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Pathophysiology - Respiratory > Introduction to Sleep and Sleep Medicine > Flashcards

Introduction to Sleep and Sleep Medicine Flashcards

1
Q

Is sleep an active or a passive process?

A

VLPO secretes GABA to inhibit waking neurotransmitters

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2
Q

What are the two opposing processes of the biologic clock?

A

Process S - homeostatic Sleep drive - builds throughout the day

Process C - Circadian arousal process - alerting effects of biologic clock. Opposes process S until the “off” biologic clock, which allows you to be very sleepy.

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3
Q

What pattern of sleep is associated with depression? Dementia?

A

Depression - Decreased sleep latency, middle insomnia (similar to alcohol). Increased REM sleep / decreased REM latency.

Dementia - flips day / night often

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4
Q

How does metabolic rate, minute ventilation, tidal volume, breathing frequency, and heart rate change with NREM sleep?

A

Due to parasympathetic increase:

Metabolic rate - decreases
Tidal volume - decreases
Minute ventilation - decreased (due to Vt drop)
Respiratory rate - unchanged
Heart rate - decreases
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5
Q

What are the stages of NREM sleep?

A

N1: light sleep, still feel partially awake
N2: true sleep, thoughts are short / fragmented. Sleep spindles and K complexes
N3: Slow wave sleep - little or no mentation

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6
Q

What happens in REM sleep?

A

Dreaming, muscle atonia (except diaphragm), cardiopulmonary instability (HR, Ve remain below wake values, but fluctuate with REM)

poikilothermic state - does not shiver or sweat to regulate temp

penile erection

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7
Q

What stage of sleep is extremely rejuvenative? When in the night does it predominate? How does it change with age?

A

Slow wave sleep (N3)
Decreases with age - our sleep doesnt feel as good

Early in the night - longer duration. Later in the night, REM is longer and there is less N3

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8
Q

When does REM occur in sleep and what is childhood sleep characterized by?

A

90 minutes into sleep onset

Childhood - characterized by longer total sleep time, and sleep of all stages

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9
Q

What are examples of parasomnias? Which ones will you remember / won’t remember??

A
  1. Arousal disorders - sleep walking, night terrors (childhood, NREM, won’t remember)
  2. REM-associated - nightmares (will remember), sleep paralysis, REM behavior disorder (acting out dreams)
  3. Sleep enuresis
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10
Q

What are the components of the polysomnography?

A

EEG, EOG (electrooculograms), EMG (for movement of chin, tibia), ECG, airflow at nose/mouth, respiratory movements, pulse ox

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11
Q

What are the three types of insomnia by time period?

A

Transient - less than 1 week, due to anxiety / emotion
Short-term: up to severeal weeks / less than three months, failure of adjustment to sleep-wake
Chronic: >3 months

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12
Q

What are common sleep-related disorders which can precipitate insomnia?

A

RLS, OSA, disruptive or irregular sleep-wake schedule, inadequate sleep hygiene

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13
Q

What is necessary to diagnose insomnia as a disorder rather than simply a complaint?

A

Presence of daytime compliants: unrefreshed, fatigued / sleepy throughout day, poor concentration / attentiveness / memory

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14
Q

What is the difference between primary / secondary insomnia?

A

Primary - not associated with other medical conditions

Secondary - associated with sleep-related disorders, medications, medical disorders (GERD, chronic pain), or psychiatric disorders

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15
Q

What are the three main theories which seems to determine a patient will have primary insomnia?

A

Hyperarousal theory - people tend to be very anxious and have more beta EEG activity

Cognitive theory - patients ruminate and excessively problem solve, worry about sleeping all day

Behavioral theory - poor sleep hygiene

Physiological factors - heightened autonomic arousal, HPA dysregulation

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16
Q

What does the stimulus control model tell you to do when trying to fall asleep?

A

If you are in bed for 15+ minutes without falling asleep, get up and go somewhere else until you’re tired
-> you don’t want to associate the bed with activities which aren’t sleeping

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17
Q

What are some Circadian rhythm disorders?

A

Delayed sleep phase disorder (sleep later in the night), time zone change syndrome (jet lag)

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18
Q

What is the most common type of primary insomnia?

A

Psychophysiologic Insomnia

  • > disorder of high tension before going to bed from learned sleep-preventing associations
  • > overly trying to fall asleep which is causing arousal
  • > can sleep better on couch or away from home
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19
Q

How is insomnia best managed?

A

Cognitive behavioral therapy - sleep hygiene, stimulus control therapy, and sleep restriction therapy

2nd line: Pharmacologic treatment - sedative hypnotics, melatonin antagonists

20
Q

What is the rough definition of EDS?

A

Excessive Daytime Sleepiness

Patient is “sleepy” in situations which alertness is warranted throughout the day, not just fatigued, lacking in energy, or depressed

21
Q

What is physiologic vs manifest sleep tendency?

A

Physiologic - your tendency to fall asleep in a dark, quiet room aka in the absence of other stimulation

Manifest - The moment to moment changes in how sleepy you are based on external factors - i.e. what sleepiness you manifest as a result of physiologic + everything else

22
Q

What are the determinants of physiological sleepiness?

