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Psychiatry > Substance Related Disorders > Flashcards

Substance Related Disorders Flashcards

1
Q

What is the DSM-IV criteria for substance abuse?

A

Abuse is a pattern of substance use leading to impairment or distress for at least 1 year w/ one or more of the following manifestations:

  • Failure to fulfill obligations at work, school or home
  • Use in dangerous situations (driving a car)
  • Recurrent substance-related legal problems
  • Continued use despite social or interpersonal problems due to the substance use
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2
Q

What is the DSM-IV criteria for substance dependence?

A

Dependence is a substance us leading to impairment or distress manifested by at least 3 of the following w/i a 12 mo period:

  • Tolerance
  • Withdrawal
  • Using substance more than originally intended
  • Persistent desire or unsuccessful efforts to cut down on use
  • Significant time spent on getting, using or recovering from substance
  • Decreased social, occupational or recreational activities because of substance use
  • Continued use despite subsequent physical or psychological problem (ex: drinking despite worsening liver problems)
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3
Q

A diagnosis of substance ________ supercedes a diagnosis of ________.

A

dependence, abuse

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4
Q

Substance dependence

  • Lifetime prevalence
  • Men vs. Women
  • Most commonly used substances
  • What symptoms are most common
A
  • Lifetime prevalence: 17%
  • Men >> Women
  • Caffeine, alcohol, nicotine
  • Depressive symptoms
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5
Q

What is the definition of withdrawal?

A

The development of a substance-specific symptom due to the cessation of substance use that has been heavy and prolonged

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6
Q

What is the definition of tolerance?

A

The need for increased amounts of the substance to achieve the desired effect or diminished effect if using the same amt of the substance.

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7
Q

______ is the most common co-ingestant in drug overdoses

A

Alcohol

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8
Q

____% of Americans are alcoholics

A

7-10%

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9
Q

Alcohol…

  • ______ GABA receptors
  • ______ serotonin receptors
  • ______ glutamate receptors
A
  • activates GABA receptors
  • activates serotonin receptors
  • inhibits glutamate receptors
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10
Q

How is alcohol metabolized?

A
  • Alcohol –> acetaldehyde
    • via alcohol dehydrogenase
  • Acetaldehyde –> acetic acid
    • via aldehyde dehydrogenase
  • Upregulation of enzymes in heavy drinkers
  • Asian people have less aldehyde DH
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11
Q

How do you screen for alcohol abuse?

A

CAGE questionnaire - 2 or more “yes” are positive; 1 “yes” should arouse suspicion of abuse

  • Have you ever wanted to cut down on your drinking?
  • Have you ever felt annoyed by criticism of your drinking?
  • Have you ever felt guilty about drinking?
  • Have you ever taken a drink as an “eye opener” (to prevent shakes)?
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12
Q

The absorption & elimination rates of alcohol depend on what factors?

A
  • Age
  • Sex
  • Body weight
  • Speed of consumption
  • Presence of food in the stomach
  • Chronic alcoholism
  • Presence of advanced cirrhosis
  • State of nutrition
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13
Q

In most states, the legal limit for alcohol intoxication is _____ mg/dL.

More than 50% of adults with BAL > ____ mg/dL show obvious signs of intoxication.

A

80-100 mg/dL

150 mg/dL

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14
Q

What is the novice drinker’s BAL for each of these clinical presentations?

  • Decreased fine motor control
  • Impaired judgment & coordination
  • Ataxic gait & poor balance
  • Lethargy; difficulty sitting upright
  • Coma in the novice drinker
  • Respiratory depression
A
  • Decreased fine motor control
    • 20-50 mg/dL
  • Impaired judgment & coordination
    • 50-100 mg/dL
  • Ataxic gait & poor balance
    • 100-150 mg/dL
  • Lethargy; difficulty sitting upright
    • 150-250 mg/dL
  • Coma in the novice drinker
    • 300 mg/dL
  • Respiratory depression
    • 400 mg/dL
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15
Q

What is the differential diagnosis for alcohol intoxication?

