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Supporting life block > Sleep& sleep deprivation > Flashcards

Sleep& sleep deprivation Flashcards

1
Q

What are the functions of sleep?

A
  • Conservation of effort& energy
  • Production of hormones
  • Augmentation of immune system
  • Memory consolidation
  • Mood regulation
  • Promotion of optimal performance
  • Cleans the brain of toxins (mainly beta amyloid, cleared on a higher rate during sleep)
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2
Q

Outline the REM stage of sleep

A
  • Occurs 90mins after being awake
  • Your body goes through several REM stages, first one is the shortest
  • Your brain& body are energized and dreaming occurs
  • Thought to be involved in the process of storing memories, learning and balancing your mood
  • Muscle tone declines during REM sleep
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3
Q

How do we enter sleep and why?

A
  • Sleep is entered through NREM.

- If it is entered through REM, the person is either depressed, sleep deprived or has narcolepsy

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4
Q

Outline the basics of sleep

A
  • SWS (slow wave sleep/deep sleep) dominates in the first third of the night
  • REM predominates in the last third of the night
  • Wakefulness in sleep is usually less than 5% of the night
  • stage 2= the majority of sleep
  • NREM= 75-80% of sleep
  • REM=20-25% of sleep
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5
Q

Describe HR in NREM vs REM sleep

A
  • NREM= regular

- REM=irregular

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6
Q

Describe BP in NREM vs REM sleep

A
  • NREM=regular

- REM=variable

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7
Q

Describe RR in NREM vs REM sleep

A 
NREM= regular
REM= irregular
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8
Q

Describe responses to o2& co2 changes in NREM vs REM sleep

A

NREM= decreased

REM=significantly depressed

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9
Q

Describe skeletal muscle tone in NREM vs REM sleep

A 
NREM= preserved
REM= absent
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10
Q

Describe brain o2 consumption & CBF in NREM vs REM sleep

A 
NREM= reduced
REM= increased
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11
Q

Describe thermoregulation in NREM vs REM sleep

A

NREM= Homeothermic

REM=poikilothermic

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12
Q

Describe penile tumescence/vaginal engorgement in NREM vs REM sleep

A

NREM= infrequent
REM= frequent
All men without physiological erectile dysfunction experience nocturnal penile tumescence, usually three to five times during the night, typically during REM sleep

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13
Q

Describe how sleep architecture changes with age.

A
  • SWS decreases by 2% per decade until age 60
  • loss of 30 mins per decade in TST(total sleep time) from 16-83 years
  • Reduced time in N3, with corresponding increases in N1& N2
  • REM sleep shifts to slightly earlier at night
  • All non-pathological changes
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14
Q

What is the deepest stage of sleep

A
  • REM

- but N3 is the deepest stage of NREM sleep

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15
Q

Describe the changes in sleep as part of the ageing process

A
  • Decrease in TST, less SWS (loss of synaptic density), advanced sleep-wake phase, less homeostatic drive, napping returns
  • Co-morbidities associated with ageing apart from age-related changes
  • Medical, psychiatric, social, environmental factors & polypharmacy may have an impact on sleep.
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16
Q

Outline what Circadian rhythm sleep disorders are

A
  • Mismatch between endogenous biological rhythms& required social time
  • This results in an impairment in sleep& wake functioning
  • Sleep is normal when patients can sleep at their desired time
  • Divided into intrinsic( primary) and extrinsic (secondary)
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17
Q

Describe Intrinsic (primary) Circadian rhythm sleep disorders.

A
  • Alterations of the circadian timekeeping system
  • May result from:
  • DSPD(delayed sleep phase disorder)=a sleep disorder that occurs when a person’s circadian ryhthm (sleep/wake cycle) is delayed from the typical day/night cycle
  • ASPD(advanced sleep phase disorder)=characterized by a recurrent pattern of early evening (e.g. 7-9 pm) sleepiness and early morning awakening.
  • Non-24h e.g in blindness
  • Irregular e.g dementia
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18
Q

Describe Extrinsic (secondary) Circadian rhythm sleep disorders.

A

-Misalignment between intrinsic& extrinsic signals
May result from:
-Shift work disorder
-Jet lag disorder

19
Q

What is delayed sleep phase?

A
  • Sleep is out of phase with socially acceptable sleep-wake times
  • Evening chronotype preference
  • About 9.25 hours of sleep required
  • Sleep deprivation may lead to worse academic performance, health & well-being
20
Q

What are the clinical features of DSPD?

A
  • Unable to sleep advance onset
  • Restriction to conventional bedtimes results in sleep deprivation
  • Insomnia &/or excessive sleepiness
  • Sleep is normal when they can sleep at their desired times
  • Symptoms are chronic
  • History of hypnotic use, alcohol at bed time, psychiatric interventions( e.g antidepressants, psychotherapy)
  • 70% will have a comorbid psychological/ psychiatric disorder
21
Q

What is the treatment of DSPD?

A

combination of:

  • Phototherapy
  • Melatonin
  • CBT-I
  • examine for psychiatric co-morbidity
22
Q

Outline shift work disorder(SWD)

A
  • Insomnia/excessive sleepiness with a recurring work schedule that overlaps the usual time for sleep
  • Symptoms are associated with work schedule for 1 month
  • Sleep disturbance is not otherwise explained by another sleep disorder, medication or substance misuse
  • Supported by sleep log or actigraphy
23
Q

What are some short-term consequences of SWD?

A
  • sleepiness at night
  • Mood disturbances
  • short day time sleep
  • Higher risks at night( e.g accidents)
  • GI problems
24
Q

What are some long-term consequences of SWD?

