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Sleep Physiology > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

What is thermoregulation regulated by?

A

Preoptic nuclei in the anterior hypothalamus

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2
Q

What does heat loss to the environment occur through?

A

Radiation, convection, conduction, evaporation

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3
Q

What is the relationship between core body temperature and sleep?

A

Increases through the day, peaks in the afternoon, drops at onset of sleep, reaches minimum during second half of night, does not depend on outside influence

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4
Q

What is the relationship between proximal and distal skin temperature and sleep?

A

*Proximal skin temp decreases until onset to sleep, spike after falling asleep

*Distal skin temp increases until onset of sleep, during sleep is equal in value to proximal temp (lower before)

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5
Q

What is DPG?

A

Distal proximal skin temperature gradient: Distal minus proximal temp

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6
Q

What is the relationship between DPG and sleep?

A

Narrowing of DPG (gets closer to zero) at sleep onset → direct relationship

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7
Q

What is the role of the POA?

A

Preoptic area integrates thermal sensory info to control thermoeffector output

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8
Q

What are the types of neurons in the POA?

A

Warm sensitive neurons (30%), cold sensitive neurons (10%) and other neurons

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9
Q

Describe warm sensitive neurons

A

GABAergic, increase firing rate in response to increases in local temperature (sleep related)

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10
Q

Describe cold sensitive neurons.

A

Increase firing rate in response to drops in local temperature (wake related)

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11
Q

How does firing rate of warm sensitive neurons change from wake → transition → NREM?

A

Increases more at each step

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12
Q

How does warming affect raphe neurons?

A

Firing rate is reduced in serotonin (5-HT) with preoptic warming

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13
Q

How does brain temperature change during wake/sleep in rats?

A

Increases throughout sleep/with REM, increases throughout wake (higher than with sleep), drops at onset of sleep

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14
Q

What are the two types of insomniacs?

A

Sleep onset insomniacs and sleep maintenance insomniacs (early morning awake)

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15
Q

How are body temperature patterns different with sleep onset insomniacs?

A

Minimum and peak body temp is delayed

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16
Q

How are body temperature patterns different with sleep maintenance insomniacs?

A

Minimum and peak body temp is advanced

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17
Q

Describe the skin temperature challenge between insomnia and healthy sleepers.

A

Warm 1 hand in water, should cause increase in skin temp and vasodilation in other hand - in insomniacs skin temp didn’t increase. Shows relationship between body temp and sleep

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18
Q

How did warming of skin temperatures affect sleep in older insomniacs?

A

Increased slow wave sleep, decreased WASO

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19
Q

What are some possible thermoregulatory remedies for decreasing sleep onset latency?

A

Wearing socks, hot back, electric blanket, exercise

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20
Q

Why do thermoregulatory remidies work?

A

Increase the magnitude of CBT peak to increase transmission of skin thermoreceptors to warm sensitive neurons in the POAH

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21
Q

Describe what happens at onset of NREM sleep.

A

Dramatic reorganization of thermoregulatory control:
1. Body temp falls driven by vasodilation
2. Decreases in metabolism contribute to energy conservation during sleep

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22
Q

Describe what happens during NREM sleep.

A

*Thermoregulatory responses to change are diminished compared to waking
*Thermoregulatory function persists, body temp is defended at a lower level

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23
Q

Describe what happens during REM sleep.

A
  1. Thermoregulatory function is severely compromised
  2. Exposure to hot/cold suppresses sleep
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24
Q

Describe the effect of temperature (cold stress) on metabolic rate in different stages of sleep.

A
  • Awake: dramatic increase in metabolic rate as temperature decreases (in POA)
  • SWS: less of an increase
  • REM: no response
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25
Q

In what temperature environments are sleep amounts maximal?

A

Mildly warm environments

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26
Q

What experiment proved this?

A

Rats chose warmer environment for sleep than wake when given the choice

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27
Q

How does circadian variation differ in core versus distal skin temp?

