Alcohol Use Disorder Flashcards
What is the DSM-5 diagnostic criteria for AWS?
2 or more of the following sx following a decrease in heavy & prolonged drinking, and causing distress or impairment
-hallucinations/illusions/delirium tremens
-autonomic hyperactivity
-seizures
-anxiety
-psychomotor agitation
-insomnia
-nausea/vomiting
-tremor
HAS A PINT
When do the symptoms of AWS peak?
day 2-3
What is the most serious complication of alcohol withdrawal?
delirium tremens
What is delirium tremens?
severe confusion, disorientation, +/- hallucinations with clouding of global sensorium, + severe autonomic hyperactivity (tachy/htn/sweating/agitation/hyperthermia)
-mortality rate 5%
What does the typical timeline look like for delirium tremens?
usually begins 48-96h after last drink
lasts 1-5 days
Which two neurotransmitters are involved in the pathogenesis of AWS?
GABA and glutamate
-the balance shifts towards glutamate
What are the risk factors for AWS?
increased quantity, frequency, and duration of use
previous withdrawal
family history of alcohol withdrawal
concurrent medical conditions
consumption of sedatives/hypnotics/anxiolytics
What are the complications of AWS?
death
seizures
arrhythmias
brain damage
prolonged hospitalization
aspiration
relapse
delirium tremens
What is the PAWSS tool?
most useful screening tool for predicting patients risk of developing severe complications related to alcohol withdrawal
-10 item risk assessment
-can be done before stopping or reducing drinking to determine risk of severe AWS complications
-could be used in ER setting
-useful to help determine level monitoring and support required
What score on PAWSS warrants outpatient management? What about the score indicating inpatient care?
3 or less: low risk of complications, outpatient
4 or more: high risk of complications, inpatient
What is the most commonly used class of medications in AWS?
benzodiazepines
What is the role of clonidine in AWS?
often used in addition to benzos (not on its own)
suppresses noradrenergic sx (anxiety/htn/tachy) that do not resolve with benzos
used for “symptomatic relief”
What are some examples of medications that have insufficient evidence to conclude benefit/harm in AWS?
CBZ
gabapentin
baclofen
beta-blockers
GHB
haloperidol
What is the MOA of benzodiazepines?
bind to the BZD binding site on GABAa receptors to increase GABA binding affinity and increase inhibitory action of GABA
Which benzodiazepines are used for AWS?
lorazepam
diazepam
Differentiate lorazepam and diazepam.
lorazepam:
-onset: 30-60 min
-t1/2: 10-14h
-metabolism: inactive metabolites
-IV/IM/SC
diazepam:
-onset: 15-30 min
-t1/2: 50-100h
-metabolism: active metabolites
-IV only
What are the side effects of benzodiazepines?
common:
-sedation
-confusion
-amnesia
-psychomotor impairment
rare:
-paradoxical reactions
-falls
-respiratory depression
-pancytopenia
What is CIWA?
10-item scale used to measure the severity of alcohol withdrawal symptoms
commonly used on inpatient settings as part of “symptom triggered dosing protocols”
Differentiate the different scores and their severity of alcohol withdrawal for CIWA.
0-9: very mild or absent
10-15: mild
16-20: moderate
>21-67: severe
What CIWA score requires treatment?
10 or greater
What are the symptoms covered by CIWA?
- nausea and vomiting
- tremors
- paroxysmal sweats
- anxiety
- agitation
- orientation
- tactile disturbances
- auditory disturbances
- visual disturbances
- headache
What are supportive care measures for AWS?
thiamine
-prevent Wernicke-Korsakoffs syndrome, peripheral neuropathy, cardiomyopathy
multivitamin
-prevent and correct micronutrient deficiency
folate
-prevent and correct anemia
electrolyte correction
-prevent elyte imbalances and life-threatening complications
fluids
-correct hypovolemia and dehydration
What are examples of medications used in AUD?
naltrexone
acamprosate
topiramate
gabapentin
What is AUD?
problematic pattern of drinking with clinically significant impairment or distress
What are the many consequences of AUD?
