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Therapeutics III > Yang Sedatives and Hypnotics > Flashcards

Yang Sedatives and Hypnotics Flashcards

1
Q

Sedative definition

A

Calms anxiety, decreases excitement and activity, does not produce drowsiness, or impair performance

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2
Q

Anxiolytic definition

A

Antianxiety, relieves anxiety without sleep or sedation (not all anxiolytics are sedatives)

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3
Q

Hypnotic definition

A

Induces sleep, implies restful, refreshing sleep, not “hypnotized”, natural sleep (sleep-inducing)

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4
Q

Narcotic definition

A

Actually means “sleep-producing” now refers to opioids or illegal drugs

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5
Q

Stages of sleep

A

-Wakefulness
-Non-rapid eye movement (NREM) slow-wave sleep
-Rapid eye movement (REM) sleep

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6
Q

Stages of NREM sleep

A

-Stage 1: dozing
-Stage 2: unequivocal sleep
-Stage 3: voltage increase, frequency decrease
-Stage 4: delta waves

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7
Q

Factors that regulate sleep

A

-Age: decreases with age due to changes in activity of reticular formation
-Sleep history: rebound of REM sleep
-Drug ingestion: acute and withdrawal produce rebound effects
-Circadian rhythms: normal sleep cycle

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8
Q

Neurotransmitters that regulate sleep

A

-Catecholamines
-Serotonin
-Histamine
-Acetylcholine
-Adenosine
-GABA

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9
Q

Neuromodulators that regulate sleep

A

-Growth hormone
-Prolactin
-Cortisol
-Melatonin
-Endogenous peptides

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10
Q

Targets for sedative-hypnotics on the GABAa receptor/chloride ion channel complex

A

-Orthosteric site
-Allosteric site
-Channel pore

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11
Q

What binds to the orthosteric site on the GABAa receptor/chloride ion channel complex?

A

GABA

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12
Q

What binds to the allosteric sites on the GABAa receptor/chloride ion channel complex?

A

-Benzodiazepines
-Barbituates
-Ethanol
-Gluccocorticoid

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13
Q

What binds to the channel pore on the GABAa receptor/chloride ion channel complex?

A

Picrotoxin

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14
Q

Benzodiazepine mechanism of action

A

Facilitate GABA action, increase frequency, require intact GABA system

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15
Q

What do Z-Hypnotics target?

A

BZ1 receptors of alpha1

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16
Q

Benzodiazepine antagonists for overdose treatment

A

Flumazenil

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17
Q

Inverse benzodiazepine agonists

A

B carbolines

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18
Q

Z-hypnotics

A

-Zolpidem
-Zaleplon
-Eszopliclone

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19
Q

BZDs with slow elimination rates

A

All have active metabolites
-Chlordiazepoxide
-Diazepam (used for seizures, accumulation of metabolites)
-Flurazepam
-Clorazepate
-Quazepam
-Prazepam

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20
Q

BZDs with intermediate elimination rates

A

-Alprazolam
-Lorazepam
-Clonazepam (anticonvulsant)
-Oxazepam
-Temazepam

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21
Q

BZDs with rapid elimination rates

A

-Midazolam
-Triazolam

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22
Q

Characteristics of BZDs with slow elimination

A

-Active metabolites
-Accumulation
-Drowsiness and sedation
-Useful in patients who “wake up”

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23
Q

Characteristics of BZDs with intermediate to rapid elimination

A

-Preferable in patients with hepatic problems
-Preferable in elderly patients
-Drugs that alter liver enzymes
-Rapid tolerance
-Rebound insomnia

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24
Q

Benzodiazepine considerations

A

-Readily absorbed (can be delayed by food)
-Have active metabolites or are converted to active forms
-Increased lipid solubility will increase speed of delivery to brain
-Redistribution to highly perfused tissue may decrease duration of action
-Cross placental barrier and are detected in breast milk
-Extensive protein binding, but not clinically significant

