate
4
Q
what NT are affected by alc
A
GABA, glutamate, dopamine and opioids
5
Q
what is the tolerance of alcohol
A
moderate
6
Q
what is the physical dependence of alcohol vs psychological dependance
A
intense vs moderate
7
Q
withdrawal symptoms of alc
A
cramps, delirium, vomiting, sweating, hallucinations, seizures and delirium tremens
8
Q
what is the schedule of alc
A
legal
9
Q
how was alc used in ancient times?
A
used as medicine: stress relief, relaxation, antiseptic properties and anesthetic
- comboed with natural botanicals
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
11
Q
what was the first distilled drink
A
in middle ages (12th century) of Italy: wine to brandy
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
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
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
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- most provinces repealed the ban in 1920s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
16
Q
what is the avg age of initiation into alc in canada: CADUMS 2012
A
18.3
17
Q
what % canadians have used alc in their life?: CADUMS 2012
A
91
18
Q
what % canadians have used alc in the past year?: CADUMS 2012
A
78
19
Q
how is brain atrophy indicated in brain structure?
A
increased sulci, and ventricle size
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)
21
Q
what determines the type of alcoholic beverage
A
the material that provides the sugar
22
Q
3 ways to increase alc concentration
A
- heating the fermented mixture
- add additional alcohol
- fractional freezing
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%
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
25
what determines absorption of alc
- presence of food
- ulcer medication
- sex differences
- hydration levels
- aspirin
- carbonation
- stress/anxiety/fear
- illness
26
2 ways alc is metabolized
1. alcohol dehydrogenase
2. enzymes from cytochrome 450 family
27
4 types of tolerance
pharmacodynamic, acute, metabolic, behavioral
28
symptoms of withdrawal from chronic alc use
- can last up to weeks:
sleep disturbance
intense anxiety
fast HR
tremors
high BP
excessive sweating
rapid breathing
nausea/vomiting
29
more severe symptoms of alc withdrawal
convulsions, delirium, hallucinations, total disorientation
30
effect of alc on CNS: judgement (low dose, social vs quiet)
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
31
effect of alc on CNS: memory (low dose vs high dose)
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)
32
effect of alc on CNS: motor skills
Reduced coordination lead to slurred speech and impaired fine motor skills and delayed RT
33
effect of alc on CNS depression
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
34
signs of alcohol poisoning
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
35
what leads to brain damage from alc
high levels of alcohol, elevated acetaldehyde, liver deficiency, and inadequate nutrition.
36
wernickes encephalopathy: cause
lack of thiamine
- thiamine is critical for brain glucose metabolism, its deficit causes cell death.
37
wernickes encephalopathy: characterization
confusion and disorientation, as well as poor coordination, tremors, weakness, and ataxia
- oculomotor dysfunction such as abnormal eye movements or double vision
38
wernickes encephalopathy: results from
lesions in the periaqueductal gray, medial thalamus, and mammillary bodies of the hypothalamus
39
wernickes encephalopathy: if treated early/without treatment
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
what is WE associated with?
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
what happens if someone survives WE
develop korsakoff syndrome
- potentially irreversible memory loss, anterograde amnesia (inability to form new memories), decreased spontaneity, confabulation, hallucinations and personality changes
42
what causes korsakoff syndrome
result of permanent damage to thalamic nuclei and brain regions involved with memory subsequent to lack of thiamine
43
examples of cell loss, unrelated to diet
- tissue shrinkage
- frontal lobe affect
- cerebellar cell loss
44
cell loss: tissue shrinkage (DEF AND PROOF)
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
cell loss: frontal lobes
most affected by cell loss, and may be responsible for the personality changes, including apathy, disinhibition, and diminished executive functioning
46
cell loss: cerebellar cell loss
correlated with ataxia and incoordination, particularly of the lower limbs.
