PULMO-SLEEP APNEA Flashcards

1
Q

Why do we sleep?

A
Brain wake and evolved
Restoration
Conservation of energy
Protein
Impacts immune system
Allow processing of input
Memory consolidation depends on sleep
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2
Q

What are the Socioeconomic Consequences?

A

40 mill Americans suffer from chronic disorders of sleep and wakefulness.

ES ,OSA-93%- W, 82% -M not clinically dx

Excessive daytime sleepiness (EDS) impairs:
Human performance that can lead to accidents home, road, career

31% drivers fall asleep-
Academic performance, learning, and judgment

Increased weight, mood disorders, stress, cardiovascular complications
Inc. infections

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3
Q

Definitions of Sleep

A

reversible behavioral state of perceptual disengagement from, and unresponsiveness to, the environment.- not aware

very complex amalgam of physiologic and behavior processes.
A process, unlike coma, that is physiologic, recurrent, and reversible.

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4
Q

Where is the body’s master “clock”

A
suprachiasmatic nucleus (SCN) of the hypothalamus. Behind eyes
Crossing some optic chiasm

Light-dark signals reach the SCN via a retinohypothalamic track fibers.

Circardian- about a day

SCN cells are circadian oscillators, exhibiting a stable, biphasic firing cycle. synchronized by exposure of light.

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5
Q

Sleep hygiene

How to keep circadian clock on time?

A

Regular wake up time-more important than sleep time
Bright light sun exposure helps more

Keep Circadian Clock on Time:
Awaken at approximately the same time each day.
Obtain bright light (e.g. sun) during desired daytime hours.

Maximize Homeostatic Sleep Drive:
Limit napping when insomnia is a problem
“siesta” or afternoon nap is fine if no trouble sleeping at night.
Go to bed only when sleepy.
Reduce Physiological and Psychological Arousal:
Limit or eliminate caffeine, chocolate, nicotine, alcohol.
Exercise long before bedtime (morning exercise works well).
Shut your day down at least 1 hour before bedtime.
Sleep in a comfortable bedroom, especially not too hot.

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6
Q

Agent blocks adenosine

A

Caffeine

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7
Q

Improve Sleep Hygiene tips

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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8
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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9
Q

The alerting effects of the biologic clock:

A

Oppose the Homeostatic Sleep Drive with its alerting effect.
Allow for a consolidated WAKE during the subjective day.
Initiate a mid-day dip in biologic clock alerting activities.

Homeostatic Sleep Drive:
It is proportional to the amount of previous WAKE and Sleep Debt.
Sleep Debt builds throughout the day.

What’s normal: Adults need 7-8 hours of sleep, Children need 9 or more hours of sleep

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10
Q

DM and HTN

A

affect sleep

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11
Q
When Patients Say They Are Tired
EDS vs. fatigue
Sleepiness: able to sleep if given a chance
Fatigue: tired but does not fall asleep 
Body is tired but mind is very active

Ask the patient: If given a chance to stretch out and sleep right now, what would happen?

A

There is a pos-test question on this. This is a simple but very important concept for primary care providers. The questions from the Epworth should guide them

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12
Q

Epidemiology of Insomnia
Overall prevalence of an insomnia symptom within the last year: ~30%
Risk factors:
Female gender
meta-analysis of 31 studies: relative risk (RR) = 1.41
Medical, psychiatric, and substance abuse issues
Social factors (many co-vary)
Possible genetic factors
Age

A
You can quickly review some specifics social factors should include:
Lower socioeconomic status
Unemployment
Marital status (divorced or widowed)
Lack of education
Race, ethnicity, country of origin
Shift work
Poor sleep hygiene
Adverse sleeping environment
Far-northern latitudes
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13
Q

Sleep-Related Arousal As a Trait

Primary insomnia

A

Markers of hyperarousal:
Reduced parasympathetic tone
Increased basal metabolism
Elevated circulating catecholamines
Increased electroencephalogram (EEG) ß activity (cortical activation)
Elevated body temperature
High activity of hypothalamo-pituitary-adrenal axis

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14
Q

Psychophysiologic: Characteristics

A

Contributed to and reinforced by poor sleep hygiene
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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15
Q

Cognitive-Behavioral Treatment of Insomnia
Counseling in sleep hygiene
Cognitive therapy and stimulus control therapy
Sleep restriction therapy

A

Improve patient’s understanding of his/her sleep
Establish realistic expectations regarding sleep
Review simple relaxation techniques
Dissuade patient from believing lack of sleep will be harmful
Most Insurance will reimburse PCPs’ for patient education not cognitive therapy
Relaxation techniques could include deep breathing, reduce stimulation, etc

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16
Q

Behavioral Management of Insomnia

Sleep Restriction Therapy

A

Set the alarm for the same time each morning, regardless of the amount of sleep obtained the night before.
No daytime naps allowed
Keep a sleep diary for at least 7 days and compute the total amount of sleep per night (total sleep time [ TST]) indicated by the diary.
Set up a schedule restricting the time spent in bed to equal the TST.
As sleep efficiency improves, bedtime is advanced (go to bed earlier) by 15- to 20-minute intervals, maintaining the same wake time.

