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Mind, Brain, and Behavior > Substance Use Disorders > Flashcards

Substance Use Disorders Flashcards

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1
Q

Dopamine reward pathway

A

Dopamine pathways that form part of the central nervous system (CNS) “reward system” have been identified in the ventral tegmental region of the forebrain and in the nucleus accumbens

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2
Q

All drugs of abuse appear to target the brain’s reward system by ___

A

All drugs of abuse appear to target the brain’s reward system by flooding the circuit with dopamine

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3
Q

Substances that do not ____ are rarely misused.

A

Substances that do not provide some form of pleasure or relief are rarely misused.

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4
Q

Symptoms and BAC in individuals without alcohol tolerance

A
  • 0–100 mg/dL: A sense of well-being, sedation, tranquility
  • 100–150 mg/dL: Incoordination, irritability
  • 150–250 mg/dL: Slurred speech, ataxia
  • >250 mg/dL: Passing out, unconsciousness
  • Higher concentrations—greater than 350 mg/dL—can lead to coma and death
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5
Q

The presence of few symptoms of alcohol intoxication in an individual with a BAC > ____ is indicative of a likely alcohol use disorder.

A

The presence of few symptoms of alcohol intoxication in an individual with a BAC > 150 is indicative of a likely alcohol use disorder.

This is an empirical demonstration that this individual has tolerance to alcohol, which is most often acquired from regular use of high doses.

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6
Q

In many jurisdictions, a motor vehicle operator is considered legally under the influence at a blood alcohol concentration of ___

A

In many jurisdictions, a motor vehicle operator is considered legally under the influence at a blood alcohol concentration of 0.08 g per 100 mL, equivalent to 80 mg/dL

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7
Q

Metabolic changes in individuals with alcohol use disorder

A
  • Elevated LDH
  • Decreased BUN (diuretic effect)
  • Decreased red cell volume with increased MCV
  • Increased uric acid
  • On liver tests:
    • Increased GGT
    • Increased AST/ALT, with AST/ALT ratio > 1 (often >2)
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8
Q

Clinical manfiestations of chronic alcohol use disorder detectable on physical exam

A
  • Acne rosacea (on an adult, not unusual on adolescent)
  • Palmar erythema
  • Painless hepatomegaly (alcoholic fatty liver disease)
  • Unexplained bruises
  • Jaundice, ascites, gynecomastia (liver failure signs)
  • Dupuytren’s contractures (very advanced AUD)
  • Testicular atrophy (males)
  • Hx Respiratory (or other) infection, periods of amnesia, or unexplained falls at home, concerns about driving skill or arrest/accident related to driving
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9
Q

What is going on in this individual’s hand?

A

Dupuytren’s contractures

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10
Q

PNS damage in alcohol use disorder

A
  • Peripheral neuropathy occurs in stocking-and-glove distribution
  • Probably the result of alcohol-induced B vitamin deficiencies
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11
Q

Cerebellar damage in alcohol use disorder

A

Common cause of dysarthria, ataxia, and instability in chronic alcohol use

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12
Q

Wernicke’s encephalopathy

A
  • The syndrome of thiamine deficiency
    • May be caused by chronic alcohol use
  • Syndrome of nystagmus, ataxia, and mental confusion that may be reversible by supplementation of thiamine
  • Wernicke-Korsakoff syndrome is when cognitive and memory impairment persists even after thiamine supplementation. These patients oftel also present with anterograde amnesia and confabulation.
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13
Q

Imaging findings of chronic alcohol use

A
  • Necrotic lesions in mamillary bodies, thalamus, other brainstem lesions
  • Enlarged cerebral ventricles and widened cortical sulci
    • This appears to be partially reversible when the individual abstains from drinking
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14
Q

Uncomplicated alcohol withdrawal

A
  • Begins 12-18 hrs post-cessation
  • Peaks at 24-48 hrs, takes ~1 week to subside
  • Minor symptoms include anxiety, tremors, and nausea and vomiting; heart rate and blood pressure may be increased.
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15
Q

