Sleep and Sleep Disorders Flashcards

1
Q

Time in life spent sleeping

A

1/3

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2
Q

Brain plasticity

A

brain remodels and purges old information during sleep

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3
Q

purpose of sleep

A
  • restoration
  • conservation of energy
  • allow processing of input
  • memory consolidation depends on sleep
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4
Q

number of Americans who suffer form sleep disorders

A

40 million

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5
Q

percent of men and women with obstructive sleep apnea who are not clinically diagnosed

A

93% of women

82% of men

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6
Q

excessive daytime sleepiness impairs:

A
  • human performance that can lead to accidents at work, at home, or on the road
  • 31% drivers fall asleep at some point
  • academic performance, learning, and judgment
  • increased weight, mood disorders, stress, CV complications
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7
Q

definition of sleep

A
  • reversible behavioral state of perceptual disengagement from and unresponsiveness to the environment
  • a very complex amalgam of physiologic and behavior processes
  • a process, unlike coma, that is physiologic, recurrent, and reversible
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8
Q

biologic clock activity

A
  • the body’s master “clock” is located in the suprachiasmatic nucleus (SCN) of the hypothalamus
  • light-dark signals reach the SCN via a retinohypothalamic track
  • SCN cells are circadian oscillators, exhibiting a stable, biphasic firing cycle
  • 24.18 hours is clock period
  • clock is mainly determined by light and dark cycles
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9
Q

alerting effects of the biological clock

A
  • oppose the homeostatic sleep drive with its alerting effect
  • allow for consolidated WAKE during the subjective day
  • Initiate a mid-day dip in biologic clock alerting activities
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10
Q

Homeostatic sleep drive

A
  • proportional to the amount of previous WAKE and sleep debt.
  • sleep debt builds throughout the day
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11
Q

amount of sleep needed for adults and children

A
  • adults = 7-8 hrs

- children = >9 hrs

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12
Q

body clock

A
  • responsible for alternating drives for wakefulness and sleepiness
  • as long as there are no rapid shifts in environmental time cues (shift work or multiple time zone travel), the body clock allows us to consolidate sleep to the night and wakefulness to the day
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13
Q

how to keep circadian clock on time

A
  • awake approximately the same time each day

- obtain bright light during daytime hours

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14
Q

how to maximize homeostatic sleep drive

A
  • limit napping

- only go to bed when you’re sleepy

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15
Q

how to reduce arousals

A
  • limit or eliminate caffeine intake

- shut down your day at least one hour before bedtime

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16
Q

principles of sleep hygiene

A

keep circadian clock on time, maximize homeostatic sleep drive, reduce arousals

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17
Q

how to improve sleep hygiene

A
  • take hot showers or baths at least 2 hours before bedtime
  • place the alarm clock where it cannot be seen
  • keep the bedroom dark, quiet, and cool, with no pets
  • avoid stressful activities in the evening
  • use the bed only for sleep and intimacy
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18
Q

Sleep ROS

A
  • do you wake up feeling rested and refreshed?
  • how long does it take you to fall asleep?
  • do you snore, or has your bed partner complained about you snoring?
  • do you have any leg discomfort at night?
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19
Q

Two issues profoundly affected by sleeping disorders

A

diabetes and cardiovascular problems

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20
Q

Excessive daytime sleepiness vs. fatigue

A
  • sleepiness: able to sleep if given a chance

- fatigue: tired but does not fall asleep (body is tired but mind is very active)

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21
Q

prevalence of insomnia

A

~30% within the last year

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22
Q

Risk factors of insomnia

A
  • female gender (RR = 1.41)
  • medical, psychiatric, and substance abuse issues
  • social factors (many covary)
  • possible genetic factors
  • age
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23
Q

Markers of hyperarousal

A
  • reduced parasympathetic tone
  • increased basal metabolism
  • elevated circulating catecholamines
  • increased electroencephalogram (EEG) beta activity (cortical activation)
  • elevated body temperature
  • high activity of HPA axis
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24
Q

characteristics contributing to or reinforced by poor sleep hygiene

A
  • tension anxiety, arousal in association with efforts to sleep, or in the usual sleeping environment
  • negative expectations regarding ability to sleep
  • clockwatching
  • ability to fall asleep when not trying to
  • better sleep away from home
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25
Q

cognitive behavioral treatment of insomnia

A
  • counseling in sleep hygiene
  • cognitive therapy and stimulus control therapy
  • sleep restriction therapy
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26
Q

sleep restriction therapy

A
  • for insomnia
  • set alarm same time each morning
  • no daytime naps
  • sleep diary for 7 days and calculate total sleep per night (total sleep time = TST)
  • set up schedule restricting time spent in bed to equal TST
  • as sleep improves, bedtime advanced by 15-20 mins to go to bed earlier
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27
Q