CNS:
-cognitive impairment, dementia, stroke
PNS:
-neuropathy, myopathy
psych:
-depression, anxiety, eating disorder
CV:
-cardiomyopathy, afib, arrhythmia, HTN
GI:
-alcoholic hepatitis, cirrhosis, pancreatitis
cancers:
-mouth, larynx, pharynx, esophagus
others:
-FAS, B12 deficiency
Describe the role of genetics in AUD.
first degree relative –> 3-4x prevalence
twin studies suggest genetics account for 50% of risk
children of alcohol dependent ppl adopted and raised by ppl not alcohol dependent remained at increased risk
theories include polymorphisms in GABA, D4, 5HT, ADH
Describe the transtheoretical model.
- precontemplation: no recognition/interest in change
- contemplation: thinking about changing
- preparation: planning for change
- action: adopting new habits
- maintenance: ongoing practice of new, healthier behavior
the patient must examine pros and cons and come to a decision themselves
What are the goals of therapy for AUD?
abstinence
prolong survival
decrease morbidity and SAEs
minimize ADRs
improve daily functioning and QoL
Which populations is AUD most common in?
males
middle aged (30-64)
early onset of drinking < 21y
single
lower income
white or Indigenous
military combat deployment
What are some clinical markers of AUD?
medical:
-MCV > 96
-elevated GGT/ALT/AST (AST:ALT > 2:1)
-HTN, GERD, DM, pancreatitis
-chronic non-cancer pain
-alcohol on breath
mental:
-cognitive impairment
-mood/anxiety/sleep disorder
-behavioral or academic change
What are Canada’s guidelines on alcohol use?
0 drinks/wk: most benefit
2 drinks/wk: likely to avoid consequences
3-6 drinks/wk: increased cancer risk
7 drinks/wk: increased CV risk
What is the AUDIT tool?
used for patients that are challenging to engage
-score of 8 or more is considered to indicate hazardous or harmful alcohol use
What are the 4 C’s of addiction?
control (loss of)
craving
compulsions
consequences
Who are the candidates for AUD pharmacotherapy?
any patient with mod-severe AUD
any patient who has undergone withdrawal management, stopped, or reduced drinking and has ongoing alcohol cravings placing them at risk of relapse
What are the goals of AUD pharmacotherapy?
prevent return to any drinking or return to heavy drinking
reduce # of heavy drinking days
reduce # of drinks per drinking day
What are the 1st line agents for AUD?
naltrexone
acamprosate
What is the MOA of naltrexone?
mu-opioid antagonist
-blocks euphoric effects to alcohol to decrease rewarding alcohol effects & reduces cravings
-prevents lapse from becoming a relapse
How is naltrexone started?
titrate slowly due to GI AE
What should naltrexone be avoided with?
concurrent opioids
What is a monitoring parameter for naltrexone?
LFTs at baseline, 1, 3, and 6 months
What is the MOA of acamprosate?
not fully understood
-thought to restore imbalance between glutamate and GABA to reduce neuronal hyperexcitability
-prevent lapse: more effective at supporting abstinence
When should acamprosate be avoided?
CrCl < 30 ml/min
-adjust if 30-50 ml/min
What is the efficacy of acamprosate and naltrexone?
safe and effective for AUD
-NNT 12-20 for return to any drinking
Describe the role of topiramate and gabapentin for AUD.
topiramate:
-decreases cravings by reducing DA release from EtOH
-BRAIN FOG!!
gabapentin:
-reduces unpleasant withdrawal symptoms
What is the MOA of disulfiram?
inhibits aldehyde dehydrogenase to block metabolism of alcohol
-results in unpleasant AE when patient drinks alcohol
Is disulfiram commercially available?
no it has to be compounded
What is the role of disulfiram in AUD?
due to severity of disulfiram rxn and weak evidence of benefit it should not be recommended for tx
-specific circumstances +/- highly motivated patients
What is a precaution of disulfiram?
do not start until abstained from EtOH x 12 hrs minimum
