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Paediatrics > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Bronchiectasis CXR findings

A

Peribronchial thickening Retained secretions Compensatory emphysema Tubular / cystic

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2
Q

Bronchiectasis causes

A

Childhood infections - Measles, pertussis Bronchial obstruction Chronic aspiration Kartagener’s syndrome - Bronchiectasis, dextrocardia, absent frontal sinuses Immune deficiency

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3
Q

Causes of pulmonary oedema

A

Cardiac failure Fluid overload Cerebral CVA, head injury, raised ICP Drowning Aspiration Radiation Thoracocentesis Drugs Inhaled toxins (smoke, hydrocarbons_ Shock lung

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4
Q

What is asthma?

A
  • Heterogenous disease usually characterised by
    • Chronic airway inflammation
    • Wheeze, SOB, chest tightness. cough
    • Variable expiratory airflow limitation
  • No SINGLE gold standard diagnostic test
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5
Q

What are the factors that increase the risk of asthma?

A

Exposure to paracetamol + antibiotics in 1st year of life

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6
Q

What is the pathophysiology of asthma?

A
  • Smooth muscle hyperplasia
  • Thick tenacious mucus plugs
  • Thickened basement membrane
  • Muscus oedema –> abnormal mucociliary clearance
  • Eosinophili of the submucosa + secretions
  • Increased mast cells in smooth muscle
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7
Q
A

Raised exhaled nitric oxide

  • Elevated in ANYONE with atopy + eczema
    • Therefore need a even high level if patient you are testing also has eczema
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8
Q
A

B

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9
Q

Asthma spirometry

A
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10
Q

Other than spirometry can you use in asthma?

A
  • Direct challenges are more likely to provoke a response
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11
Q

At what age do we diagnose asthma?

A
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12
Q

Does inhaled corticosteroids affect growth?

A

YES

Frequent use can reduce height by 1.5-2cm

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13
Q

What questions do you ask for asthma control?

A
  • Daytime asthma symptoms > 2 /week
  • Any night waking?
  • Reliever needed for symptoms >2/weel
  • Any activity limitation due to asthma
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14
Q

Spacer vs mask use in asthma

  • When to use + effect on lung deposition
A
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15
Q
A

Check inhaler technique + adherence

Montelukast side effect: ADHD like behaviour, suicidal ideation, sleep difficulties

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16
Q
A
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17
Q

What is the treatment algorithm for preschool wheeze with frequent symptoms?

A

If this does not work requires further investigation for CF/ bronchiectasis / immune deficiency

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18
Q

Why don’t we give LABA’s without ICS?

A

LABA increase the risk of sudden death + severe exacerbations therefore ALWAYS need to give them with ICS

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19
Q

What is the treatment algorithm for asthma?

A
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20
Q
A

D: ultrafine doubles the potency

Fluticasone 1/2 as potent as beclomethasone

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21
Q

What are the concerns about SABA only treatment in asthma?

A
  • SABA only treatment is associated with increased risk of exacerbations + lower lung function
  • Regular use increases allergic responses + airway inflammation
  • Beta receptor down regulation, decreased bronchoprotection, rebound hyperresponsiveness, decreased bronchodilatory response
  • Over use of SABA (e.g. > 3 canisters / year) is associated with increased risk of severe exacerbations
  • >12 canisters / year is associated with increased risk of asthma related death
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22
Q
A

A wrong- would make it worse

B wrong- binds to IgE in the blood but doesn’t work if IgE levels are > 1500

  • Would give this if IgE wasn’t so high

C Mepolizumab

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23
Q

What is the mechanism of action of omalizumab (anti IgE)

A

10 % risk of anaphylaxis

1st time the dose is given need to be in hospital for 4hrs post

Subseqent doses requires to wait 25min post administration

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24
Q

What is the mechanism of action of mepolizumab, reslizumab + benralizumab (anti IL5)?

A
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25
Q

How do sleep disorders usually present in childhood?

A
  • Anxious
  • Irritable
  • Impulsive
  • Inattentive
  • Poort concentration
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26
Q

What are the screening questions for sleep disorders?