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25
Q

BZD pharmacologic properties

A

-Anxiolytic
-Decrease in REM
-Decrease stage 3 and 4
-Anticonvulsant activity
-Muscle relaxant
-Cardiovascular and respiratory depression
-Anterograde amnesia
-Unable to recall events that occurred

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26
Q

BZD side effects

A

-Sedation (confusion, ataxia, daytime sedation)
-Weakness
-Headache
-Vertigo
-Nausea
-Paradoxical effects

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27
Q

BZD precaution and interactions

A

-Other sedatives
-Alcohol
-Pregnancy/breast-feeding

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28
Q

BZD abuse potential

A

-Low vs barbiturates
-Small kick

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29
Q

Flumazenil therapeutic use

A

Treat BZD overdose

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30
Q

Flumazenil dosing

A

-0.2 mg IV over 30 seconds
-If desired consciousness is not obtained, increase to 0.3 mg IV over 30 seconds

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31
Q

Flumazenil max cumulative dose

A

3 mg

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32
Q

Flumazenil side effects

A

-Induce convulsions
-Panic attacks
-Agitation
-Confusion
-Nausea an vomiting
-Headache

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33
Q

Z-hypnotic site of binding

A

Act at BZD binding site

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34
Q

When to use zolpidem

A

-Short-term treatment of insomnia
-With difficulty of sleep-onset
-Ambien CR for sleep maintenance

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35
Q

Zaleplon clinical pearls

A

-Short-term treatment of insomnia (7-10 days)
-Rapid acting, rapidly eliminated
-Little tolerance or dependance

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36
Q

Eszopiclone clinical pearls

A

-Active enantiomer of zopiclone (50 times greater affinity)
-Treatment of insomnia (approved for long-term use)

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37
Q

How are z-hypnotics metabolized?

A

CYP3A4 to some extent

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38
Q

Side effects of z-hypnotics

A

-Daytime drowsiness
-Dizziness
-Ataxia
-Nausea
-Vomiting
Sleep-driving
-Sleep-cooking
-Sleep-eating
-Sleep-sex
-Less negative side effects on sleep-patterns vs BZDs

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39
Q

Illicit sedative/hypnotics that target the benzodiazepine binding site

A

-Flunitrazepam
-Clonazepam
-Zolpidem

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40
Q

Why is flunitrazepam considered illicit?

A

-Not available in the US
-Roofies
-DEA recommends changing it to a control schedule 1
-Anterograde amnesia (dangerous aid for sexual assault)

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41
Q

Why is zolpidem considered illicit?

A

-A-minus and zombie pills
-Dangerous aid for sexual assault
-Teen party drug

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42
Q

Long acting barbiturate use

A

Anticonvulsant

43
Q

What are the long-acting barbiturates?

A

Phenobarbital

44
Q

Short to intermediate acting barbiturate use

A

Sedative-hypnotics

45
Q

What are the short to intermediate acting barbiturates?

A

Pentobarbital

46
Q

Ultra short acting barbiturate use

A

IV anesthetics

47
Q

Barbiturate sleep physiology

A

-Comparable to BZD
-Decrease REM
-Slow deep sleep

48
Q

Barbiturate side effects

A

-Idiosyncratic excitement and pain
-Cardiovascular depression at high doses
-Respiratory depression leading to death
-Enzyme interactions
-Dependence
-Tolerance
-Abuse
-Withdrawal
-Overdose
-Hangover
-Accumulation

49
Q

Barbiturate duration of action

A

Inversely proportional to lipid solubility

50
Q

Barbiturate mechanism of action

A

-Bind to all GABAa alpha1-5
-Increase the duration of channel opening
-Direct effects on GABAa channel (high doses)
-Higher risk

51
Q

Benzodiazepine mechanism of action

A

-Bind to all GABAa alpha1-5
-Increase frequency of GABAa channel opening
-Medium risk

52
Q

Z-hypnotic mechanism of action

A

-Bind to GABAa BZ1 receptors of alpha1
-Increase frequency of GABAa channel opening
-Lower risk

53
Q

What kind of coupled receptor is GABAb?

