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PMCOL 305 > alcohol 3 > Flashcards

alcohol 3 Flashcards

1
Q

what are bed spins (simple defintion)

A

positional alcohol vertigo

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2
Q

what is altered physiologically that causes bed spins

A

buoyancy of the cupula with respect to surrounding endolymph fluid

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3
Q

what is the cupula

A

inner ear component

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4
Q

what happens to the ear at BAC around 0.04

A

ethanol diffuses into cupula and makes it lighter than surrounding endolymph

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5
Q

what BAC is required for ethanol to diffuse into cupula

A

0.04

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6
Q

what happens to cupula when alcohol enters

A

it makes it lighter than surrounding endolymph

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7
Q

how long does it take to get BAC to 0.04

A

30min

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8
Q

what happens to ear when drinking increases (3-5hrs, more than 0.04)

A

endolymph is also affected by ethanol, so now its density matches cupula

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9
Q

what happens when drinking stops to ear

A

ethanol diffuses out of cupula first, so it is heavier than endolymph (hangover, 5-10hours)

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10
Q

what causes the bed spins (physiologically)

A

difference in density of cupula (heavier) than endolymph (lighter) tricks brain into thinking its spinning

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11
Q

in bed spins, what is affected(enter) by ethanol first

A

cupula

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12
Q

in bed spins, what is affected(enter) by ethanol second

A

endolymph

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13
Q

in bed spins, where does alcohol LEAVE first

A

cupula

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14
Q

in bed spins, where does alcohol LEAVE second

A

endolymph

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15
Q

is bed spins caused by a more dense endolymph or cupula

A

more dense cupula

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16
Q

what places are most likely to get cancer from ethanol

A

GI tract, liver, colorectal, breast

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17
Q

what % of upper GI cancer is caused by alcohol

A

50%

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18
Q

what are the main culprits of ethanol caused cancer

A

acetaldehyde and reactive oxygen species

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19
Q

what is the safe threshold for drinking

A

non for some cancers (esophagus)

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20
Q

what type of cancer is most prominent with ethanol use

A

esophagus

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21
Q

order these cancers in descending order with cancer and alcohol intake

  • colorectal
  • oral cavity/pharynx
  • pancreas
  • larynx
  • esophagus
A
  • esophagus
  • oral cavity/pharynx
  • larynx
  • colorectal
  • pancreas
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22
Q

what does acetaldehyde do to DNA repair enzymes

A

binds to and inactivates them

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23
Q

what does acetaldehyde do to DNA bases

A

covalently modify

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24
Q

what happens when acetaldehyde inactivates DNA repair enzymes and modifies DNA bases

A

mutations and chromosomal abnormalities

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25
Q

which base can be modified by acetaldehyde 2 ways

A

deoxygaunosine

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26
Q

is it ethanol or acetaldehyde that modifies deoxyguanosine + how did they find out

A

it was the acetaldehyde because they used an ADH inhibitor to figure it out

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27
Q

what are the two types of reactions that happen with acetaldehyde and deoxyguanosine

A

one with 1 and one with 2 acetaldehydes

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28
Q

what is made with 1 acetaldehyde and 1 deoxyguanosine

A

N^2 ethylidene - deoxyguanosine

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29
Q

what is made with 2 acetaldehyde and 1 deoxyguanosine

A

propano-deoxyguanosine

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30
Q

what happens if the propano-deoxyguanosine ring does close and aldehyde group remains

A

it can form covalent links with other DNA strands and/or proteins (DNA interstrand crosslinks or DNA-protein crosslinks)

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31
Q

why is there so much cancer in the upper-digestive tract

A

ethanol is metabolized to acetaldehyde by microbes in saliva (10-100X higher conc of acetaldehyde in saliva than blood)

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32
Q

how does the concentration of acetaldehyde compare to in the blood

A

10-100X higher in saliva

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33
Q

what does poor dental hygiene do to acetaldehyde amounts + Why

A

increases the concentration as there are more microbes with worse hygiene

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34
Q

what does smoking to do the microbes in mouth

A

shifts the types of microbes to the types that produce high (50%) acetaldehyde levels`

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35
Q

what causes ethanol induced liver cancer

A

ROS from CYP2E1 and catalase, activated from immune cells

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36
Q

what does ROS do to cause cancer

A

lipid damage creates reactive lipid species which covalently modify DNA - mutagenic

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37
Q

what is the role of retinoic acid/ vitamin A

A

negative regulator of malignant cells (prevent proliferation)

