Sleep and Consciousness Flashcards

1
Q

What are the different stages of consciousness according to the Glasgow Coma Scale (GCS)

A

Coma, unconsciousness, sleep, drowsy wakeful, normal wakeful and high arousal

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2
Q

What is an EEG?

A

Electroencephalograph

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3
Q

What does an EEG represent?

A

Consists of very small voltages that are recorded from the scalp and this represents the average activity of thousands of nerve cells

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4
Q

What are EEGs commonly used for?

A

Detecting seizure activity and sleep/coma

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5
Q

How does a coma present on an EEG?

A

No electrical activity to note

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6
Q

Which structure coordinates sleep and wakefulness?

A

Reticular formation in the pons

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7
Q

What are the 5 stages of sleep?

A

Normal sleep (four stages) and then REM sleep

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8
Q

When is growth hormone mainly secreted?

A

In normal/slow-wave sleep

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9
Q

How are cortisol levels affected by sleep?

A

Decrease during sleep

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10
Q

Why does BP reduce during sleep?

A

Reduced sympathetic output

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11
Q

How is leptin affected by sleep?

A

Leptin is released from fat cells during normal sleep which provides satiety

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12
Q

How may sleep deprivation lead to perpetual hunger?

A

Leptin isn’t being secreted by fat cells to signal satiety

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13
Q

What is the function of REM sleep?

A

Memory consolidation (short to long-term) and removing junk and defragmenting memories

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14
Q

How long is a sleep cycle?

A

90 minutes

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15
Q

Which molecules increase sleepiness in the body?

A

High CCK (satiety) and high adenosine levels

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16
Q

Which molecules inhibit sleepiness in the body?

A

Increased ghrelin (hunger hormone) and low blood glucose

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17
Q

How does caffeine keep us awake?

A

Caffeine antagonises A1 adenosine receptor to prevent sleepiness

18
Q

How do hunger hormones and adenosine affect our arousal and sleepiness?

A

Blood brain barrier is more permeable around the medial and ventrolateral pre optic nuclei in the thalamus so molecules can cross

19
Q

How do the pre-optic nuclei in the thalamus regulate sleep?

A

By modulating the activity of the tuberomamillary nucleus (TMN) histaminergic neurones

20
Q

What is the consequence of a lesion to the suprachiasmatic nucleus?

A

Destroys the diurnal sleep rhythm in animals

21
Q

Explain why we stay awake during the day and sleep at night (diurnal rhythm).

A

Suprachiasmatic nucleus lies above optic chiasm and receives input from the retina (specifically photoreceptors send action potentials constantly during daylight) which then project to the TMN

22
Q

What is narcolepsy?

A

Disorder due to abnormal sleep tendencies, excessive daytime sleepiness and pathological REM sleep

23
Q

What is thought to be the cause of narcolepsy?

A

Insufficient orexigens (appetite stimulants) due to autoimmune T-cell attack

24
Q

Where are orexigenic neurones located?

A

Posterior hypothalamus

25
How do orexigens work to stimulate wakefulness?
From posterior hypothalamus project to brainstem nuclei to stimulate release of amine transmitters (acetylcholine, NA, serotonin and dopamine)
26
When does sleep onset occur?
When the signals from preoptic nuclei (blood chemicals) and suprachiasmatic nucleus (day/light cycles) inhibit the histamine and orexin neurones to inhibit excitatory drive to monoamine neurones of pontine reticular formation
27
In the context of the sleep/wake cycle: where are dopaminergic cells found?
Ventral tegmental area
28
In the context of the sleep/wake cycle: where are cholinergic cells found?
Pedunculopontine nucleus
29
In the context of the sleep/wake cycle: where are noradrenergic cells found?
Locus coeruleus
30
In the context of the sleep/wake cycle: where are serotonergic cells found?
Raphe nuclei
31
How is the cholinergic system affected by the sleep/wake cycle?
Decreased firing except for in REM sleep where ACh is released to allow activation of thalamus and cortex
32
How is the noradrenaline system affected by the sleep/wake cycle?
Reduced firing in all sleep, implicated in why we don't remember our dreams
33
How is the dopaminergic system affected by the sleep/wake cycle?
Reduced firing in all forms of sleep
34
Why are we paralysed in REM sleep?
Dopamine levels are low; nigrostriatal dopamine systems are required to activate the basal ganglia so that we can move (change motor programmes)
35
How do amphetamines and cocaine prevent sleep?
Cause continual release of dopamine and noradrenaline
36
How is the serotonergic system affected by the sleep/wake cycle?
Completely inactive in REM
37
How does the serotonergic system create dreams?
Lack of serotonin activity means thalamus can't transmit messages from sensory receptors to the cortex, so the cortex 'freewheels' and generates its own images and perceptions to create dreams
38
How do SSRIs and SNRIs affect sleep?
Decrease in sleep efficiency and suppresses REM sleep
39
How do tricyclic antidepressants affect sleep?
Promote sleep by blocking H1 and preventing noradrenaline uptake
40
How do MAO inhibitors affect sleep?
Structurally similar to amphetamines so can cause insomnia
41
How may insomnia be treated?
Antihistamines (nytol), benzodiazepines and Z drugs
42
What is sleep apnoea?
When the motor innervation to the respiratory muscles ceases during REM sleep leading to airway obstruction --> individual wakes due to CO2 build up --> hyperventilation and agitation