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NMSP Exam 3 > Sedative and Hypnotic Drugs > Flashcards

Sedative and Hypnotic Drugs Flashcards

1
Q

What is anxiolysis?

A
  • Relief of anxiety
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2
Q

What is sedation?

A
  • Producing relaxation, calmness, and decreased motor activity without loss of consciousness
  • A side effect of many drugs that are not general CNS depressants (antidepressants, antihistamines, antipsychotics, transient with opioids)
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3
Q

What is hypnosis?

A
  • Inducing drowsiness and a depressed state of consciousness resembling natural sleep, with decreased motor activity and impaired sensory responsiveness from which person is easily aroused
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4
Q

What is anesthesia?

A
  • Cause a state of unconsciousness from which patient cannot be aroused
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5
Q

What are some clinical uses for sedative-hypnotics?

A
  • Relief of anxiety
  • Insomnia
  • Sedation and amnesia before and during medical surgical procedures
  • Treatment of epilepsy and seizure states
  • Component of balanced anesthesia
  • Control of ethanol or other sedative-hypnotic withdrawal states
  • Muscle relaxation in specific neuromuscular disorders
  • Diagnostic aids or for treatment in psychiatry
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6
Q

What is insomnia?

A
  • Inability to fall asleep, stay asleep, get refreshed by sleeping, etc
  • Widespread, affecting ~1/3 of population
  • More common in women
  • More common in elderly, affecting ~1/2
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7
Q

What is the MOA of benzodiazepines?

A
  • Work to facilitate GABA interaction with its GABAa receptor, exact mechanism uncertain, but increases frequency of Cl- channel opening in response to GABA and gives a greater postsynaptic response to released GABA causing local hyperpolarization, meaning cell is less likely to fire
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8
Q

What are some clinically useful effects of benzodiazepines?

A
  • Anti Anxiety
  • Sedative-hypnotic
  • Anticonvulsant
  • Used to assist with alcohol withdrawal
  • Amnestic
  • Skeletal muscle relaxant properties
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9
Q

How do benzodiazepines affect the CNS?

A
  • Produce dose dependent suppression of CNS –> drowsiness/sedation can be side effect or the desired effect
  • Differences in kinetics make some agents a better hypnotic agent than anti-anxiety agent
  • Anxiety relief in humans/taming in experimental animals correlates with effects in the limbic system
  • Some benzodiazepines produce anterograde amnesia, the failure to retain memory for some time after drug administration
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10
Q

How do benzodiazepines affect the cardiovascular system?

A
  • In healthy adults, little effect on either cardiac output or blood pressure with therapeutic doses
  • Large doses cause clinically insignificant decreases in blood pressure and cardiac output
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11
Q

How do benzodiazepines affect the respiratory system?

A
  • Normal doses have little effect
  • Midazolam (versed), used for intravenous sedation, can cause respiratory depression and apnea
  • Respiratory depressant effects are additive with other CNS depressant drugs such as opioids
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12
Q

What are the elimination ranges of benzodiazepines?

A
  • 1.5-2 hours to >100 hours
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13
Q

What is the metabolism of benzodiazepines?

A
  • Most undergo phase I reactions (CYP3A4) and then glucuronidation (phase II)
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14
Q

What are some common side effects of benzodiazepines?

A
  • Lack of coordination
  • Confusion
  • Muscle weakness
  • Slurred speech
  • Apathy
  • Dizziness
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15
Q

Who is most likely to suffer from side effects of benzodiazepines?

A
  • Elderly
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16
Q

Who is most likely to be resistant to side effects of benzodiazepines?

A
  • Alcoholics

- Barbiturate drug abusers

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17
Q

What are some paradoxic reactions in benzodiazepines?

A
  • Excitement leading to nightmares
  • Hyperactivity
  • Insomnia
  • Irritability
  • Agitation
  • Hostility/rage
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18
Q

Which benzodiazepines are most likely to cause amnesia?

A
  • Short acting
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19
Q

What birth defects can benzodiazepines cause?

A
  • Cleft lip
  • Use during labor and delivery can cause respiratory depression
  • Hypotonia
  • Hypothermia in the infant
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20
Q

What mental and emotional changes do benzodiazepines cause?

