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Psychiatry Part 2 > Substance-Related Disorders > Flashcards

Flashcards in Substance-Related Disorders Deck (95)
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1
Q

Substance Use Disorder

A

Using large amounts or for longer time than intended
Persistent desire or unsuccessful attempts to cut down or control use
Great deal of time obtaining, using, or recovering
Craving
Fail to fulfill major roles (work, school, home)
Persistent social or interpersonal problems caused by substance use
Important social, occupational, recreational activities given up or reduced
Use in physically hazardous situations
Use despite physical or psychological problems caused by use
Tolerance
Withdrawal

2
Q

Which substances have no withdrawal even after repeated use?

A

PCP, inhalants, hallucinogens

3
Q

Severity of disorder

A

Depends on # of symptom criteria endorsed
Mild: 2-3 symptoms
Moderate: 4-5 symptoms
Severe: 6 or more symptoms

4
Q

Specifiers of substance use disorder?

A

In early remission: no criteria for > 3 months but < 12 months (except craving)
In sustained remission: no criteria for > 12 months (except craving)
In a controlled environment: access to substance restricted (e.g. jail)

5
Q

Intoxication

A

REVERSIBLE substance-specific syndrome due to recent ingestion
Behavioral/psychological changes due to effects on CNS after ingestion (e.g. disturbances of perception, wakefulness, attention, thinking, judgement, psychomotor behavior and interpersonal behavior)
Not due to another medical condition or mental disorder
* Does not apply to tobacco

6
Q

Withdrawal

A

Substance-specific syndrome due to stopping or reducing prolonged use
Physiological & cognitive components
Significant distress in social, occupational or other important areas of functioning
Not due to another medical condition or mental disorder

7
Q

Substance-Induced Mental Disorder

A

Can be due to any of the 10 classes of substances
During or within 1 month of use
Not an independent mental disorder (can’t have preceded onset of use or persist for substantial time after use)

8
Q

10 classes of substances?

A
Alcohol
Caffeine
Cannabis
Hallucinogens (e.g. PCP)
Inhalants
Opioids
Sedatives, hypnotics, anxiolytics
Stimulants
Tobacco
Other (gambling??)
9
Q

Neuroadaptation

A

Underlying CNS changes that occurs after repeated use such that person develops tolerance and/or withdrawal

10
Q

Pharmacokinetic neuroadaptation

A

Adaptation of metabolizing system

11
Q

Pharmacodynamic neuroadaptation

A

Ability of CNS to function despite high blood levels

12
Q

Tolerance

A

Need to use an increased amount of substance in order to achieve desired effect
OR
Markedly diminished effect with continued use of same amount of substance

13
Q

Rates of substance abuse by age

A

1% of 12 y/o
25 % of 21 y/o
1% of 65 y/o

14
Q

Does starting substance use at earlier age matter?

A

Starting at earlier age (<15 y/o), more likely to become addicted
e.g. alcohol addiction is 18% if started use before 15 y/o vs. 4% if started at 18 y/o or older

15
Q

Demographics associated with substance abuse?

A
Men
American Indians and whites
Unemployed
Large metro areas
Parolees
16
Q

Alcohol epidemiology

A

$300 billion/year spent on alcohol
13 million require tx for alcohol
(vs. 5.5 million require tx for drug use)

17
Q

What percent of population reported using Rx meds non-medically within past month?

A

2.5%

18
Q

What percent of hospital admissions have alcohol or drugs associated?

A

40%

19
Q

What percent of hospital deaths have alcohol or drugs associated?

A

25% = 100,000 deaths per year

20
Q

Intoxication is associated with what % of MVAs, DV cases, murders?

A

50% of all MVAs
50% of all DV cases
50% of all murders

21
Q

ER visits due to substances?

A
1.2 million = non-medical use of pharmaceuticals!!
660 K = alcohol
425 K = cocaine
380 K = marijuana
210 K = heroin
93 K = stimulants
22
Q

Is substance abuse a “brain disease”?

A

Changes in structure and neurochemistry transform voluntary drug-using to compulsive using
Changes are not necessary/sufficient (drug-dependent person changes behavior in response to positive reinforcers)

23
Q

Psychodynamic etiology?

A

Disturbed ego function (inability to deal with reality)

24
Q

Self-medication etiology?