Alcoholic withdrawal seizure

A
  • May occur 7-38 hours post-cessation
  • Peak risk is 24-48 hours
  • The patient may have a single burst of one to six generalized seizures; status epilepticus is rare.
  • Withdrawal seizures occur primarily as a consequence of severe, long-term alcohol misuse.
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16
Q

Alcoholic hallucinosis

A
  • Begin within ~48 hrs post-cessation
  • Occur in the presence of a clear sensorium
  • Vivid and unpleasant auditory, visual, or tactile hallucinations
  • The hallucinations typically last about 1 week but can become chronic. Like withdrawal seizures, they are a sign of severe alcohol misus
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17
Q

Alcohol withdrawal delirium

A
  • 5% of individuals hospitalized with AUD
    • 1/3 of those with withdrawal seizures
  • Symptoms include confusion, agitation, perceptual disturbance, mild fever, and autonomic hyperarousal
  • 2-3 days post-cessation, or 4-5 days after a decrease in consumption rate
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18
Q

When interviewing a patient with a diagnosis of AUD, you should always ask. . .

A

. . . what symptoms they have when they are intoxicated and in withdrawal

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19
Q

Management of alcohol withdrawal

A
  • general support (i.e., adequate food and hydration, careful medical monitoring, electrolytes)
  • nutritional supplementation (oral thiamine, folic acid, multivitamin, some may be administered intramuscularly if oral intake not feasible)
  • Use of benzodiazepines
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20
Q

Best pharmacologic treatment for symptoms of alcohol withdrawal

A

Chlordiazepoxide

A benzodiazepine especially good for this use. Benzos are cross-tolerant with alcohol, and are one of the only other depressants that can be used for this indication.

Intermediate- or short-acting benzodiazepines (e.g., lorazepam, oxazepam) are generally preferred in patients with liver damage or in elderly patients because these benzodiazepines lack metabolites and are renally excreted

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21
Q

Drugs approved for treating chronic alcohol use disorder (not acute toxicosis/withdrawal)

A
  • Disulfiram: Inhibits aldehyde dehydrogenase, an enzyme necessary for the metabolism of alcohol. Inhibiting this enzyme leads to the accumulation of acetaldehyde when alcohol is consumed. Acetaldehyde is toxic and induces noxious symptoms, such as nausea, vomiting, palpitations, and hypotension. Disulfiram should be prescribed only after careful consideration and with the full cooperation of the patient.
  • Naltrexone: μ-opioid antagonist that appears to reduce the pleasurable effects of alcohol. The drug is generally well tolerated but can produce nausea, headache, anxiety, or sedation. Unfortunately, it cannot be given to patients with severe liver disease.
  • Acamprosate: Glutamate receptor modulator, also reduces craving. Acamprosate is generally well tolerated, although some patients report headache, diarrhea, flatulence, and nausea. Needs to be taken 3x/day.
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22
Q

___ is first-line for psychotic symptoms of alcoholic hallucinosis

A

Haloperidol or second generation antipsychotic is first-line for psychotic symptoms of alcoholic hallucinosis

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23
Q

Physical signs that may accompany opioid intoxication

A
  • Flushing
  • Pupillary constriction (miosis)
  • Slurred speech
  • Respiratory depression
  • Hypotension
  • Hypothermia
  • Bradycardia
  • Constipation
  • Nausea/vomiting
24
Q

Opioid withdrawal syndrome

A
  • May begin 10 hours post-cessation for short acting opioids, or longer for longer for longer-acting
  • Minor symptoms include lacrimation, rhinorrhea, sweating, yawning, piloerection, hypertension, and tachycardia
  • More serious symptoms include hot and cold flashes, muscle and joint pain, nausea, vomiting, and abdominal cramps
  • Psychological symptoms include severe anxiety and restlessness, irritability, insomnia, and decreased appetite.
25
Q