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38
Q

what metabolizes retinoic acid/ Vit A

A

CYP2E1

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39
Q

what does low retinoic/VIit A cause

A

less RA receptors, so a change in levels of proteins involved in gene regulation and proteins involved in liver cell proliferation (whole pathway less active, bad bad)

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40
Q

what 6 things cause brain damage from alcohol

A

acetaldehyde, ROS, nutritional deficiency, head trauma, neuroinflammation, excitotoxicity (Ca influx-excess glutamatergic)

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41
Q

what causes excitotoxiticy

A

hyperactivity of glutamatergic system-excess calcium influx causing inappropriate activation of calcium-sensitive signalling pathways and cell death

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42
Q

why does nutritional deficiency happen a lot in alcoholics

A

no nutritional value in ethanol

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43
Q

what is wernickes disease

A

B1 (thiamine) deficiency

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44
Q

is wernickes disease reversible

A

partially

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45
Q

what causes wenickes disease

A

bad B1/thiamine absorption from GI due to inflammation

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46
Q

what is thiamine/B1 involved in

A

myelin formation, glucose utilization and amino acid production

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47
Q

what are symptoms of wenickes disease

A

confusion, ataxia, abnormal eye movement (shaky or paralyzes eyes)

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48
Q

what is korsakoffs psychosis symptoms

A

short and long term memory loss, inability to learn new info

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49
Q

is korsakoffs psychosis reversivle

A

no

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50
Q

what causes korsakoffs psychosis

A

neuronal loss - progression of wernikes

51
Q

what can help reverse wernickes

A

increase B1 intake

52
Q

what does low ethanol dose do to HDL

A

increases it (its the good cholesterol)

BUT only really in cell culture

53
Q

what does low ethanol dose do to platelet aggregation and coagulation

A

decreases (less likely to have clots) (but this data is kinda not sure if real)

54
Q

what does low ethanol dose do to blood vessel inflammation

A

decrease (kinda weird and contradictory…)

55
Q

what does low ethanol dose do to endothelial function, in what way is it changed

A

improved balance between blood vessel constriction and dilation

56
Q

are the cardioprotective effects of alcohol real? do they translate into a measureable clinical benefit?

A

not really, there is an increase in moderate/heavy users of heart issues like BP

57
Q

what does high dose of ethanol do to heart

A

toxic-cardiomyopathy (disease of heart muscle)

58
Q

what does alcohol do directly to the myocardium

A

directly depresses it

59
Q

what does acetaldehyde do to myocyte function and how

A

inhibits by altering calcium homeostasis and myocardial protein synthesis

60
Q

how does acetaldehyde change calcium homeostatis

A

ca release from SR is inhibited - negative effect on calcium sensitive contractility proteins

61
Q

what does ethanol metabolites do to mitochondria

A

causes dysfunction and poor energy usage

62
Q

what was the main issue with the study that claimed alcohol was fine in moderation

A

that the abstainer group included previous drinkers and alcoholics (got so sick that they quit)

63
Q

how many people (that drink 1 drink a day) out of 100 000 with experience 1 of 23 alcohol related issues

A

918

64
Q

how many people (that drink 0 drink a day) out of 100 000 with experience 1 of 23 alcohol related issues

A

914

65
Q

how many people (that drink 2 drink a day) out of 100 000 with experience 1 of 23 alcohol related issues

A

977`

66
Q

what is the leading cause of brain damage in USA

A

fetal alcohol spectrum disorder (1 in 10 births) (i think 1 in 10 of brain damage births)

67
Q

what is fetal alcohol syndrome

A

the severe end of the spectrum

68
Q

what week in human development does the face and forebrain develop

A

week 3

69
Q

what are the ways kids with FASD look different

A

thin upper lip
small head
small eye openings
no ridge b/w nose and lips

70
Q

what are some symptoms of FASD

A

poor impulse control&planning, impaired mental function, seizures

71
Q

when does synaptogenesis occur

A

third trimester

72
Q

when is fetal alcohol exposure most harmful to brain and why

A

third trimester because thats when synaptogenesis occurs

73
Q

what happens to the neurons in the third trimester with alcohol there

A

they dont form synapses-they may just go to the wrong place or never make connections

74
Q

what can binge exposure of ethanol do to fetus

A

massive apoptosis (programmed cell death)

75
Q

were all brain regions sensitive to ethanol at the same times

A

no, different regions are sensitive to ethanol during different stages within the time period (diff timing of the development and making connections between regions)

76
Q

is the hypothalamus sensitive to early mid or late third trimester ethanol exposure