A

Alcohol - panic
Opioids - anger
Amphetamines - depression

25
Q

Genetic etiology?

A

Well-established with alcohol

26
Q

Conditioning etiology?

A

Behavior is maintained by its consequences:

  • Terminate aversive state (pain, anxiety, withdrawal)
  • Special status
  • Euphoria
  • Secondary reinforcers (e.g. paraphernalia)
27
Q

What happens to cellular receptors with substance abuse?

A

Too little endogenous opioid activity (i.e. low endorphins) OR too much endogenous opioid antagonist activity = increased risk of dependence
It’s a normal endogenous receptor BUT long-term use modulates it = need exogenous substance to maintain homeostasis

28
Q

Learning and physiological basis for dependence?

A

Using drugs or stopping use leads to depleted state resulting in dysphoria and/or cravings, reinforcing the use of more drug
Brain cells respond by downregulating receptors and/or decreasing production of neurotransmitters that are in excess of normal levels

29
Q

Comorbidity of substance use disorders with other psych disorders?

A

Up to 50% of addicts have comorbid psychiatric disorder (antisocial PD, depression, suicide)

30
Q

What percent of patients are eventually able to abstain or decrease use to not meet criteria after treatment?

A

70%

31
Q

When to treat in hospital?

A

Drug OD, risk of severe withdrawal, medical comorbidities, requires restricted access to drugs, psychiatric illness with SI

32
Q

When to treat in residential treatment unit?

A

No intensive medical/psychiatric monitoring needs
Require restricted environment
Partial hospitalization

33
Q

When to treat in outpatient program?

A

No risk of med/psych morbidity

Highly motivated patient

34
Q

Behavioral interventions

A

Must target internal and external reinforcers
Motivation to change (MI), group therapy, individual therapy, contingency management, self-help recovery groups (AA), therapeutic communities, aversion therapy, family involvement/therapy, twelve-step facilitation, relapse prevention

35
Q

Alcohol intoxication

A

Blood alcohol level 0.08 g/dL
Progresses from mood lability, impaired judgment, and poor coordination to increased level of neurologic impairment (severe dysarthria, amnesia, ataxia, obtundation)

36
Q

How can alcohol intoxication be fatal?

A

Loss of airway protective reflexes
Pulmonary aspiration
Profound CNS depression

37
Q

Symptoms of early alcohol withdrawal?

A

Anxiety, irritability, tremor
Headache, insomnia, nausea
Tachycardia, HTN, hyperthermia
Hyperactive reflexes

38
Q

Symptoms of late alcohol withdrawal?

A
Seizures (24-48 hours), usually grand mal
Delirium tremens (48-72 hours) with altered mental status, hallucinations, marked autonomic instability, LIFE THREATENING
39
Q

What is CIWA?

A

Clinical Institute Withdrawal Assessment for Alcohol

  • Score orientation, n/v, tremor, sweating, anxiety, agitation, tactile/auditory/visual disturbances, headache
  • Total score >10 indicates severe withdrawal
40
Q

Inpatient treatment for alcohol withdrawal?

A
  • Benzodiazepines - cross-tolerant with alcohol, reduce risk of seizures, provide comfort/sedation
  • Anticonvulsants (carbamazepine, valproate) - reduce risk of seizures and maybe kindling, good for protracted withdrawal
  • Thiamine supplementation - risk of thiamine deficiency (Wernicke/Korsakoff)
41
Q

Medications used for alcohol use disorder

A

Disulfiram, Naltrexone, Acamprosate

42
Q

Disulfiram (Antabuse)

A

250-500 mg PO daily
Inhibits aldehyde dehydrogenase and dopamine beta hydroxylase
Aversive reaction when alcohol ingested (vasodilatation, flushing, n/v, hypotension/HTN, coma/death)
Watch out for disguised forms of alcohol (cologne, sauces, mouth wash, OTC cough meds)

43
Q

Disulfiram side effects?

A
  • Hepatotoxicity - check LFTs and h/o hep C
  • Neurologic - polyneuropathy/paresthesias that increase over time, increased risk with higher doses
  • Psychiatric - psychosis, depression, confusion, anxiety
  • Dermatologic - rashes, itching
44
Q

Naltrexone

A
50 mg PO daily
Opioid antagonist (blocks mu receptors?)
Reduces intoxication euphoria and cravings
Hepatotoxicity at high doses - check LFTs
45
Q

Acamprosate (Campral)

A

666 mg PO TID
Unknown MOA
Stabilizes neuron excitation and inhibition?
Interacts with GABA and glutamate receptor?
Cleared renally - check kidney fx

46
Q

Benzodiazepine/barbiturate intoxication?

