Alcohol Use Disorder Flashcards

1
Q

what is the DSM-5 criteria for alcohol withdrawal syndrome?

A

2 or more of the following symptoms after a decrease in heavy and prolonged drinking and causing distress or impairment
HAS A PINT

Hallucinations/illusions/delirium tremens
Autonomic hyperactivity (sweats, HR >100)
Seizures
Anxiety
Psychomotor agitation
Insomnia
Nausea/vomiting
Tremor of the hand

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2
Q

when do symptoms of AWS start and how long does it last?

A

can appear as early as 4-12 hours after last drink, usually around 6-24h
peak on day 2-3, improved by day 5
may continue at low levels for 3-6 months

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3
Q

when is seizure risk at the highest in AWS?

A

first 72 hours

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4
Q

when is the peak of AWS?

A

day 2-3

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5
Q

what is the mortality rate of delirium tremens?

A

5%

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6
Q

what is delirium tremens?

A

severe confusion, disorientation, +/- hallucinations with clouding of global sensorium (decrease LOC) + severe autonomic hyperactivity (tachycardia, HTN, hyperthermia, agitation, sweating)

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7
Q

what is the most serious complication of AWS?

A

delirium tremens

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8
Q

how long does delirium tremens last for?

A

1-5 days

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9
Q

what 2 neurotransmitters are key to the pathogenesis of AWS?

A

GABA and glutamate

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10
Q

what does acute alcohol intoxication do to NT balance?

A

increases inhibitory effects of GABA and suppresses excitatory effect of glutamate

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11
Q

what does chronic and regular alcohol use to do NT balance? what are the consequences then in withdrawal?

A

brain develops tolerance and GABA receptors become less sensitive (downregulation) and glutamate receptors become more sensitive (upregulation), so that when alcohol is consumed, there is less overall suppression of the CNS

abrupt withdrawal of alcohol: downregulated GABA system cannot compensate for the rapid increase in glutamate activity resulting in a state of CNS hyper-excitation

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12
Q

what are risk factors for AWS?

A

increase quantity, frequency and duration of alcohol use
previous alcohol withdrawal
family history of alcohol withdrawals
concurrent medical conditions
consumption of sedatives/hypnotics/anxiolytics

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13
Q

what are complications of AWS?

A

death
brain damage
prolonged hospitalisation
delirium tremens
seizures
arrhythmias
aspiration
relapse

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14
Q

what scale is used to predict the risk of severe symptoms of AWS?

A

prediction of alcohol withdrawal severity scale (PAWSS)

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15
Q

what is the interpretation of PAWSS score?

A

a score of 3 or less indicates low risk and outpatient management is suitable
a score of 4 or more indicates a patient might be at high risk for developing complications of alcohol withdrawal and should be admitted to an inpatient setting

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16
Q

what is the first line treatment for AWS?

A

benzodiazepines: lorazepam or diazepam

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17
Q

when is clonidine used in AWS?

A

in addition to benzos

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18
Q

what is the role of clonidine in AWS?

A

suppress noradrenergic symptoms (anxiety, HTN, tachycardia) that do not resolve with benzos
used for symptomatic relief

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19
Q

what is the dosing of clonidine in AWS?

A

0.1-0.3 mg TID x 5d

20
Q

what are other treatments (other than benzos/clonidine) that can be used for AWS?

A

carbamazepine
gabapentin
baclofen
beta-blockers
haloperidol
GHB

21
Q

what is the MOA for benzos in AWS?

A

bind to BZD binding sites on GABA-A receptors to increase GABA binding affinity and increase the inhibitory action of GABA

22
Q

what scale is used to asses the severity of AWS?

A

clinical institute withdrawal assessment for alcohol (CIWA)

23
Q

what CIWA score constitutes treatment?

A

10 or more

24
Q

what is the max CIWA score?

A

67

25
Q

what are some things that are used in supportive care in AWS?

A

thiamine
folate
multivitamin
electrolyte correction
fluids

26
Q

why is thiamine used in AWS?

A

to prevent Wenicke-Korsakoff’s syndrome, peripheral neuropathy, and cardiomyopathy

27
Q

what are some consequences of AUD?

A

cognitive impairment, dementia, stroke
neuropathy, myopathy
depression, anxiety, eating disorders
cardiomyopathy, afib, arrhythmias, HTN
alcoholic hepatitis, cirrhosis, pancreatitis
mouth, esophagus, pharynx and larynx cancer
fetal alcohol spectrum disorders
vitamin B12 deficiency

28
Q

what is the definition of alcohol use disorder?

A

problematic pattern of drinking with clinically significant impairment or distress

28
Q

what is the transtheoretical model?

A

assess an individuals readiness to act on a new healthier behaviour, and provides strategies, or processes of change to guide the individual through the stages of change to action and maintenance

precontemplation –> contemplation –> preparation –> action –> maintenance

29
Q

what are some medical markers of AUD?

A

MCV >96
elevated GGT, AST, ALT (especially AST:ALT >2:1)
GERD, HTN, diabetes, pancreatitis
chronic non-cancer pain
alcohol on breath

30
Q

what are some mental markers of AUD?

A

cognitive impairment or decline
mood, anxiety, sleep disorder
significant behavioural or academic change

31
Q

what are the 4 C’s of addiction?

A

loss of control
consequences
compulsions
cravings

32
Q

who is a candidate for AUD treatment?

A

any patient with moderate-severe AUD
any patient who has undergone withdrawal management, stopped, or reduced drinking and has ongoing alcohol cravings placing them at risk of relapse

33
Q

what is the MOA of naltrexone?

A

mu opioid antagonist
blocks euphoric effects to alcohol to decrease rewarding alcohol effects and reduces cravings
“prevents lapse from becoming a relapse”

34
Q

what is the dosing of naltrexone?

A

start at 12.5 mg daily and increase by 12.5 mg every 4 days to target of 50 mg

35
Q

what needs to be monitored with naltrexone therapy?

A

LFTs at baseline, 1, 3 and 6 months

36
Q

what is the MOA of acamprosate?

A

not fully understood
though to restore imbalance between glutamate and GABA to reduce general neuronal hyperexcitability
“prevents lapse - more effective at supporting abstinence”

37
Q

what is the dosing of acamprosate?

A

666 mg TID

333 mg TID if renal impairment, CrCl 30-50 mL/min

38
Q

what is a CI of acamprosate?

A

CrCl </= 30 mL/min

39
Q

how does topiramate work in AUD?

A

decreases cravings by reducing DA release when ETOH consumed

40
Q

how does gabapentin work in AUD?

A

reduces unpleasant withdrawal symptoms

41
Q

which treatment of AUD is a deterrent?

A

disulfram

42
Q

what is the MOA of disulfram?

A

aversive agent that inhibits alcohol dehydrogenase enzyme and blocks the metabolism of alcohol
results in unpleasant s/e if patient drinks alcohol

43
Q

what is the dosing of disulfram?

A

initial: 500 mg Od x1-2 weeks
maintenance: 250 mg OD

44
Q

when should disulfram NOT be used

A

must be abstained from alcohol for at least 12 hours

45
Q
A