A

BEARS

Bedtime problems

Excess daytime sleepiness

Awakening at night

Regularity + duration of sleep

Snoring + apnoea

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27
Q

What happens during sleep?

A
  • Reduction in BP
  • Reduction in temperature
  • Decreased tone;
    • Upper airway resistance increases (x 2 in REM)
    • Tidal volume decreases (1/2 in REM)
  • Any impairment of ventilation when awake will be worse when asleep
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28
Q

What is the function of sleep

A
  • Immune restoration
  • Hormonal/growth
  • Consolidate learning
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29
Q

What are the different stages of sleep?

A
  • REM“dream sleep” decreased tone (chin EMG), rapid eye movement, partial paralysis, vivid dreams, irregular breathing, increased upper airway resistance, decreased tiday volume
  • N1 transition to light sleep, easily roused
  • N2 light sleep (K complexes + spindles)
  • N3 deep sleep or “slow wave sleep”, still, very hard to rouse. Very regular breathing.
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30
Q

How do you tell if it is a breathing or sleeping question on PSG?

A
  • Breathing: 1 or 2 min / page
  • Sleeping: 30 sec / page
    • Are there eye movements (Yes- awake or REM)
    • What is the chin tone? (Big- awake, small- REM)
    • Are there K complexes or spindles?
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31
Q

What stage of sleep is this?

A

N2 sleep: sleep spindles + K complexes present + medium chine EMG

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32
Q

What stage of sleep is this?

A

N3 sleep

33
Q

What stage of sleep is this?

A

REM sleep

34
Q

Normal sleeping times

A

Approximate = 16 - age (from birth to sleep time of 8-9hrs)

  • Birth = 16 hours
  • 2 years = 14 hours
  • 6 years = 10 hrs
35
Q

Normal napping

A

1 year old = 2 naps / day

2 year old = 1 nap / day

5year old = no napping

36
Q
A
37
Q

Type of waves in each phase of wakefullness/ sleep

A

BATS Drink Blood

  • Awake- beta waves
  • Relaxed wakefulness- alpha waves
  • NON REM
    • N1: theta waves
    • N2: spindles (memory consolidation) + K complexes
    • N3: delta waves
  • REM: beta waves
    • Dreams
    • Active sympathetic system: rise in HR + body temp
    • Eyes rapidly move but rest of body is paralysed
38
Q

What is the MOST restful sleep?

A

N3 (slow wave sleep)

Entered into relatively quickly after the onset of sleep

Preserved in the face of reduced total sleep

Increases (rebounds) after a night of restricted sleep

39
Q

During which stage of sleep do night terrors + bed wetting occur?

A

Slow wave sleep: N3 (during in SWS peaks during early childhood which explains why sleep waking / bedwetting / night terrors is MOST common in preschool age children)

40
Q

When during the night do you have more

  • Non- REM sleep
  • REM sleep
A
41
Q

Does REM sleep % increase or decrease as you age?

A
42
Q

What hormones are deficient in narcolepsy?

A

Hypocretin + orexin

43
Q

Characteristics of narcolepsy

A

Multiple sleep latency SHORT with > 2 REM onsets

  • Abnormal latency < 8 min

Features

  • Can have cataplexy = sudden + temporary loss of muscle tone
  • Sleep paralysis
  • Hypnagogic hallucinations
  • Sleepiness

Narcolepsy special tests

  • HLA for DR2, DRB1 1501, DQB1*0602
  • Hypcretin levels = low
44
Q

What is the definition of apnoea?

A

>90% decrease baseline flow for > 2 breaths

  • Obstructive: continued effort
  • Central: absence of effort
  • Mixed: starts central + ends obstructive
45
Q

What is the defition of hypopnoea?

A
  • >30% decreased baseline flow for 2 or more respiratory cycles with O2 desat of 3%
46
Q

What sort of apnoea is this?

A

CENTRAL

You have see complete absence of effort + air flow (which lasts > 2 breaths) just prior to the desat

47
Q

What sort of apnoea is this?

A

OBSTRUCTIVE

Also note paradoxical movement of abdomen + thorax

48
Q

What event is this?

A

Hypopnoea

> 30% decrease in airflow signal that lasts > 90% duration of > 2 normal breaths

49
Q

What is the prevalence of OSA in children?

