Task 3 Flashcards

1
Q

Adult obstructive sleep apnea

  • Diagnosis and definitions
  • Jordan
A
  • obstructive sleep apnea (OSA) repetitive pharyngeal collapse during sleep
  • apnea= airflow reduced to less than 10% for more than 10sec, obstructive if respiratory effect is present
  • hypopnea=airflow reduced to less than 30% for more than 10sec
  • report snoring, witnessed apneas, waking up with a chocking sensation and excessive sleepiness
  • indicators are family history and physical attributes
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2
Q

Adult obstructive sleep apnea

  • pathophysiology and risk factors
  • Jordan
A
  • problem of upper airway anatomy
  • stability of the respiratory control system important causative factor
  • the arousal treshold
  • long volume causative factor
  • factors that impair upper airway anatomy or muscle function are predisposed factors to OSA
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3
Q

Adult obstructive sleep apnea

  • obese gender and age
  • Jordan
A
  • Male major risk
  • obese risk factor because affecting anatomy of airways as fat is disposed in surrounding structures and influence long volume and therefore stability of respiratory control
  • age risk factor because reduced tethering of upper airway due to loss of elastic recoil in lung, reduced arousal treshold and efficiency might fall with age
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4
Q

Adult obstructive sleep apnea

  • nasal continuous positive airway pressure
  • CPAP and other treatment
  • Jordan
A
  • Nasal continuous positive airway pressure (CPAP) treatment for adults with sleep apnea (60-70%)
  • education and support improve adherence
  • nasal difficulties and type of mask
  • hypnotherapy when using CPAP
  • alternatives are oral devices, upper airway surgery, positional therapy and other conservative measure (avoidance of depressants such as alcohol)
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5
Q

DSM-V Obstructive sleep apnea hypopnea

-DSM-V

A

A either 1 or 2
1. evidence by PSG of at least 5 obstructive apneas
or hypopneas per hour of sleep and following
symptoms
a. nocturnal breathing disturbances: snoring,
gasping or breathing pauses during sleep
b. daytime sleepiness, fatigue, not explained by
another mental disorder of medical condition
2. evidence by PSG of 15 or more apneas per hour of
sleep regardless of accompanying symptoms

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6
Q

Restless leg syndrome

-Rama

A
  • characterised by unpleasant sensations in the legs, occuring at rest, especially in bed
  • accompanied by urge to move the limbs –>relief
  • urge to move or unpleasant feeling worsened during periods of sleep or inactivity
  • not explained by something else
  • idiopathic and hereditary condition –>primary RLS
  • associated with other conditions –> secondary RLS
  • occur at any age and is chronic and worsen with age
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7
Q

Periodic limb movement disorder

-Rama

A
  • PLMD characterised by limb movements while asleep result in insomnia and excessive daytime sleepiness
  • predominant in first half and declne through course of the night
  • diagnosis by PSG utilizing EMG recordings from leg muscles
  • movements counted if they last 0,5-5s and occur in series of 4 or more at intervals of 5-90s
  • 5 per hour in childeren, 15 in adult cases
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8
Q

Difference RLS and PLMD

-Rama

A
  • RLS occurs while awake as well as when asleep, voluntary response to uncomfortable feeling
  • PLMD is involuntary, and patients often unaware of these movements
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9
Q

Pathology RLS

-Rama

A
  • RLS highly responsive to dopaminergic agents (L-dopa)
  • L-dopa can cross the blood-brain barrier
  • RLS worse during night when dopamine levels are at their lowest
  • Iron critical factor biosynthesis of dopamine
  • decreased iron concentrations in substantia nigra
  • hypocretin-1 levels were increased
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10
Q

Treatment RLS and PLMD

-Rama

A
  • Levodopa or dopamine agonists improve RLS and PLMD

- proper sleep hygiene and avoid exacerbating factors

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11
Q

Kleine-levin syndrome

  • what is it
  • Arnulf
A

A recurrent hypersomnia
1 excessive sleepiness 2 days - 4 weeks
2episodes once per year
3between episodes and hypersomnia normal
B one of the following next to hypersomnia criteria
cognitive abnormalities, abnormal behavior,
hyperphagia, hypersexuality
-increasingly tired aften identifiable triggering event
-hypersomnia and at least one of confusion, apathy and derealisation

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12
Q

Kleine-Levin syndrome

  • presentation and symptoms during episodes
  • Arnulf
A
  • exhausted, sleeping with no clear circadian rhythm
  • apathetic, having or showing no or little feeling
  • impaired communication, concentration, decision making and memory
  • derealisation in all patients
  • repetitive or depressed moods and anxiety
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13
Q

Kleine-Levin syndrome

  • abnormal findings
  • possible pathophysiological mechanisms
  • Arnulf
A
  • widespread abnormalities seen on SPECT
  • hypoperfusion seen in thalamus, basal ganglia, medial temporal lobe and frontal lobe
  • encephalopathy (disorder of the brain) occurs during episodes of KLS
  • Temporal-lobe dysfunction explain derealisation
  • frontal-lobe involvement explain apathy and disinhibition
  • thalamus explains hypersomnia
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14
Q

