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CMOD > Sweatman Alcohol: Use and Abuse > Flashcards

Sweatman Alcohol: Use and Abuse Flashcards

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1
Q

toxicants

A

ethanol
methanol
ethylene glycol

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2
Q

antidotes for ethanol

A

disulfuram

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3
Q

antidote for methanol

A

fomepizole or ethanol

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4
Q

antidote for ethylene glycol

A

ethanol or fomepizole

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5
Q

drugs for ethanol withdrawal

A

diazepam

thiamine (B1)

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6
Q

drugs for chronic alcoholics

A

disulfiram
naltrexone
acamprosate

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7
Q

tx for acute methanol or ethylene glycol poisoning

A

ethanol or fomepizole

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8
Q

break down of ethanol

A

ethanol–>acetaldehyde–>acetate

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9
Q

ethanol to aldehyde enzyme

A

ALCOHOL dehydrogenase

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10
Q

aldehyde to acetate enzyme

A

Acetaldehyde dehyrogenase

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11
Q

order kinetics for alchohol

A

zero order

*constant mass–> different proportion

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12
Q

Is alcohol metabolism CYP mediated

A

very little unless chronic alcholism–>some cyp induction can occur and become more substantiative

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13
Q

Alcohol dehydrogenase blocker

A

fomepizole

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14
Q

aldehyde dehydrogenase blocker

A

disulfiram

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15
Q

metabolism of ETOh requires excess of what

A

NAD+

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16
Q

zero order kinetics

A

ethanol
phenytoin
aspirin (high dose)

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17
Q

disulfiram MOA

A

aldehyde dehydrogenase atangonist–> leads to accumulation of acetaldehyde–> nause flushed skin

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18
Q

encourages abstinence from alcohol (antebuse)

A

disulfiram

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19
Q

Aian flush

A

SNP’s in acetaldehyde dehydrogenase enzyme–> result is loss of functionality and build up of acetaldehyde–> nasuea, vomiting and flushing of skin

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20
Q

Why some alcoholics find acetaldehyde pleasurable

A
  • unplaseant in periphery

* in the VTA it can lead to dopamine release –> CONDENSES WITH DOPAMINE TO FORM SALSOLINOL–> REINFORCING AGENT

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21
Q

ETHANOL IS AN IMPORTANT INDUCER OR

A

CYP 2E1

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22
Q

ETOH induction of CYP leads to increased amounts of

A

NAPQI–> highly toxic

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23
Q

acetominophin is metoblized in three ways

A

Sulfate conjugation–>major and non-toxic
Glucuronide–> major and non-toxic
NAPQI–> minor and highly toxic (quickly converted to non-toxic thang if GSH stores are high)

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24
Q

mechanism for acetominophen toxicity in chronic alcoholic

A

etoh induces CYP 2E1–> over production of NAPQI–> GSH stores run out and unable to conjugate NAPQI to non-toxic intermediate–>hepatotoxicity

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25
antedote for acetominophen toxicity
N acetyl cystein--> restores conjugate substrate for metab to non-toxic intermediate
26
level with limited muscular incoordination
< 50
27
pronounced incoordinatio
50-100
28
mood and personality changes, intoxication over legal limit in most states
100-150
29
nusea vomiting, ataxia, amnesia, dysarthria
150-400
30
coma, resp failure, death
>400
31
ETOH receptors in the brain
NONE --modulates other pathways
32
Key pathways modulated by ETOH in brain
1. reinforcement of inhibitory actions of GABA | 2. inhibition of stimulatory actions of Glutamate
33
blackouts are because of what
inhibition of stimulatory actions of glutamate system
34
other acute effects of ETOH
relaxes uterine smooth muscle relaxes vascular smooth muscle ->vasodilation, hypthermia, increased gastric blood flow CV depressant
35
can alcohol in small doses prevent premature labor
yes
36
within body ETOH distribution depends on
total body water | 0.5-0.7 L/Kg
37
does alcohol distribute to body fat
NO
38
higher BMI=
high BAL | *alcohol would be excluded from this compartment
39
more weight=
lower BAL | *larger total volume of distribution
40
female sex=
higher BAL * weight is less * more fat * increased absoprtion
41
Most common neurologic defect in the alcoholic
peripheral neuropathy
42
thiamine deficiency results in
Wernicke-Korsakoff syndrome
43
classic WK tirad
>occulomotor defects (nystagmus) 30% >ataxia cerebellar dysfunction >confusion altered mental state 80%
44
Ultimate consequence of thiamine deficiency
inability to synthesize and replenish critical amino acids and proteins, especially those in the brain *brought on by poor diet, and inadequate storage in the liver
45
modest ETOH can
increase HDL's
46
binge drinking can cause
arrhythmias
47
chronic alcoholics are susceptible to
infection pneumonia
48
CV risks with chronic ETOH
HTN anemia dilated cardiomyopathy
49
ETOH levels in the fetus reflect
maternal blood levels
50
does ETOH cross placenta
hell yeah mane
51
charcteristics of FAS
``` microcephaly poor coordination intrauterine growth retardation flattened face *1st trimester is mose devastating due to organogenesis ```
52
How to deal with intoxicated pt.
- monitor vital signs and airway patency - thiamine (prevent WK) - then dextrose (compensate for hypoglycemia) - fix electrolyte imbalances
53
why thimaine before dextrose
dextrose can exacerbate WK syndrome
54
How to deal with withdrawal pt.
BNZo to control withdrawal symptoms -thiamine (b1) -correct electrolyte issues `
55
symptoms of ETOH withdrawal
DT's, seizures, n/v, diarrhea, arrhythmias, insomnia, tremor
56
preferred BNZo for withdrawal
long acting diazepam | *lorazepam if hepatic function impaired
57
acetominiphen toxicity with ETOH is an example of
Pharmacodynamic intercation drug on body increses toxicity of Acetominiphen
58
disulfiram -like effects
anything that causes build up of acetaldehyde * doesnt refer to chronic alcoholism tx. * dont take alcohol with these drugs
59
3 drugs for tx of alcoholism
1. disulfiram-->acetaldehyde antagonist 2. Naltrexone--> opiate receptor antagonist 3. acamprosate--> gaba agonist
60
Both methanol and ethylene glycol are broken down initially by
alcohol dehydrogenase
61
ethylene glycol toxicity
acidosis | nephrotoxicity
62
methanol toxicity
severe acidosis | retinal damage
63
drugs to prevent conversion of methanol/ethylene glycol to toxic intermediates
1. fomepizole--> alcohol dehydrogenase antagonist 2. ethanol--> competitive inihibitor for alcohol dehydrogenase(want a BAL of 100 mg/dL * greater renal elimination

CMOD (19 decks)

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