Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Respiratory > Sleep disorders > Flashcards

Sleep disorders Flashcards

1
Q

OSA and OHS - people typically wake up with …

A

Headache due to high CO2 levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Pathophysiology of OHS

A

1) Leptin resistance (leptin is a powerful ventilatory stimulus)
2) Increased mechanical load (extrathoracic fat) on lungs
3) Chronic renal compensation by increasing serum bicarb –> reduce acidaemia –> normal pH

= Blunted ventilatory response –> persistent high CO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Symptoms of OSA/OHS

A
  • SOBOE
  • Headache - specifically morning headaches may be secondary to retained CO2
  • Snoring
  • Poor quality sleep
  • Mental cloudiness, fatigue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What screening tools are available for OSA?

A

STOP BANG

  • Are you tired?
  • Good sensitivity and NPV. Not specific.

Epworth sleepiness scale

  • Are you likely to knock off?
  • Not sensitive or specific to OSA. Weak correlation with all measurements of OSA severity.

FOS-Q
- Can be used to track improvements in QOL after treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Define OHS

A

TRIAD of
Obesity (BMI ≥30) +
Daytime hypercapnia (ABG with pCO2 ≥45mmHg) +
Sleep disordered breathing

Must exclude other causes of hypoventilation
85% have OSA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Things to look for on exam OHS

A

Central obesity (increased waist to hip ratio, increased neck circumference)
Mallampati score 3 or 4
Signs of cor pulmonale (lower extremity oedema, clubbing)
Daytime oxygen saturation - low-mid 90s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Can OHS and COPD coexist?

A

Yes

But you technically can’t call it OHS because its a diagnosis of exclusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Define OSA

A

Apnoeas (stop breathing for ≥10 seconds) or hypopneas (decreased airflow ≥10 seconds) associated with desaturation or arousal

OSA is at least 5 episodes of apnoea or hypopneas per hour of sleep + symptoms
5-15 episodes = mild
15-30 episodes = moderate
30+ episodes = severe

Alternatively, its ≥15 episodes +/- symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the proportion of OHS that has OSA?

A

70-90%

The greater the AHI (in OSA) the greater the risk of OHS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Pathophysiology of central sleep apnoea?

A

Overly brisk ventilatory response (overbreathe) to small changes in CO2 –> breathing exceeds what’s necessary
E.g. cheyne-stokes breathing in HF, or periodic breathing in opioid use or high altitude

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How is central sleep apnoea diagnosed?

A

Only on sleep study

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Investigations to get in OHS

A

1) ABG pCO2 >45

2)
Serum bicarbonate <27 = unlikely to have hypercapnia in low-to-moderate OHS patients

3) RFTs
- Rule out obstructive lung disease (if present, can be cause of hypoventilation)
- Rule out neuromuscular disease - increased FRC, ERV and RV
- Severe obesity/OHS - extrinsic restriction with mildly reduced TLC, preserved DLCO, low FRC and very low ERV (fat pushing on diaphragm so you can’t breathe out as easily)

4) CXR

5) TTE
- ?Pulmonary HTN

6) In Lab Sleep study
- To evaluate OHS and titrate PAP treatment +/- oxygen
- Cf OSA get usually get away with home sleep study

7) Polycythaemia on FBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Treatment for severe OSA (>30 AHI) that is also associated with OHS

A

CPAP is equal to biPAP in terms of CO2 reduction, improvement in hypoxemia and QOL overtime

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

When do you give oxygen monotherapy to OHS?

A

Never - may worsen hypercapnia

Can give it together with PAP therapy if needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What’s the difference between APAP, CPAP and biPAP?

