Substance use disorder Flashcards
SUDs DSM -5 mild
2-3 criteria
SUDs DSM -5 moderate
4-5 criteria
SUDs DSM -5 severe
6+ criteria
Risk Factors for SUD
Cultural attitudes
Onset of use at an early age
Early evidence of aggressive behavior
Intra-familial disturbances
Environment (high substance use among peers/family)
Family history of SUD
Psychiatric co-morbidities
Trauma
SUD subtypes
Alcohol
Opioid
SUD subtypes
Alcohol
Opioid
Etiology
Dose-dependent central nervous system (CNS) depression
Neurotransmitters affected
GABA (inhibitory)
Glutamate (excitatory)
Dopamine (reward)
Alcohol-induced euphoria is enhanced by the dopamine reward system
Reinforces more use
GABA and glutamate affected by alcohol consumption
play a role in withdrawal symptoms
Alcohol Pharmacokinetics Mechanism
GABA agonist
Standard drinking size
12 fl oz beer = 8-9 fl oz malt liquor = 5 fl oz wein = 1.5 fl oz shot
Alcohol absorption
Starts within 10 min
peak effects 30-90 minutes after last drink
alcohol distribution
Freely throughout the body
Rapidly crosses blood-brain barrier
alcohol metabolism
Mostly by the liver (90%) via alcohol dehydrogenase
Remainder is eliminated via lungs, urine, and sweat
Acute Effects of Alcohol Use
impaired balance, speech, vision, reaction time, hearing,
Euphoria
mental confusion,
Chronic effects of alcohol use
CNS problems
CV problems
GI problems
CNS problems
Memory impairment
Seizures (w/d)
Periph. neuropathy
Ataxia
Insomnia
Wernicke syndrome
CV problems
Palpitations
Cardiomyopathy
Hypertension
Anemia (increase MCV)
GI problems
Dyspepsia
N/V/D
Pancreatitis
GIB
Liver disease
Wernicke-Korsakoff Syndrome
Caused by thiamine deficiency –> leads to eventual cell death –> causes eventual injury to brainstem
Korsakoff psychosis
later manifestation of Wernicke’s
Treatment for Wernicke-Korsakoff
banana bag
Thiamine + folate + MVI
prophylaxis Wernicke-Korsakoff
Thiamine 100-500 mg daily IV/IM x3-5 days, then oral
Treatment Wernicke-Korsakoff dose
Thiamine 100-500 mg IV/IM TID x 5+days, then oral
Goals of treatment
Prevent/treat withdrawal
Achieve abstinence or reduce heavy drinking
Maintain abstinence with continued treatment
Non-Pharm Treatment
CBT
motivational enhancement therap
community reinforcement
cue exposure and relation training
group therapy, family therapy
self help
12 step program
Maintenance medications
Disulfiram
Oral Naltrexone
injectable naltrexone
Acamprosate
Disulfiram MOA
block acetaldehyde dehydrogenase
Causes acetaldehyde build up
Disulfiram reaction classic symptoms
Flushing
Throbbing in head/neck
Respiratory difficulty/dyspnea/hyperventilation
N/V
Diaphoresis
Thirst
Chest pain
Palpitations, tachycardia, hypotension
Syncope
Weakness
Vertigo
Blurred Vision
Confusion
Disulfiram reaction severe
Respiratory depression
Cardiovascular collapse
Arrhythmias
Myocardial infarction
Acute CHF
Unconsciousness
Seizures
Death
Disulfiram when to take
wait 12 hrs after last drink to start
Disulfiram efficiacy
reduction in alcohol consumption
not as much on cravings
Disulfiram ADE
Dermatitis, garlic-like or metallic aftertaste, hepatitis, optic neuritis, peripheral neuropathy, psychosis, HA, fatigue, drowsiness
Disulfiram DDI
Disulfiram metabolite inhibits CYP3A4
Metronidazole & EtOH-containing products (e.g. cough syrup, mouthwash, hand sanitizer) disulfiram-like rxn
Disulfiram counseling
Can take up to 14 days for liver enzymes to return to baseline after stopping Avoid metronidazole & all EtOH-containing products during this time period
Disulfiram considerations
RCTs have not shown disulfiram advantage over placebo in achieving total abstinence, delaying relapse, or improving employment status or social stability
Naltrezone MOA
block activation of opioid receptors
Naltrexone efficacy
EtOH consumption/craving, non-pharmacologic treatment adherence
Naltrexone ADEs
N/V, HA, anxiety, insomnia, fatigue, increased ALTs, syncope, opioid-withdrawal type syndrome (rare unless opioid-dependent), injection site reactions (naltrexone IM)
Naltrexone DDI
Opioids may precipitate withdrawal in opioid-dependent patients
Naltrexone counseling
NO opioids in past 7-10 days! Review potential AEs; ensure pt understands traditional pain meds won’t work in emergency
Naltrexone considerations
Role in treatment – anti-craving
Effective for achieving & maintaining abstinence
Effective for reducing quantity consumed
REMS program for IM formulation
IM injection useful for patients with concerning med adherence
Acamprosate MOA
Seems to increase GABA activity & decrease glutamate
Acamprosate dose adjustments
Dose adjustments: consider lower dose (333mg PO TID) in patients with renal impairment (CrCl 30-50mL/min, avoid if CrCl <30mL/min), body weight less than 60 kg, or a history of response to a lower dose
Acamprosate efficacy
alcohol consumption/cravings, non-pharmacologic treatment adherence
Acamprosate ADE
Diarrhea (10-17%), nausea, depression, anxiety
Acamprosate Considerations
Best at helping maintain abstinence
4 – 8 weeks until efficacy onset
Theoretically acamprosate + naltrexone may increase abstinence (conflicting evidence)
High likelihood of non-adherence
