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28 Cards in this Set
- Front
- Back
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In the waking state, what does the thalamus do? x3
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1. Cortical activation
2. Sleep spindles 3. EEG synchronization |
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What provides the sleep/wake switch?
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Hypothalamus
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What provides the REM/SWS switch?
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ARAS/Brainstem
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What provides the circadian clock in our brains?
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Suprachiasmatic nucleus
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In Sleep/Wake, where do the following NT's come from?
- Histamine - Dopamine - Serotonin - Norepinephrine |
TMN Tuberomammillary nucleus
VTA Ventral Tegmental Area Raphe's nucleus Locus Ceruleus |
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Hypocretins are made where?
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Lateral hypothalamus
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What does hypocretin system do?
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Maintains/reinforces alertness
by increasing activity of all major ascending arousal systems. |
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T/F - Hypocretin receptors (Hcrt-1 and Hcrt-2) are always excitatory.
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True
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Where is the major sleep promoting area of the brain, and how does it promote sleep?
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VLPO of the anterior hypothalamus
uses GABA to inhibit all major wake-promoting regions. |
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What are the major wake promoting regions? x4
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Thalamus
Hypothalamus Brainstem Suprachiasmatic nucleus |
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REM sleep is controlled by a subpopulation of _________ neurons in the __________ . These are called " ________ " neurons.
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Cholinergic
PPT/LDT REM-on |
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What does it mean that the REM sleep system is of "dual projections."
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Cholinergic REM-on neurons activate the thalamocortical system , leading to fast EEG resembling waking state EEG.
REM-on neurons also descend to activate neurons in the medial medulla to inhibit motor neurons using Glycine and GABA. |
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What are the key differences between REM sleep and wakefulness.x2
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1. Complete absence of activity in the wakefulness-promoting aminergic pathway during REM sleep.
2. Loss of muscle tone (atonia) during REM sleep. |
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Aminergic neurons can be found where?
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Brainstem and posterior hypothalamus
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Modafinil does what?
Give example of Modafinil. |
Block reuptake of dopamine (wakefulness promoting) and NE (inhibits sleep promotion), thus promoting wakefulness by hitting that shit on both sides.
Provigil. |
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T/F - Alerting agents improve and normalize sleepiness.
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False - Improving sleep yes, but not normalize.
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Use of alerting agents such as amphetamines and methylphenidate leads to what? x2
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Tolerance
Rebound hypersomnolence |
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Mechanism of Benzodiazepines.
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Binds to BZD1, BZD2, and BZD3 nonspecifically.
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Mechanism of Nonbenzodiazepines (Z drugs).
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Preferential binding to BZD-1
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Which BZD receptor is primary for sedative and hypnotic effects?
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BZD-1
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What do hypnotic drugs do to sleep stages.
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Decrease stage 1, 3, and 4
Increase stage 2 Decrease percentage and density of REM sleep, while increasing REM latency. |
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What are the clinical implications of hypnotic short half-life?
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Rebound Insomnia
Anterograde Amnesia Tolerance |
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What are the clinical implications of hypnotic long half-life?
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Daytime Sedation
Hangover |
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Contraindications for hypnotic use. x3
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Sleep Apnea
EtOH excessive Potential for alertness during sleep periods. |
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When would you recommend Flurazepam (Dalmane)?
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For patients who need early morning awakening, and needing to deal with anxiety.
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Which sleep med has a potential for amnesia, anxiety, and rebound insomnia?
a.) Flurazepam b.) Zolpidem c.) Zaleplon d.) none of the above |
c.) Zaleplon (Sonata)
is the shortest half life hypnotic. May cause all these symptoms including headache, weakness, drowsiness, and dizziness. |
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What are the treatment strategies x2 for transient insomnia?
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1.) use lowest effective dose of BZD
2.) half life matches the desired duration |
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Zolpidem (Ambien) binds to which receptor?
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BZ1 mostly
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