A

Quantity / quality of sleep (sleep debt), Circadian rhythms, drugs, and CNS

23
Q

What is multiple sleep latency test and how is it useful for diagnosing EDS?

A

Measures tendency to fall asleep while lying in a quiet, dark bedroom at 4 times during the day

Normal daytime sleep latency should be greater than 15 min in well-rested adults, and no REM should occur in a 20 min nap

24
Q

What scale is used to track a patient’s daytime sleepiness overtime, and will decrease with treatment?

A

Epworth Sleepiness Scale

-> survey measures chance of dosing off in several situations

25
Q

What is the apneic threshold? How does it tend to differ between men and women? What stage of sleep does it occur in?

A

The level of CO2 at which breathing will stop during NREM sleep (lower threshold is better, because you won’t stop breathing til very low CO2 concentrations, allowing for some degree of hyperventilation)

Threshold is higher in men -> more prone to apnea

26
Q

How does breathing change as we sleep and why is this such a problem?

A

N1: irregular and periodic
N2: Regular
REM: irregular with the rapid eye movements

Problem because although BMR decreases in sleep, breathing does moreso and PaCO2 will rise -> need to keep breathing to blow off CO2

27
Q

What happens to the upper airway during sleep?

A

Dilator activity decreases, especially in REM (muscle atonia)

  • > decreased response to negative pressure
  • > increased airway resistance due to smaller lumen, with greater collapsibility
28
Q

What is obstructive sleep apnea vs obstructive sleep apnea syndrome?

A

OSA - being awoken by sleep due to upper airway collapse / obstruction during sleep. Recurrent O2 desurations and arousal from sleep

OSA syndrome - when associated with daytime sequellae

29
Q

What is the definition of apnea, and how can central vs obstructive be told apart?

A

Cessation of airflow for >10 seconds

Central: no ventilatory effort at all (seen in CHF)
Obstructive - persistent ventilatory effort seen with abdomen and chest moving

30
Q

What is a hypopnea?

A

20-50% reduction in airflow which causes either an awakening or a 2-4% drop in O2 saturation

31
Q

How is the severity of OSA determined?

A

Apnea-hypopnea index

-> sum total of apneic and hypopneic events per hour. <5 events is normal. >30 events is severe

32
Q

What might there be a familial tendency to OSA?

A

Craniofacial skeletal abnormalities like retrognathia and micrognathia can contribute to airway obstruction

33
Q

What commonly causes OSA in child and adults?

A

Children - adenotonsillar hyperplasia

Adults - Obesity

34
Q

What cardiovascular morbidity is associated with OSA?

A

Hypertension
Metabolic syndrome: insulin resistance, HTN, proinflammatory state, oxidative stress, hyperlipidemia
Heart disease
CVA

35
Q

What are common daytime symptoms of OSA?

A

Excessive daytime sleepiness
Nonrefreshed feeling on waking
Problems with memory / concentration

36
Q

What are the conservative measures to control OSA?

A

Weight loss, alcohol avoidance, sleeping on side, treatment of sinus congestion

37
Q

What are the more aggressive treatments for OSA?

A

CPAP (splint the upper airway with positive pressure), dental devices, surgery (especially with adenotonsillar hyperplasia)

38
Q

What is the definition of narcolepsy?

A

Uncontrollable urges to sleep for short duration, with patient quickly falling into REM sleep

39
Q

What is the pathophysiology of narcolepsy?

A

Loss of orexin neurons in hypothalamus. It is associated with a specific HLA allele, but is not believed to be autoimmune.

40
Q

What are the symptoms of narcolepsy?

A

**Cataplexy - sudden brief loss of muscle control following strong emotions (laughter, surprise, anger)

EDS

Sleep paralysis

Hypnagogic hallucinations

Automatic behavior - wake up and realize they’ve been doing something (driving, cooking)

41
Q

What will narcoleptic patients show by polysomnography and MSLT?

A

Polysomnography - onset to REM less than 60 minutes

MSLT - sleep latency is <5 minutes, with 2 or more naps having REM onset within 10 min

42
Q

How is narcolepsy treated? Include EDS, cataplexy, and behavioral.

A

EDS - treated with stimulants like modafinil, methylphenidate, and dextroamphetamine

Cataplexy - TCAs, SSRIs, or sodium oxybate (GHB derivative)

Behavioral - scheduled naps, good sleep hygiene

43
Q

What are the features of restless leg syndrome (RLS)? How will sleep be different?

A

Urge to move due to uncomfortable sensations in legs, especially at night. Worsened by relaxation

Sleep is also involved with periodic limb movements and much more messing up of covers

44
Q

What conditions are associated with RLS and why?

A 
Iron deficiency (ferritin < 50)
Renal insufficiency and pregnancy (low iron states)
Parkinson's (low dopamine state)

Iron is required for production of dopamine, RLS is associated with low dopamine levels

45
Q

What drugs are used to treat RLS?

A

Dopamine agonists: Pramipexole and ropinirole

Anticonvulsants: Gabapentin

Pathophysiology - Respiratory (24 decks)

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