A
  • Hypoglycemia
  • Hypoxia
  • Mixed EtOH-drug overdose
  • Ethylene glycol or methanol poisoning
  • Hepatic encephalopathy
  • Psychosis
  • Psychomotor seizures
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16
Q

What is the diagnostic evaluation for alcohol intoxication?

A
  • Serum EtOH level
  • Expired air breathalyzer
  • CT scan of the head
    • Rule out subdural hematoma or other brain injury
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17
Q

How is acute alcohol intoxication treated?

A
  • Ensure adequate airway, breathing, circulation; monitor electrolytes & acid-base status
  • Obtain finger-stick glucose level to exclude hypoglycemia
  • Thiamine (prevent/treat Wernicke’s encephalopathy), naloxone (reverse opioid effects if ingested), folate administered
  • GI evacuation (gastric lavage, charcoal) no role in treatment of EtOH overdose (mixed drug-EtOH)
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18
Q

How is long-term alcohol dependence treated?

A
  • Alcoholics Anonymous - self-help group
  • Disulfiram (Antabuse) - aversive therapy; inhibits aldehyde dehydrogenase, causing violent retching when person drinks
  • Psychotherapy & SSRIs
  • Naltrexone - opioid antagonist; reduces cravings for EtOH
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19
Q

The earliest symptoms of EtOH withdrawal being btwn ___ & ___ hrs after the pts last drink and depend on the _______ & _______ of EtOH consumption.

A

6-24 hrs

duration, quantity

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20
Q

Clinical presentation: mild vs. severe alcohol withdrawal

A
  • Mild
    • Irritability, insomnia
  • Severe
    • Fever, disorientation, seizures, hallucinations, delirium
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21
Q

What are the signs/symptoms of alcohol withdrawal syndrome?

A
  • Insomnia
  • Anxiety
  • Tremor
  • Irritability
  • Anorexia
  • Tachycardia
  • Hyperreflexia
  • Hypertension
  • Fever
  • Seizures
  • Hallucinations
  • Delirium
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22
Q

What is delirium tremens?

How many pts experience it?

What are the symptoms?

A
  • Most serious form of EtOH withdrawal
  • Begins w/i 72 hrs of cessation of drinking
  • Only 5% of pts hospitalized for EtOH withdrawal
  • 15-20% mortality rate if untreated
  • Symptoms
    • Delirium
    • Visual/tactile hallucinations
    • Gross tremor
    • Autonomic instability
    • Fluctuating levels of psychomotor activity
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23
Q

How is alcohol withdrawal diagnostically evaluated?

A
  • Accurate & frequent assessment of vitals
    • Autonomic instability may occur
  • Careful attention to level of consciousness
  • Possibility of trauma should be investigated
  • Signs of hepatic failure may be present
    • Ascites, jaundice, caput medusae, coagulopathy
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24
Q

What is the differential diagnosis of alcohol withdrawal?

A
  • Alcohol-induced hypoglycemia
  • Acute schizophrenia
  • Drug-induced psychosis
  • Encephalitis
  • Thyrotoxicosis
  • Anticholinergic poisoning
  • Withdrawal from other sedative-hypnotic type drugs
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25
Q

How is alcohol withdrawal treated?

A
  • Tapering doses of benzodiazepines
    • chlordiazepoxide, lorazepam
  • Thiamine, folic acid, multivitamin to treat nutritional deficiencies
  • Mg sulfate for postwithdrawal seizures
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26
Q

Wernicke-Korsakoff syndrome is caused by….

A
  • Thiamine (vitamin B1) deficiency
  • Poor diet of alcoholics
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27
Q

What is Wernicke’s encephalopathy?

A
  • Acute & reversed by thiamine therapy
  • Triad
    • Ataxia
    • Confusion
    • Ocular abnormalities (nystagmus, gaze palsies)
  • May progress to Korsakoff’s syndrome if left untreated
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28
Q

What is Korsakoff’s syndrome?

A
  • Progression from Wernicke’s encephalopathy
  • Chronic, often irreversible
  • Triad
    • Impaired recent memory
    • Anterograde amnesia
    • +/- confabulation
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29
Q

What is confabulation?