A
  • Confusion
  • Disorientation
  • Fuzzy thoughts
  • Impaired memory
  • Depression
  • Emotional numbness
  • Impaired judgement
  • Losing one’s inhibitions
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21
Q

What physical changes do benzodiazepines cause?

A
  • Altered vision
  • Dry mouth
  • Impaired motor coordination
  • Poor reflexes
  • Sedation
  • Vertigo
  • Withdrawal
  • Changes in breathing
  • Fatigue
  • Low BP
  • Nausea and/or vomiting
  • Speech troubles
  • Unexplainable drowsiness
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22
Q

What is the MOA of diazepam?

A
  • Binds to specific GABA-A receptor subunits at CNS neuronal synapses facilitating GABA-mediated chloride ion channel opening frequency
  • Enhances membrane hyperpolarization
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23
Q

What are the effects of diazepam?

A
  • Dose-dependent depressant effects on the CNS including:
    1. Sedation
    2. Relief of anxiety
    3. Amnesia
    4. Hypnosis
    5. Anesthesia
    6. Coma
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24
Q

What are the toxicities of diazepam?

A
  • Concomitant use of benzodiazepines and opioids may result in profound sedation, respiratory depression, coma, and death
  • Reserve concomitant prescribing of these drugs for use in patients for whom alternative treatment options are inadequate, and limit dosages and durations to the minimum required. Follow patients for signs and symptoms of respiratory depression and sedation
  • Extensions of CNS depressant effects… drowsiness is common –> dangerous to operate machinery
  • Dependence liability
  • Interactions: additive CNS depression with ethanol and many other drugs –> death
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25
Q

What are some labeled clinical indications of benzodiazepine?

A
  • Alcohol withdrawal syndrome
  • Anxiety, acute/severe
  • Management of anxiety disorders
  • Muscle spasm, spasticity and/or rigidity
  • Procedural anxiety, premedication in patients undergoing surgical/endoscopic procedures
  • Seizures, acute/active
  • Status epilepticus
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26
Q

What are some off-label clinical indications of benzodiazepine?

A
  • Hydroxychloroquine/chloroquine toxicity
  • Sympathomimetic intoxication
  • Neuroleptic malignant syndrome
  • Opioid withdrawal
  • Serotonin syndrome
  • Treatment of acute vertigo
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27
Q

What is the MOA of alprazolam?

A
  • Bind to specific GABA-A receptor subunits at CNS neuronal synapses facilitating GABA-mediated chloride ion channel opening frequency
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28
Q

What are some effects of alprazolam?

A
  • Dose-dependent depressant effects on the CNS including:
    1. Sedation
    2. Relief of anxiety
    3. Amnesia
    4. Hypnosis
    5. Anesthesia
    6. Coma
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29
Q

What are some toxicities of alprazolam?

A
  • Concomitant use of benzodiazepines and opioids may result in profound sedation, respiratory depression, coma, and death
  • Reserve concomitant prescribing of these drugs for use in patients for whom alternative treatment options are inadequate, and limit dosages and durations to the minimum required. Follow patients for signs and symptoms of respiratory depression and sedation
  • Extensions of CNS depressant effects… drowsiness is common –> dangerous to operate machinery
  • Dependence liability
  • Interactions: additive CNS depression with ethanol and many other drugs –> death
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30
Q

What are some clinical applications of alprazolam?

A
  • Generalized anxiety disorder
  • Short term anxiety
  • Anxiety associated depression
  • Panic disorder +/- agoraphobia
  • Vertigo
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31
Q

What is the MOA of temazepam?

A
  • Bind to specific GABA-A receptor subunits at CNS neuronal synapses facilitating GABA-mediated chloride ion channel opening frequency
32
Q

What are some effects of temazepam?

A
  • Dose-dependent depressant effects on the CNS including:
    1. Sedation
    2. Relief of anxiety
    3. Amnesia
    4. Hypnosis
    5. Anesthesia
    6. Coma
33
Q

What is a clinical application of temazepam?

A
  • Insomnia
34
Q

What are some toxicities of temazepam?

A
  • Concomitant use of benzodiazepines and opioids may result in profound sedation, respiratory depression, coma, and death
  • Reserve concomitant prescribing of these drugs for use in patients for whom alternative treatment options are inadequate, and limit dosages and durations to the minimum required. Follow patients for signs and symptoms of respiratory depression and sedation
  • Extensions of CNS depressant effects… drowsiness is common –> dangerous to operate machinery
  • Dependence liability
  • Interactions: additive CNS depression with ethanol and many other drugs –> death
35
Q

What is the MOA of midazolam?

