87b - Circadian Rhythms and Sleep Flashcards

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1
Q

What EEG pattern will you see if a patient is in Stage N1 sleep?

A

Theta waves

In general, the waves are slowing down

N1 = “light sleep”

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2
Q

Where is the primary circaidan pacemaker located?

From where does it receive input?

A

Suprachiasmatic nucleus in the hypothalamus

Receives photic input from the retinohypothalamic tract

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3
Q

What EEG pattern will you see if a patient is in Stage N3 sleep?

A

Larger slower waves at delta frequency (5-6 Hz)

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4
Q

What is the FDA-approed medication for the treatment of non-24h sleep wake disorder/

A

Hetlioz (tasimelteon)

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5
Q

In general, what is the treatment for circaidan rhythm sleep disorders?

A

Timed light and/or melatonin exposure

Planned sleep schedules

Hypnotics are not recommended; they can help with sleep, but will not re-set the circadian rhythm

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6
Q

Describe the molecular clock and associated feedback loop

A

The following process takes ~24h, thus providing the basis for our intrinsic circadian rhythm

  • CLOCK and BMAL1 are synthesized
  • They exit the nucleus and dimerize
  • CLOCK/BMAL1 dimer acts as a transcription factor that promotes the transcription of PER and CRY
  • They exit the nucelus and dimerize
  • They are phosphorylated by CK1ε/δ​
    • This is the rate limiting step
  • Phosphorylated PER/CRY dimer acts as a transcription factor that inhibits its own transcription
  • When enough Phosphorylated PER/CRY gets into the nucleus transcription of PER and CRY stops, thus allowing it to start being transcribec again
    *
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7
Q

The VLPO [activates/inhibits] orexinergic nuclei

This stabilizes [wakefulness/sleep]

A

The VLPO inhibits orexinergic nuclei

This stabilizes sleep

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8
Q

The [ARAS/VLPO] dominates when we are asleep, while the [ARAS/VLPO] dominates when we are awake

A

The VLPO dominates when we are asleep, while the ARAS ​dominates when we are awake

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9
Q

When does the “biological morning” start?

A

After the core body temperature minimum (which is usually ~2h before wake)

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10
Q

Which neuromodulator stabilizes the “awake” state?

A

Orexin (aka hypocretin)

@scientists y tho ¯_(-_-)

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11
Q

Inhibiting the VLPO results in [sleep/wakefulness]

A

Inhibiting the VLPO results in wakefulenss

  • The VLPO usually inhibits wake-promoting nuclei
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12
Q

Orexinergic nuclei stabilize the [ARAS/VLPO]

This results in [wakefulness/sleep]

A

Orexinergic nuclei stabilize the ARAS

This results in wakefulness

  • The VLPO inhibits orexinergic nuclei, resulting in sleep
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13
Q

When do you give melatonin to treat:

  • Delayed sleep/wake disorder:
  • Non-24h sleep/wake disorder:
A
  • Delayed sleep/wake disorder:
    • Give melatonin ~5h before bedtime
  • Non-24h sleep/wake disorder:
    • Give melatonin ~1h before bedtime
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14
Q

What EEG pattern will you see if a patient is in REM sleep?

A

Theta waves (just like Stage N1 sleep), may also see beta waves (like awake state)

But also:

  • Atonia
  • Rapid eye movements behind closed eyelids
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15
Q

Which neurotransmitters are most active in wakefulness?

A

ACh

Monoamines (NE, Serotonin, Dopamine)

Orexin

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16
Q

What EEG pattern will you see if a patient is in Stage N2 sleep?

A

Sleep spindles

K complexes

Theta waves will still be present

17
Q

Describe the two process model that controls sleep

A

Process S (sleep) and Process C (circadian) work together

  • Process S
    • Homeostatic sleep need
    • The longer we are awake, the more we need to sleep
  • Proces C
    • Helps us stay awake in the afternoon when our sleep drive is high, but we’re supposed to be awake
    • Falls at night, allowing process S to knock us out
18
Q

Which system modulates arousal?

A

Ascending reticular activating system

  • Nuclei of monoamines
  • Inhibits the VLPO
19
Q

Traveling from Hawaii to Chicago will result in jet lag, with symptoms similar to which circadian rhythm sleep disorder?

How would you minimize these symtoms?

A

Similar to delayed sleep/wake disorder

  • Light in the biological morning when you arrive in Chicago
    • After the core body temp minimum, usually about 2h before wake time
  • Melatonin ~5h before bedtime
20
Q

Which neurotransmitters are most active in NREM sleep?

A

VLPO

Some monoamines (Serotonin, NE, Dopamine)

21
Q

Which neurotransmitters are most active in REM sleep?

A

ACh

MCH

VLPO

22
Q

Light exposure at night and melatonin in the morning [advance/delay] the circadian clock

A

Light exposure at night and melatonin in the morning delay the circadian clock

Note: to treat advanced sleep/wake disorder, planned sleep schedule + light exposure in the evening. Usually don’t give melatoin in the morning

23
Q

Light exposure in the biological morning and melatonin at night [advance/delay] the circadian clock

A

Light exposure in the biological morning and melatonin at night advance the circadian clock

24
Q

ACh is active in [Wakefulness/NREM sleep/REM sleep]

A

ACh is active in wakefulnes and REM sleep

25
Q

What EEG pattern will you see if a patient is in “relaxed wakefulness?”

A

Alpha waves

26
Q

REM sleep occurs when monoamines levels are [low/high] and ACh levels are [low/high]

A

REM sleep occurs when monoamines levels are low and ACh levels are high

MCH and VLPO activity are also high