Approved pharmacologic agents for opioid use disorder

A
  • Methadone
  • Buprenorphine
26
Q

“Phases” of clinical management of substance use disorders

A
  1. Detoxification
  2. Rehabilitation
27
Q

DSM-V diagnostic criteria for SUD

A
  • Of the following 11 symptoms (2-3 mild, 4-5 moderate, 6 or more severe):
    • Symptoms of impaired control
      • Use more than intended
      • Wish to decrease use
      • Time consuming
      • Craving
    • Symptoms of social impairment
      • Major role obligations not fulfilled
      • Continued use despite social/interpersonal problems
      • Social/occupational activities reduced or given up
    • Symptoms of risky use
      • Continued use in physically hazardous situations
      • Continued use despite physical or psychological problems caused or worsened by use
    • Pharmacologic criteria
      • Evidence of drug tolerance
      • Evidence of withdrawal symptoms
        • Exception: not those that occur as part of medical therapy
28
Q

Prevalence of SUD in US

A

~7% of population

29
Q

Four C’s of addiction

A
  • Compulsive use
  • Loss of Control
  • Craving
  • Consequences
30
Q

“At risk” drinking

A
31
Q

A patient with alcoholic hallucinosis is often not ___.

A

A patient with alcoholic hallucinosis is often not delirious.

Alcoholic hallucinosis and delerium tremens are separate. They can co-occur, but they do not by any means go together.

32
Q

Caine criteria

A
  • Criteria for assessing clinical suspicion of thiamine deficiency
    • Not just for alcohol, but other etiologies of nutritional deficiency as well
  1. Cerebellar signs
  2. Mild memory impairment or confusion
  3. Signs of poor nutrition
  4. Occular signs (cranial nerve 6 specifically)
33
Q

Assessing thiamine level

A
  • Very difficult to accurately gauge what the CSF level of thiamine is
    • Blood values do not necessarily reflect this
    • So, if we suspect someone may be thiamine deficient, we will usually just give them a thiamine bolus to be safe. If they aren’t actually deficient, this won’t do any harm.
34
Q

SUD pharmacology summary table

A
35
Q

The Iron Law of Prohibition

A

If a substances is outlawed, those who continue to produce and distribute it illicitly will produce more and higher purity substances as they are not taking on any additional risk by doing so for a greater financial benefit.

36
Q

No study has ever shown that ___ is an effective strategy for opioid use disorder.

A

No study has ever shown that detoxification programing is an effective strategy for opioid use disorder.

Buprenorphine and methadone are far, far, far, far, FAR superior in outcomes. Not offering these is not offering these patients the appropriate, evidence-based medical treatment.

37
Q

Despite being approved for treatment of OUD, ___ is not actually effective in practice due to ___.

A

Despite being approved for treatment of OUD, oral naltrexone is not actually effective in practice due to poor adherance.

Ideally, this drug should only be utilized as a long-acting, once/month injection.

38
Q

RCTs comparing and contrasting psychosocial treatment vs pharmacotherapy vs combination for OUD have shown. . .

A

. . . psychosocial therapy is useless, it doesn’t even lead to better outcomes when in combination. All that matters is the treatment drug for this particular disorder.

39
Q

Neurochemical hypothesis for why adolescents are at greater risk for substance use disorders

A

During adolescence, due to the faster development of limbic regions relative to regulatory prefrontal cortices, the striatal reward/motivation and limbic-emotional circuits are hyperactive, leading to greater emotional reactivity and reward-seeking behaviors

Additionally, early exposure to neuroactive substances may impair prefrontal cortex development, exacerbating the problem.

40
Q

During the craving stage, the conditioned stimuli (drug cues) themselves . . .

A

During the craving stage, the conditioned stimuli (drug cues) themselves elicit dopamine release in the striatum, triggering the motivation to seek and consume the drug

41
Q

Neurobiological changes caused by ACEs

A

ACEs can result in delayed prefrontal limbic connectivity, which is associated with behavioral impulsivity. This is one biological mechanism by which ACEs predispose to substance use and other psychiatric conditions.