47
what plays a central role in brain changes due to cell loss
glutamate-induced hyperexcitability of neurons during abstinence
48
effect of alc on cardiovascular system
Dilation of peripheral blood vessels: brings them closer to skin surface and makes the person feel warm and looked flushed
49
what does superficial vasodilation tell us
superficial vasodilation means that heat is actually being lost from the body rather than being retained
50
vasodilation within the brain
vasodilation may improve cognitive function in older adults
51
how much alc can reduce the risk of heart disease and why
low to moderate dose
- it increases the amount of “good” cholesterol in the blood while reducing the “bad”
-Reduces blood clots and stroke
52
effect of alc on renal-urinary system
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
effect of alc on reproductive system
Believed to enhance sexual arousal and lower inhibitions (expectations play a role on sexual response)
54
alc effect on male reproductive system
low doses of alcohol enhanced arousal to a small extent, but higher blood levels reduced the sexual response
55
what happens to males reproductive system if alc use is heavy and chronic
males may become impotent and may show atrophy of the testicles, reduced sperm production, and shrinkage of the prostate and seminal vesicles
56
alc effect on female reproductive system
Physiological measures of sexual arousal decreased with increasing alcohol levels; however, reported subjective arousal was increased
57
what happens to the female reproductive system when women misuse alc
experience disrupted ovarian function and show a higher-than-normal incidence of menstrual disorders
58
effect of alc on GI system
increases salivation and secretion of gastric juices, which may explain its ability to increase appetite and aid digestion
59
how does higher conc of alc affect the GI system
irritates the stomach lining
60
how does chronic vs heavy use of alc affect the GI system
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
what is the most damaging effect of heavy chronic alc consumption
liver dysfunction
62
what 3 disorders does liver dysfunction lead to
fatty liver
alc induced hepatitis
alc induced cirrhosis
63
fatty liver
involves the accumulation of triglycerides inside liver cells
64
alc induced hepatitis
death of liver cells
65
alc induced cirrhosis
further progression of hepatitis, includes inflammation of the liver, fever, jaundice, pain, and scar tissue
66
what is the most effective treatment for sever liver damage
liver transplant surgery
67
fetal alcohol syndrome
a condition in a child that results from alcohol exposure during the mother's pregnancy
68
fetal alcohol spectrum disorders
a group of conditions that can occur in a person who was exposed to alcohol before birth
69
symptoms of FAS
Intellectual disability and other developmental delays
Low birthweight (below 10th percentile)
Neurological problems
Distinctive craniofacial malformations
Other physical abnormalities
- cardiac, testes and kidney
70
why are correlational epidemiological studies with humans are much more difficult to conduct because
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
prevalence of alc use: what % of americans drink how much
10% - 60% of alc
10% - 20% of alc
30% - no alc
50% - 20%
72
what happens in regards to diffusion of ethanol when there is a greater conc of alc consumed
absorption movement is faster from GI to blood
73
is alc less distributed in fatty acids
yes
BAC is lower in females who have higher fat/lower blood volume
74
how does alc cross in the body vs BBB vs placenta
freely, in all cases
*fetal BAC is the same as the drinking mother
75
induction
= 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
when does BAC peak and decline
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
how much alc is eliminated by breaking down into metabolites
90%
the rest 2-10% is excreted in breath, sweat or urine
78
factors that do not affect metabolism/elimination
caffeine, cold showers, exercise, sleep
79
BAC effect on behavior: 0.02-0.03 VS 0.05-0.06
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
BAC effect on behavior: 0.08-0.10 VS 0.14-0.16
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
BAC effect on behavior: 0.15-0.18
this is when ones body would vomit in response the bad feeling
82
BAC effect on behavior: 0.20-0.25 VS 0.30
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
BAC effect on behavior: 0.45
this is the LD50
- coma, death for 50% of the population
84
what does the intensity/duration of withdrawal signs depend on?
the amount and duration of drug taking
(this is true with any drug)
85
alcohol withdrawal timeline (5 phases)
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
why is ethanol a dirty drug
it can interact on many body parts and has many effects (specific and nonspecific)
87
specific vs nonspecific effects
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
cognitive control circuit
prefrontal cortex - anterior cingulate coretex
89
reward prediction and pleasure circuit
ventral pallidum - nucleus accumbens
90
motivations, drive and salience eval circuit
orbitofrontal cortex
91
learning and memory circuit
amygdala - hippocampus
