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Dana's Exam Learning. > Respiratory and Sleep Medicine > Flashcards

Respiratory and Sleep Medicine Flashcards

1
Q

Other than sleepiness, how can children with sleep disorders present?

A

Anxiety, irritability, impulsive, inattentive or have poor concentration

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2
Q

DIMS (Sleep)

A

Disorders of initiation and maintenance of sleep

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3
Q

DOES (sleep)

A

Disorders of excess sleepiness

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4
Q

What is a parasomnia?

A

f

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5
Q

Screening tool for sleep

BEARS

A 
B - Bedtime problems
E - Excessive daytime sleepiness
A - Awake at night
R - Regularity and duration of sleep
S - Snoring and Apnoea
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6
Q

How common are sleep problems in well children?

A

10-30% of children

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7
Q

What are the normal physiological changes that occur in sleep?

A

Changes in blood pressure and body temperature
Decreased tone - leads to upper airwat resustence (x 2 in REM) + reduction in tidal volume.
- Any impairment of ventilation when awake will be worse in sleep

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8
Q

What is the function of sleep?

A

Unclear - beneficial in learning, consolidation, restoration

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9
Q

Effects of sleep depreivation

A

Tremor, reflex changes
Blunted hormone secretion (GH, prolactin)
Elevated pro-inflammatory cytokines
Impaired psychomotor performance
Behavioural changes (pre-frontal cortex + executive function
Associated with obesity

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10
Q

How does sleep deprivation lead to obesity?

A

Add picture of sleep + obesity (males)

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11
Q

What are the elements of Polysomnography?

A 
EEG 
EMG
Airflow to detect apnoea
Effort (obstructive / central)
Oxygen saturations, CO2, heart rate
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12
Q

What are the stages of Sleep?

A

N1 - transition to light sleep, easily roused
N2 - light sleep (K complexes + spindles)
N3 - Deep sleep “slow wave sleep”, still, very hard to rouse, regular breathing - big triangluar waves
“ if in a dingy on the ocean , you would be sea sick”
REM - “dream sleep” , decreased tone, partial paralysis, vivid dreams, irregular breathing, increased upper airway resistance

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13
Q

Stages of sleep in newborns + cycle length

A

Active sleep = N1,2 and REM
Quiet sleep = N3
= 40 minute cycle

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14
Q

How long is the adult sleep cycle?

A

90 minutes

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15
Q

Which part of the night is REM sleep more prevalent?

A

2nd half of the night

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16
Q

Which part of the night is DEEP sleep more prevalent?

A

1st half of the night

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17
Q

Example of sleep spindle + K-complex

A

Image

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18
Q

What percentage of children stop daytime sleep by 5?

A

95%

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19
Q

Behavioural insomnia (3 types)

A

Type 1 - Sleep association type (poor sleep hygiene)
- not innate to know how to fall asleep
Type 2 - Limit setting disorder type (if parents have issues setting limits during the day, the night is even worse
Type 3 - Mixed

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20
Q

Management of behavioural insomina

A

Manage as if mixed

  • exclude physiological causes (restless legs, OSA< reflux, eczema
  • Day time behaviour / limit problems?
  • Sleep hygiene and new sleep associations

Evidence Based Techniques:

1) Sudden / graduation extinction (controlled crying)
2) Fading with positive bedtime routines (20 mins quiet play / reading) - routine + regularity!

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21
Q

ADHD and sleep

A

Also hyperactive in sleep
Easily wake, move more
daytime sleepiness
? due to OSA ? due to stimulants ? not enough stimulants
- consider atomoxetine, clonidine or melatonin + behavioural therapy

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22
Q

Autism and sleep

A

up to 80% have issues with sleep
Difficulty settling
Waling between 1-5am + wake entire house
- Early morning waking
Behavioural therapy - look at perpetuating factors
Melatonin - short half life (may need long acting) - have issues swallowing tablets

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23
Q

What is delayed sleep phase?