A

making up answers when memory has failed

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30
Q

What is the mechanism of cocaine?

A
  • Blocks dopamine reuptake from the synaptic cleft
  • Stimulant effect
  • Dopamine plays a role in behavioral reinforcement (“reward” system of the brain)
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31
Q

What is the clinical presentation of cocaine intoxication?

A

“flight or fight” response

  • Euphoria
  • Increased/decreased BP
  • Tachycardia/bradycardia
  • Nausea
  • Dilated pupils
  • Weight loss
  • Psychomotor agitation & depression
  • Chills
  • Sweating
  • Respiratory depression
  • Seizures
  • Arrhythmias
  • Hallucinations (tactile)
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32
Q

Cocaine’s vasoconstrictive effect may result in _____ or _____.

A

Myocardial infarction

Cerebrovascular accident

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33
Q

What is the differential diagnosis of cocaine intoxication?

A
  • Amphetamine or PCP intoxication
  • Sedative withdrawal
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34
Q

What is the diagnostic evaluation for cocaine intoxication?

A
  • Urine drug screen
  • Positive for 3 days, longer in heavy users
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35
Q

How is cocaine intoxication treated?

A
  • Mild-to-moderate agitation: benzodiazepines
  • For severe agitation or psychosis: haloperidol
  • Symptomatic support
    • Control HTN, arrhythmias, etc.
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36
Q

How is cocaine dependence treated?

A
  • Psychotherapy, group therapy
  • TCAs
  • Dopamine agonists (amantadine, bromocriptine)
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37
Q

How does cocaine withdrawal present clinically?

How is it treated?

A
  • Abrupt abstinence is not life threatening but produces a dysphoric “crash”
  • Malaise, fatigue, depression, hunger, constricted pupils, vivid dreams, psychomotor agitation or retardation
  • Treatment usually supportive; let pt sleep off crash
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38
Q

What are the 3 classic amphetamines?

A
  • Dextroamphetamine (Dexedrine)
  • Methylphenidate (Ritalin)
  • Methamphetamine (Desoxyn, ice, speed, “crystal meth”, “crack”)
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39
Q

What are the 2 substituted “designer” amphetamines?

A
  • MDMA (ecstasy)
  • MDEA (eve)
40
Q

What is the mechanism of classic amphetamines?

A
  • Release dopamine from nerve endings
  • Stimulant effect
  • Used medically in treatment of narcolepsy, ADHD & depressive disorders
41
Q

What is the mechanism of designer amphetamines?

A
  • Release dopamine & serotonin from nerve endings
  • Have both stimulant & hallucinogenic properties
42
Q

Amphetamine intoxication causes symptoms similar to those of ______.

A

cocaine

43
Q

What is the differential diagnosis of amphetamine intoxication?

A
  • Cocaine or PCP intoxication
  • Chronic use in high doses may cause a psychotic state similar to schizophrenia
44
Q

What is the diagnostic evaluation for amphetamine intoxication?

A
  • UDA (positive for 1-2 days)
  • Negative routine drug screen doesn’t rule it out
    • Most assays not of adequate sensitivity
  • Negative drug screen can NEVER completely rule out substance abuse or dependence
45
Q

Treatmentof amphetamine intoxication/withdrawal of amphetamines is similar to ____.

A

cocaine

46
Q

What is the mechanism of PCP?

A
  • “angel dust”
  • Hallucinogen that antagonizes N-methyl-D-aspartate (NMDA) glutamate receptors & activate dopaminergic neurons
  • Ketamine similar to PCP (anesthetic agents)
47
Q

__________ is pathognomonic for PCP intoxication.

More than with other drugs, intoxication w/ PCP results in _______.

A

Rotary nystagmus

violence

48
Q

How does PCP intoxication present?

Overdose?

A
  • Intoxication
    • Recklessness
    • Impulsiveness
    • Impaired judgment
    • Assaultiveness
    • Rotatory nystagmus
    • Ataxia
    • HTN
    • Tachycardia
    • Muscle rigidity
    • High tolerance or pain
  • Overdose
    • Seizures, coma
49
Q

How is PCP intoxication treated?