A
  • Bind to specific GABA-A receptor subunits at CNS neuronal synapses facilitating GABA-mediated chloride ion channel opening frequency
36
Q

What are the effects of midazolam?

A
  • Dose dependent depressant effects on the CNS including sedation and relief of anxiety
    1. Amnesia
    2. Anesthesia
    3. Hypnosis
    4. Coma
    5. Respiratory depression
37
Q

What are the clinical applications of midazolam?

A
  • Preoperative sedation, anxiolysis, amnesia for:
    1. Bronchoscopy
    2. Gastroscopy
    3. Cystoscopy
    4. Coronary angiography
    5. Cardiac catheterization
    6. Oncology procedures
    7. Radiologic procedures
    8. Suture of lacerations
  • Induction of general anesthesia
38
Q

What are some toxicities of midazolam?

A
  • IV midazolam has been associated with respiratory depression and respiratory arrest, especially when used for sedation in noncritical care settings
39
Q

What is the MOA of zolpidem?

A
  • Binds selectively to BZ1 receptors, a subgroup of GABA-A receptors, acting like benzodiazepines to enhance membrane hyperpolarization
40
Q

What are the effects of zolpidem?

A
  • Rapid onset of hypnosis with few amnestic effects or day-after psychomotor depression or somnolence
  • No anxiolytic, anesthetic, anticonvulsant, muscle relaxing, respiratory, or cardiovascular effects
41
Q

What are the clinical applications of zolpidem?

A
  • Insomnia

- Safe in pregnancy

42
Q

What are some toxicities of zolpidem?

A
  • Complex sleep behaviors including sleep-walking, sleep-driving, and engaging in other activities while not fully awake may occur following the use of zolpidem
  • Some of these events may result in serious injuries, including death
  • Other complex sleep behaviors (eg, preparing and eating food, making phone calls, having sex) while asleep have also been reported
  • Abnormal thinking/behavior
  • Extensions of CNS depressant effects, may affect machinery operation
  • Lower dependence liability than benzodiazapines
43
Q

What is the MOA of flumazenil?

A
  • Antagonist at benzodiazepine-binding sites on the GABA-A receptor
44
Q

What are the effects of flumazenil?

A
  • Blocks actions of benzodiazepines and zolpidem

- Does not block other sedative-hypnotic drugs like barbiturates, alcohol, ramelteon, suvorexant

45
Q

What are the clinical applications of flumazenil?

A
  • Management of benzodiazepine overdose

- Reversal of benzodiazepine induced sedation during surgical procedures, reverses in 1-2 minutes

46
Q

What are some toxicities of flumazenil?

A
  • Has been associated with the occurrence of seizures, especially in people who have been long-term sedation or were treated with TCAs –> watchful waiting preferred if patient stabilized
  • Agitiaton, confusion
  • Can precipitate withdrawal symptoms in benzodiazepine dependence
47
Q

What is the MOA of barbiturates?

A
  • Binds to the GABA-A receptor, increases the duration of GABA-related channel openings
  • Increases chloride influx, increase hyperpolarization, decrease number of action potentials
  • At higher doses, could lead to Cl- channel opening in absence of GABA
48
Q

What do barbiturates cause?

A
  • Diminished psychological performance and responsiveness to external stimuli
  • Patients to experience relaxation, feeling of well-being, drowsiness
  • Loss of REM sleep, which is “made up” upon discontinuation giving a sense of restless sleep… see potential for a vicious cycle
  • Effects at all levels of the CNS, but the reticular activating system is particularly affected
49
Q

What are the cardiovascular effects from barbiturates?

A
  • No effects at sedative doses
  • Mild hypotension at hypnotic doses
  • Progressive decline in blood pressure as barbiturates are raised above hypnotic doses
50
Q

What are the respiratory effects from barbiturates?

A
  • Little effect at sedative doses
  • Increasing dosage leads to progressive depression of medullary respiratory center
  • Respiratory reflex activity such as cough, hiccough, sneezes, and laryngospasm are increased, complicating use during anesthesia
51
Q

What is the solubility of barbiturates?