A

Similar to alcohol but less cognitive/motor impairment
Variable rate of absorption (lipophilic), onset of action, and duration in CNS
* More lipophilic and shorter duration of action = more “addicting”

47
Q

Benzodiazepine withdrawal symptoms?

A

Similar to alcohol but time frame depends on half-life

Anxiety, irritability, tremor, sweating, insomnia, fatigue, headache, poor concentration

48
Q

Benzodiazepine withdrawal treatment?

A

Convert short half-life BZD to long half-life BZD, then slowly taper (common mistake is tapering too fast, symptoms worse at end of taper)
Outpatient taper: decrease dose every 1-2 weeks and not more than 5 mg diazepam dose equivalent
Consider carbamazepine or valproate if doing rapid taper

49
Q

5 mg diazepam is equal to what?

A

0.5 mg alprazolam = 25 mg chlordiazepoxide = 0.25 mg clonazepam = 1 mg lorazepam

50
Q

Which BZDs are not affected by age or hepatic insufficiency?

A

Oxazepam, temazepam, lorazepam

Metabolized through only glucuronidation in liver

51
Q

Which BZD is least lipophilic?

A

Chlordiazepoxide

Half-life 30-100 hrs

52
Q

Which BZD is most lipophilic (more addicting)?

A

Diazepam

Half-life 30-100 hrs

53
Q

Opioid MOA

A

Bind mu receptors in CNS to modulate pain

54
Q

Opioid intoxication

A

Pinpoint pupils, sedation, constipation, hypotension, bradycardia, decreased RR

55
Q

Opioid withdrawal

A

Not life threatening unless severe medical illness
Extremely uncomfortable
Dilated pupils, lacrimation, goosebumps, n/v, diarrhea, myalgias, arthralgias, dysphoria or agitation

56
Q

Opioid withdrawal treatment

A

Symptomatically
Antiemetic, antacid, antidiarrheal
Muscle relaxant (methocarbamol)
NSAIDs, clonidine, maybe BZD

57
Q

Opioid neuroadaptation

A

Increased dopamine

Decreased NE

58
Q

Medications used for opiate use disorder

A

Methadone, Naltrexone, Buprenorphine

59
Q

Naltrexone

A

Opioid blocker, mu antagonist

50 mg PO daily

60
Q

Methadone

A

Mu agonist
Start at 20-40 mg, titrate up to 80-100 mg daily
Needs to be enrolled in a certified opiate substitution program

61
Q

Buprenorphine

A

Partial mu agonist with ceiling effect
Any physician can Rx after taking certified ASAM course
Helpful for highly motivated people who do not need high doses

62
Q

Acute stimulant intoxication

A

Psychological: euphoria, enhanced vigor, gregariousness, hyperactivity, restlessness, interpersonal sensitivity, anxiety, tension, anger, impaired judgment, paranoia
Physical: tachycardia, papillary dilation, HTN, n/v, diaphoresis, chills, weight loss, chest pain, cardiac arrhythmias, confusion, seizures, coma

63
Q

Chronic stimulant intoxication

A

Affective blunting, fatigue, sadness, social withdrawal, hypotension, bradycardia, muscle weakness

64
Q

Stimulant withdrawal

A

Not severe but have exhaustion with sleep (crash)

Treat with rest and support

65
Q

Cocaine use?

A

Nasal, IV, smoked
Vasoconstrictive effects (may outlast use), increased risk for CVA and MI - get EKG
Rhabdomyolysis with compartment syndrome from hypermetabolic state
Psychosis associated with intoxication (resolves)
No medications FDA-approved for tx of use disorder

66
Q

Cocaine neuroadaptation

A

Prevents reuptake of dopamine

67
Q

Amphetamine use?

A

Oral, IV, nasal, smoked
Similar intoxication syndrome to cocaine but usually longer
No vasoconstrictive effects
Chronic use = neurotoxicity from glutamate and axonal degeneration?
Permanent amphetamine psychosis with continued use
No medication treatment (atypical antipsychotics?)