A

early

77
Q

is the PFC sensitive to early mid or late third trimester ethanol exposure

A

late

78
Q

is the thalamus sensitive to early mid or late third trimester ethanol exposure

A

mid

79
Q

rank thalamus, hypothalamus and PFC in order of early to late in trimester most likely to die with ethanol

A

hypothalamus, thalamus, PFC

80
Q

is severity of apoptosis linked to total dose or peak concentration

A

peak concentration

81
Q

what BAC triggered apoptosis (and for how long) in rat embryo experiment

A

0.2 for 4 hours

82
Q

what causes ethanol induced apoptosis

A

combination of GABA A receptor activation and NMDA receptor block

83
Q

when does most of the ethanol induced apoptosis occur

A

third trimester

84
Q

what is MK-801

A

NMDA receptor antagonist

85
Q

what is phenobarbital

A

GABA-A receptor activator

86
Q

how did they use phenobarbital and MK-801 to see what causes apoptosis

A

MK-801 antagonizes NMDA receptor,

phenobarbital activates GABA -A receptor, so both of those effects combined showed the same results as ethanol exposure

87
Q

what does ethanol do to ERK and cause does this cause

A

causes a lack in ERK phosphorylation - mitochondrial damage

88
Q

what does ERK do normally

A

help cause neuroplasticity

89
Q

what do caspase 3 and 9 do

A

enzymes that trigger apoptosis

90
Q

what does ethanol do to caspase 3 and 9

A

activates them, which triggers apoptosis

91
Q

is there more or less caspase 3 and 9 when theres ethanol around

A

more

92
Q

what does prenatal ethanol do to surviving neurons

A

alters their migration

93
Q

what are heterotopias

A

clumps of neurons in the wrong part of the brain

94
Q

genes for which receptors are affected by prenatal ethanol

A

thyroid hormone and retinoid acid

95
Q

what does the affected genes with thyroid hormone and retinoid acid cause

A

increased biological reactions to stress-poor coping, anxiety and depression

96
Q

what is in stage 1 withdrawal (6)

A

tremors, rapid HR, hypertension, sweating, no appetite, insomnia

97
Q

what is in stage 2 withdrawal (1)

A

hallucinations

98
Q

what is in stage 3 withdrawal (4)

A

delusions, delirium, disorientation, amnesia

99
Q

what is in stage 4 withdrawal (1)

A

seizures

100
Q

what is mortality rate in alcohol withdrawal when not supervises/treated

A

1/7

101
Q

what are delirium tremens

A

stage 3,4

-delusions, delirium, disorientation, amnesia, seizures

102
Q

when do delirium tremens occur

A

peak 3-4 days after last drink

103
Q

how can benzodiazepines help with withdrawal

A

prevent stages 3 and 4 - especially seizures

104
Q

what is clonidine

A

agonist and alpha2 receptors (adrenergic)

105
Q

how can clonidine help with withdrawal

A

prevents excessive NT release

106
Q

what is propranolol

A

beta adrenergic antagonist

107
Q

how can propranolol help with withdrawal

A

blocks excess sympathetic activity, slows HR and reduces tremors

108
Q

what are 2 drugs +1 drug class used for withdrawal

A

clonidine, propranolol, benzos (sedatives)can

109
Q

what is disulfiram/how does it work

A

prevents aldehyde dehydrogenase from working

110
Q

when is disulfiram used./why

A

to prevent alcohol use-makes you throw up, nausea

111
Q

what does disulfiram do

A

results in high levels of acetaldehyde (prevents aldehyde dehydrogenase from working)

112
Q

does disulfiram work long term

A

questionable

113
Q

does disulfiram stop cravings

A

no!

114
Q

what is naltrexone

A

mu-opioid receptor antagonist

115
Q

what does naltrexone do

A

prevents beta endorphin from activating presynaptic receptors

116
Q

what does naltrexone do to GABA release in VTA

A

prevents inhibition of GABA release in VTA

117
Q

can naltrexone help with cravings

A

some studies say yes

118
Q

what is a downside of naltrexone

A

may cause negative mood

119
Q

what does alcohol do to endorphin and where

A

increases it in VTA and NA

120
Q

what is acamprosate

A

glutamate receptor antagonist

121
Q

how does acamprosate work

A

prevents glu acting at its receptors, stops the hyperexcitability due to glu up-regulation (esp in withdrawal)

122
Q

what does acamprosate do to craving

A

helps prevent

123
Q

when is acamprosate best and why

A

in withdrawal because it prevents glu binding to its receptor and causing hyperexcitability (due to gluR upregulation)

PMCOL 305 (26 decks)

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