A

Gi/o-coupled receptor

54
Q

Location of the GABAb receptors?

A

-Brain
-Limbic system

55
Q

What does inhibition of GABAb do?

A

-Presynaptic - decrease Ca2+ conductance
-Postsynaptic - increase K+ conductance

56
Q

GABAb agonists

A

-Baclofen
-Gamma-hydroxybutyric acid (GHB)

57
Q

GABAb antagonists

A

-Phaclofen
-Saclofen
-2-hydroxysaclofen

58
Q

Xyrem (sodium oxybate, GHB) clinical pearls

A

-Liquid form is only used for medical use other forms for illicit use
-Available only to prescribers enrolled in the Xyrem Patient Success Program

59
Q

Actions of Xyrem

A

-Decreases excessive daytime sleepiness and increases daytime wakefulness with concomitant stimulant use
-Decrease cataplexy

60
Q

Xyrem receptor targets

A

GABAb, GABAa, and GHB rceptors

61
Q

Concerns regarding Xyrem

A

-Questionable mechanism of action
-Combined with other agents
-Red tape
-Abuse and misuse

62
Q

GHB street names

A

-Liquid ecstasy
-Liquid X
-Juice
-Grievous bodily harm
-Scoops
-Georgia home boy

63
Q

GHB effects

A

-Dose-dependent CNS depression
-Patients often awaken spontaneously

64
Q

Acute effects of GHB

A

-Loss of consciousness
-Amnesia
-Nausea and vomiting
-Headache
-Seizures
-Death

65
Q

GHB concerns

A

-No antagonist
-Use with other sedative-hypnotics - including alcohol
-Amnesia
-Date rape

66
Q

What are the melatonin agonists?

A

-Ramelteon
-Tasimelteon

67
Q

Ramelteon mechanism of action

A

-High affinity for MT1 and MT2 melatonin receptors
-Receptors located in the suprachiasmatic nucleus (SCN)

68
Q

Ramelteon metabolism

A

CYP1A2 substrate

69
Q

What does ramelteon treat?

A

Insomnia characterized by difficulty with sleep onset

70
Q

Ramelteon clinical pearls

A

-Non-controlled substance sleep aid
-No abuse, withdrawal, or dependency
-Negligible risk for next-day “hangover” effects

71
Q

Tasimelteon mechanism of action

A

High affinity for MT1 and MT2 melatonin receptors

72
Q

What does tasimelteon treat?

A

Non-24-hour sleep wake disorder in blind individuals

73
Q

Tasimelteon clinical pearls

A

Orphan product registration

74
Q

Orexin receptor antagonists

A

Suvorexant

75
Q

Suvorexant mechanism of action

A

-High affinity antagonist for OX1 and OX2 orexin receptors
-Receptors located in the hypothalamus
-Decrease arousal and attention via receptors in locus coeruleus and the raphe
-Reduce rewarding stimuli (DA release) via receptors that modulate the mesolimbic projections between the VTA and the nucleus accumbens

76
Q

What does suvorexant treat?

A

Insomnia

77
Q

Suvorexant clinical pearls

A

-Morning impairment likely/possible (use the lowest dose possible)
-Scheduled CIV

78
Q

What information needs to be included on the labeling of all sleep disorder drug products?

A

-Sleep-driving
-Cooking and eating food while sleeping
-Making phone calls while sleeping

79
Q

Miscellaneous sedative drugs

A

-Trazodone
-Antihistamines

80
Q

Herbal/natural sedative hypnotics

A

-Tryptophan
-Melatonin
-Lemon balm
-Valerian
-Chamomile
-Kava kava

81
Q

Causes of sedative-hypnotic overdose

A

-Suicide and suicide gesture
-Drug abuse

82
Q

Signs and symptoms of sedative-hypnotic overdose

A

-Depressed respiration
-Blood pressure
-Reflexes
-Hypothermia

83
Q

Treatment of sedative-hypnotic overdose

A

-Supportive treatment
-Maintain respiration
-Maintain cardiovascular function
-Flumazenil for benzodiazepines or z-hypnotics

84
Q

What is anxiety?

