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Psychopharmacology > Chapter 10: Disorders of sleep and their tx > Flashcards

Chapter 10: Disorders of sleep and their tx Flashcards

1
Q

what is the arousal spectrum regulated by

A

histamine
dopamine
norepinephrine
serotonin
acetylcholine
GABA
orexin

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2
Q

sx of deficient arousal

A

inattention
cognitive dysfunction
sleepiness

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3
Q

sx of excessive arousal

A

hypervigilance
cognitive dysfunction
panic/fear
hallucinations/psychosis

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4
Q

how do wake-promoting drugs target histamine

A

enhancement of histamine release

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5
Q

how do sleep-promoting drugs target histamine

A

blockage of H1 receptors

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6
Q

which 2 enzymes terminate the action of histamine

A

-MAOB converts N-methylhistamine to N-methyltransferase
-in the periphery it is terminated by diamine oxidase

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7
Q

what is best known as targets for antihistamines

A

postsynaptic H1 receptors

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8
Q

what are well known targets of heartburn medicine

A

postsynaptic H2 receptors

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9
Q

which receptor functions as an autoreceptor for histamine

A

presynaptic H3 receptors

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10
Q

what does histamine do at NMDA receptors

A

alter the action of glutamate

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11
Q

where do all histamine neurons arise

A

small area in the hypothalamus called the tuberomammillary nucleus

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12
Q

what brain structure regulates arousal, wakefulness, and sleep

A

tuberomammillary nucleus in the hypothalamus

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13
Q

what is the difference between orexin and hypocretin

A

nothing. 2 scientists discovered at the same time and named two different things

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14
Q

what does hypocretin usually refer to

A

gene or genetic products

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15
Q

what does orexin typically refer to

A

peptide neurotransmitters themselves

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16
Q

which neurons are localized exclusively in hypothalamic areas

A

orexin/hypocretin

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17
Q

what happens when there is diminished release of orexins/hypocretins onto downstream wake-promoting neurotransmitters

A

destabilized wakefulness

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18
Q

which neurons degenerate in narcolepsy

A

orexin/hypocretin

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19
Q

what receptors regulate the postsynaptic actions of orexin A and B

A

orexin1 and orexin 2 receptors

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20
Q

which type of orexin binds to orexin 1 receptors and what does that do

A

orexin A binds and leads to increased intracellular calcium and activation of the sodium-calcium exchanger

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21
Q

which orexins bind to orexin recepto 2 and what does that do

A

orexin A and B
either increased expression of NMDA glutamate receptors or inactivation of G-protein-regulated potassium channels

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22
Q

what functions does orexin play a role in

A

stabilizing wakefulness and regulating feeding behavior and reward

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23
Q

how do orexin neurons fire during wakefulness

A

fire with tonic frequency to maintain arousal

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24
Q

where does orexin stimulate acetylcholine release from

A

basal forebrain
pendunculopontine and laterodorsal tegmental area

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25
Q

where does orexin stimulate dopamine release from

A

VTA

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26
Q

where do orexins stimulate release of norepinephrine from

A

locus coeruleus

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27
Q

where does orexins stimultate srotonin release from

A

raphe nuclei

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28
Q

where does orexin stimulate release of histamine from

A

tuberomammillary nucleus

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29
Q

how does the homeostatic sleep drive work

A

adenosine starts to accumulate as as the person tires throughout the day which ultimately lead to disinhibition of ventrolateral preoptic nucleus and release of GABA in the sleep circuit

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30
Q

what mediates the circadian wake drive

A

light acting on the suprachiasmatic nucleus

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31
Q

what happens when light acts on the suprachiasmatic nucleus

A

stimulates release of orexin which enhances release of other wake-promoting neurotransmitters

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32
Q

where is histamine released in the circadian wake drive and what does that do

A

released onto neurons throughout the cortex and VLPO and it inhibits the release of GABA