Restless leg syndrome

A

-distressing need/urge to move the legs, usually accompanied by an uncomfortable, deep-seated sensation in the legs that is: 1. brought on by rest, 2. relieved with moving or walking, 3. worse in the night or evening (circadian)

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28
Q

Primary RLS

A

primary (idiopathic)

  • no precipitating factor
  • younger age onset
  • genetic association
  • autosomal dominant
  • chromosome 12/14
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29
Q

secondary RLS

A
  • iron deficiency (~25%)
  • Pregnancy (~25%)
  • Renal failure (up to 60%)
  • Drugs (antidepressants, SSRIs)
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30
Q

RLS and pregnancy

A
  • extremely common in pregnancy
  • ~11-50%
  • severity increases in 3rd trimester
  • etiology could be anemia, abdominal distention, inactivity
  • no increase in fetal risk
  • parity increases risk in mothers in dose dependent way
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31
Q

management of RLS

A
  • discontinue use of: SSRIs, tricyclics (amitriptyline), dopamine antagonists (risperidone), antihistamines
  • treat secondary causes: iron deficiency (ferritin <50ng/mL), renal disease
32
Q

pharmacologic management of RLS

A
  • dopamine agonists (pramipexole, ropinirole) are first-line treatment
  • start low and slowly increase to effective dose
  • dose (30-90 mins) before bed
  • antivipate augmentation and rebound
33
Q

drug options for treating RLS

A
  • dopaminergic agents
  • iron, if ferritin <50ng/mL
  • anticonvulsants (gabapentin)
  • low-potency opiates
  • benzodiazepines
34
Q

circadian rhythm sleep disorders

A
  • jet lag
  • delayed sleep phase (sleep onset insomnia)
  • advanced sleep phase (sleep maintenance insomnia)
  • shift work sleep disorder
  • irregular sleep-wake rhythm
35
Q

special populations of circadian rhythm sleep disorders

A

-shift workers, adolescents, elderly and chronically hospitalized, travelers, physicians and nurses

36
Q

most common sleep disorder

A

-insomnia

37
Q

pathogenesis of insomnia

A

-behavioral, cognitive, physiologic

38
Q

treatment of insomnia

A
  • cognitive behavioral therapy

- pharmocologic (benzodiazepine receptor agonists, melatonin receptor agonist)

39
Q

REM behavior disorder

A
  • normal REM sleep associated with inhibition of skeletal muscles to prevent “acting out” dreams
  • RBD involves failure of the inhibition
  • now shown to be a precursor to certain degenerative neurologic conditions such as parkinson’s disease in a significant percent (40%) of these patients
  • responds well to conazepine
40
Q

Narcolepsy

A
  • Excessive Daytime Sleepiness
  • Cataplexy: brief emotionally triggered episodes of muscle weakness (50%)
  • Sleep paralysis (40-80%)
  • Hypnogogic and hypnopompic hallucinations (40-80%)
  • Fragmented sleep
  • Mild obesity
41
Q

parasomnias

A
  • Sleep walking
  • Night terrors
  • Bed Wetting
  • Nocturnal eating
42
Q

Obstructive sleep apnea

A
  • Most common form of SDB (sleep disorder breathing)
  • partial or complete collapse of upper airway
  • muscles controlling soft palate and tongue relax
  • common mechanism for the deadly triad: CV disease, diabetes, cancer
  • defined as AHI >/= 5
43
Q

prevalence of OSA

A
  • 1 in 5 has mild OSA, 1 in 15 has moderate to severe OSA
  • 9% of women, 25% of men in middle-aged working population have OSA
  • 75% severe SDB patients not diagnosed (SDB = sleep disorder breathing)
44
Q

apnea

A

-cessation of airflow for >/= 10 seconds (obstructive, central, mixed)

45
Q

obstructive apnea

A

no airflow (apnea) but with continued effort to breathe in both abdominal and thoracic tracings