A
  • Sleep disorder
  • Mood disorder
  • Cardiovascular risk
  • Alcohol/drug abuse
  • Cancer(breast- circadian disruption appears to be carcinogenic
25
Q

Define sleep deprivation

A

-A sufficient lack of restorative sleep over a cumulative period so as to cause physical or psychiatric symptoms and affect daily performance

26
Q

What are some effects of sleep deprivation

A
  • irritability
  • Cognitive impairment
  • Memory lapses/loss
  • Impaired moral judgement
  • Severe yawning
  • Hallucinations
  • Symptoms similar to ADHD
  • Impaired immune system
  • Risk of diabetes type 2
  • Increased HR variability
  • Decreased reaction time& accuracy
  • Tremors
  • Aches
  • Growth suppression
  • risk of obesity
  • Decreased temp.
27
Q

Outline hallucinations in sleep deprivation

A
  • Occur at the sleep/wake transition
  • Hypnagogic hallucinations= occur on going to sleep
  • Hypnopompic hallucinations= occur on waking from sleep
  • May occur with isolated sleep paralysis
  • Simple visual or auditory hallucinations
  • Can be frightening, but insight is retained, and there’s no delusional expansion vs those hallucinations occurring in psychotic illnesses
28
Q

Are visual hallucinations in psychotic illnesses common?

A

NO!

29
Q

What are parasomnias?

A
  • Abnormal behaviours that occur in association with sleep
  • occur during NREM & REM sleep
  • Diagnostically challenging due to: poor patient recall; limited history if no witness account; routine investigations are often normal
30
Q

Outline NREM parasomnias

A
  • occur in the first 1/3rd of the night
  • frequency varies
  • Onset in childhood
  • Confusional arousal
  • Sleep walking (somnabulism)
  • Night terrors (pavor nocturnus)
  • Sleep-related eating disorders
  • Sexsomnia
31
Q

How can we treat night terrors?

A

-Education. CBT-I to stabilise sleep-wake patterns
-scheduled awakening
-keep the room safe; be aware of new environments
-Only wake fully if the episode lasts>45 mins
Pregablin, Clonazepam

32
Q

How can we distinguish night terrors from nocturnal panic attacks

A

With nocturnal panic attacks there is…

  • Physiologic warning (HR or breathing changes)
  • Daytime symptoms of anxiety, panic or agoraphobia
33
Q

How can we distinguish night terrors from nightmares

A
  • Usual recollection

- Often during REM sleep

34
Q

What are some of the characteristics of NREM parasomnias?

A
  • Family history
  • Exacerbated by sleep deprivation, stress, alcohol, OSA(obstructive sleep apnea), fever
  • Patient is often amnesic for the event, but may have partial recollection
  • partner may describe tearfulness or confusion
35
Q

How can we treat NREM parasomnias?

A
  • Reassurance (benign)
  • Education-CBT-I to improve sleep pattern
  • avoid triggers
  • safety
  • anti-depressants(e.g Fluoxetine, Trazadone)
  • Clonazepam
  • Melatonin
36
Q

Outline REM parasomnias

A
  • Second half of the night
  • 1-2 episodes per night
  • Frequency varies
  • REM sleep behavior disorder
  • Nightmares-Rx: stop causative meds( e.g Beta-blockers,L-Dopa), CBT, Prazosin
  • Catathrenia-nocturnal groaning
37
Q

What are the characteristics of REM sleep behaviour disorder?

A
  • 2nd half of the night
  • Usually a single episode per night
  • frequency varies
  • Mean age of onset 50-65 years
  • Loss of muscle atonia during REM sleep and a history of abnormal behaviours during sleep
  • Often correlate with recalled vivid dreams- usually aggressive
  • May injure bed partner
38
Q

What can contribute to REM sleep behavior disorder?

A
  • Male gender predilection
  • Mean onset age range is 50-65years
  • unknown prevalence
  • Post-mortem studies suggest Lewy body pathology
  • A significant proportion of patients with idiopathic RBD( IRBD) may have mild cognitive impairment at diagnosis
  • Anti-depressants can induce RBD or make it worse
  • Appears that the anti-depressants unmask a subclinical RBD (except buproprion)
39
Q

What is the association between RBD and Parkinson’s disease?

A
  • RBD is the most robost non-motor predictor of developing Parkinson’s disease, and it is a predictor of early cognitive impairment
  • Present in other neurodegenerative conditions(mainly synucleopathies) such as MSA &DLB
  • IRBD could convert to a neurodegenerative disease- risk increases as time since diagnosis increases
  • Coexistence of mild cognitive impairment indicates the progression to dementia in less than 5 years
40
Q

How can RBD be diagnoses?

A

-Clinical history may be highly suggestive but a v-PSG (visual polysomnography) would confirm the diagnosis ( catching an episode or REM without atonia)

41
Q

List some RBD mimics

A
  • Severe OSA
  • severe PLMS, RMD
  • Sleep talking, confusional arousals, night terrors(possible overlap disorders
  • Nocturnal seizures
  • Nocturnal dissociative episodes
42
Q

How can we treat RBD?

A
  • Patient education
  • If possible, discontinue meds which may be contributing
  • Safety e.g separate beds
  • Simple home oximetry in the sleep
  • medication if necessary…
  • Clonazepam (cons= daytime sedation possible, worsens OSA and symptoms return on stopping)
  • Melatonin ( typical doses=2-8mg, long lasting symptom relief, better tolerated, restores atonia)
43
Q

Why may melatonin be used to treat a pt with DSPD?

A
  • Hormone made naturally by your body

- Lets your body know it’s night time so that you can relax and fall asleep easier

Supporting life block (28 decks)

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