Kleine-Levin syndrome

  • Treatment
  • Arnulf
A
  • no effective pharmacological

- benefit from reassurance, maintenance of a simple hygiene routine and management at home

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15
Q

Narcolepsy

  • what is it
  • van der heide
A
  • Narcolepsy with cataplexy is a disturbed hypocretin transmission
  • narcolepsy without cataplexy is excessive daytime sleepiness (EDS) in combination with abnormal expressions of REM sleep on PSG
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16
Q

Narcolepsy

  • Excessive daytime sleepiness
  • van der heide
A
  • EDS leading symptom narcolepsy
  • Monotonous activities increase sleepiness
  • sleep attacks less than 20 min and 1-10 times each day
17
Q

Narcolepsy

  • cataplexy
  • van der heide
A
  • charaterized by sudden bilateral loss of muscle tone, with preserved consciousness, elicited by emotions
  • complete attacks cause falls
  • provoked by emotional trigger
  • attack last seconds to half a minute
18
Q

Narcolepsy

  • hypnagogic hallucinations
  • van der heide
A
  • HH are vivid, dreamlike experiences
  • extremely unpleasant and frightening
  • occurrence during transition between wakefulness and sleep
19
Q

Narcolepsy

  • sleep paralysis
  • van der heide
A

-the inability to move at awakening or when falling asleep while being subjectively awake and conscious

20
Q

Narcolepsy

  • disturbed nocturnal sleep
  • van der heide
A
  • sleep latency is very short in narcolepsy

- frequent awakenings

21
Q

Narcolepsy

  • associated symptoms
  • van der heide
A
  • automatic behavior
  • memory complaints
  • obesity –> hypocretin deficiency, decreased activity
22
Q

Narcolepsy

  • comorbidities
  • van der heide
A
  • sleep apnea and parasomnias
  • PLMS and RBD higher prevalence
  • depression
23
Q

Narcolepsy

  • diagnosis narcolepsy with cataplexy
  • van der heide
A

A. complaint excessive daytime sleepiness for at least 3 months
B. history of cataplexy
C. confirmed by PSG, MSLT and hypocretin-1 measure
D. not explained by another disorder

24
Q

Narcolepsy

  • differential diagnosis narcolepsy without cataplexy
  • van der heide
A

A. complaint excessive daytime sleepiness for at least 3 months
B. no cataplexy
induced by chronic sleep deprivation
low hypocretin can prove diagnosis

25
Q

Narcolepsy

  • The hypocretin system
  • van der heide
A
  • hypocretin system includes two peptides (hypocretin 1 and 2) and two receptors
  • hypocretin-1 has equal affinity for both receptors, hypocretin-2 binds to hypocretin receptor-2
  • produces in dorsolateral hypothalamus but project throughout whole brain
26
Q

Narcolepsy

  • sleep switch
  • van der heide
A
  • nuclei for promoting wakefulness and sleep located in dorsal and medial raphe nuclei, the LC, the ventral periaqueductal gray matter (vPAG) and the PPT and LDT
  • ascending arousal system (AAS) = TMN and 2 branches
  • choninergic branch–>the PPT/LDT project to thalamic reticular nucleus and activate cerbral cortex
  • Monoaminergic branch–>the rest project to the cortex of entire hemisphere
  • wakefulness both branches active
  • ventrolateral preoptic nucleus (VLPO) facilitates sleep
  • during NREM both inhibited by the VLPO
  • during REM only monoaminergic inhibited
27
Q

Narcolepsy

  • flip flop
  • van der heide
A
  • VLPO and monoaminergic nuclei have a reciprocal inhibition (sleep switch)
  • feedback loop with a self-reinforcing firing pattern resulting in two possible states
28
Q

Narcolepsy

  • state boundary control
  • van der heide
A
  • all systems narcolepsy explained by ‘loss of state boundary control’
  • no sleep or wake state can be maintained for a normal length of time
  • phenomena occur out of context
29
Q

Narcolepsy

  • treatment behavioral modification
  • van der heide
A
  • hypocretin substitution not because cannot cross blood-brain barrier easily
  • live regular life
  • more sensitive to sleep-inducing properties of carbohydrates
  • alcohol consumption should be avoided
30
Q

Narcolepsy

-pharmalogical treatment

A
  • Sodium oxybate only available improving drug
  • long term improvement nocturnal sleep with SO
  • stimulants treatment of EDS, but side-effects and tolerance
  • SO effective in reducing EDS
  • SO and tricyclic antidepressants most effective
  • TCA REM sleep inhibitor
  • SO inhibitor of cataplexy
  • nocturnal sleep short term benzodiazepines
31
Q

SO improves excessive daytime sleepiness

-Black

A
  • dosis of modafinil (placebo) and SO (placebo)
  • after 4 weeks PSG and Maintenance of Wakefulness test
  • SO and modafinil both effective, together additive effect
  • SO beneficial as both monotherapy and adjunctive therapy