46
Q

central apnea

A

no airflow (apnea) with NO effort to breathe

47
Q

mixed apnea

A

combination of central and obstructive apneas with the central component always appearing first

48
Q

hypopnea

A

decrease in airflow lasting >/= 10 seconds with 30% reduction in airflow and with at least 4% O2 desaturation from baseline

49
Q

flow limitation

A
  • Upper airway narrowing

- Earliest sign of impending upper airway closure

50
Q

RERA

A
  • Respiratory Effort Related Arousal

- Flow limitation leading to arousal

51
Q

AHI

A

Apnea/hypopnea index

  • Number of apneas and/or hypopneas per hour of sleep (or study time)
  • Reflects the “severity” of the SDB (AHI 0-4 = Normal range, AHI 5-14 = Mild sleep apnea, AHI 15-30 = Moderate sleep apnea, AHI > 30 = Severe sleep apnea)
52
Q

airway collapse: repeated asphyxia cycle

A

state shift to sleep > upper airway collapse > hypoxia and obstruction > respiratory effort related arousal

53
Q

arousal threshold

A
  • transient arousal that changes the physiology from sleep to wake with consequent increase in muscle tone and opening up of the airway
  • arousal threshold of O2 saturation is 88% in non-REM and 70% in REM
54
Q

physiologic consequences of OSA

A
  • hypoxia, hypercapnia, and arousal all lead to sympathetic nervous system activation
  • activation of SNS releases norepinephrine and this can have deleterious cardiovascular consequences
55
Q

incidence of OSA

A
  • most serious common sleep disorder
  • 5-9% of adults in western countries
  • 2% per hear for AHI >/= 15
  • same prevalence as asthma in general population
56
Q

Risk factors for OSA

A
  • Obesity associated with adult OSA
  • Snoring
  • Male gender (until about age 50)
  • Postmenopausal state
  • Upper airway anatomic obstruction (including nose)
  • Ethnicity: black, Asian, or Hispanic
57
Q

negative effects of sleep-disordered breathing

A
  • Neurocognitive impairment (memory loss)
  • Daytime sleepiness
  • Impaired quality of life
  • Metabolic effects
  • Cardiovascular effects
  • Cancer
58
Q

signs and symptoms of OSA

A
  • Snoring
  • Unrefreshing sleep/daytime sleepiness
  • Witnessed apneas
  • Insomnia
  • Restless sleep
  • Nocturnal heartburn
  • Morning headache
  • Nocturia
  • Dry mouth, sore throat, sinus and nasal congestion
  • Mood, memory, and learning problems
  • Parasomnias
  • Impotence
  • Enuresis
  • Many with almost no symptoms
59
Q

Cardiovascular effects of OSA

A
  • Systemic hypertension
  • Pulmonary hypertension (with sustained hypoxemia)
  • Arrhythmias, especially atrial fibrillation
  • Coronary artery disease
  • Congestive heart failure
  • Stroke and transient ischemic attacks (TIA)
  • Mortality
60
Q

OSA and metabolic dysfunction

A
  • associated with glucose intolerance and insulin resistance, independent of potential confounders
  • OSA is independent risk factor for metabolic syndrome
  • hypoxemia may be presdisposing factor to metabolic alterations associated with OSA
  • CPAP improves insulin sensitivity in some patients with OSA
61
Q

OSA severity by AHI

A
  • > /= 5 = mild
  • > /= 15 = moderate
  • > /= 30 = severe
62
Q

tests to identify sleep apnea patients

A
  • Berlin
  • ESS
  • STOP BANG
  • HST
  • PSG
63
Q

Epworth sleepiness scale (ESS)

A
  • Self-administered, eight questions
  • Rate sleepiness from 0-3
  • Measures the average sleep propensity in those eight different situations
  • ESS scores >10 can be said to represent excessive daytime sleepiness
64
Q

STOP BANG

A
  • Do you Snore loudly (louder than talking or loud enough to be heard through the closed door) ?
  • Do you often feel Tired, fatigued or sleepy during daytime?
  • Has anyone Observed you stop breathing during your sleep?
  • Do you have or are you being treated for high blood Pressure?
  • BMI :Is your body mass index greater than 35
  • Age :Are you 50 years old or older
  • Neck : Is your neck circumference >17” (male) or > 16”(female)
  • Gender : Are you a male
  • STOP: 2/4 significant chance of OSA
  • STOP +BANG: Very likely moderate to severe OSA
65
Q