A

“permanent jet lag”

Common in adolescent due to decreased and delayed melatonin peak

  • promoted by late homework, TV, texting, internet
  • TAKE AWAY DEVICE

Exam Q - actigraphy - delayed sleep phase

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24
Q

Treatment of delayed sleep phase

A 
Sleep hygiene
- dim light before bed, no computer / TV in room
No steroe, texting
Bright light when should be awake
Advance bedtime by 15 mins each 3 mights
Melatonin as adjuvant
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25
Q

Disorders of sleep with movements

A

Sleep stage specific

Non-sleep stage specific

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26
Q

Parasomnias

A

= Confusional arousals, night-terrors and seep walking

    • partial awakening from N3 (SWS) - usually 60-90 minutes into sleep, 1-2 x per night
    • strong family history
    • Thinks of causes of abnormal arounsal (OSA)
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27
Q

Night terror

A

N3
Child is unable to be comforted, goes straight back to sleep, cannot recall event, usually in deep sleep (60-90 mins from sleep onset)

39% of children occasionally
3% persistent
Clonazepam if extreme

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28
Q

Night mare

A

Able to be comforted, recall event in the morning, waking from REM sleep

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29
Q

Frontal lobe seizures

A

Stereotypical features of pointing and pelvic thrusting, more likely to stand, sudden onset, ALWAYS THE SAME MOVEMENTS
- Post-ictal state can look like parasomina / night terror

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30
Q

Sleep walking

A

N3
Occasional 15%, frequent 3%
Primary + preschool age
- primary concern is safety (lock doors) - direct to bed
Dont try to wake them up
Clonazepam if extreme - especially if anticipatory awakening

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31
Q

Rhythmic movement disorder

= head dropping / head banging

A

Normal variant
Just before sleep onset / stage 1
increased in autism and developmental delay
may result in injury

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32
Q

Periodic limb movements of sleep

A

Part of spectrum of Restless leg syndrome
- increased frequency of leg movements in sleep
Partial iron deficiency in CNS - aim ferritin > 50 (PO or IV)

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33
Q

Definition of Restless legs syndrome

A

AKA - Willis-Ekbom Dx
- Common, treatable neurological disorder impacting sleep, often co-existing with ADHD, mood and anxiety disorders
Diagnostic Criteria
–> Urge to move the leg, usually accompanied by uncomforatble sensation in the legs
- Symptoms worsen / begin with inactivity and relieved by movement
– Occur exclusively / predominatly at night / evening
– can not be attributed to by another medical or behavioural condtion

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34
Q

Hypersomnias = excess sleepiness

A

Fall asleep at inappropriate circumstances
Process S - sleep homeostasis
Process C - circadian alerting (work together)
= constantly fighting sleep or falling asleep in inappropriate situations
* most common cause is lack of sleep *
Duration, routine, regularity

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35
Q

Orexin - hypocretin 1 - involved in …..

+ treatment

A

Narcolepsy
high levels of orexin
Treatment - scheduled naps (30 mins), regular sleep routine, methylphenidate / dexamphetamine or modafinil (best)

Catoplexy - extreme emotions (sadness, laughing)
Tx - sodium Oxybate (GHB), SSRI’s, TCA, Venlafaxine

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36
Q

Primary hypersomnia

- constant vs periodic

A 
Constant = narcolepsy (+/- cataplexy); primary idiopathic hypersomnia
Periodic = Klein Levin Sx, (obese, 5-7 days of increased sleepiness and sexual behaviours);  menstrual-related hypersomnia
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37
Q

What is a multiple sleep latency test

A

Measure time to go to sleep in a dark room
- normal = 1-2 , no rem, > 8 minutes
Short latency + REM = narcolepsy
Short latency + no rem = hypersomnia

  • Don’t forget hypothalamic tumour *
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38
Q

Melatonin effect on gonads

A
  • In Rats * testicular cancer, brings estrous forward, can delay puberty
  • lowers seizure threshold
  • being tired also reduces seizure threshold + stimulated immune system (contraindicated post transplant)
39
Q

Cystic Fibrosis

  • Incidence (Australia)
  • Inheritance pattern
A

Autosomal recessive
1:2500 (Australia)
Asia 1:300,000
Carrier 1:25

40
Q

Cystic Fibrosis

- Gene and protein involved

A

CFTR - Cystic Fibrosis Transmembrane conductance Regulator
= CFTR Gene (Chr 7), 27 exons (large)
- Encodes chloride channel in apical membrane of exocrine epithelial cells, when faulty, have abnormal secretions