A

Fear or apprehension of something dreadful

85
Q

When to treat anxiety

A

-When it interferes with normal life
-When it interferes with part of another disease

86
Q

Types of anxiety

A

-Generalized anxiety disorder
-Panic disorder
-Social anxiety disorder or social phobia
-Obsessive-compulsive disorder
-Post-traumatic stress disorder
-Anxiety associated with other medical issues (autism, depression, etc.)

87
Q

Drugs that can induce anxiety

A

-Cocaine
-Beta agonists
-Psychostimulants
-Corticosteroids

88
Q

Diseases that can induce anxiety

A

-CHF
-COPD
-Diagnosis of terminal diseases

89
Q

What can cause anxiety from withdrawal?

A

-Antidepressants
-Anxiolytics
-Drugs of abuse
-Cell phone/social media

90
Q

How does norepinephrine effect anxiety?

A

-Over-active locus coeruleus-release NE
-Stimulate autonomic nervous system
-Dysregulated in GAD and other types of anxiety
-Projects to the amygdala (fear center)

91
Q

How does the GABAergic system effect anxiety?

A

-Normally counteracts/balances stimulatory effects of excess NE
-Hypothesis proposes reduced GABAergic signaling. Agents that increase GABA signaling are anxiolytic
-GABA/glutamate (inhibitory/excitatory) (glutamate is converted to GABA by glutamic acid decarboxylase - GAD in the CNS)
-Involved in GAD and panic disorder

92
Q

How does serotonin effect anxiety?

A

-May reflect tone at multiple receptors/SSRIs have efficacy
-Partial agonist of 5HT1A receptors effective
-May involve amygdala and balance with NE
-GAD, panic, OCD, social anxiety

93
Q

How does corticotropin-releasing factor and the HPA axis effect anxiety?

A

-Hyperregulation
-Suppression after treatment in PTSD

94
Q

Drugs used to treat anxiety

A

-BZDs (quick acting, effective)
-Antidepressants (SSRIs, SNRIs, TCAs, takes weeks)
-New breakthrough: ketamine (nasal spray esketamine, very quick acting, game changer)
-Buspirone (Buspar)
-Beta blockers

95
Q

Buspirone mechanism of action

A

-Partial agonist on brain 5HT1A receptors
-Moderate affinity for brain dopamine D2 receptors

96
Q

Buspirone clinical pearls

A

-Low abuse potential, no or little withdrawal
-Longer onset of action compared to BZD (adaptive response)

97
Q

Uses of buspirone

A

-GAD, social anxiety, comorbid depression
-Adjunct use with OCD, PTSD
-Not good for panic disorders (BZD is much faster)

98
Q

Which beta blockers are used in anxiety?

A

Propranolol

99
Q

Uses of propranolol

A

-Social anxiety
-Nightmares associated with PTSD

100
Q

Propranolol clinical pearls

A

-CNS penetration - lipophilic
-Decreased peripheral symptoms of anxiety
-Monitor cardiovascular effects

101
Q

Propranolol side effects

A

-Hallucinations
-Vivid dreams
-Lethargy
-Impotence

102
Q

Miscellaneous anxiolytics

A

-Hydroxyzine (H1 antagonist)
-Clonidine (alpha2 agonist)

103
Q

Investigational anxiolytics

A

-Ondansetron (5HT3 antagonist)
-Ketanserin (5HT2 antagonist)
-Tiagabine (GABA uptake blocker)
-Partial benzodiazepine receptor agonists
-NDMA receptor modulators: d-cycloserine, memantine (glutamatergic agent)
-mGluR5 antagonist: fenobam (glutamatergic agent)
-mGluR2/3 agonist: LY354740 (glutamatergic agent)

Therapeutics III (42 decks)

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