Substance use disorder Flashcards

1
Q

SUDs DSM -5 mild

A

2-3 criteria

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2
Q

SUDs DSM -5 moderate

A

4-5 criteria

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3
Q

SUDs DSM -5 severe

A

6+ criteria

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4
Q

Risk Factors for SUD

A

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

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5
Q

SUD subtypes

A

Alcohol
Opioid

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6
Q

SUD subtypes

A

Alcohol
Opioid

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7
Q

Etiology

A

Dose-dependent central nervous system (CNS) depression

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8
Q

Neurotransmitters affected

A

GABA (inhibitory)
Glutamate (excitatory)
Dopamine (reward)

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9
Q

Alcohol-induced euphoria is enhanced by the dopamine reward system

A

Reinforces more use

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10
Q

GABA and glutamate affected by alcohol consumption

A

play a role in withdrawal symptoms

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11
Q

Alcohol Pharmacokinetics Mechanism

A

GABA agonist

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12
Q

Standard drinking size

A

12 fl oz beer = 8-9 fl oz malt liquor = 5 fl oz wein = 1.5 fl oz shot

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13
Q

Alcohol absorption

A

Starts within 10 min
peak effects 30-90 minutes after last drink

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14
Q

alcohol distribution

A

Freely throughout the body
Rapidly crosses blood-brain barrier

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15
Q

alcohol metabolism

A

Mostly by the liver (90%) via alcohol dehydrogenase
Remainder is eliminated via lungs, urine, and sweat

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16
Q

Acute Effects of Alcohol Use

A

impaired balance, speech, vision, reaction time, hearing,
Euphoria
mental confusion,

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17
Q

Chronic effects of alcohol use

A

CNS problems
CV problems
GI problems

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18
Q

CNS problems

A

Memory impairment
Seizures (w/d)
Periph. neuropathy
Ataxia
Insomnia
Wernicke syndrome

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19
Q

CV problems

A

Palpitations
Cardiomyopathy
Hypertension
Anemia (increase MCV)

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20
Q

GI problems

A

Dyspepsia
N/V/D
Pancreatitis
GIB
Liver disease

21
Q

Wernicke-Korsakoff Syndrome

A

Caused by thiamine deficiency –> leads to eventual cell death –> causes eventual injury to brainstem

22
Q

Korsakoff psychosis

A

later manifestation of Wernicke’s

23
Q

Treatment for Wernicke-Korsakoff

A

banana bag
Thiamine + folate + MVI

24
Q

prophylaxis Wernicke-Korsakoff

A

Thiamine 100-500 mg daily IV/IM x3-5 days, then oral

25
Q

Treatment Wernicke-Korsakoff dose

A

Thiamine 100-500 mg IV/IM TID x 5+days, then oral

26
Q

Goals of treatment

A

Prevent/treat withdrawal
Achieve abstinence or reduce heavy drinking
Maintain abstinence with continued treatment

27
Q

Non-Pharm Treatment

A

CBT
motivational enhancement therap
community reinforcement
cue exposure and relation training
group therapy, family therapy
self help
12 step program

28
Q

Maintenance medications

A

Disulfiram
Oral Naltrexone
injectable naltrexone
Acamprosate

29
Q

Disulfiram MOA

A

block acetaldehyde dehydrogenase
Causes acetaldehyde build up

30
Q

Disulfiram reaction classic symptoms

A

Flushing
Throbbing in head/neck
Respiratory difficulty/dyspnea/hyperventilation
N/V
Diaphoresis
Thirst
Chest pain
Palpitations, tachycardia, hypotension
Syncope
Weakness
Vertigo
Blurred Vision
Confusion

31
Q

Disulfiram reaction severe

A

Respiratory depression
Cardiovascular collapse
Arrhythmias
Myocardial infarction
Acute CHF
Unconsciousness
Seizures
Death

32
Q

Disulfiram when to take

A

wait 12 hrs after last drink to start

33
Q

Disulfiram efficiacy

A

reduction in alcohol consumption
not as much on cravings

34
Q

Disulfiram ADE

A

Dermatitis, garlic-like or metallic aftertaste, hepatitis, optic neuritis, peripheral neuropathy, psychosis, HA, fatigue, drowsiness

35
Q

Disulfiram DDI

A

Disulfiram metabolite inhibits CYP3A4
Metronidazole & EtOH-containing products (e.g. cough syrup, mouthwash, hand sanitizer)  disulfiram-like rxn

36
Q

Disulfiram counseling

A

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

37
Q

Disulfiram considerations

A

RCTs have not shown disulfiram advantage over placebo in achieving total abstinence, delaying relapse, or improving employment status or social stability

38
Q

Naltrezone MOA

A

block activation of opioid receptors

39
Q

Naltrexone efficacy

A

EtOH consumption/craving, non-pharmacologic treatment adherence

40
Q

Naltrexone ADEs

A

N/V, HA, anxiety, insomnia, fatigue, increased ALTs, syncope, opioid-withdrawal type syndrome (rare unless opioid-dependent), injection site reactions (naltrexone IM)

41
Q

Naltrexone DDI

A

Opioids may precipitate withdrawal in opioid-dependent patients

42
Q

Naltrexone counseling

A

NO opioids in past 7-10 days! Review potential AEs; ensure pt understands traditional pain meds won’t work in emergency

43
Q

Naltrexone considerations

A

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

44
Q

Acamprosate MOA

A

Seems to increase GABA activity & decrease glutamate

45
Q

Acamprosate dose adjustments

A

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

46
Q

Acamprosate efficacy

A

alcohol consumption/cravings, non-pharmacologic treatment adherence

47
Q

Acamprosate ADE

A

Diarrhea (10-17%), nausea, depression, anxiety

48
Q

Acamprosate Considerations

A

Best at helping maintain abstinence
4 – 8 weeks until efficacy onset
Theoretically acamprosate + naltrexone may increase abstinence (conflicting evidence)
High likelihood of non-adherence