Importantly, this is still amenable to intervention in early childhood, decreasing likelihood of psychiatric disease later in life.

42
Q

Neurobiological changes caused by social isolation

A

Social isolation and exposure to social environments with limited support are associated with reduced dopamine D2 receptor expression in the striatum, which is linked with greater vulnerability for impulsivity and compulsive drug use

43
Q

Biased opioid agonists

A

Biased opioid agonists that are developed as analgesics target the G-coupled protein “Gi” intracellular pathway, which is believed to underlie analgesia, while not engaging the β-arrestin pathway, which is associated with tolerance and the respiratory-depressing effects of opioid agonists

A pharmaceutical goal, but still mostly under development and testing.

44
Q

Nasal oxytocin

A

Shown to be effective ro reduce cravings and drug-seeking behavior for a large array of addictive drugs

45
Q

There are still no good pharmacologic therapies for ___ use disorders.

A

There are still no good pharmacologic therapies for stimulant use disorders.

46
Q

Drugs approved for SUD involving alcohol, opioids, and nicotine

A
  • Alcohol: Antabuse (disulfiram), Revia/Vivitrol (naltrexone), Campral (acamprosate)
  • Opioids: methadone, Suboxone(buprenorphine), Vivitrol(naltrexone)
  • Nicotine: Nicorette(nicotine), Zyban(bupropion), Chantix(varenicline)
47
Q

Summary of AUD meds

A
48
Q

Summary of OUD meds

A
49
Q

Summary of NUD meds

A
50
Q

Korsakoff syndrome vs Wernicke’s encephalopathy

A
  • Wernicke: Caused by acute thiamine deficiency. Characterized by confusion, ophthalmoplegia, and cerebellar ataxia. Amenable to thiamine supplement.
  • Korsakoff: Caused by chronic thiamine deficiency. Characterized by anterograde and/or retrograde amnesia with confabulation. Not amenable to thiamine supplement, permanent deficit.
  • Wernicke-Korsakoff: When the two syndromes occur together.
51
Q

Alcohol use may induce psychiatric symptoms like. . .

A

. . . depression and panic attacks (both specifically after drinking as BAL is falling)

52
Q

CIWA

A

The CIWA-Ar for alcohol withdrawal is an evaluation tool (consisting of 10 questions) designed by Sullivan et al. in 1989, as a mean of assessing the severity of acute alcohol withdrawal symptoms. This is one of the evaluations used before detoxification protocol is started.

53
Q

COWS

A

Clinical opiate withdrawal scale

54
Q

Wernicke’s is amenable to __, but Korsakoff is not.

A

Wernicke’s is amenable to thiamine supplementation, but Korsakoff is not.

Korsakoff is the manifestation of permanent damage to the mamillary body from repeated episodes of Wernicke’s.

55
Q

Alcohol-induced seizures occur ___. Alcohol-induced delirium tremens occurs ___.

A

Alcohol-induced seizures occur within the first ~48 hours post cessaiton. Alcohol-induced delirium tremens occurs ~72 hours post cessation.

56
Q

Patient is arrested following driving incident and found to have BAL over 0.27%, was brought to the ER. On post-OP day 3, the patient’s nurse notices that she is disoriented, believing she’s on a naval ship and seeing an “army of children” around her. She pulls out her Foley catheter and starts trying to get out of bed.

Vital signs are: T 98.0, HR 124, RR 12, BP 150/90, 02 sat 98%. Her skin is sweaty. On cranial nerve exam, she doesn’t track your finger with her eyes either to the left or the right.

What is the differential and appropriate treatment?

A
  • Differential:
    • Wernicke’s encephalopathy (eye movement abnorm)
    • Delirium tremens w/ alcohol induced hallocinosis
    • Alcohol-induced seizure
  • Plan:
    • Fluids, folate, thiamine, multivitamin
    • CIWA exam
    • Benzodiazepine (chlordiazepoxide)
    • Haloperidol
    • EEG

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