A

APAP is auto-titrating PAP - a range of pressures can be delivered. Machine detects whether there is snoring or flow limiting then adjusts the pressure accordingly

CPAP is continuous positive airway pressure = airway stent (increases pressure at mouth and nose to keep the airway open)

BiPAP

  • Type of NIV
  • Expiratory pressure (ePAP) like CPAP
  • Inspiratory pressure (iPAP) is higher than expiratory pressure; initiated when patient attempts to breathe in
  • ePAP keeps the airway open, while the iPAP kicks in when the patient inhales to assist with work of breathing/increase tidal volume
  • The difference between iPAP and ePAP is what’s driving the ventilation and decreasing the WOB
  • Synchronised: every time you take a breath, the breath is made bigger
  • Time-synchronised: if you don’t breathe at all like in central sleep apnoea, its going to give you a breath
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How do you monitor progress of OSA/OHS on treatment?

A

Monitor ABG (bicarb) and daytime oxygenation and symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What’s a typical BIPAP setting for OHS?

A

Much higher delta pressure 8-15mmHg needed

Might have a lower ePAP but a bigger difference between iPAP and ePAP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Management of OHS

A

Lose weight
Avoid BZDs
BIPAP
- CPAP usually first choice if significant co-existing OSA (monitor over 2-3/12 with sx, ABG)
- If minimal/mild OSA but significant OHS/respiratory failure, NIV may be first choice
- If presenting with acute on chronic T2RF, NIV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Patients admitted with concern for OHS that have not yet had the diagnosis confirmed should be managed how?

A

NIV +/- oxygen (goal is to control the acidosis)

Discharge them on NIV/bipap while they wait for sleep study (within 3 months) –> titrate PAP accordingly after sleep study

When acidosis normalises, may be able to downgrade to CPAP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

If patients have central sleep apnoea on sleep study, how do you manage them?

A 
BiPAP ST (time-synchronised) - likely lifelong as it is unlikely to resolve
Decrease opioids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the goals of treatment for OHS?

A

1) Improvement/normalisation of pCO2
2) Improvement/normalisation of pH
3) Improvement/normalisation of bicarb (often elevated before therapy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What’s the delta pressure?

A

The difference between iPAP and ePAP on biPAP/NIV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Are men or women more likely to have OHS and OSA?

A

Men > women OSA
Men = women OHS (women may be more likely to present later in their course, and thus present with more advanced disease/need to be hospitalised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Which part of a sleep study report should you look at in OSA?

A

AHI
Oxygen desaturation index (ODI) - Number of times oxygen desaturation falls by >4% in one hour of sleep
T90 - time spent below SpO2 90%

Data suggests that it is not the number of hypopneas/apneas but rather the time spent hypoxemic (T90) that most strongly correlates with outcomes such as CV disease, malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Why use home study instead of IP lab study in OSA?

A

Data suggests data from home sleep study is non-inferior to traditional lab-run polysomnography

Sleep better at home
Much better access
Less expensive
People tend to adhere to CPAP better after home sleep study ?unsure why

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Do all severities of OSA require CPAP?

A

Mild OSA may not require treatment unless they have excessive daytime sleepiness
Asymptomatic patients with mild OSA who are started on CPAP and have bad experiences may be much more difficult to reach in the future should their disease worsen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Causes of OSA

A

Majority of people are heavy and have metabolic syndrome

But you don’t need to be heavy to have OSA
Other reasons: hypothyroidism, receding chin, Down’s syndrome or Treacher-Collins (pharynx is narrowed), genetic predisposition, post menopausal women (tissue laxity including palate), children with large tonsils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Benefits of CPAP in OSA

A

Improves sleepiness, depression, cognitive function, QOL
Reduces BP
Reduces MVA

No RCT evidence that it decreases CV mortality (despite lots of observational data)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Other than CPAP, what are interventions are effective in OSA?

A

Weight loss!!
Reduce ETOH
Avoid opioids, BZD (controversial)
Positional therapy - highly effective for those with only positional OSA (up to 25%)

Oral appliance (mouth guards fit by dentist) - moderate effectiveness, $$$

Surgery may be a rescue option in those who don’t tolerate CPAP or oral appliance
Hypoglossal nerve stimulation
Tonsillectomy
Bariatric surgery
Radical maxillofacial/ENT surgery - “last resort”, variable efficacy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

When would you do an in-lab polysomnography rather than home sleep study?