A
  • Monitor BP, temp, electrolytes
  • Acidify urine w/ ammonium chloride & ascorbic acid
  • Benzodiazepines or dopamine antagonists to control agitation & anxiety
  • Diazepam for muscle spasms & seizures
  • Haloperidol to control severe agitation or psychotic symptoms
50
Q

What is the differential diagnosis for PCP intoxication?

A
  • Acute psychotic states
  • Schizophrenia
51
Q

What is the diagnostic evaluation for PCP intoxication?

A
  • Urine drug screen (positive for >1 wk)
  • Creatine phosphokinase (CPK) & aspartate aminotransferase (AST) are often elevated
52
Q

How does PCP withdrawal clinically present?

A
  • No withdrawal syndrome
  • “Flashbacks” may occur
53
Q

What types of sedatives/hypnotics are typically abused?

A
  • Benzodiazepines
    • Used to treat anxiety disorders
    • Obtained via prescription
    • Potentiates GABA by increasing frequency of chloride channel opening
  • Barbiturates
    • Used to treat epilepsy; anesthetic
    • Potentiates GABA by increasing duration of chloride channel opening
    • High doses: act as direct GABA agonists; lower margin of safety compared to BDZs
  • Benzos & Barbs are synergistic in their complementary effect on GABA channel opening
  • Respiratory depression can be a complication
54
Q

What is Gamma-hydroxybutyrate (GHB)?

A

“Grievous Bodily Harm”

  • Dose-specific CNS depressant that produces memory loss, respiratory distress, coma
  • Commonly used as a date-rape drug
55
Q

What is the clinical presentation of sedative-hypnotic intoxication?

Symptoms are augmented when combined with ____.

A
  • Drowsiness
  • Slurred speech
  • Incoordination
  • Ataxia
  • Mood lability
  • Impaired judgment
  • Nystagmus
  • Respiratory depression
  • Coma/death in overdose (esp barbs)
  • Symptoms augmented w/ EtOH
  • Long-term sedative use causes dependence
56
Q

What is the differential diagnosis for sedative-hypnotic intoxication?

A
  • Alcohol intoxication
  • Generalized cerebral dysfunction (ex: delirium)
57
Q

What is the diagnostic evaluation for sedative-hypnotic intoxication?

A
  • Urine or serum drug screen (positive for 1 wk)
  • Electrolytes
  • ECG
58
Q

How is sedative-hypnotic intoxication treated?

A
  • Maintain airway, breathing, circulation
  • Activated charcoal to prevent further GI absorption
  • For barbiturates only
    • Alkalinize urine w/ sodium bicarbonate to promote renal excretion
  • For benzos only
    • Flumazenil in overdose
  • Supportive care
    • Improve respiratory status, control hypotension
59
Q

What is Flumazenil?

A
  • Very short-acting BDZ antagonist
  • Use w/ caution when treating overdose, as it may precipitate seizures
60
Q

What is the clinical presentation of sedative-hypnotic withdrawal?

A
  • Autonomic hyperactivity (tachycardia, sweating)
  • Insomnia
  • Anxiety
  • Tremor
  • Nausea/vomiting
  • Delirium
  • Hallucinations
  • Seizures may occur (can be life-threatening)
61
Q

In general, withdrawal from drugs that are ________ is life threatening, while withdrawal from ______ & _______ is not.

A

sedating

stimulants, hallucinogens

62
Q

How is sedative-hypnotic withdrawal treated?

A
  • Admin of long-acting benzodiazepine (chlorodiazepoxide, diazepam) w/ tapering of the dose
  • Tegretol or valproic acid may be used for seizure control
63
Q

____________ is a common ingredient in cough syrup.

A

dextromethorphan

64
Q

Opiates

  • Examples
  • Mechanism of action
  • Endogenous vs. exogenous
A
  • Heroin, codeine, dextromethorphan, morphine, methadone, meperidine (Demerol)
  • Stimulate opiate receptors (mu, kappa, delta) which are stimulated by endogenous opiates
  • Analgesia, sedation, dependence
  • Mediates addictive & rewarding properties through effects on the dopaminergic system
  • Endogenous opiates: endorphins, enkephalins
65
Q

What is the clinical presentation of opiate intoxication?

