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CMOD > Sweatman Alcohol: Use and Abuse > Flashcards

Sweatman Alcohol: Use and Abuse Flashcards

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
Q

antedote for acetominophen toxicity

A

N acetyl cystein–> restores conjugate substrate for metab to non-toxic intermediate

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26
Q

level with limited muscular incoordination

A

< 50

27
Q

pronounced incoordinatio

A

50-100

28
Q

mood and personality changes, intoxication over legal limit in most states

A

100-150

29
Q

nusea vomiting, ataxia, amnesia, dysarthria

A

150-400

30
Q

coma, resp failure, death

A

> 400

31
Q

ETOH receptors in the brain

A

NONE –modulates other pathways

32
Q

Key pathways modulated by ETOH in brain

A
  1. reinforcement of inhibitory actions of GABA

2. inhibition of stimulatory actions of Glutamate

33
Q

blackouts are because of what

A

inhibition of stimulatory actions of glutamate system

34
Q

other acute effects of ETOH

A

relaxes uterine smooth muscle
relaxes vascular smooth muscle
->vasodilation, hypthermia, increased gastric blood flow
CV depressant

35
Q

can alcohol in small doses prevent premature labor

A

yes

36
Q

within body ETOH distribution depends on

A

total body water

0.5-0.7 L/Kg

37
Q

does alcohol distribute to body fat

A

NO

38
Q

higher BMI=

A

high BAL

*alcohol would be excluded from this compartment

39
Q

more weight=

A

lower BAL

*larger total volume of distribution

40
Q

female sex=

A

higher BAL

  • weight is less
  • more fat
  • increased absoprtion
41
Q

Most common neurologic defect in the alcoholic

A

peripheral neuropathy

42
Q

thiamine deficiency results in

A

Wernicke-Korsakoff syndrome

43
Q

classic WK tirad

A

> occulomotor defects (nystagmus) 30%
ataxia cerebellar dysfunction
confusion altered mental state 80%

44
Q

Ultimate consequence of thiamine deficiency

A

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
Q

modest ETOH can

A

increase HDL’s

46
Q

binge drinking can cause

A

arrhythmias

47
Q

chronic alcoholics are susceptible to

A

infection pneumonia

48
Q

CV risks with chronic ETOH

A

HTN
anemia
dilated cardiomyopathy

49
Q

ETOH levels in the fetus reflect

A

maternal blood levels

50
Q

does ETOH cross placenta

A

hell yeah mane

51
Q

charcteristics of FAS

A 
microcephaly
poor coordination
intrauterine growth retardation
flattened face
*1st trimester is mose devastating due to organogenesis
52
Q

How to deal with intoxicated pt.

A
  • monitor vital signs and airway patency
  • thiamine (prevent WK)
  • then dextrose (compensate for hypoglycemia)
  • fix electrolyte imbalances
53
Q

why thimaine before dextrose

A

dextrose can exacerbate WK syndrome

54
Q

How to deal with withdrawal pt.

A

BNZo to control withdrawal symptoms
-thiamine (b1)
-correct electrolyte issues
`

55
Q

symptoms of ETOH withdrawal

A

DT’s, seizures, n/v, diarrhea, arrhythmias, insomnia, tremor

56
Q

preferred BNZo for withdrawal

A

long acting diazepam

*lorazepam if hepatic function impaired

57
Q

acetominiphen toxicity with ETOH is an example of

A

Pharmacodynamic intercation

drug on body
increses toxicity of Acetominiphen

58
Q

disulfiram -like effects

A

anything that causes build up of acetaldehyde

  • doesnt refer to chronic alcoholism tx.
  • dont take alcohol with these drugs
59
Q

3 drugs for tx of alcoholism

A
  1. disulfiram–>acetaldehyde antagonist
  2. Naltrexone–> opiate receptor antagonist
  3. acamprosate–> gaba agonist
60
Q

Both methanol and ethylene glycol are broken down initially by

A

alcohol dehydrogenase

61
Q

ethylene glycol toxicity

A

acidosis

nephrotoxicity

62
Q

methanol toxicity

A

severe acidosis

retinal damage

63
Q

drugs to prevent conversion of methanol/ethylene glycol to toxic intermediates

A
  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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