A

3%

50
Q

How is OSA best diagnosed?

A

Polysomnograpghy = gold standard

51
Q

What are the most common consequences of OSA in children?

  • Decrements of memory + attention
  • Excessive daytime tiredness
  • FTT
  • Pulmonary hypertension
A

Decrements of memory + attention

  • Causes defects of executive function
52
Q
A
53
Q

What are the adverse effects of OSA?

A
  • Defects in executive functioning
  • Disrupts sleep
  • Hard to wake
  • Daytime sleepiness
  • Inattention, impulsive, irritable, poor concentration, poor academic performance
  • Hypertension
  • Elevated lipids
  • Insulin resistance
  • Severe: FTT, pulmonary hypertension, cor pulmonale
54
Q

What is the role of oximetry in diagnosis OSA?

A
  • Good positive predictive value
  • Poor negative predictive value
    • IF negative test is inconclusive
  • CANNT differentiate between central + obstructive sleep apnoea
  • MUST have a 2 second averaging time

Cluster = >5 desats within 30 minute period

Positive = > 3 clusters with > 3 desaturations (>3% drop in SpO2)

55
Q

A 3 year old is referred because his parents are concerned about his breathing during sleep. He snores loudly most nights, is restless and wakes frequently. During the day he is a mouth breather and said to be “on the go” all the time.

Investigation?

Treatment?

A

Polysomnography

Adenotonsillectomy: 80-85% near or total cure (50% if obese)

  • Improves behaviour + QOL
  • Does NOT improve IQ

Nasal corticosteroids HALVE the PSG score + may cure mild OSA

CPAP: reserved for moderate pos surgical disease, severe on waitlist or contraindications to surgery

56
Q

What are the risk factors for respiratory compromise post adenotonsillectomy?

A
  • Obesity
  • Age < 3 years
  • Underlying syndrome
  • Severe OSA
  • Complications of OSA
57
Q

Obesity + OSA

A
  • In childhood normally an issue of tonsils + adenoids not obesity but this is changing due to the obesity pandemic
  • Obesity causes;
    • Decreased lung volumes (fat pressing of the chest)
    • Decreased airway tension
    • Fatty deposits around pharynx narrowing the airway
    • Combined effect increased pharyngeal collapsibility
58
Q

Can adenoids + tonsils re-grow

A

Adenoids can

Tonsils CANNOT

59
Q

What is the definition of respiratory failure?

A
  • Type 1: hypoxic
    • O2 <8 (60mmHg)
  • Type 2: hypercarbnoea
    • CO2 > 7kPA (55mmHg)
60
Q

Which of the following has NIV NOT been shown to improve NMD?

  • Episodes of chest infection
  • Quality of life
  • Blood gas abnormalities
  • Survival
  • Spirometry
A

Spirometry

61
Q

Which of the following is NOT an indication for NIV in NMD?

  • Recurrent chest infection
  • Abnormal lung function
  • Symptoms of chronic alveolar hypoventilation/ respiratory failure
  • Elevated daytime CO2
A

Abnormal lung function

62
Q

What is the mean survival in NMD for;

  • Nocturnal hypoventilation
  • Daytime respiratory failure
A
  • Nocturnal hypoventilation: 50 months
  • Daytime respiratory failure: 9-10 months
63
Q

Congenital central hypoventilation syndrome (Ondine’s curse)

A
  • Hypoventilation which is WORSE during sleep
  • Autosomal dominant
  • PHOX2B mutation
    • Polyalanine repeats proportional to severity
      • Normal 20/20
      • Mild 20/24 20/25
      • Severe 20/27 20/33
  • Absent or near absent response to hypercarbia + hypoxia awake + asleep
  • Usually presents in infancy with apniea + cyanosis
  • Ventilation is BETTER awake + in REM due to cortical inputs
  • Ventilation is WORSE in non-REM
  • MOST infants require trachey-ventilation
  • Don’t have drive to breathe themselves
64
Q

What is Ondine’s curse associated with?