Home vs in lab sleep testing

A

Home:

  • Less intimidating so patient more likely to agree to testing
  • Less expensive
  • Useful in ruling IN sleep apnea, not ruling it out so mainly in patients with likely moderate to severe sleep apnea
  • Do not detect RERA

In Lab:

  • More intimidating, strange environment impacts sleep experience
  • More expensive
  • Measures sleep directly so first choice in assessing daytime sleepiness of uncertain etiology
  • Detect RERA
  • Technician present so can correct problems
  • ALLOWS TRIAL of CPAP
66
Q

indications for home sleep testing

A
  • Patient resistant to coming to lab
  • Long travel time to lab
  • Physical limitations in patient
  • Completely negative history but need clearance for job
  • Follow up after treatment with Oral Appliance
  • If negative you still need to deal with symptomatic patient
67
Q

methods of SDB treatment

A

-Positive airway pressure (PAP) is generally accepted as the gold standard of treatment for SDB

Alternatives:

  • Surgery (UPPP, LAUP, mandibular advancement)
  • Dental appliances
  • Drug therapies
  • Tracheostomy
  • Pacing (upper airway, cardiac)
68
Q

PAP for OSA

A
  • Newer machines smaller and almost silent
  • Heated humidifier and tubing help comfort
  • Many more mask options
  • Nasal pillows
  • Nasal masks
  • Full face masks
  • Main barrier is often psychological
69
Q

Oral appliances for OSA

A
  • Hold mandible forward clearing airway
  • Can be as effective as PAP but usually isn’t
  • Hard to predict level of success
  • Better accepted than PAP overall
  • Impact on quality of life and BP equal to PAP
  • Main issue is comfort, jaw discomfort, tooth movement
  • indicated for mild to moderate sleep apnea
70
Q

surgery for OSA

A
  • Tracheostomy
  • UPPP (uvulopalatopharyngealplasty)
  • Pillar Procedure
  • MMA (maxillomandibular advancement)
  • Inspire
71
Q

Sleep apnea prevalence in comorbidities

A
  • Drug resistant hypertension (80%)
  • obesity (77%)
  • pacemakers (59%)
  • congestive heart failure (50%)
  • atrial fibrillation (50%)
  • diabetes (50%)
  • all hypertension (35%)
  • coronary artery disease (30%)
72
Q

sleep apnea and diabetes

A
  • OSA is typically associated with conditions of metabolic syndrome such as hypertension, obesity and diabetes
  • 50% of patients with type 2 diabetes have sleep apnea
  • Sleep apnea is an independent contributing factor to insulin resistance, previously attributed to obesity
  • New studies have shown that CPAP may improve glucose control and insulin sensitivity; previous studies were mixed
  • CPAP may reduce cardiovascular risk (the leading cause of death among diabetes sufferers)
73
Q

sleep apnea and CV disease

A

High prevalence of sleep apnea in cardiovascular disease patients
-30% to 80% of patients for common CVD states

Proven benefits from sleep apnea therapy in lowering blood pressure
-4mm Hg to 10mm Hg reduction with CPAP therapy

Proven benefits from sleep apnea therapy in improving cardiovascular health
-Left ventricular ejection fraction, six-minute walk, VO2 max, afterload, BNP

74
Q

why treat sleep apnea before any surgery

A
  • Sleep apnea and hypertension are the leading independent predictors of complications in bariatric surgery after surgeon’s skill
  • Decrease complication rate
  • Decrease impact of comorbidities
  • Increase adherence to exercise/nutritional/diet guidelines post surgery
  • 37% of patients will continue to need PAP despite surgical success
75
Q

OSA: diagnosis and management

A
  • All children should be screened for snoring. Snoring in children is not normal!
  • Complex high-risk patients should be referred to a subspecialist.
  • Patients with cardiorespiratory failure cannot await elective evaluation.
  • Diagnostic evaluation is useful in discriminating between primary snoring and OSA, the gold standard being polysomnography.
  • Adenotonsillectomy is the first-line treatment for most children, and CPAP is an option for those who are not candidates for surgery or do not respond to surgery.
  • High-risk patients should be monitored as inpatients postoperatively.
  • Patients should be re-evaluated postoperatively to determine whether additional treatment is required.
76
Q

prevalence of SDB

A
  • ~42 million of general population
  • 30-80% of cardiovascular disease patients
  • 50% of patients with diabetes