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33
Q

what happens in the circadian wake drive when light fades

A

NE and 5HT are released onto neurons in the hypothalamus causing negative feedback to inhibit orexin release. Without orexin wakefulness is no longer stabilized

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34
Q

how many times do ultradian cycles repeat during one night

A

4-5 times

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35
Q

what are the 5 ultradian cycles

A

REM
NREM stages 1-4

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36
Q

which regions of the brain are activated during REM sleep

A

thalamus
visual cortex
limbic regions

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37
Q

Role of GABA in ultradian cycles

A

it is on all night and rises for the first few hours of sleep, plateaus, and steadily declines before arousal

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38
Q

role or orexin in ultradian cycles

A

decreases during first few hours of sleep, plateaus, then steadily rises before arousal

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39
Q

acetylcholine levels in ultradian cycles

A

lowest levels during stage 4 NREM
levels peak during REM

40
Q

levels of dopamine, norepinephrine, serotonin, and histamine in ultradian cycles

A

lowest during REM
peaks during stage 2 NREM

41
Q

what effect can disordered sleep have on your health

A

circulating levels of leptin (anorectic) and ghrelin (orexigenic) are disrupted leading to dysfunctional insulin, glucose, and lipid metabolism that increases risk for DM, obesity, cardio disease

42
Q

cognitive effects of disordered sleep

A

24h sleep deprivation same as legal intoxication

43
Q

what does REM sleep modulate

A

memory consolidation

44
Q

what is NREM sleep good for

A

declarative and procedural memory

45
Q

neurobiological effects of sleep disturbance

A

impairs hippocampal neurogenesis which may explain the behavioral effects of sleep disturbance

46
Q

what happens in insomnia in relation to sleep/wake circuits

A

more a problem with not being able to shut off arousal circuits than inability to initiate sleep circuits

47
Q

what subunits must receptors contain to be sensitive to benzodiazepines

A

two B subunits
a Y subunit
two A subunits

48
Q

where do benzodiazepine bind to GABAA receptors

A

allosteric sites

49
Q

how do benzodiazepines work to improve sleep

A

facilitate GABA neurotransmission in inhibitory sleep circuits arising from the hypothalamus and the VLPO

50
Q

what receptor subunit is targeted by all GABAA PAMs

A

a1

51
Q

what are the 2 dual orexin receptor antagonists (DORAs)

A

suvorexant
lemborexant

52
Q

how does suvorexant work differently than benzos and Z drugs

A

inhibits ability of orexin to promote release of wake-promoting neurotransmitters rather than increase GABA

53
Q

what type of inhibitor are suvorexant and lemborexant

A

reversible. Inhibition is reversed as natural orexin builds up in the morning

54
Q

what is the serotonergic hypnotic used for insomnia

A

trazadone

55
Q

what receptors does trazadone antagonize

A

5HT2A, a1, and H1

56
Q

how does Trazadone work

A

blocks serotonin, norepinephrine, and histaine to reduce arousal rather than stimulate sleep drive

57
Q

what is the H1 receptor antagonist that is used as a hypnotic

A

doxepin at low doses

58
Q

GABAA receptor occupancy threshold for inducing sleep

A

25-30%

59
Q

DORA receptor occupancy threshold for sleep induction

A

around 65%

60
Q

behavioral treatments for insomnia

A

sleep hygiene
relaxation training
stimulus control therapy
sleep restriction therapy
intensive sleep retraining

61
Q

what is one of the most common causes of daytime sleepiness

A

obstructive sleep apnea

62
Q

central disorders of hypersomnolence

A

idiopathic hypersomnia
narcolepsy

63
Q

diagnostic criteria for idiopathic hypersomnia

A

-excessive daytime sleepiness for at least 3 months
-short sleep-onset latency period
-fewer than 2 periods of REM at onset of sleep (polysomnography)

64
Q

what is cataplexy

A

sudden loss of muscle tone often triggered by strong emotions

65
Q

why does cataplexy occur in narcolepsy

A

profound loss of orexin neurons in the hypothalamus causes low daytime levels which destabilizes motor function resulting in intrusion of motor inhibition and loss of motor tone during wakefulness