A
  • Core: low during sleep, high during day
  • Distal: peaks at beginning of sleep, low during day, high during sleep
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28
Q

What were the effects of caffeine on temperature after ingestion?

A
  1. Caffeine decreased DPG by vasoconstriction (wider)
  2. Lower dorsal foot temp due to vasoconstriction
  3. Greater increase in CBT
  4. No change in infraclavicular temp
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29
Q

What were the effects of caffeine on temperature during recovery sleep?

A

Core body temp was higher with caffeine during recovery sleep (many hours after ingestion), DPG was larger (more negative) in the caffeine group

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30
Q

What were the effects of caffeine on recovery sleep?

A

Less SWS, lower sleep efficiency

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31
Q

Where are the central pattern generators responsible for breathing?

A

Pons and medulla (brainstem)

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32
Q

What inputs does the pattern generator receive?

A

Input from central chemoreceptors, etc

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33
Q

Where does the pattern generator project to?

A

Motor neurons innervating upper airway muscles and motor neurons innervating respiratory pump muscles

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34
Q

What are the three respiratory centers and where are they located?

A
  • Rhythmicity center - medulla oblongata
  • Apneustic center - pons
  • Pneumotaxic center - pons
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35
Q

What groups and neurons are in the medullary rhythmicity center?

A
  • I (inspiratory) neurons in the dorsal respiratory group
  • E (expiratory) neurons in the ventral respiratory group
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36
Q

Describe the I neurons.

A

Regulate activity of diaphragm and external intercostal muscles

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37
Q

Describe the E neurons.

A

Controls motor neurons to the internal intercostal muscles

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38
Q

Describe the apneustic center.

A

Activates inspiration: excitatory, sends nerve impulses to inspiratory center of the medulla

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39
Q

Describe the pneumotaxic center.

A

Continuously transmits inhibitory impulses to inspiratory area that limit duration of inspiration (3 seconds)

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40
Q

What do breathing patterns look like during quiet wakefulness?

A

Relatively regular, metabolically regulated (breathe faster if hot), variability increases when respiratory muscles are used for other behaviors (speech, swallowing) or with various emotional inputs

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41
Q

What do breathing patterns look like during slow wave sleep?

A

Breathing becomes deeper, slower, and very regular, end-expiratory CO2 (amount gotten rid of) increases slightly

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42
Q

What do breathing patterns look like during REM sleep?

A

Respiratory rate and depth vary greatly from breath to breath, brief suppressions, ventilation is at times dissociated from metabolism

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43
Q

How does sleep increase risk of apnea?

A

ACh involved in reduction in 5-HT and NE during REM which results in loss of activation to motor neurons → upper airway is more collapsible → more likely to have apneas

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44
Q

Describe the peptides in control of breathing.

A

Released when rate of action potentials is high - may play important role in control of breathing during active wakefulness and REM sleep

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45
Q

Which peptides are important in control of breathing?

A

TRH and substance P

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46
Q

Where are peptides that are important in control of breathing synthesized and why?

A

Serotonin containing cells - increased activation during wakefulness - respond to extracellular CO2 increases or pH declines

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47
Q

How does sleep affect peptides that are in charge of breathing?

A

Reduced activity during SWS and lost during REM (lose descending drive)

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48
Q

Describe the effect of increased CO2 on the Raphe nucleus.

A

Increased firing rate of Raphe neurons → TRH, 5-HT, SP released onto the dorsal respiratory group, motor neurons, and ventral respiratory group (pre Botzinger complex)

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49
Q

Describe SIDS.

A

Sudden infant death syndrome: sudden and unexpected death of infant under 1 year old - onset apparently occurs during sleep, cause of death remains unexplained

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50
Q

What has been done to try to decrease SIDS incidence?

A

Back to sleep campaign (baby should sleep on back) - decreases the risk significantly

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51
Q

When is SIDS most likely to occur?

A

Rarely occurs before 1 am or after 6 am - mostly between 2-4 months

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52
Q

What are some risk factors for SIDS?