> 2000 mutations, most common F508del G542X

41
Q

Cystic Fibrosis

- Pathophysiology

A

Excessive sodium into the cell, drys out ciliary layer causing thick sticky mucous
* Insert picture of channels *

42
Q

CFTR malfunctioning classes (6 types and genetic mutations)

A

*Insert picture of malfunctioning proteins *
Type 1 - NO PROTEIN - G542X
Type 2 - defective endoplasmic reticulum processing F508D
Type 3 - protein at cell surface but non functioning G551D
Type 4/5/6 - Increasing levels of protein but may be less stable * milder mutations *

43
Q

c.1521_1253delCTT mutation

A

F508delta

44
Q

Newborn screening for CF

A 
4-6 weeks average age of diagnosis
Tests IRT (Immune reactive trypsin) - 
\+ 4 genes (F508del, G551D, G542X, R117H)
Picks up 95% of cases
Can pick up carriers
Leads to early diagnosis and ? better outcomes (no evidence)
45
Q

Diagnosis of classical CF

A

2 Genetic mutations
Positive sweat test
Pancreatic elastase (low)

46
Q

CFSPID

A

Cystic Fibrosis Screen Positive Inconclusive Diagnosis

  • either mild or no disease
  • close follow up
47
Q

Sweat Test

A

Chloride measurement
>60 = Cystic Fibrosis
40-60 - borderline

Need to be >2kg and after 2 months of age
Need Sweat weight >75mg (trad) or >15microL macroduct

48
Q

Causes of False positive and false negative sweat tests

A
  • Insert table *
49
Q

Flow chart of pathophysiology of CFTR dysfunction

A
  • Insert picture *
50
Q

Clinical manifestations of CF (Lung and ENT)

A

Lung

  • Increased thick, sticky mucous
  • Chronic, productive cough
  • Chronic Bronchitis (bacterial / fungal)
  • Obstructive airways on lung function
  • Bronchiectasis

ENT

  • Nasal Polyps
  • Sinusitis
51
Q

Common Pathogens in CF

A

Most common = Staph Aureus (60-80%)
Pseudomonas (20% under 2, 50% by 18)

  • Insert graph *
52
Q

CF Treatment approach

A

Treat infection (antibiotics)
Keep inflammation under control (azithomycin)
Increase airway clearance (physio, hypertonic saline, pulmozyme nebs )

53
Q

CF Treatment - Staph Aureus

A

Some centres use prophylaxis until age 2
Exacerbation - Fluclox 2-4 weeks
Staph Eradication - IVABS - usually 2 x anti-staph agents for one month

54
Q

CF Treatment - Pseudomonas

A

First Isolation - eradication trial (IV Tobramycin + Ceftazidime 2 weeks, or oral cipro 3 weeks + Tobra nebs 2 months)

  • Chronic infection - suppress it
  • -> lung function declines

Oral - Ciprofloxacin
Neb - Tobramicin,
IV - Tobramycin, ceftazidime, meropenem

55
Q

CF Treatment - Burkholderia capacia complex

A

First isolation - IV eradication (meropenem, temocillin, bactrim
Chronic - Nebulised tobra, oral doxy
Mild Sx - Bactrim

56
Q

CF Treatment - Non TB mycobacteria

A 
MAC  (Mycobacetium avium)
M Abscessus
Consider in non-improving cases
Need smear / bronchoalveolar lavage
Treatment - 12-15 months from first negative culture - need 2-3 anti TB drugs (lots of side effects )
57
Q

CF Treatment - Viral infections

A

Treat more aggressively, admit for RSV bronch
Ensure flu vaccine
Give Tamiflu if Flu +

58
Q

CF Fungal infections

A

Aspergillus fumigatus 40-60% - no invasive disease, IgE mediated disease

  • hypersensitivity disease, avoid high damp areas (building sites, hay, compost)
    • tick sputum with brown/black bronchial cast, increased wheeze, high serum IgE, eosinophillia, pulmonary infiltrates, positive asperigillus IgG and IgE
  • Treat with steroids (oral, pulse melthyl pred), Itraconazole
  • Invasive disease - IV caspofungin