66
Q

which polymorphism is present in 90% of those with narcolepsy

A

HLA DQB1-0602

67
Q

4 circadian rhythm disorders

A

shift work disorder
advanced sleep phase disorder
delayed sleep phase disorder
non-24-hour sleep-wake disorder

68
Q

what does shift work disorder increase your risk of

A

cardiometabolic issues
cancer
GI disease
mood disorders

69
Q

what is advanced sleep phase disorder

A

go to sleep earlier than desired
wake earlier than desired
usually by 6h outside normal sleep/wake times

70
Q

how do you dx advanced sleep phase disorder

A

sleep and/or actigraphy for at least 1wk
morningness-eveningness questionnaire (MEQ)

71
Q

what is delayed sleep phase disorder

A

unable to sleep until early morning hours then sleep late into the day

72
Q

delayed sleep phase disorder is associated with polymorphisms in what gene

A

CLOCK

73
Q

who is primarily affected by non-24-hour sleep-wake disorder

A

blind people

74
Q

circadian treatment for delayed sleep phase disorder and shift work disorder

A

morning light/evening melatonin

75
Q

circadian treatment for advance sleep phase disorder

A

early evening light and early morning melatonin

76
Q

how does melatonin regulate circadian rhythm

A

acts at M1 and M2 sites on the suprachiasmatic nucleus

77
Q

melatonergic hypnotic that improves sleep onset but not necessarily maintenance

A

ramelteon

78
Q

Classification of ramelteon

A

M1/M2 agonist

79
Q

what is the worlds most widely consumed psychoactive drug

A

caffeine

80
Q

how does caffeine promote wakefulness

A

blocks the effects of adenosine buildup and restores affinity of D2 for dopamine over adenosine. Enhanced dopamine is wake-promoting

81
Q

which neurotransmitters are enhanced by amphetamine and methylphenidate

A

dopamine
norepinephrine

82
Q

wake-promoting action of methylphenidate

A

NDRI

83
Q

wake-promoting action of amphetamines

A

dopamine releasers and competitive VMAT2 inhibitors

84
Q

what is approved for the treatment of narcolepsy but not OSA or shift work disorder

A

amphetamine

85
Q

what is approved for treatment of narcolepsy AND OSA and shift work disorder

A

Modafinil
armodafinil

86
Q

modafinil and DAT

A

weak inhibitor with incomplete occupancy

87
Q

what properties of modafinil allow it to promote wakefulness without promoting abuse

A

slow rise in plasma levels w/ incomplete DAT occupancy

88
Q

how does dopamine release from modafinil cause arousal

A

cortex is aroused by dopamine release leading to downstream release of histamine and further activation of lateral hypothalamus with orexin with orexin release

89
Q

does modafinil still work in patients with a loss of hypothalamic orexin neurons in narcolepsy

A

yes

90
Q

effectiveness of modafinil for narcolepsy

A

effective but not as much as methylphenidate or amphetamine

91
Q

wake-promoting NDRI that is more potent than wellbutrin but less potent than amphetamines and has a short half-life

A

solriamfetol

92
Q

classification of pitolisant

A

H3 presynaptic antagonist

93
Q

how does pitolisant work

A

blocks normal action of presynaptic H3 autoreceptors to inhibit histamine release. This causes disinhibition of presynaptic histamine which is wake-promoting

94
Q

what is the thought behind why sodium oxybate (GHB) works to treat disorders of hypersomnia

A

rather than waking you up, it promotes such good sleep you are more alert during the day

95
Q

how is GHB formed

A

from GABA

96
Q

actions of sodium oxybate

A

full agonist at GHB receptors
partial agonist at GABAB receptors

97
Q

what med can reduce hypnagogic hallucinations and sleep paralysis

A

sodium oxybate

Psychopharmacology (13 decks)

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