Sleep and Consciousness Flashcards

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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
Q

How do orexigens work to stimulate wakefulness?

A

From posterior hypothalamus project to brainstem nuclei to stimulate release of amine transmitters (acetylcholine, NA, serotonin and dopamine)

26
Q

When does sleep onset occur?

A

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
Q

In the context of the sleep/wake cycle: where are dopaminergic cells found?

A

Ventral tegmental area

28
Q

In the context of the sleep/wake cycle: where are cholinergic cells found?

A

Pedunculopontine nucleus

29
Q

In the context of the sleep/wake cycle: where are noradrenergic cells found?

A

Locus coeruleus

30
Q

In the context of the sleep/wake cycle: where are serotonergic cells found?

A

Raphe nuclei

31
Q

How is the cholinergic system affected by the sleep/wake cycle?

A

Decreased firing except for in REM sleep where ACh is released to allow activation of thalamus and cortex

32
Q

How is the noradrenaline system affected by the sleep/wake cycle?

A

Reduced firing in all sleep, implicated in why we don’t remember our dreams

33
Q

How is the dopaminergic system affected by the sleep/wake cycle?

A

Reduced firing in all forms of sleep

34
Q

Why are we paralysed in REM sleep?

A

Dopamine levels are low; nigrostriatal dopamine systems are required to activate the basal ganglia so that we can move (change motor programmes)

35
Q

How do amphetamines and cocaine prevent sleep?

A

Cause continual release of dopamine and noradrenaline

36
Q

How is the serotonergic system affected by the sleep/wake cycle?

A

Completely inactive in REM

37
Q

How does the serotonergic system create dreams?

A

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
Q

How do SSRIs and SNRIs affect sleep?

A

Decrease in sleep efficiency and suppresses REM sleep

39
Q

How do tricyclic antidepressants affect sleep?

A

Promote sleep by blocking H1 and preventing noradrenaline uptake

40
Q

How do MAO inhibitors affect sleep?

A

Structurally similar to amphetamines so can cause insomnia

41
Q

How may insomnia be treated?

A

Antihistamines (nytol), benzodiazepines and Z drugs

42
Q

What is sleep apnoea?

A

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