A
  • High lipid solubility which means that they will get to brain rapidly
  • Organs with high blood flow also get higher initial concentrations
52
Q

What do barbiturates do in the liver?

A
  • Induce CYP3A4
  • Long term use cause an increase in liver microsomal activity –> increasing the rate of metabolism of many drugs besides the barbiturates
53
Q

What are some adverse effects/drug interactions of barbiturates?

A
  • High risks for dependence and development of drug tolerance
  • Cause respiratory depression, do not use if compromised respiration
  • Cause sneezing, cough, laryngospasm, hiccough
  • Confusion, somnolence, impaired psychomotor performance
  • Unusual behavioral reactions can occur, but rarely: attitudinal depression and manic behavior, anxiety, hositility
  • Possible severe consequences if combined with other CNS depressants
54
Q

What is the MOA of buspirone?

A
  • A nonbenzodiazepine anxiolytic

- Mechanism uncertain: partial agonist at 5-HT receptors but interactions with other receptors also possible

55
Q

What are the effects of buspirone?

A
  • Slow onset of anxiolytic effects

- Minimal psychomotor impairment– no additive CNS depression with sedative hypnotic drugs

56
Q

What are the clinical applications of buspirone?

A
  • Generalized anxiety states
  • Useful to augment partial response to antidepressant
  • Lack tolerance, dependence, and withdrawal
57
Q

What are the toxicities of buspirone?

A
  • Typical side effects: insomnia, agitation, nausea
  • Also risk of: tachycardia, paresthesias, GI distress
  • Interactions: CYP3A4 inducers and inhibitors
58
Q

What is the MOA Of ramelteon?

A
  • Activates MT1 and MT2 receptors in suprachiasmatic nuclei in the CNS
59
Q

What are the effects of ramelteon?

A
  • Rapid onset of sleep with minimal rebound insomnia or withdrawal symptoms
60
Q

What are the clinical applications of ramelteon?

A
  • Sleep disorders, especially those characterized by difficulty in falling asleep
  • No abuse, withdrawal, or dependency so not a controlled substance
  • Efficacy can be disappointing… not a top 300 drug
61
Q

What are the toxicities of ramelteon?

A
  • Dizziness
  • Fatigue
  • Endocrine changes
  • Interactions: fluvoxamine inhibits metabolism
62
Q

What is the MOA of suvorexant?

A
  • Blocks binding of orexins, neuropeptides that promote wakefulness
63
Q

What are the effects of suvorexant?

A
  • Promotes sleep onset and duration
64
Q

What are the clinical applications of suvorexant?

A
  • Sleep disorders, especially those characterized by difficulty falling asleep
65
Q

What are some toxicities of suvorexant?

A
  • Some next day somnolence and driving impairment
  • Generally well tolerated
  • Some abuse potential
66
Q

What is the MOA of doxepin?

A
  • Antagonizes H1 receptors

- Inhibits reuptake of NE and 5-HT

67
Q

What are the effects of doxepin?

A
  • Causes sedation
68
Q

What are some clinical applications of doxepin?

A
  • Insomnia, sleep maintenance only

- Treatment resistant major unipolar depressive disorder

69
Q

What are the toxicities of doxepin?

A
  • Black box warning of all antidepressants related to increased suicidal ideation
  • Generally well tolerated but possible
  • Anticholinergic effects
  • CNS depression impairing ability to operate machinery
70
Q

What is generalized anxiety disorder (GAD)?

A
  • Persistent and excessive worry that interferes with daily activities +/- physical symptoms
  • Worries often focus on everyday things
71
Q

What are some treatment options for GAD?

A
  • Try CBT if available and patient is willing
  • SRIs
  • Buspirone
  • Pregabalin
  • Benzodiazepines
72
Q

What is panic disorder?

A
  • Core symptom is recurrent panic attacks
  • An overwhelming combination of physical and psychological distress
  • Many people, due to the symptoms, think they are having a heart attack
73
Q

What is agoraphobia?

A
  • Fear of being in situations where escape may be difficult or embarrassing, or help might not be available
  • Fear is out of proportion to the actual situation
74
Q

When do benzodiazepines come into the conversation when treating phobias?

A
  • Late stage

- Need to jump through a lot of hurdles

75
Q

How is separation anxiety treated?

A
  • CBT +/- SSRI

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