Candida Albicans 75-90% - usually from mouth

59
Q

GIT manifestations of CF (x 6)

A

Meconiium ileus (20%), DIOS (Distal intestinal obstruction syndrome
GORD
Pancreatic insufficiency (90%) - creon
Pancreatitis (in pancreatic sufficient patients )
Malabsorption - often bacterial overgrowth, poor intake of creon
CF liver disease (cirrhosis with portal hypertension)

60
Q

Endo manifestations of CF (x 4)

A

CF related diabetes (50% by age of 30) 0 usually pancreatic insufficient
Poor growth, delayed puberty and low bone mineral density
Fertility - 95% male infertility- congenital bilateral absence of Vas deference; 20% female infertility - normal tract

61
Q

Rheumatoid manifestations of CF ( x 2)

A

CF related arthropathy (10%)

  • Episodic arthritis with pain and swelling of large joints, occasionally low grade fever and rash
  • treat with NSAIDS

Hypertrophic pulmonary osteoarthropathy (HPOA) - arthritis, joint effusion, tenderness and pain over long bones - treat with anti-inflammatory

NOTE - Ciprofloxacin can cause arthropathy

62
Q

Pseudo-Bartter’s syndrome

A

Metabolic alkalosis with ow K, Cl Na

- in hot weather with inadequate salt and fluid replacement, may be preceeded by gastro, not clinically dehydration

63
Q

Mechanism of action

- Ivacaftor / Lumacaftor / Elexacaftor

A

Ivacaftor

  • Type 3 mutations, partially correct channel defect allowing chloride transport (potentiator)
  • $250K/yr, 10 % improvement in lung function

Lumacaftor/Tezacaftor
- Improved protein folding and increased trafficking to cell surface

Elexacaftor
- Improves trafficking to cell surface

ORKAMBI - Lumacaftor and ivacaftor

64
Q

Trikafta mechanism of action

- % improvement in lung function

A

TRIKAFTA - elexacafrot, tezacaftor, ivacaftor
* Insert image *
reduced exacerbations, improved BMI, reduced sweat chloride, reduced symptom scores (14.3% improvement maintained)

65
Q

CF related diabetes

  • when it presents
  • how to diagnose
A

Presents in second decade of life
Does not usually present with DKA
Diagnosed by fasting glucose and HbA1C
Girls > Boys

66
Q

When to go to lung transplant for CF

A 
FEV1 less than 30% Pred Lung function
Poor exercise tolerance / nutritional status
Rapid decline in lung function
Major life threatening complications
Quality of Life complications
67
Q

Child presents with large volume greazy stools, 3 months of weakness, poor coordination, mild ataxia, decreased vibratory sense, bilateral hyporeflexia
–> Which vitamin is deficient?

A

Vitamin E

- weakness, hypotonia ? cerebellar component

68
Q

Definition of Asthma

A

Variable, chronic airway inflammation, periods of exacerbation and remission

  • Reversible airway obstruction
  • Increased mucous production (mucous plugging)
  • Bronchospasm
    • Thickened and inflammed bronchial walls
  • -> Hyperinflation

10% prevalence in Aus/NZ

69
Q

Contribution to development of asthma

A 
Family History (only 4% explained)
Tobacco Smoke
Air Pollution
Mould / Damp
Animals (reduces prevalence)
Antibiotics ? Paracetamol
Diet/obesity
Breast feeding
70
Q

Naive T-Cells –> Atopic response pathway (3 x interleukins)

A

Th2 cells
- produce IL 4, 5, 13 –> B-Cell production –> Atopy (IgE dominance and eosinophillic inflammation
Th2 suppressed by interferon gamma

Only explains 50% of children

71
Q

Naive T-Cells –> NON-atopic response pathway (2 cytokines)

A

Th1 cells

–> Produce IL-2 and interferon Gamma –> IgG dominant and cell mediated immune response

72
Q

Natural history of asthma

A

Even children who lose overt symptoms of asthma have persistent airway obstruction

  • airway inflammation may persist in the absence if symptoms
  • Frequently reoccurs
73
Q

