Introduction to Sleep and Sleep Medicine Flashcards
Is sleep an active or a passive process?
VLPO secretes GABA to inhibit waking neurotransmitters
What are the two opposing processes of the biologic clock?
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.
What pattern of sleep is associated with depression? Dementia?
Depression - Decreased sleep latency, middle insomnia (similar to alcohol). Increased REM sleep / decreased REM latency.
Dementia - flips day / night often
How does metabolic rate, minute ventilation, tidal volume, breathing frequency, and heart rate change with NREM sleep?
Due to parasympathetic increase:
Metabolic rate - decreases Tidal volume - decreases Minute ventilation - decreased (due to Vt drop) Respiratory rate - unchanged Heart rate - decreases
What are the stages of NREM sleep?
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
What happens in REM sleep?
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
What stage of sleep is extremely rejuvenative? When in the night does it predominate? How does it change with age?
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
When does REM occur in sleep and what is childhood sleep characterized by?
90 minutes into sleep onset
Childhood - characterized by longer total sleep time, and sleep of all stages
What are examples of parasomnias? Which ones will you remember / won’t remember??
- Arousal disorders - sleep walking, night terrors (childhood, NREM, won’t remember)
- REM-associated - nightmares (will remember), sleep paralysis, REM behavior disorder (acting out dreams)
- Sleep enuresis
What are the components of the polysomnography?
EEG, EOG (electrooculograms), EMG (for movement of chin, tibia), ECG, airflow at nose/mouth, respiratory movements, pulse ox
What are the three types of insomnia by time period?
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
What are common sleep-related disorders which can precipitate insomnia?
RLS, OSA, disruptive or irregular sleep-wake schedule, inadequate sleep hygiene
What is necessary to diagnose insomnia as a disorder rather than simply a complaint?
Presence of daytime compliants: unrefreshed, fatigued / sleepy throughout day, poor concentration / attentiveness / memory
What is the difference between primary / secondary insomnia?
Primary - not associated with other medical conditions
Secondary - associated with sleep-related disorders, medications, medical disorders (GERD, chronic pain), or psychiatric disorders
What are the three main theories which seems to determine a patient will have primary insomnia?
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
What does the stimulus control model tell you to do when trying to fall asleep?
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
What are some Circadian rhythm disorders?
Delayed sleep phase disorder (sleep later in the night), time zone change syndrome (jet lag)
What is the most common type of primary insomnia?
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
How is insomnia best managed?
Cognitive behavioral therapy - sleep hygiene, stimulus control therapy, and sleep restriction therapy
2nd line: Pharmacologic treatment - sedative hypnotics, melatonin antagonists
What is the rough definition of EDS?
Excessive Daytime Sleepiness
Patient is “sleepy” in situations which alertness is warranted throughout the day, not just fatigued, lacking in energy, or depressed
What is physiologic vs manifest sleep tendency?
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
What are the determinants of physiological sleepiness?
Quantity / quality of sleep (sleep debt), Circadian rhythms, drugs, and CNS
What is multiple sleep latency test and how is it useful for diagnosing EDS?
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
What scale is used to track a patient’s daytime sleepiness overtime, and will decrease with treatment?
Epworth Sleepiness Scale
-> survey measures chance of dosing off in several situations
What is the apneic threshold? How does it tend to differ between men and women? What stage of sleep does it occur in?
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
How does breathing change as we sleep and why is this such a problem?
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
What happens to the upper airway during sleep?
Dilator activity decreases, especially in REM (muscle atonia)
- > decreased response to negative pressure
- > increased airway resistance due to smaller lumen, with greater collapsibility
What is obstructive sleep apnea vs obstructive sleep apnea syndrome?
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
What is the definition of apnea, and how can central vs obstructive be told apart?
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
What is a hypopnea?
20-50% reduction in airflow which causes either an awakening or a 2-4% drop in O2 saturation
How is the severity of OSA determined?
Apnea-hypopnea index
-> sum total of apneic and hypopneic events per hour. <5 events is normal. >30 events is severe
What might there be a familial tendency to OSA?
Craniofacial skeletal abnormalities like retrognathia and micrognathia can contribute to airway obstruction
What commonly causes OSA in child and adults?
Children - adenotonsillar hyperplasia
Adults - Obesity
What cardiovascular morbidity is associated with OSA?
Hypertension
Metabolic syndrome: insulin resistance, HTN, proinflammatory state, oxidative stress, hyperlipidemia
Heart disease
CVA
What are common daytime symptoms of OSA?
Excessive daytime sleepiness
Nonrefreshed feeling on waking
Problems with memory / concentration
What are the conservative measures to control OSA?
Weight loss, alcohol avoidance, sleeping on side, treatment of sinus congestion
What are the more aggressive treatments for OSA?
CPAP (splint the upper airway with positive pressure), dental devices, surgery (especially with adenotonsillar hyperplasia)
What is the definition of narcolepsy?
Uncontrollable urges to sleep for short duration, with patient quickly falling into REM sleep
What is the pathophysiology of narcolepsy?
Loss of orexin neurons in hypothalamus. It is associated with a specific HLA allele, but is not believed to be autoimmune.
What are the symptoms of narcolepsy?
**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)
What will narcoleptic patients show by polysomnography and MSLT?
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
How is narcolepsy treated? Include EDS, cataplexy, and behavioral.
EDS - treated with stimulants like modafinil, methylphenidate, and dextroamphetamine
Cataplexy - TCAs, SSRIs, or sodium oxybate (GHB derivative)
Behavioral - scheduled naps, good sleep hygiene
What are the features of restless leg syndrome (RLS)? How will sleep be different?
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
What conditions are associated with RLS and why?
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
What drugs are used to treat RLS?
Dopamine agonists: Pramipexole and ropinirole
Anticonvulsants: Gabapentin