A
  • Smoking during pregnancy and second hand smoke
  • Cosleeping (bed sharing, especially with parents who use alcohol or drugs)
  • Sleeping in their own room
  • Soft bedding, pillows, bumpers
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53
Q

What are some possible causes of SIDS?

A

Deficits in the serotonin system - affect control of breathing and thermoregulation

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54
Q

How are sleep and immune function related?

A

Bidirectional links: proinflammatory cytokines (little immune function) promote sleep, full blown sickness disturbs sleep, sleep loss disturbs immune function

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55
Q

What causes the time of day pattern in immune cells?

A

Cortisol

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56
Q

How do mild bacterial and viral infections affect sleep?

A

Increases SWS (NREM)

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57
Q

How do chronic conditions affect sleep?

A

More wakefulness and sleep fragmentation, less NREM sleep and REM sleep

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58
Q

How does sleep restriction affect immune function?

A

Alters immune molecules to increase drive to sleep - increases IL-6 and CRP (adequate sleep would decrease them), greater risk for sickness

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59
Q

What factors of sleep increase risk of illness?

A

Sleep duration (short), sleep disorder, sleep disturbance

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60
Q

How do proinflammatory and antiinflammatory cytokines affect sleep?

A

Proinflammatory cytokines promote NREM while antiinflammatory cytokines reduce it

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61
Q

Describe IL-1β.

A

Interleukin-1β: primary proinflammatory cytokine (released when pathogen is present to promote inflammation), induces fever and sleep, increases during sleep deprivation

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62
Q

How does IL-1β affect sleep?

A

Increases NREM (SWS) in the dorsal raphe nucleus, decreases REM in the LDT, increases brain temperature

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63
Q

How does IL-1β affect wake/sleep neurons?

A

Wake neurons: reduces discharge rates of wake-active POA neurons (no effect on sleep related neurons), also inhibits wake promoting neurons in the dorsal raphe nucleus
Sleep neurons: reduces discharge rates of cholinergic neurons in the LDT (REM)

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64
Q

How does sleep deprivation affect IL-1 levels?

A

Increases - contributes to sleep pressure

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65
Q

Define IL-1ra.

A

Interleukin 1 receptor antagonist: produced by immune cells, competitively binds to the IL-1 receptor to inhibit its actions (anti inflammatory), reduces NREM

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66
Q

Define IL-6.

A

Interleukin-6: primarily proinflammatory; increased in response to antigens/inflammation/ stress; stimulates production/release of CRP; may have indirect antiinflammatory effects

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67
Q

What are IL-6 levels affected by?

A

Insomnia and sleep deprivation elevate IL-6 levels

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68
Q

Define TNF-ɑ?

A

Tumor necrosis factor-alpha: produced in response to bacteria and stress, stimulates IL-1 production, increases NREM sleep (blocking it decreases NREM)

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69
Q

What is TNF-ɑ affected by?

A

Elevated with insomnia

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70
Q

Define IL-10.

A

Interleukin-10: most important antiinflammatory cytokine, inhibits the synthesis of many proinflammatory cytokines (including IL-1, TNFɑ, IL-6), reduces NREM sleep

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71
Q

Define CRP.

A

C reactive protein: inflammation causes white blood cells to release cytokines that stimulate the liver to produce/release CRP, higher levels = more inflammation (unhealthy)

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72
Q

How does sleep restriction affect CRP?

A

Increases → increases the risk for heart disease (CRP is a biomarker)

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73
Q

Describe risk factors in obese people.

A

Those with more severe sleep apnea show more inflammation (higher CRP and IL-6) - sleep apnea is comorbid with obesity

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74
Q

Describe how heart disease risk is affected by LDL and CRP.

A

Both show an increased risk for heart disease (both biomarker), greater risk with greater CRP levels, worst is combo

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75
Q

What is the circadian rhythm of IL-6?

A

High during the day, lowest right when wake up

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76
Q

Do immune cells have circadian clocks?

A

Yes

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77
Q

How is the response to pathogens affected by time of day?

A

Lower inflammatory response during biological night - circadian rhythm

78
Q

Who does this affect and how?

A

Shift workers have greater risk of sickness - they are exposed during their biological night

79
Q

How does sleep affect the adaptive immune response?

A

Supports its initiation (body produces more antibodies quicker if exposed before)

80
Q

What are the effects of prior sleep deprivation on response to immunization?

A

Still have immune response but less antibodies produced - vaccine less effective

81
Q

What are the effects of subsequent sleep deprivation on response to immunization?

A

Produces less antibody - less clinically protected (vaccine is less effective)

82
Q

How do different levels of exposure affect NREM and REM?

A

Low levels: increase NREM
Medium levels: increase NREM, reduce REM
High levels: reduce both NREM and REM

83
Q

What factors of sleep, when deprived, result in a greater likelihood of illness?

A

Sleep duration and efficiency

84
Q

What is the general diagnostic criteria for disorders of arousal?

A
  1. Recurrent episodes of incomplete awakening from sleep
  2. Inappropriate or absent responsiveness to efforts of to others to intervene or redirect the person during the episode
  3. Limited (e.g., a single visual scene) or no associated cognitions or dream imagery
  4. Partial or complete amnesia for episode
  5. Not explained by another sleep disorder, mental disorder, medical condition, medication or substance use
85
Q

Describe sleep terrors.

A

Piercing scream, few minutes long, no recollection of dream or memory of scream

86
Q

Who is affected by sleep terrors?

A

Affects 3% of children (mainly in late childhood and adolescence) and 1% of adults

87
Q

When is the onset and duration of sleep terrors?

A

If they start before age 7, last ~4 years
If they start later, last longer

88
Q

What are the genetic factors influencing sleep terrors?

A
  • 35% of children with both NT and sleep disordered breathing have at least 1 immediate relative with parasomnia
  • 96% had 1 or more relatives in the pedigree with NT or sleepwalking
  • 60% risk if both parents were affected
89
Q

Describe somnambulism.

A

Sleepwalking: partial arousal out of deep NREM sleep (SWS) mainly in the first third of the night, can’t be easily awakened, episodes last <10 minutes, risk of falling downstairs, driving a car, etc

90
Q

Who is affected by somnambulism?

A

~18% of children, mainly between 4-8 years old, ceases spontaneously by adolescence

91
Q

Describe adult somnambulism.

A

Has a later age of onset (~9.9 years), lasts much longer, happens more often, can be related to psychological and stress factors

92
Q

What are the causes of sleepwalking?

A
  • Genetic factors (much more likely if parents sleepwalk)
  • Development (ends at the end of adolescence - suggests link to body maturation)
  • Stress
  • Drugs
  • Sleep disordered breathing
92
Q

Which parts of the brain are involved during sleepwalking?

A
  • Cerebellum (movement) and posterior cingulate (internal cognitions - thinking to self)
  • Less involvement of frontal and parietal association areas (reduced engagement with the world - don’t remember these events)
93
Q

Describe somniloquy.

A

Sleep talking: no awareness, most likely during SWS and least during REM

94
Q

Describe nocturnal enuresis.

A

Intermittent urinary incontinence while sleeping after expected age of development of urinary control

95
Q

When should nocturnal enuresis be a concern?

A

Older than ~5 years

96
Q

What stage of sleep is nocturnal enuresis most common in?

A

NREM sleep, may be restricted to stage 3/4

97
Q

Is there a genetic predisposition to nocturnal enuresis?

A

Yes

98
Q

How is nocturnal enuresis treated?

A

No treatment before 5-6 years old, but afterward:
* Daytime bladder training (delay using the bathroom when they need to)
* Postponing micturition (pee then stop then pee then stop)
* Alarm systems (sense urination, wake up child, hopefully child will eventually wake up themselves before peeing)
* Mediations (act like vasopressin)

98
Q

What are contributing factors to nocturnal enuresis?

A

Small bladder functional capacity, decreased capacity to inhibit spontaneous bladder contractions, decreased nocturnal secretion of vasopressin, decreased central arousal and control of micturition

99
Q

Describe bruxism.

A

Teeth grinding usually occurring during sleep, usually not aware, happens in NREM, tends to be associated with stress

100
Q

Define bruxomania.

A

Neurotic habit performed in the daytime

101
Q

How is bruxism treated?

A

Mouthpiece from dentist that can withstand grinding, addressing stressors in their life

102
Q

Describe sleep related eating disorder.

A

Partial arousal from NREM, involuntary eating and drinking during sleep, sometimes inedible things, can get injured, sometimes have insomnia, morning anorexia

103
Q

Who is more affected by sleep related eating disorder?

A

Eating disorders, college students, females

104
Q

Describe night eating syndrome.

A

Change in behavioral pattern of eating - 25% of food intake after dinner, aware of behavior, associated with obesity, morning anorexia

105
Q

Define each term.

Apnea:
Hypopena:
Respiratory effort related arousals:
AHI:

A

Apnea: no to very little flow
Hypopnea: 30-50% reductions in flow
Respiratory effort related arousals: brief arousal upon restoration of breathing, associated with worse apnea
AHI: apnea hypopnea index - number of events per hour

106
Q

What tests can diagnose sleep apnea outside of the clinic?

A
  • OCST: out of center sleep testing
  • HST: home sleep test
107
Q

Define obstructive sleep apnea.

A

Loss of patency (keeping it open) in the airway despite respiratory effort

108
Q

Define central sleep apnea.

A

Cessation of respiratory effort

109
Q

Who is more likely to get OSA?

A

Obese people, men, people with large necks, women in menopause, physical abnormality of the upper airway

110
Q

What kind of facial abnormalities can lead to OSA?

A

Enlarged uvula, tongue, tonsils, soft palate, mandible too far back, thick neck

111
Q

What problems can occur in children with OSA?

A

More likely to have problems with hyperactivity, attention disruptive behaviors, communication, competency, self-care, learning problems, obesity

112
Q

How does OSA affect bed partners?

A

Very disruptive- patient can have loud snoring, gasping, choking

113
Q

When is sleep apnea most likely to occur?

A

During REM - muscle atonia

114
Q

How is apnea graded to determine severity?

A

5 or less events per hour (AHI): no issue
5-10 AHI: mild
Greater than 10: apnea

115
Q

Where, geographically, is apnea prevalence higher?

A

At altitude

116
Q

How does overall sleep look in sleep apnea patients?

A

No slow wave sleep, very little stage 2, very fragmented sleep

117
Q

How does sleep apnea affect the body?

A

Reduced arterial oxygen saturation, increased cardiac activity (stress on heart), excessive daytime sleepiness and fatigue (more in men than women)

118
Q

Describe the process of activating the genioglossus.

A

Tonic inputs (descending drive) and inspiratory drive activate the hypoglossal motoneuron which activates the genioglossus (tongue) to move forward and open airway

119
Q

Describe the process of activating the upper airway muscles.

A

Tonic inputs (more when awake) and very little inspiratory drive activate the trigeminal motoneuron which activates muscles

120
Q

Describe the CPAP machine.

A

Constant positive air pressure: keeps airway open with forced air - need the specific pressure determined by sleep test, can get rid of apnea/solve problem

121
Q

Describe oral pressure therapy.

A

Sucks air inside mouth to pull tongue etc. forward; helps some people but not others

122
Q

Describe upper airway stimulation for sleep apnea.

A

Surgical treatment that involves a lead that innervates the hypoglossal nerve - stimulates tongue to push forward

123
Q

Describe oral appliance therapy.

A

Pulls lower jaw forward opening the airway, only works for mild → moderate sleep apnea

124
Q

Describe surgical treatment of sleep apnea.

A

Remove portion of soft palate and uvula, very painful, often doesn’t work

125
Q

By what pathways does sleep apnea contribute to type II diabetes

A

Sleep apnea –> hypoxemia, (arrows go both directions) obesity, sleep deficiency

sleep deficiency -causes-> obesity

hypoxemia, obesity, and sleep deficiency –cause–> inflammation oxidative stress, impaired glucose tolerance, insulin resistance —> TYPE 2 DIABETES

126
Q

explain why there is a spike in skin temperature following onset of sleep

A

because when you fall asleep your core body temperature decrases but the skin temperature increases (proximal and distal temperatures become closer - less difference)

  • as core temp decreases blood flow to the extremities increases causing an increase in skin temp temporarily == SPIKE
127
Q

What does sleep apnea indicate? treatment?

A

Treating sleep apnea can be used to treat type II diabetes and improve metabolic health

128
Q

What do leptin and ghrelin levels look like in sleep apnea patients?

A

Both are higher

129
Q

How is this affected by CPAP treatment?

A
  • Ghrelin levels decrease rapidly to healthy control levels
  • Leptin levels decrease over 8 weeks (without weight loss) to healthy levels
130
Q

What do cortisol levels look like in sleep apnea patients and with treatment?

A
  • Sleep apnea: increased at beginning of sleep
  • With treatment: decreased at beginning of sleep - SWS suppressed cortisol
131
Q

What do growth hormone levels look like in sleep apnea patients and with treatment?

A

*Sleep apnea: very low
* With treatment: rapid increase in levels (restores SWS)

132
Q

How is blood pressure affected by sleep apnea?

A

OSA associated with sheer stress and an increase in blood pressure

133
Q

How does treatment affect blood pressure?

A

Lower blood pressure as long as patients use it correctly and often enough

134
Q

What do levels of CRP and IL-6 look like in sleep apnea patients and with treatment?

A
  • sleep apnea: increased
  • with treatment: lowered
135
Q

How does sleep apnea affect performance?

A

People with mild - moderate untreated sleep apnea performed worse than those with 0.06% BAC, risk of crashes is increased between 2 and 10 fold

136
Q

What chemical does narcolepsy affect?

A

Hypocretin (orexin) from the lateral hypothalamus is reduced (normally stabilizes wakefulness and reduces likelihood of REM by activating REM-off)

137
Q

What is the diagnostic criteria for type 1 narcolepsy?

A

Both of the following must be met:

A. Daily periods of intense need to sleep or daytime lapses into sleep for at least 3 months
B. The presence of one or both of the following:
a) Cataplexy, mean sleep latency of less than 8 minutes, two or more sleep onset REM periods
b) CSF hypocretin-1 concentration is low

138
Q

Define cataplexy.

A

Loss of muscle tone/muscle weakness like in REM, triggered by stress/emotional stim

139
Q

What are some common symptoms in narcolepsy?

A

Excessive daytime sleepiness, cataplexy, hypnagogic (REM-like) hallucinations, sleep paralysis

140
Q

When does narcolepsy often get diagnosed?

A

Second decade of life
– young adulthood

141
Q

Is there a genetic component of narcolepsy?

A

Yes - increased risk of first degree relatives

142
Q

How is narcolepsy diagnosed?

A

Sleep study at a sleep center:
* Medical and physical exam
* Polysomnography
* Multiple sleep latency test
* Daytime sleepiness tests and sleep diaries (including Epworth sleepiness scale)

143
Q

Describe canine narcolepsy.

A

Daytime sleepiness, cataplexy, sleep onset REM periods, genetic, mutation in hypocretin receptor

144
Q

Describe mouse narcolepsy.

A

Loss of hypocretin/hypocretin neurons, genetic, behavioral arrest

145
Q

Describe the autoimmune theory for narcolepsy.

A

Genetic disposition - antibodies attack hypocretin neurons - piece of a flu protein is similar to hypocretin so T cells react to both is exposed

146
Q

What are some predisposing genes for narcolepsy?

A

HLA (immune gene), COMT (dopamine gene), TNFR2 (mutation in receptor for TNFɑ)

147
Q

How is narcolepsy treated?

A
  • Education (know risks, considered disability, naps are effective)
  • Behavioral treatment (kids wear helmet, take naps, avoid sleep deprivation and nicotine)
  • Medications
148
Q

What medications are available for narcolepsy?

A

Stimulant (alerting) medications, wake promoting medications (modafinil), anticataplectic medications (antidepressants, xvrem (sodium oxybate)

149
Q

What are the criteria for insomnia?

A
  • Disturbance in sleep quality or quantity due to problems initiating sleep, problems maintaining sleep, or early morning awakenings
  • Causes distress or impairment
  • Occurs 3 nights/week for at least 3 months
  • Occurs even with adequate sleep opportunity
  • Not due to another sleep disorder or effects of a substance
150
Q

Is insomnia associated with other medical problems?

A

Yes - people with insomnia have much higher prevalence rates of medical conditions

151
Q

How is insomnia related to psychiatric disorders?

A

Insomnia predicts subsequent psychiatric disorders - contributes to the risk

152
Q

How is insomnia prevalence affected by age?

A

More prevalent as people age

153
Q

How does insomnia relate to dementia?

A

Sleep maintenance insomnia has increased risk, short sleep duration has increased risk in older women

154
Q
A

Stress is the number one cause of short term sleep difficulties, excitement, new environment, noise, temperature, bed partners, altitude

155
Q

What drugs cause insomnia?

A

Alcohol, stimulants, bronchodilators, heart medications

156
Q

What are the two models of insomnia?

A

Physiological and behavioral

157
Q

What is the physiological model of insomnia based on?

A

Hyperarousal - too much activity in the brain/body causes sleep initiation/maintenance problems and nonrestorative sleep → insomnia

158
Q

How is hyperarousal seen in an EEG?

A

More beta and gamma waves (associated with wake) during sleep in insomniacs

159
Q

How is hyperarousal seen in an fMRI?

A

Overactivity seen in the ascending reticular activating system (wake promoting region) and insula (emotion, awareness, info processing) during sleep

160
Q

What does an fMRI show in insomnia patients during wake?

A

Reduced brain arousal in the prefrontal cortex (cognitive) and the ascending reticular activating system (doesn’t promote wakefulness as much)

161
Q

How does the endocrine system respond to insomnia?

A

Overactivity of the HPA axis - stress hormones such as cortisol are too high when trying to fall asleep (beginning of night)

162
Q

What is seen metabolically in patients with insomnia?

A

What is seen metabolically in patients with insomnia?

163
Q

What is sleep reactivity and how is it related to insomnia?

A

How vulnerable someone is to stressors during their sleep - patients with insomnia are much more reactive and a major stressor can affect them without recovery

164
Q

What factors contribute to the behavior model of insomnia?

A
  • Predisposing factors: risk factors for insomnia that make you more vulnerable - don’t go over the threshold of causing insomnia
  • Precipitating factors: stressors cause symptoms to start to develop - surpass threshold
  • Perpetuating factors: behaviors to compensate for loss or try to get more sleep - maintain insomnia chronically after initial stressors go away
165
Q

What are the problems with perpetuating factors?

A

Mismatch between time in bed and sleep duration, stimulus dyscontrol, conditioned arousal (bed elicits arousal instead of sleep)

166
Q

Define stimulus dyscontrol.

A

Associating bed/bedroom with things other than sleep/sex - learned association, results in low probability that getting in bed will yield sleep

167
Q

What are treatment options for insomnia?

A

Cognitive behavioral therapy for insomnia (CBTI) and prescription hypnotic medications

168
Q

List and define the three critical components of CBTI.

A
  • Stimulus control: limits time spent awake in bed: go to bed only when sleepy, avoid behavior in bedroom other than sleep/sex, leave if awake for more than 15 minutes
  • Sleep restriction: limit sleep opportunity to current sleep duration - increase sleep pressure
  • Sleep hygiene: (non effective alone) exercise regularly, comfy temp, don’t watch clock
169
Q

List and define the three optional components of CBTI.

A
  • Cognitive therapy: reduce preoccupation with insomnia
  • Relaxation/mindfulness: reduce physiological arousal in pre-sleep period
  • Light therapy: reduce circadian phase delay/advance
170
Q

How effective is CBTI?

A

Gold standard treatment, reduces SOL and WASO, improvements last 24 months

171
Q

What pharmacological treatments are available for insomnia?

A

Monoamines and DORAs (inhibit wake centers), zolpidem/ambien and melatonin (activate sleep centers)

172
Q

Compare CBCT and hypnotics.

A

Similarly effective short term, CBTI is more effective long term, medications have risk of tolerance and undesirable side effects - if taken together, have faster initial response but no benefit long term

173
Q

What are some false beliefs about insomnia?

A
  • It is a normal part of aging
  • Everyone needs 8 hours of sleep every night
  • I can’t function after a sleepless night
  • I should stay in bed and try harder to fall asleep if I’m having trouble
174
Q

what is a common diagnositc test used in the diagnosis fo hypersomnia

A

MSLT – can tell how sleepy someone is

175
Q

What is jet lag?

A

Being awake to trying to sleep at inappropriate circadian time, sleep disruption surrounding flight to a new time zone, internal desynchrony

176
Q

How do the internal clocks in different parts of the body adapt to jet lag?

A

The SCN adapts quickly, liver and lung take longer to adapt → different tissues take different amounts of time to adapt

177
Q

How can you pre adjust to jet lag?

A

Dim lights at night, go to bed earlier, bright lights in the morning, melatonin in late afternoon/evening to phase advance - opposite to phase delay

178
Q

What are some health consequences of shift work?

A

Accidents/injury, cardiovascular disease/stroke, metabolic syndrome, overall obesity and abdominal obesity, gastrointestinal disorders, reproductive problems, increased cancer risk

178
Q

What is shift work defined as?

A

Work performed during the typical time for sleep - thought to be a higher risk for shift work disorder because it goes against our biology

178
Q

What are symptoms like in shift work disorder versus just shift work?

A

Shorter sleep duration, higher rates of ulcers, more sleep related accidents, more absenteeism, more depression

179
Q

How does shift work affect the balance between circadian rhythm and sleep?

A

Normally, circadian drive for wakefulness overrules homeostatic drive for sleep but with shift work, circadian and homeostatic drives for sleep cause impaired wakefulness during work hours

180
Q

What are some management strategies for shift work disorder?

A

Schedule design and education, circadian adaptation, promote sleep duration and quality, promote wakefulness,

181
Q

When should night shift workers sleep?

A

Major anchor sleep post-shift plus prophylactic nap in late afternoon, don’t nap during the night shift, take pre-nap caffeine

182
Q

How can shift workers promote wakefulness?

A
  • Caffeine - prior and during night shift, no energy drinks, no nicotine
  • Modafinil is recommended, can combine bright light, caffeine, naps, modafinil
183
Q

What is non-24 hour sleep wake syndrome?

A

Failure of circadian rhythm to entrain to the 24 hour light dark cycle - bed and wake times get later each day due to delay of melatonin

184
Q

What can be used to treat non 24 hour sleep wake syndrome?

A

melatonin daily

185
Q

what is irregular slep wake rhythm disorder

A

no circiadian rhythm - leads family members to admit people into care –> very disruptive

186
Q

Define delayed sleep phase syndrome

A

Delayed sleep time and reduced sleep duration during school week, sleep onse insomnia, later circadian melatonin phase, catch up sleep on weekends which pushes even further back

187
Q

How can delayed sleep phase syndrome be treated?

A

bright light exposure in the morning, dim light exposure in the evening- must deep this schedule 7 days/wk

Sleep Physiology (6 decks)

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