A

Not suitable for complex sleep pathology

CI: neuromuscular weakness or hypoventilation, intellectual impairment, seizures, parasomnias (abnormal behaviours during sleep)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Sleep is divided into NREM and REM sleep. Explain the difference.

A

NREM

  • Makes up 80% of sleep
  • Divided into N1/N2/N3 - progressively ‘deeper’ sleep. N3 (slow wave sleep) mostly occurs in the first half of the night.

REM

  • Makes up 20% of sleep
  • Characterised by atonia (EMG), tonic/phasic eye movements (EOG)
  • Predominantly 2nd half of night
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Does narcolepsy involve NREM or REM sleep?

A

REM - intrusion of REM sleep into wakefulness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Define apnoea

A

Cessation of airflow for ≥10 seconds

Central vs obstructive vs mixed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Define hypopnea

A

Reduction of airflow by 30% for ≥10 seconds followed by:

  • 4% oxygen desaturation
  • EEG arousal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Define apnoea-hypopnea index (AHI)

A

Number of apnoea and hypnoea events per hour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What’s respiratory effort related arousal (RERA)?

A

Increased respiratory effort for ≥10 seconds associated with EEG arousal BUT don’t meet criteria for hypopnea

37
Q

What’s respiratory disturbance index (RDI)?

A

AHI + RERAs

38
Q

What is the definition of sleep hypoventilation?

A

Abnormal increase in PaCO2 during sleep
E.g. neuromuscular disorders, OHS

Transcutaneous CO2 increases to >55mmHg for ≥10 minutes
OR
≥10mmHg increase in transcutaneous CO2 to value >50mmHg for ≥10 minutes

39
Q

What is the definition of Cheyne Stokes respiration?

A

Central apnoeas/hypopneas alternating with a respiratory phase (crescendo-decrescendo pattern of flow)
Long cycle length >45 seconds

40
Q

In what conditions do you get Cheyne strokes respiration?

A

CCF
Post stroke
Terminal phase

41
Q

Pathophysiology of OSA

A

Narrow collapsible upper airway

42
Q

What questions are listed in STOP BANG?

A 
S - snoring
T - tiredness
O - observed apnoea
P - blood pressure
B - BMI
A - age
N - neck circumference
G - gender
  • Are you tired?
  • ≥3 intermediate risk
  • ≥5 high risk
43
Q

What score in epworth sleepiness score is likely pathological?

A

≥10 is likely pathological

44
Q

Risk factors for OSA

A 
Male
Older age
BMI - strongest risk factor 
Increased neck circumference
Snoring
Witnessed apnoeas
Menopause 
Craniofacial abnormalities e.g. short mandible, tonsilar hypertrophy
45
Q

Complications of untreated OSA

A 
MVA 
Cardiovascular disease - HTN, CAD, CCF, AF
CVA
Pulmonary HTN
Diabetes, poor BSL control 
Mortality
46
Q

What are the 2 kinds of PAPs that can be used in OSA?

A

APAP

CPAP

47
Q

Complicated of untreated OHS

A

CV disease - HTN, pulmonary HTN, RHF

Increased mortality

48
Q

What types of sleep disordered breathing can you get in HF?

A

Cheyne strokes respiration

OSA

49
Q

Rx sleep disordered breathing in HF

A

Optimise HF therapy

Treatment is controversial
Treatment options include CPAP, O2, NIV
Adaptive servo ventilation is CI in those with EF <45%

50
Q

Pathophysiology of narcolepsy

A

Autoimmune destruction of hypothalamic neurons that produce hypocretin (orexin) that keeps up awake

51
Q

What’s cateplexy?

