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CDM 4 Exam 2 > Substance use disorder > Flashcards

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
Treatment Wernicke-Korsakoff dose
Thiamine 100-500 mg IV/IM TID x 5+days, then oral
26
Goals of treatment
Prevent/treat withdrawal Achieve abstinence or reduce heavy drinking Maintain abstinence with continued treatment
27
Non-Pharm Treatment
CBT motivational enhancement therap community reinforcement cue exposure and relation training group therapy, family therapy self help 12 step program
28
Maintenance medications
Disulfiram Oral Naltrexone injectable naltrexone Acamprosate
29
Disulfiram MOA
block acetaldehyde dehydrogenase Causes acetaldehyde build up
30
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
31
Disulfiram reaction severe
Respiratory depression Cardiovascular collapse Arrhythmias Myocardial infarction Acute CHF Unconsciousness Seizures Death
32
Disulfiram when to take
wait 12 hrs after last drink to start
33
Disulfiram efficiacy
reduction in alcohol consumption not as much on cravings
34
Disulfiram ADE
Dermatitis, garlic-like or metallic aftertaste, hepatitis, optic neuritis, peripheral neuropathy, psychosis, HA, fatigue, drowsiness
35
Disulfiram DDI
Disulfiram metabolite inhibits CYP3A4 Metronidazole & EtOH-containing products (e.g. cough syrup, mouthwash, hand sanitizer)  disulfiram-like rxn
36
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
37
Disulfiram considerations
RCTs have not shown disulfiram advantage over placebo in achieving total abstinence, delaying relapse, or improving employment status or social stability
38
Naltrezone MOA
block activation of opioid receptors
39
Naltrexone efficacy
EtOH consumption/craving, non-pharmacologic treatment adherence
40
Naltrexone ADEs
N/V, HA, anxiety, insomnia, fatigue, increased ALTs, syncope, opioid-withdrawal type syndrome (rare unless opioid-dependent), injection site reactions (naltrexone IM)
41
Naltrexone DDI
Opioids may precipitate withdrawal in opioid-dependent patients
42
Naltrexone counseling
NO opioids in past 7-10 days! Review potential AEs; ensure pt understands traditional pain meds won’t work in emergency
43
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
44
Acamprosate MOA
Seems to increase GABA activity & decrease glutamate
45
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
46
Acamprosate efficacy
alcohol consumption/cravings, non-pharmacologic treatment adherence
47
Acamprosate ADE
Diarrhea (10-17%), nausea, depression, anxiety
48
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

CDM 4 Exam 2 (13 decks)

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