A
  • Drowsiness
  • Nausea/vomiting
  • Constipation
  • Slurred speech
  • Constricted pupils
  • Seizures
  • Respiratory depression
  • Coma/death in overdose
66
Q

What is serotonin syndrome?

How is it caused?

A
  • Caused by combination of meperidine & monoamine oxidase inhibitors
  • Hyperthermia, confusion, hyper/hypo-tension & muscular rigidity
67
Q

What is the differential diagnosis for opiate intoxication?

A
  • Sedative-hypnotic intoxication
  • Severe EtOH intoxication
68
Q

What is the diagnostic evaluation for opiate intoxication?

A
  • Rapid recovery of consciousness following the admin of IV naloxone (opiate antagonist)
  • Urine & blood tests remain positive for 12-36 hrs
69
Q

How is opiate intoxication treated?

A

Ensure adequate airway, breathing, circulation

70
Q

How is opiate overdose treated?

A

Admin of naloxone or naltrexone (opiate antagonists)

  • Will improve respiratory depression
  • May cause severe withdrawal in an opiate-dependent patient; ventilatory support may be required
71
Q

How is opiate dependence treated?

A
  • Oral methadone once daily, tapered over months to years
  • Psychotherapy, support groups (Narcotics Anonymous, etc)
72
Q

_________ is the exception to opioids producing miosis.

A

Meperidine

“Demerol dilates pupils)

73
Q

What is the classic triad of opioid overdose?

A

“Rebels Admire Morphine”

  • Respiratory depression
  • Altered mental status
  • Miosis
74
Q

What is the clinical presentation for opiate withdrawal?

A
  • Not life threatening
  • Dysphoria
  • Insominia
  • Lacrimation
  • Rhinorrhea
  • Yawning
  • Weakness
  • Sweating
  • Piloerection
  • Nausea/vomiting
  • Fever
  • Dilated pupils
  • Muscle ache
75
Q

How is opiate withdrawal treated?

A
  • Moderate symptoms
    • Clonidine and/or buprenorphine
  • Severe symptoms
    • Detox w/ methadone tapered over 7 days
76
Q

What are some examples of hallucinogens?

What effects do they have?

A
  • Psilocybin (mushrooms), mescaline, lysergic acid diethylamide (LSD)
  • Pharmacological effects vary
  • LSD known to act on serotonergic system
  • Tolerance to hallucinogens develops quickly but reverses rapidly after cessation
  • Don’t cause physical dependence or withdrawal
77
Q

What is the clinical presentation and treatment of hallucinogen intoxication?

A
  • Perceptual changes, papillary dilation, tachycardia, tremors, incoordination, sweating, palpitations
  • Guidance & reassurance (“talking down” the patient) are usually enough
  • Severe cases: antipsychotics or benzos
78
Q

Describe hallucinogen withdrawal

A
  • No withdrawal syndrome is produced
  • Patients may experience “flashbacks” later in life (recurrence of symptoms due to reaborption from lipid stores)
79
Q

What do methyl pemolines produce?

A
  • 92C-B, U4EUH, Nexus
  • Classic psychedelic distortion of senses
  • Feeling of harmony, anxiety, paranoia, panic
80
Q

What can Ketamine produce symptomatically?

A

“special K”

  • Tachycardia, tachypnea w/ hallucinations at higher doses
  • Amnesia & numbed confusion
81
Q

What is the main component of marijuana?

What is the mechanism of action?

How is it used?

A
  • THC (tetrahydrocannabinol)
  • Cannabinoid receptors in the brain inhibit adenylate cyclase
  • Effects increased when used w/ EtOH
  • Marijuana shown to successfully treat nausea in cancer patients & increase appetite in AIDS patients
  • No dependence or withdrawal syndrome has been shown
82
Q

What are the clinical symptoms of marijuana intoxication?