How to diagnose asthma

A

Recurrent / persistent wheeze / nocturnal cough / chest tightness
Triggers - exercise, cold air, allergen, viral infections, stress, aspirin, recurrent / seasonal
Family Hx asthma / atopy
Absence of physical findings suggesting alternative diagnosis
Tests that support diagnosis (spirometry in children)
Response to bronchodilators / preventers

74
Q

Preschool Wheeze

A

Preschool asthma - multitrigger wheeze - usually respond to ICS
Infrequent
Frequent

75
Q
  • Insert image*
A

Normal lung function

76
Q
  • Insert image *
A

Obstructed intrapulmonary airways

  • concave shape to exhalation
  • Reduction in FEV1 and FEV1/ FVC ratio
77
Q
  • Insert image*
A

Restrictive lung disease

- Normal shape but squashed

78
Q
  • Insert image *
A

Fixed central or upper airways obstruction

- Flattend loops

79
Q

Insert image

A

Variable upper airway obstruction

80
Q

Insert image

A

Inadequate effort

- common - not really a curve at all

81
Q

Insert image

A

Incomplete exhalation

82
Q

Asthma spirometry

A 
Concave pattern
FEV1 reduced
FEV1/FVC reduced
Bronchodilator responsive - FEV1 increase of at least 12% from baseline
Normal does not exclude asthma
83
Q

Direct challenge test

A

Inhalation of increasing concentrations of histamine or methacholine - falling FEV1 of >20%

84
Q

Indirect challenge test

A
  • Exercise - negative response to an exercise challenge test is helpful excluding asthma in children with exercise related breathlessness
  • Inhaled mannitol
85
Q

Peak expiratory flow monitoring

A

Variability of up to 20% in children

- not good diagnostically but a trend can show worsening disease activity (still not well correlated)

86
Q

Fractional exhaled nitric oxide (FeNO)

A

Positive - suggests eosinophillic inflammation and provides supportive but not conclusive evidence of asthma (> 35PPB, some use 25)
–> not for diagnosis
FeNO higher in :
- Asthma, atopic children, eosinophillic bronchiitis

FeNO lower in:
- smokers, early phase allergic response, neutrophilic asthma

Difficult to do in under 8-9 year olds

87
Q

Long acting beta agonists

A

Formeterol / salmeterol
Always use with ICS
Not for use under age 4
Should not be initiated when clinically unstable

Cause reduction of b-receptors

88
Q

SMART / AIR therapy

A

Use the same puffer for preventer and reliever

  • Low dose budesonide / formeterol (symbicort)
  • 1 puff BD (maintenance), up to 1 puff QUD for reliever
  • use salbutamol as needed
  • not used in young children

S/E: Fine tremor, palpitations, arrhythmia, tachycardia, paradoxical bronchospasm

89
Q

Gina report - 2019

A

Adolescents
Recommend no longer just use ventolin alone to manage acute symptoms
increased risk of severe exacerbations by 2/3 if you do not also use steroid
Increases allergic response
B-receptor down-regulation, decreased broncho-protection, rebound hyperresponsiveness, reduced response

90
Q

MoA - Omalizumab

A

Binds to IgE - stops IgE binding to receptors and reduction in allergic response, reduced high-affinity receptors
S/C injection 4 weekly
When treatment stopped, asthma often never as bad
Need to be on maximum asthma treatment

91
Q

MoA - Mepolizumab, ( Resilizumab, Benralizumab)

A

Anti - IL-5
Inhibits proliferation of eosinophils
Need high eosinophils and over age 12
Need to be on maximum asthma treatment

92
Q

When do you use nasal nitric oxide test?

A

Primary ciliary dyskinesia (PSD)
Use from age 5
nNO - sensitivity 97.5% Specificity 96.4%
- false positive in acute viral infection / sinusitis
- Need to repeat on two seperate occasions

93
Q

How to diagnose ciliary dyskinesia

A 
nasal Nitric Oxide (1st) - functional
Electron Microscopy (invasive) - structural
Gene testing - 30 genes (panel - 93.9% sensitive)

Dana's Exam Learning. (17 decks)

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