A

Sudden + transient muscle weakness associated with conscious awareness usually triggered by emotions e.g. laughing

52
Q

Definition of narcolepsy

A

Excessive daytime sleepiness for at least 3 months + positive mean sleep latency test +/- cataplexy

53
Q

Rx narcolepsy

A

Dexamphetamine or armodafinil

SSRI/SNRI for cataplexy

54
Q

How to diagnose narcolepsy?

A

Mean sleep latency test (MSLT)

1) PSG to ensure at least 6 hour sleep before MSLT

2) MSLT during the day in sleep lab
- x5 20 minute naps set 2 hours apart
- <8 minutes associated with 2 sleep onset REM periods = highly suggestive of narcolepsy

55
Q

Most common cause of restless leg syndrome

A

Iron deficiency

56
Q

What is the difference between restless leg syndrome and periodic limb movement disorder?

A

PLMD occurs during sleep and people are unaware of it (seen in sleep study), while RLS occurs when a person is awake and asleep.
80% of people with RLS also have PLMS, but not the reverse.

57
Q

What is parasomnia?

A

Abnormal behaviours during sleep

E.g. REM sleep disorder, occurs in Parkinson’s

58
Q

Is RLS related to genetics?

A

Yes

Autosomal dominant

59
Q

Phenotypes of RLS

A

Primary (early onset)
Younger, slowly progressive, FHx, idiopathic

Secondary
Iron deficiency, ESKD, pregnancy, medications that block the DA pathway (AD, antihistamine, lithium, D2 receptor blocker)

60
Q

Pathophysiology RLS

A

Reduced CNS iron

Iron important for DA synthesis –> reduced CNS DA

61
Q

Diagnosis RLS

A

Clinical diagnosis
Iron studies
Pregnancy
Renal function

BUT if you do a sleep study, may see periodic limb movements (non-specific)

62
Q

Rx RLS

A

Lack robust evidence

Stop caffeine, nicotine, ETOH
Iron replacement if ferritin <75

1st line: DA agonist (pramipexole or ropinorole)
Side effects: augmentation with time
(paradoxical worsening RLS during the day), impulsive behaviours

1st line: pregabalin/gabapentin
Side effects: suicidal ideation, weight gain, sleepiness

2nd line: opioids, BDZ

63
Q

Periodic limb movements disorder

A 
RARE. Controversial diagnosis. 
Diagnosis of exclusion
Period limb movements on sleep study
Marked sleep disturbance and daytime sleepiness
No other sleep disorder
64
Q

Explain normal sleep

A

Early part of the night: deep sleep (NREM)
Late part: REM sleep

NREM–>REM–>NREM–REM (x4 cycles)

65
Q

NREM parasomnia

A

Undesirable behaviour or phenomenon occurring during NREM sleep

Partial arousal from sleep
Some genetic susceptibility

Can be related to zolpidem, sleep deprivation, emotion stress

Common in children

Happens first part of night

66
Q

Types NREM parasomnia

A

Sleep walking

Confusional arousal - sexsomnia

Sleep terrors - wake up, high pitched screaming

67
Q

Treatment NREM parasomnia

A

Generally grow out of it
Reverse exacerbating factors

Rx: clonazepam in difficult to treat (no RCT)

68
Q

REM behaviour disorder (REM parasomnia) associated with

A

Alpha synucleopathies

PD
DLB
MSA

Within 16 years, 80% of them will develop alpha synucleopathies/neurodegeneration.

69
Q

REM behaviour disorder diagnosis

A

REM sleep loss of muscle atonia
+
Abnormal behaviour during REM often as dream enactment behaviour that can cause injury

Diagnosis requires both

EMG
- Sustained muscle activity during REM

70
Q

REM behaviour disorder Rx

A

Clonazepam (90% response) +/- melatonin

Safe home environment
Avoid changes in sleep routine
Avoid antidepressants (TCAs, SSRI)
Neuro assessment

71
Q

Clinical features REM behaviour disorder

A

30 seconds - 3 minutes
Fighting, violent during REM sleep
M>F
Rapid return to baseline +/- recall (tend to remember it)

72
Q

What’s narcolepsy?

