Substance Abuse Disorders - Cooley Flashcards

1
Q

a primary, chronic disease of brain reward, motivation, memory and related circuitry

  • seeking pain relief, seeking drugs for euphoric effects
  • pathologically pursuing reward and/or relief by substance use and other behaviors
A

addiction

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2
Q

result of DA-system malfunction

  • malfunction is complicit in vulnerability to addiction
  • helps us understand the compulsive use that characterizes addiction vs physical dependency
A

reward deficiency syndrome

  • most well-known evidence that supports an addiction syndrome
  • the neurobiological circuitry of the central nervous system is the ultimate common pathway for addictive behaviors
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3
Q

what do genetic studies show regarding reward deficiency syndrome?

A

common molecular mechanisms for drug addiction and compulsive running behavior

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4
Q

strictly conceptual model used for risk assessment and treatment planning

genetic hx of:

  • addictive disorders
  • intractable mood disorders
  • personality disorder or habitual criminal behavior

personal/family hx of:

  • polysubstance use
  • trauma
  • chronic psychosocial stressors starting at young age
A

addictophrenia spectrum

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5
Q

what are common comorbidities seen with substance abuse?

A
  • antisocial PD
  • depression
  • suicide
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6
Q
  • using larger amounts of substances, or for longer time than intended
  • persistent desire or unsuccessful attempts to cut down/control use
  • great deal of time obtaining, using, or recovering
  • craving
  • fail to fulfil major roles (work, school, home)
  • persistent social or interpersonal problems caused by substance use
  • important social, occupational, recreational activities given up/reduced
  • use in physical or psychological problems caused by use
  • tolerance
  • withdrawal
A

substance use disorder KNOW this

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7
Q

what is considered mild substance use disorder?

A

2-3 symptoms

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8
Q

what is considered moderate substance use disorder?

A

4-5 symptoms

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9
Q

what is considered severe substance use disorder?

A

6+ symptoms

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10
Q

what is considered early remission for substance use disorder?

A

no criteria (except craving) for >3 months but <12 months

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11
Q

what is considered sustained remission for substance use disorder?

A

no criteria (except craving) for >12 months

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12
Q

the disorder represents a clinically significant symptomatic presentation of a relevant mental disorder

there is evidence from the hx, PE, or lab findings of both of the following:

  1. the disorder developed during or within 1 month of a substance intoxication or withdrawal or taking a medication
  2. the involved substance/medication is capable of producing the mental disorder
A

substance-induced mental disorder

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13
Q

the disorder is not better explained by an independent mental disorder

  • the disorder preceded the onset of severe intoxication/withdrawal or exposure to the medication
  • the full mental disorder persisted for a substantial period of time after the cessation of acute withdrawal or severe intoxication

the disorder does not occur exclusively during the course of a delirium
the disorder causes clinically significant distress or impairment in social, occupational, or other important areas of functioning

A

substance-induced mental disorders

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14
Q

reversible substance-specific syndrome d/t recent ingestion of a substance

  • behavioral/psychological changes d/t effects on CNS after ingestion
  • not d/t another medical condition/mental disorder
  • does not apply to tobacco
A

intoxication

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15
Q

substance-specific syndrome problematic behavioral change d/t stopping or reducing prolonged use

  • physiological and cognitive components
  • significant distress in social, occupational or other important areas of functioning
  • not d/t another medical condition or mental disorder
A

withdrawal

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16
Q

refers to underlying CNS changes that occur following repeated use such that person develops tolerance and/or withdrawal

A

neuroadaptation

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17
Q

what is pharmacokinetic neuroadaptation?

A

adaptation of metabolizing system

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18
Q

what is pharmacodynamic neuroadaptation?

A

ability of CNS to function despite high blood levels

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19
Q

need to use an increased amount of a substance in order to achieve the desired effect
OR
markedly diminished effect with continued use of the same amount of the substance

A

tolerance

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20
Q

what treatment option for substance abuse did Cooley stress?

A

motivational interviewing in the primary care setting

  • twelve step facilitation (AA, NA, etc)
  • also treat co-occurring psychiatric disorders (50% will have another psychiatric disorder)
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21
Q

what is the legal intoxication level of alcohol?

A

blood alcohol 0.08 g/dL

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22
Q

what are the signs of early alcohol withdrawal?

A

anxiety, irritability, tremor, HA, insomnia, nausea, tachycardia, HTN, hyperthermia, hyperactive reflexes
- seizures (generally seen 24-48 hours)

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23
Q

what is withdrawal delirium?

A

altered mental status, hallucinations, marked autonomic instability

  • life threatening
  • generally seen between 48-72 hours
24
Q

the most severe manifestation of alcohol withdrawal, occurs 3-10 days following the last drink
- agitation, profound global confusion, disorientation, hallucinations, fever, HTN, diaphoresis, autonomic hyperactivity (tachycardia)

A
Delirium Tremens (DT)
- medical emergency with high mortality rate
25
Q

chronic alcohol use causes increased release of which NT?

A

GABA - the inhibitory NT, which leads to up-regulation of NMDA receptor
- during withdrawal, loss of GABA stimulation is associated with tremors, diaphoresis, tachycardia, anxiety

26
Q

what is the CIWA?

A

clinical institute withdrawal assessment for alcohol

  • assigns numerical values to orientation, N/V, tremor, sweating, anxiety, agitation, tactile/auditory/visual disturbances and HA
  • total score of >10 indicates more severe withdrawal
  • based on severity of withdrawal or hx of previous withdrawal seizures or DT’s, med therapy can be scheduled or symptom triggered
27
Q

what is the med tx for alcohol withdrawal?