17
Q

RLS

A

A distressing need/urge to move the legs, usually accompanied by an uncomfortable, deep-seated sensation in the legs that is:

Brought on by rest
Relieved with moving or walking
Worse in the night or evening (circadian

18
Q

Primary (idiopathic):

A
No precipitating factor
Younger age onset ("growing pains)
Genetic association
Autosomal dominant
Chromosome 12/14
19
Q

Secondary:

A
Iron deficiency (~25%)
Pregnancy (~25%)
Renal failure (up to 60%)
Drugs
Antidepressants
20
Q
RLS is common
Prevalence: 
Etiologies of RLS:
Treatment
Anticipate augmentation and rebound
A

3% to 15% of the general population
Up to 25% of primary care patients

Most cases are primary and hereditary
Secondary etiologies: Iron deficiency, end-stage renal disease (ESRD), peripheral neuropathies

Identify and treat precipitants: Drugs, iron deficiency, sleep deprivation, renal failure
Dopamine agonists are first-line pharmacologic agents
Pramipexole and ropinirole are FDA-approved for RLS
Dopaminergic agents
Iron, if ferritin < 50 ng/mL
Anticonvulsants (gabapentin)
Low-potency opiates
Benzodiazepines (clonazepam)

21
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
Shift workers
Adolescents
Elderly and chronically hospitalized
Travelers
Physicians and nurses
22
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 clonazepine

23
Q

Narcolepsy

A

Excessive Daytime Sleepiness

Cataplexy: brief emotionally triggered episodes of muscle weakness, Laughter trigger muscle weakness- sleep paralysis comes on when wide awake (50%)

Sleep paralysis (40-80%)

Hypnogogic and hypnopompic hallucinations (40-80%)

Fragmented sleep

Mild obesity

Multiple types

DX-sleep study

24
Q

Parasomnias

A
Deep sleep
Sleep walking- less w/ age, slow wave sleep dec.
Night terrors
Bed Wetting
Nocturnal eating
Hypersomnia
Nocturnal Seizures
25
Q

Prevalence of SDB and OSA

sleep disorder breathing

A

Approximately 42 million American adults have SDB

9% women and 25% men in the middle-aged working population have OSA

OSA defined as AHI > 5

30% a primary care office may have OSA d/t relationship of morbidities

~75% of severe SDB patients are not diagnosed Young Sleep 2008

DM, CA, CVD

26
Q

OSA

A

most common/most predominant.
anyone with AHI > 5

Causes airway to narrow = snoring and breathing difficulties

Relaxing too much may become blocked completely = OSA

MC of SDB
Partial or complete collapse of upper airway
Muscles controlling soft palate and tongue relax

Apnea- cessation of airflow for > 10 seconds
obstruction, central, mixed

Hypopnea- A decrease in airflow lasting > 10 seconds with a 30% reduction in airflow and with at least a 4% oxygen desaturation from baseline

Flow limitation
Upper airway narrowing
Earliest sign of impending upper airway closure

RERA
Respiratory Effort Related Arousal, interferes w/ sleep
Flow limitation leading to arousal

27
Q

Classification of SDB

A

AHI (Apnea/Hypopnea Index)
Number of apneas
“severity” of the SDB
10 sec of not breathing every 2min

AHI = 0-4 Normal
AHI = 5-14 Mild
AHI =15-30 Moderate
AHI > 30 Severe

Measured by polysogram

28
Q

Name the effects of transient arousals.

A
hypoxia
hypercapnia 
Arousal
Neurocognitive impairment (memory loss)
Daytime sleepiness
Impaired quality of life
Metabolic effects
Cardiovascular effects
Cancer

result in activation of sympathetic nervous system___release of norepinephrine with deleterious cardiovascular consequences.

29
Q

Major factors include:

A
Obesity 
Snoring
Male gender (until about age 50)
Postmenopausal state
Overbite
Upper airway anatomic obstruction (including nose)
AA, Asian, or Hispanic
30
Q

Signs and Symptoms of OSA: History

A
Snoring
Unrefreshing sleep/daytime sleepiness
Witnessed apneas
Insomnia
Restless sleep
Nocturnal heartburn
Morning headache- common
Nocturia- apnea, will wake then urinate
Dry mouth, sore throat, sinus and nasal congestion
Mood, memory, and learning problems
Parasomnias
Impotence
Enuresis	
Many with almost no symptoms-idiopathic
31
Q

Cardiovascular Effects of OSA

A

Systemic hypertension
Pulmonary hypertension (with sustained hypoxemia)
atrial fibrillation-OSA trigger
Coronary artery disease
Congestive heart failure
Stroke and transient ischemic attacks (TIA)
Mortality

32
Q

OSA and Metabolic Dysfunction

A

glucose intolerance and insulin resistance
50% DM have sleep apnea
independent contributing factor

HCP must screen

Hypoxemia

CPAP improves insulin sensitivity, CVD
10mmHG reduction
Atrial fib- sleeps

33
Q

Epworth Sleepiness Scale (ESS)

A

average sleep propensity

> 10 excessive daytime sleepiness

no cause
no apnea related

34
Q

STOP BANG Obstructive Sleep Apnea

A
Snore
Tired
Observed apnea
Pressure
BMI
Age >older
Neck circumference
Gender
2 out 4 
92% apnea sensitive
35
Q

Positive airway pressure (PAP)

A

generally accepted as the gold standard
Inc. pressure inc. size of airway

Alternatives:
Surgery (UPPP, LAUP, mandibular advancement)
Dental appliances-some affect
Drug therapies
Tracheostomy 
Pacing (upper airway, cardiac)
36
Q

Why Treat Sleep Apnea Before Any Surgery?

ss

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 succe

37
Q

OSA: Diagnosis and Management

Recommendations from the American Academy of Pediatrics 2002:

A
Trouble school 
underdeveloped
Sleeping
30% ADHD
Large tonsils and Adenoids-removal
Nasal congestion- serious early
mouth breathers- high arch narrow jaw
Max mandibular expansion
referred to a subspecialist.