68
Q

Amphetamine neuroadaptation

A

Inhibits reuptake of DA, NE, 5HT - greatest effect on DA

69
Q

Most important preventable cause of death/disease in the U.S.?

A

Tobacco

70
Q

How many current tobacco smokers? Ex-smokers?

A

25% current smokers, 25% ex-smokers

71
Q

Percent of all U.S. deaths attributed to tobacco?

A

20%

72
Q

How many smokers die of tobacco-induced disorder?

A

45%

73
Q

What percent of schizophrenic patients smoke tobacco?

A

75-90%

74
Q

Drug interactions with tobacco?

A

Induces CYP1A2 - watch for interactions with olanzapine

75
Q

Tobacco intoxication, tolerance, withdrawal?

A

No intoxication diagnosis! (dizziness, headache, nausea)
Rapid tolerance
Withdrawal: dysphoria, irritability, anxiety, decreased concentration, insomnia, increased appetite

76
Q

Tobacco neuroadaptation?

A

Nicotine ACh receptors on dopamine neurons in ventral tegmental area release dopamine in nucleus accumbens

77
Q

Tobacco use disorder treatment?

A

CBT
Agonist substitution therapy (nicotine gum or lozenge, transdermal patch, nasal spray)
Meds: bupropion 150 mg PO BID, varenicline 1 mg PO BID

78
Q

Hallucinogens

A

Naturally occurring mescaline, magic mushroom

Synthetic - LSD, DMT, STP, MDMA

79
Q

MDMA (ecstacy) effects

A

Enhanced empathy, personal insight, euphoria, increased energy
3-6 hour duration

80
Q

MDMA intoxication

A

Illusions, hyperacusis, sensitivity of touch/taste/smell, “oneness with the world”, tearfulness, euphoria, panic, paranoia, impaired judgment

81
Q

MDMA tolerance/dependence?

A

Tolerance develops quickly

Unpleasant side effects (teeth grinding) = dependence less likely

82
Q

MDMA neuroadaptation

A

Affects 5HT, dopamine, NE but predominantly 5HT2 receptor agonist

83
Q

MDMA psychosis

A

Hallucinations generally mild
Paranoid psychosis with chronic use
Serotonin neural injury associated with panic, anxiety, depression, flashback, psychosis, cognitive changes

84
Q

MDMA withdrawal

A

Unclear syndrome

Maybe similar to mild stimulants - sleepiness and depression due to 5HT depletion

85
Q

What is the most commonly used illicit drug in the U.S.?

A

Cannabis

86
Q

Cannabis blood levels?

A

THC levels peak in 10-30 min

Lipid soluble = long-half life of 50 hours

87
Q

Cannabis intoxication

A

Appetite and thirst, colors/sounds/tastes are clearer, increased confidence and euphoria, relaxation, increased libido, transient depression/anxiety/paranoia
Tachycardia, dry mouth, conjunctival injection
Slow reaction time/motor speed
Impaired cognition, psychosis

88
Q

Cannabis neuroadaptation

A

CB1, CB2 cannabinoid receptors in brain/body are coupled with G proteins and adenylate cyclase to Ca2+ channels, inhibiting Ca2+ influx
Neuromodulator effect = decreased uptake of GABA and DA

89
Q

Cannabis withdrawal

A

Insomnia, irritability, anxiety, poor appetite, depression, physical discomfort
No pharmacological treatment

90
Q

PCP (“Angel Dust”) MOA

A

Anesthetic

Similar to ketamine - NMDA antagonist

91
Q

PCP intoxication

A

Severe dissociative reactions (paranoid delusions, hallucinations, agitation/violence with decreased awareness of pain)
Cerebellar symptoms - ataxia, dysarthria, nystagmus (vertical and horizontal)

92
Q

Severe PCP overdose?

A

Mute, catatonic, muscle rigidity, HTN, hyperthermia, rhabdomyolysis, seizures, coma, death

93
Q

PCP treatment?

A

Antipsychotic drugs or BZD if needed
Low stimulation environment
Acidify urine if severe toxicity/coma

94
Q

PCP neuroadaptation

A

Opiate receptor effects

Allosteric modulator of glutamate NMDA receptor

95
Q

PCP tolerance/withdrawal?

A

NO tolerance or withdrawal!