A

benzo’s:

  • GABA-agonist, reduce risk of seizure
    anticonvulsants: (carbamazepine or valproic acid)
  • reduce risk of seizure, helpful for protracted withdrawal
  • *thiamine supplementation**
  • risk of thiamine deficiency (wernicke/korsakoff)
28
Q

when would Naltrexone be appropriate to give?

A

alcohol use disorder (also for eating disorders)
- is an opioid antagonist, thought to block mu receptors reducing intoxication, euphoria and cravings

NOTE: acamprosate can also be given. unknown mech but thought to stabilize neuron excitation and inhibition (may interact with GABA)

29
Q

what meds?

  • similar to alcohol but less cognitive/motor impairment
  • variable rate of absorption (lipophilia) and onset of action and duration in CNS
  • the more lipophilic and shorter the duration of action, the more addicting
A

benzo’s and barbiturates

30
Q

what is the withdrawal of benzo’s like?

A

similar to alcohol with anxiety, irritability insomnia, fatigue, HA, tremor, sweating, poor concentration

  • common detox mistake is tapering too fast, sx worse at end of taper
  • convert short elimination of benzo’s to longer elimination half life drug then taper slowly (decrease doese every 1-2 weeks)
31
Q

what is the half life of alprazolam?

A

6-20 hrs

32
Q

what is the half life of oxazepram?

A

8-12 hrs

33
Q

what is the half life of temazepam?

A

8-20 hrs

34
Q

what is the half life of clonazepam?

A

18-50 hrs

35
Q

what is the half life of lorazepam?

A

10-20 hrs

36
Q

what is the half life of chlordiazepoxide?

A

30-100 hrs

37
Q

what is the half life of diazepam?

A

30-100 hrs

38
Q

what drug class binds to the mu receptors in the CNS to modulate pain?

A

opioids

  • intoxication: pinpoint pupils, sedation, constipation, bradycardia, hypotension, decreased RR
  • withdrawal: not life threatening unless severe medical illness, but extremely uncomfortable. dilated pupils, lacrimation, goosebumps, N/V, diarrhea, arthralgia, dysphoria/agitation
39
Q

what meds can be used for opiate use disorder?

A
  • methadone (opioid substitution)
  • naltrexone
  • buprenorphine (opioid substitution)
40
Q

what medication is considered HIGH RISK

  • can be deadly when used with a benzo
  • frequently causes QTC prolongation - sometimes fatal
  • dangers increase when used with another 3A4 substrate
  • is a mu agonist, oral solution only
A

methadone

NOTE: do NOT use with benzo’s or other 3A4 substrates

41
Q

what med:

  • partial mu agonist with a ceiling effect
  • any physician can Rx after taking certified ASAM course
  • helpful for highly motivated people who do not need high doses
A

buprenorphine

42
Q

what drug class causes:

  • euphoria, enhanced vigor, gregariousness, hyperactivity, restlessness, interpersonal sensitivity, anxiety, tension, anger, impaired judgement, paranoia
  • tachycardia, papillary dilation, HTN, N/V, diaphoresis, chills, weight loss, chest pain, cardiac arrhythmias, confusion, seizures, coma, hyperthermia
A

stimulants

43
Q

affective blunting (narrowed range of emotional responses), fatigue, sadness, social withdrawal, hypotension, bradycardia, muscle weakness

A

chronic intoxication of stimulants

44
Q

which drug:

  • has vasoconstrictive effects that may outlast use and increase risk of CVA and MI
  • can get rhabdomyolisis with compartment syndrome from hypermetabolic state
  • can see psychosis associated with intoxication
A

cocaine

45
Q

cocaine mainly prevents the reuptake of which NT?

A

dopamine

46
Q

what drug type:

  • chronic use results in neurotoxicity possibly from glutamate and aonal degeneration
  • can be fatal at lower doses in setting of Brugada syndrome
  • tx similar as for cocaine but no known substances to reduce cravings
A

amphetamines

47
Q

amphetamines inhibit reuptake of which NT’s?

A

DA (mainly), NE, 5HT

48
Q

what are the main drug interactions with tobacco?

A

induces CYP1A2

- watch for interactions when starting or stopping (Olanzapine)

49
Q

nicotine interacts with which NT receptors?

A

Ach receptors on DA neurons in ventral tegmental area

- release DA in nucleus accumbens

50
Q

what meds can be given for tobacco use disorder?

A
  • bupropion (150mg bid)

- varenicline (1mg po)

51
Q

which drug:

  • tachycardia, sweating, muscle spasms, EXTREMELY HIGH FEVER
  • in severe toxicity, high fever can progress to rhabdomyolysis, renal failure, seizures, disseminated intravascular coagulopathy, cardiac arrhythmias and death
A

MDMA

52
Q

MDMA interacts with which NTs?

A

5HT (mainly), DA, NE

53
Q

what is the half life of cannabis?

A

50 hours

- lipid soluble molecule, reaches peak effectiveness 10-30min

54
Q

cannabis interacts with which receptors in brain/body?

A

CB1, CB2

  • coupled with G proteins and adenylate cyclase to Ca-channels, inhibiting Ca influx
  • decreases uptake of GABA and DA
55
Q

what drug:

  • dissociative anesthetic
  • similar to ketamine
  • severe dissociative reactions: paranoid delusions, hallucinations, can become very agitated/violent with decreased awareness of pain
  • NYSTAGMUS, ataxia, dysarthria
  • with severe overdose: mute, catatonic, muscle rigidity, HTN, hyperthermia, rhabdomyolysis, seizures, coma, death
A

phenacyclidine (PCP), aka Angel Dust

56
Q

what is the tx for PCP?

A
  • antipsychotic drugs or benzo’s
  • low stimulation environment
  • acidify urine if severe toxicity/come
57
Q

PCP interactions with which receptor type?

A
  • opioid receptors

- allosteric modulator of glutamate NMDA receptor