A
  • Euphoria
  • Impaired coordination
  • Mild tachycardia
  • Conjunctival injection
  • Dry mouth
  • Increased appetite
83
Q

What is the treatment & diagnostic evaluation for marijuana intoxication?

A
  • Supportive & symptomatic
  • Urine drug screen is positive for up to 4 wks in heavy users (released from adipose stores)
84
Q

What is the clinical presentation & treatment of marijuana withdrawal?

A
  • No withdrawal syndrome
  • Mild irritability, insomnia, nausea, decreased appetite in heavy users
  • Treatment: supportive & symptomatic
85
Q

What are some examples of inhalants?

A
  • Solvents, glue, paint thinners, fuels, isobutyl nitreates (“rush”, “locker room”, “bolt”)
  • Inhalants generally act as CNS depressants
  • User is typically an adolescent male
86
Q

What is the clinical presentation of inhalent intoxication?

A
  • Impaired judgment, belligerence, impulsivity, perceptual disturbances, lethargy, dizziness, nystagmus, tremor, muscle weakness, hyporeflexia, ataxia, slurred speech, euphoria, stupor, coma
  • Overdose may be fatal
    • Respiratory depression
    • Arrhythmias
  • Long-term use may cause permanent damage
    • CNS, PNS, liver, kidney, muscle
87
Q

What is the diagnostic evaluation & treatment for inhalent intoxication?

A
  • Serum drug screen (positive for 4-10 hrs)
  • Treatment
    • Monitor airway, breathing, circulation
    • Symptomatic treatment as needed
    • Psychotherapy & counseling for dependent patients
88
Q

What is the clinical presentation of inhalent withdrawal?

A
  • Withdrawal syndrome does not usually occur
  • Symptoms may include
    • Irritability
    • Nausea/vomiting
    • Tachycardia
    • Occasional hallucinations
89
Q

What is the mechanism of caffeine?

A
  • Most commonly used psychoactive substance in the US (coffee, tea)
  • Adenosine antagonist
  • Increases cAMP
  • Stimulates dopaminergic system
90
Q

How much caffeine is in one cup of coffee? tea?

A
  • One cup of coffee: 100-150 mg
  • One cup of tea: 40-60 mg
91
Q

What is the clinical presentation of caffeine intoxication?

How is it treated?

A
  • >250 mg caffeine
    • Anxiety, insomnia, twitching, rambling speech, flushed face, diuresis, GI disturbance, restlessness
  • >1 g caffeine
    • Tinnitus, severe agitation, cardiac arrhythmias
  • >10 g caffeine
    • Death secondary to seizures & respiratory failure
  • Treatment: supportive & symptomatic
92
Q

What is the clinical presentation & treatment of caffeine withdrawal?

A
  • Withdrawal symptoms resolve w/i 1 wk
  • Headache, nausea/vomiting, drowsiness, anxiety, depression
  • Treatment
    • Taper consumption of caffeine-containing products
    • Use analgesics to treat headaches
    • Short course of benzos for anxiety (rare)
93
Q

What is the mechanism of action of nicotine?

A
  • Derived from the tobacco plant
  • Stimulates nicotinic receptors in autonomic ganglia of the sympathetic & parasympathetic nervous systems
  • Cigarette smoking poses many health risks
  • Nicotine rapidly addictive through effects on dopaminergic systems
94
Q

Cigarette smoking during pregnancy is associated with…..

A

low birth weight

persistent pulmonary HTN of newborn

95
Q

What is the clinical presentation & treatment of nicotine intoxication?

A
  • CNS stimulant
  • Restlessness, insomnia, anxiety, increased GI motility
  • Improved attention, improved mood, decreased tension
  • Treatment: cessation
96
Q

What is the clinical presentation & treatment of nicotine withdrawal?

A
  • Intense craving, dysphoria, anxiety, increased appetite, irritability, insomnia
  • Treatment: smoking cessation with…
    • Behavioral counseling
    • Nicotine replacement therapy (gum, transdermal patch)
    • Zyban: antidepressant that helps reduce cravings
    • Clonidine
  • Relapse after abstinence is common

Psychiatry (18 decks)

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