A

Don’t have neat NREM–>REM sleep cycle
Its all over the place
Young people get it

73
Q

Forms of narcolepsy

A

3 forms

1) NT1 (with cataplexy)
- Well studied
- Low CSF hypocretin (lateral hypothalamus)
- HLA positive 98%

2) NT2 (without cataplexy)
- May improve spontaneously
- Some have normal CSF hypocretin

3) Secondary narcolepsy (rare)
- CNS tumour, brain trauma

74
Q

What’s cateplexy?

A

Brought on by emotion
Transient loss of muscle tone - may be subtle like drooping of mouth or slumping to the ground. No LOC.

Possible REM sleep intruding into wakefulness

75
Q

What’s hypocretin?

A

Maintains wakefulness

Maintains sleep stages

76
Q

Symptoms narcolepsy

A

Daytime sleepiness
Irresistible urge to fall asleep
+/- cataplexy
Go into REM sleep very quickly (normally it takes 60-90 minutes)

77
Q

Pathophysiology narcolepsy

A

Genetic predisposition and environmental factors (e.g. pandemic H1N1 in Finland)

78
Q

Diagnosis narcolepsy

A

Sleep study - exclude other sleep disorders
MSLT - how long it takes for you to fall asleep during the day (<8 minutes)
How soon before ongoing into REM sleep?
Consider CSF hypocretin

79
Q

Treatment narcolepsy

A

Schedule naps
Modafinil or armodafinil
Amphetamines

Cataplexy
Sodium oxybate (similar to date rape drug so very hard to access) - only drug that improves sleep consolidation
Antidepressants

80
Q

Insomnia management

A

CBT works just as well as pharmacotherapy
However access to psychologist is difficult

BZD have significant side effects and safety concerns
Most other alternatives have not been systemically evaluated for efficacy or safety

81
Q

Types of sleep study

A

Level 1 - in hospital, monitored
- Do this in patients with hypoventilation

Level 2 - at home, similar to level 1

  • Similar outcomes to level 1
  • Helpful in selected patients

Level 3
- Measures oximetry, airflow

Level 4

  • Simple screening
  • Oximetry only
82
Q

2 patterns of presentation OHS

A

1) acute on chronic respiratory failure
- Often have RHF, pulmonary HTN
- Need BIPAP in ICU

2) Chronic (stable)
- Part of routine assessment for OSA
- May get away from simple CPAP

83
Q

What’s central sleep apnoea?

A

Cessation of airflow

No effort to breathe

84
Q

Causes of central sleep apnoea

A 
CCF (50%)
Stroke
Drugs e.g. opioids 
Neuromuscular disorders
CNS disorder e.g. MS, Arnold-Chiari 
Iatrogenic - when you over ventilate people (blow off CO2 too much)
85
Q

Treatment central sleep apnoea

A

Treat underlying cause

Consider
Oxygen
Adaptive seroventilation (controversial)

86
Q

What’s nocturnal hypoventilation syndrome?

A

Hypoventilation at night, most severe during REM
Increased PaCO2 (reduced PaO2)
Reduced or absent effort

Prone to RHF, pulmonary HTN, respiratory arrest (especially if they have pneumonia on top of that)

87
Q

Causes nocturnal hypoventilation syndrome

A

Nocturnal hypoventilation syndrome is always caused by something else!!

OHS
Severe COPD
Neuromuscular disease e.g. severe scoliosis
CNS disorders
Congenital central hypoventilation syndrome (No PHOX 2B gene)

88
Q

Diagnosis nocturnal hypoventilation syndrome

A

Severe desaturation, sustained, particularly in REM sleep

Rise in PaCO2

89
Q

Stable hypercapnic COPD PaCO2 >52, not acidotic
Without overlay OSA, HF, opioids
Without exacerbation

Management

A

Long-term NIV

Better outcomes

Respiratory (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions