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Pharmacology III > Substance Abuse > Flashcards

Substance Abuse Flashcards

1
Q

What is A chronic disorder characterized by the compulsive use of substance resulting in physical, psychological, or social harm to be user and continued use despite the harm?

A

Addiction

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2
Q

What is the physiological adaptation to the effect of drugs so as to diminish effects with constant dosages or to maintain the intensity and duration of effects through increased dosage?

A

Tolerance

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3
Q

What is the development of a substance-specific syndrome due to the cessation use that has been heavy and prolonged?

A

Substance withdrawal

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4
Q

What is reversible substance-specific syndrome due to a recent ingestion or exposure to a substance?

A

Substance intoxication

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5
Q

What is substance intoxication?

A

Clinically significant maladaptive behavior or psychological changed due to the effect of the substance on the CNS
Develops during or shortly after use of the substance
Not due to a general medical condition or another mental disorder.

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6
Q

All abused substance appear to activate what?

A

The same brain reward pathway.

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7
Q

What are the key components in the pathophysiology of abuse?

A

DA in mesocorticolimbic system
Nucleus Accumbens (NA) to prefrontal cortex, amygdala and olfactory tubule.
Cocaine and stimulants block DA reuptake
Opioids activate μ receptors resulting in increased release of DA in NA
Nicotine also interacts with the opioid pathway
Marijuana’s active component, tetrahydrocannabinol (THC), binds to cannabinoid-1 (CB1) receptors resulting in activation of DA neurons in mesolimbic system

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8
Q

How does chronic substance use affect DA?

A

General decrease in DA neurotransmission

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9
Q

What are the 2 explanations for development of substance dependence?

A

Sensitization– Increased response following repeated intermittent administration of a drug, in contrast to tolerance to drug effects that occur secondary to continuous exposure to a drug

Counteradaptation– Initial positive reward feeling followed by the opposing development of tolerance

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10
Q

What is substance abuse via the DSM-IV?

A

Any 1 of:
Recurrent use causing failure to fulfill major role obligations at work/home/school
Recurrent use when physically hazardous
Recurrent substance-related legal problems
Continued use despite persistent social/interpersonal problems due to substance use

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11
Q

What is Substance dependence via the DSM-IV?

A 
Any 3 of:
Tolerance
Withdrawal
Uses more or longer than intended
Unable to cut down
Use consumes a great deal of time
Important social/work activities given up
Continued use despite physiological or physical problems know to be caused by substance
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12
Q

Alcohol- MOA

A 
CNS depressant
Works in a dose dependent fashion
Sedative, sleep, unconsciousness, coma, respiratory depression and CV collapse
Affects GABA, glutamate and dopamine
Affects endogenous opioids (release)
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13
Q

How is current use of alcohol use defined? Binge use? heavy use?

A

Current use- at least one drink in the past 30 days (includes binge and heavy use)
Binge use- five or more drinks on the same occasion at least once in the past 30 days
Heavy use- five or more drinks on the same occasion on at least 5 different days in the past 30 days.

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14
Q

What is the neurobiology of alcohol involving glutamate?

A

Major excitatory system in CNS
Four principal receptor subtypes
NMDA receptor
NMDA receptor activation → excitation
Acute ethanol intoxication → inhibition
NMDA R inhibited (↓glutamate activity)
Sedative, incoordinating, amnestic, and anxiolytic effects of alcohol
Chronic ethanol intoxication → hypersensitivity
Up-regulation of NMDA R number and function
Enhancement of NMDA R stimulated intracellular Ca2+ levels

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15
Q

What is the neurobiology of alcohol involving GABA?

A

Gamma-aminobutyric Acid (GABA)
Major inhibitory system in CNS
Two principal receptor subtypes
GABAA receptor subtypes
GABAA R activation→ inhibition
Acute ethanol intoxication→ activation
Potentiates GABAA inhibition
Sedative, incoordinating, amnestic, and anxiolytic effects of alcohol
Chronic ethanol intoxication→ hyposensitivity
Down-regulation of GABAA R number and function

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16
Q

What is the neurobiology of alcohol involving dopamine (DA)?

A

Ethanol activates mesolimbic DA systems→
increases DA release in nucleus accumbens (NAc)
Positive reinforcement and pleasurable effects of ethanol

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17
Q

What are the sx and tx of mild-moderate intoxication (BAL 0.08-0.1%)

A

Lower limits of legal intoxication
Do not require formal treatment
Mood labilty, loud or inappropriate behavior, slurred speech, incoordination, unsteady gait

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18
Q

What are the sx and tx of sever intoxication?

A

(BAL 0.2-0.3%) confusion, depressed consciousness, vomiting
(BAL 0.3-0.4%) stupor, coma
(BAL > 0.4%) cardiac arrhythmias, respiratory depression, death
If consciousness is impaired then thiamine should be given IV or IM for at least 3 days

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19
Q

What does CAGE stand for and what does it assess?

A

Assesses alcohol dependence
Have you ever felt the need to Cut Down on your drinking?
Have you ever been Annoyed by criticism of your drinking?
Have you ever felt Guilty about your drinking?
Have you ever needed an Eye Opener to get going in the morning?

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20
Q

What are the drugs used to treat alcohol dependence?

A

Disulfiram – Antabuse®
Naltrexone – Revia®
Acamprosate- Campral®

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21
Q

Disulfiram- Antabuse®- MOA

A

Acetaldehyde dehydrogenase (ALDH) inhibitor (irreversible)

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22
Q

Disulfiram- Antabuse®- ETOH reaction

A 
Nausea/Vomiting
HA
Hypotension
MI
Weakness
Tachycardia
SOB
Sweating
Dizziness
Blurred vision
Confusion
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23
Q

Disulfiram – Antabuse®- treatment recommendations

A

250mg PO QD
Range from 125-500mg/d
Start when abstinent from ETOH for at least 12 hours
Full “protective” effect in 12-14 hours
2 weeks wash-out before alcohol interaction

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24
Q

What are the predictors of success with disulfiram?

A 
Motivated
Compliant
High risk situations (e.g. weddings) where behavior is important
Contingencies (e.g. loss of license)
Supervised administration
Stable home life
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25
Q

Naltrexone- Rivia®- indications

A

Narcotic abuse

Alcohol dependence

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26
Q

Naltrexone- Rivia®- MOA

A

Competitive mu (µ) opioid receptor antagonist
Naltrexone blocks ß- endorphin which stimulates dopamine release
Naltrexone blocks ethanol- induced DA release in NAC
» May attenuate rewarding effects of alcohol

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27
Q

Naltrexone- Rivia®- effectiveness

A

Moderate effects at best
More recent study in VA population found naltrexone no different than placebo on time to relapse, % of drinking, or # of drinks per drinking day
Long-term effectiveness???
One study has shown beneficial effects diminish gradually over time
Long-acting injectable: one study has shown effects sustained during 6 months of treatment

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28
Q

Acamprosate- Campral® - Indication

A

Approved to maintain abstinence after detoxification

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29
Q

Acamprosate- Campral® - MOA

A

Unknown
“restores balance” between glutamate and GABA
May ↓ glutamate overactivity
Binding to allosteric polyamine site on NMDA R and ↓ polyamine modulation of NMDA activity
Binding postsynaptic metabotropic glutamate receptors (mGluR5) and alter NMDA Receptor number and function
Binding to presynaptic mGluR5 and ↓ glutamate release
May ↓ ability of ethanol to activate mesolimbic dopamine system

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30
Q

Acamprosate- Campral® - effectiveness

A

Moderate effects at best
Similar decreases in drinking frequency, and similar relapse rates as naltrexone
13 trials, mostly European

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31
Q

Acamprosate- Campral® - Long-term effectiveness

A

In long-term trials, 16-30% of subjects completely abstinent at 48 and 52 week endpoints

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32
Q

Acamprosate- Campral® - ADRs

A

Only ADR reported in > 10% patients and at a rate > placebo was transient diarrhea
Asthenia (6%)
Anxiety (6%)
Insomnia (7%)

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33
Q

Acamprosate- Campral®- contraindications

A

Renally eliminated

Should not be used if CCI < 30 dl/ml

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34
Q

Is pharmacologic management required for patients with no significant withdrawal signs/sx of ETOH?

A

Nope

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35
Q

What are the signs and sx of ETOH withdrawal with minor withdrawal sx?

A 
Tremor
GI (nausea/vomiting)
Mild diaphoresis
Vital signs increase (mild)
Sleep disturbance
Hallucinations
Seizures (7%)
36
Q

What is the incidence and time course of ETOH withdrawal with minor withdrawal sx?

A 
Incidence:
>/= 1 sign/symptom
95%
Time Course:
Onset: 8-12 Hours
Peak:  24-36 Hours
Duration:  60-72 hours(important!)
37
Q

What are the signs/sx of alcohol withdrawal with major withdrawal sx?

A 
Delirium
Delirium Tremems
	(DT’s)
Hallucinations
Agitation
Tremors
Vital signs increased (Marked)
Diaphoresis (marked)
Sleep disturbance
38
Q

What is the incidence and time course of alcohol withdrawal with major withdrawal sx?

A 
Incidence:
5%
Time Course:
Onset: 48-60 hours
Peak: 72 hours
Duration: 120-168 hours (Important!)
39
Q

What are the treatment goals of alcohol withdrawal?

A 
Prevent withdrawal symptoms including
Seizures
Delirium Tremens
Medical and psychological complications
Encourage long-term abstinence
Encourage/refer to outpatient treatment
(AA, 12 step programs, etc.)
40
Q

What is the DOC for uncomplicated withdrawal?

A

Benzodiazepine

41
Q

What is the criteria for the Mild, moderate, and severe clinical institute withdrawal assessment-alcohol revised (CIWA-Ar)

A

Mild: less than 8 on CIWA no pharmacological therapy
Moderate: 8-15 Use medication
Severe: 15 Use medication (enough to control symptoms) and monitor closely

42
Q

When should patients be monitored during withdrawal?

A

Monitoring patient every 4-8 h
CIWA-Ar until score has been < than 8for 24 h
Use additional assessments as needed

43
Q

What drugs should be administered when CIWA-Ar is Greater than or equal to 8?

A

Administer 1 of the following medications every hour when CIWA-Ar is ≥ to 8
Chlordiazepoxide 50-100 mg
Diazepam 10-20 mg
Lorazepam 2-4 mg
Repeat CIWA-Ar 1 after every dose to assess need to further medication

44
Q

Are short or long acting benzodiazepines preferred for alcohol withdrawal treatment?

A

Long acting

45
Q

What are the long acting benzodiazepines used in alcohol withdrawal tx?

A

Preferred: Long-acting
Chlordiazepoxide (Librium)
Diazepam (Valium)

46
Q

What are the short acting benzodiazepines used in alcohol withdrawal tx?

A

Severe liver disease: Short-acting
Lorazepam (Ativan)- used frequently
Oxazepam (Serax)

47
Q

What should be used to treat complicated alcohol withdrawal?

A

Complicated withdrawal
Patient NPO/vomiting
Parenteral BZD
Chlordiazepoxide 50mg PO = lorazepam 2-4mg IM
Supplement with lorazepam 2-4mg IM q1h for breakthrough signs/symptoms

48
Q

What is used to tx seizures from alcohol withdrawal?

A 
Benzodiazepines drug of choice
IV diazepam 5-10mg may repeat q 5min till termination seizure
IM lorazepam 4mg 
Correction of Electrolyte Imbalances
IV magnesium 1g q hours for 1st day
IV thiamine  (as in intoxication)
49
Q

What is used to treat delirium tremens (DTs) in alcohol withdrawal?

A

IV Benzos ‘till light somnolence is achieved
Haloperidol- given only for severe agitation unresponsive to benzos
IV thiamine

50
Q

How should benzodiazepines be tapered?

A 
Simple taper
25% dose reduction per week until 50% of original dose is reached
Then decrease dose by 1/8 every 4-7 days
If therapy > 8 weeks
2-3 week taper is recommended
If therapy > 6 months
4-8 week taper should be used
If therapy > 1 year
Strong consideration should be given to using long-acting agents (Diazepam, Clonazepam)
51
Q

What can sudden discontinuation of benzodiazepines result in?

A

Rebound anxiety

Recurrence or relapse of symptoms

Withdrawal symptoms
Onset
Short-acting agents ~ 1-2 days
Longer-acting agents ~ 2-4 days

52
Q

What are the common sx of benzodiazepine withdrawal?

A 
Anxiety
Insomnia
Restlessness
Muscle tension
irritability
53
Q

What are the rare sx of benzodiazepine withdrawal?

A

Seizures
Hallucinations
Paranoid delusions
Confusion

Less frequently- nausea, malaise, blurred vision, diaphoresis, nightmares, ataxia, hyperreflexia

54
Q

When do short acting and long acting benzo agents have withdrawal?

A

Short-acting agents
~3 days after discontinuation
Longer-lasting agent
~1 week after discontinuation

55
Q

What are the risk factors for benzodiazepines?

A

High BDZ doses
Long duration of therapy
Concurrent meds/drugs that lower seizure threshold

56
Q

What are signs of intoxication of stimulants-cocaine,methamphetamine?

A 
Restlessness/anxiety
Euphoria
Grandiosity
Hypervigilance
Tachycardia/elevated blood pressure
Mydriasis
Sweating and/or chills
Nausea, vomiting, diarrhea
Psychosis
Cardiovascular collapse
death
57
Q

What are the signs of abuse of stimulants-cocaine,methamphetamine?

A
  • Dilated pupils (high dose)
    - Dry mouth
    - Bad breath
    - Frequent lip licking
    - Decreased appetite and sleep
    - Irritable, argumentative
    - Talkative but tangential
    - Runny/bloody nose
    - Paraphenalia
58
Q

How do you treat intoxication of stimulant?

A

Treat and monitor medical problems
Hyperthermia, Hypertension, Cardiac arrhythmias, Stroke
Psychiatric Problems
Benzodiazepines for anxiety
History and drug screen 1st because often used in combo with ethanol, opioids so benzos can increase sedation and respiratory depression

59
Q

How do you treat intoxication of stimulant?

A

Dependence
Therapy, groups, etc 12 step program
No proven pharmacotherapy, Disulfiram shows some promise with cocaine

60
Q

What should be used for severe sx in the first 24 hours of stimulant withdrawal?

A

For severe symptoms in first 24 hours benzodiazepines or antipsychotics might be helpful for delusions, paranoia, compulsive behavior

61
Q

What are the life threatening complications associated with stimulant withdrawal?

A

Seizures
Hyperthermia
Ischemic chest pain
Suicide

62
Q

What are the signs of opioid intoxication?

A 
Euphoria
Dysphoria
Apathy
Motor retardation
Sedation
Attention impairment
Miosis
63
Q

What are the signs of opioid withdrawal?

A 
Lacrimation
Rhinorrhea
Mydriasis
Piloerection
Diarrhea
Yawning
Insomnia
Muscle aching
64
Q

What is the treatment for opioid intoxication?

A

Reverse intoxication with naloxone 0.4-2mg IV q 2-3 min up to 10mg
Secure airway

65
Q

What is the treatment for opioid dependence?

A

Opioid agonists

Opioid antagonists

66
Q

What do opioid inhibit?

A 
Opioids inhibit cyclic AMP system
Chronic use discontinuation
Leads to cyclic AMP in the adrenergic neurons becomes overactive
Noradrenergic brain activity increases
Contributes to withdrawal symptoms
Adrenergic autoreceptors
When stimulated decrease neural activity
67
Q

What are the Mild (grade I)of opioid sx?

A 
Yawning
Lacrimation
Rhinorrhea
Perspiration
Restlessness
Insomnia
68
Q

What are the moderate (Grade II) of opioid withdrawal?

A 
Tremors
Dilated Pupils
Goosebumps
Anorexia
Muscle Twitching
Myalgia/arthralgia
Abdominal pain
69
Q

What are the marked (grade III) of opioid withdrawal?

A 
Nausea
Extreme
Restlessness
Vital Signs ↑ 
Tachycardia
Hypertension
Fever
Hot/Cold Flashes
70
Q

What are the severe (Grade IV) of opioid withdrawal?

A 
Vomiting
Diarrhea
Weight loss
Dehydration
Hypotension
71
Q

When is opioid withdrawal fatal?

A

With a medical complication (still great discomfort, incapacitating)

72
Q

Clonidine- MOA

A

Alpha adrenergic autoreceptors

73
Q

Clonidine- Indications

A

Heroin: 10 day treatment
Methadone: 14 day treatment
Clonidine taper in both cases

74
Q

When should vital signs be checked with methadone tx for opioid withdrawal?

A

Vital signs before each dose

Titration: ↑ 5-10mg QOD as tolerated

75
Q

Methadone (Dolophine®)- MOA

A

Mechanism of action
µ and ō opioid withdrawal agonist
Suppresses opioid withdrawal symptoms
Blocks effect of other opioids

Use for detox limited to a licensed treatment facility

76
Q

Methadone (Dolophine®)- side effects

A

Constipation, sweating, urinary retention

Respiratory depression in intolerant individuals

77
Q

Buprenorphine(Subutex®, Suboxone®)- MOA

A

µ receptor partial agonist and weak K receptor antagonist
Similar effects as methadone
Opioid antagonist at higher doses
Controls cravings
Still some sense of euphoria
Safer than heroin
Not as addictive, little risk of overdose

78
Q

Naltrexone (ReVia®)

A

Should not be initiated until patient is opioid free for 7-10d
Poor compliance and high drop-out rates limit usefulness

79
Q

What CNS neurotransmitters affected by nicotine?

A

DA, NE, 5-HT, glutamate, GABA, and endogenous opioid peptides
Activates nicotinic acetylcholine receptors in the brain

80
Q

What are the nicotine replacement therapies?

A 
Patch
Gum
Lozenge
Nasal Spray
Inhaler
81
Q

What are the smoking cessation pharmacotherapies?

A

Buproprion
Varenicline
Clonidine
TCA’s

82
Q

When is combining nicotine replacement therapies more effective?

A

In refractory smokers

83
Q

Buproprion (Zyban®, WellbutrinSR®)- MOA

A

Blocks reuptake of DA and NE
Acts as a noncompetitive antagonist on nAch receptor
Reduces nicotine reinforcement, withdrawal, and craving

84
Q

Varenicline (Chantix®)- MOA

A

agonizes and blocks nicotinic acetylcholine receptors

85
Q

Varenicline (Chantix®)- ADRs

A

Black Box Warning
Neuropsychiatric Symptoms and Suicidality
Weigh varenicline risks vs. benefits of smoking cessation

86
Q

What are the 2nd line therapies for smoking cessation?

A

Clonidine
Modest efficacy in smoking cessation trials

TCA’s
Nortriptyline (inhibit reuptake NE and 5-HT)
Significant disadvantages
Anticholinergic burden
Cardiac side effects

Pharmacology III (19 decks)

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