A
  • Failure to develop fever when unwell
  • Cardiac arrhythmias
  • Sudden death
  • Hirschprung’s
  • Neural crest tumours
  • Iris problems

Require lifelong ventilation + supervision

65
Q

What is the association between Prader Willisyndrome + sudden death?

A
  • ~60% deaths related to respiratory problems (mainly infection)
  • Hypoventilation due to
    • Hypotonia
    • Kyphoscoliosis
    • Decreased CO2 responsiveness
  • 75% of deaths occur within first 7-9 months of commencing growth hormone therapy
    • Due to IGF1 adenotonsillar hypertrophy
    • Therefore should be assessed for OSA prior to commencing GH + then early in treatment
    • Adenotonsillectomy not always curative in PWS
  • Children with normal PSG may still suffer sudden death. They may also die on CPAP
66
Q

Carrier frequency of CF

A

1/25

67
Q

What is the 1st + 2nd most common cause of bronchiectasis?

A

CF is the MOST common

Primary immunodeficiency is the 2nd most common

68
Q

Which of the following drugs may be taken up to 8 hours prior to a histamine bronchial challenge?

  • Montelucast
  • Salbutamol
  • Salmeterol
  • Nedocromil sodium
  • Theophylline
A

Salbutamol

69
Q
A
70
Q

An eight year old boy is admitted with an episode of acute asthma. His oxygen saturation is 92% in air. He is prescribed prednisolone 1mg/kg and hourly salbutamol 12 puffs. Three hours later his O2 saturation in air has dropped to 89%. He looks well and is less distressed than when admitted. He has widespread wheeze with good air entry.

Based on these findings what is the most appropriate next step in his management?

  • Add ipratropium bromide
  • Blood gas analysis
  • Change to IV salbutamol
  • CXR to rule out a pneumothorax
  • Reduce frequency of salbutamol
A

Reduce frequency of salbutamol

  • Need to look at the whole picture it seems he is clinically improving
  • Don’t just focus on O2 saturations
  • Reducing frequency of salbutamol may improve V/Q mismatch which will improve O2 saturations
71
Q

Omalizumab is a biological product (monoclonal antibody) used in the treatment of severe asthma. What is its specific molecular target?

  • Circulating IgE
  • Eosinophilic basic protein
  • Eotaxin 1
  • IL5
  • Leukocyte immunoglobulin like receptor 7
A

Circulating IgE

72
Q

An 8 year old boy with previous eczema is now having exercise induced wheeze. Which finding below is the most consistent with a diagnosis of asthma?

  • FVC 85%, FEV1 83% FEV1/FVC 95%
  • Exhaled NO 70 (normal 5-20)
  • Widespread bronchial wall thickening on CXR
  • Nasal NO 80 (normal >250)
  • Total serum IgE 125
A
  • FVC 85%, FEV1 83% FEV1/FVC 95%: more of a restrictive pattern
  • Exhaled NO 70 (normal 5-20)
  • Widespread bronchial wall thickening on CXR: more in keeping with bronchiectasis
  • Nasal NO 80 (normal >250): low which is seen in PCD
  • Total serum IgE 125
73
Q

What are the 5 phases of lung development?

A

Embryonic (26 days to 6 weeks gestation)

Pseudoglandular (6 to 16 weeks gestation)

Canalicular (16-28 weeks gestation)

Saccular (28-36 weeks gestation)

Alveolar (36 weeks through to infancy)

74
Q

Key features of PJP infection

A
  • O2 saturation strikingly lower than would be expected from symptoms
  • Unicellular fungi
  • PCP is identified by staining of cysts with methenamine silver nitrate, or toluidine blue, which stains dark bodies within the cysts
  • Pneumocystis pneumonia is most often observed when the CD4+ T helper cell count falls below 200 cells/mm3. CD4+ T cells are absolutely critical for resolution of Pneumocystis, having an essential role in the recruitment and activation of effector cells against the organism.
75
Q

Of the following, the strongest risk factor associated with SIDS is:

Smoking by the mother in the prenatal period

Smoking by the father in the prenatal period

Exposure of the infant to environmental tobacco smoke after he or she is born

Smoking by the mother prenatally only in association with alcohol use

There is no association between smoking and SIDS

A

Smoking by the mother in the prenatal period

76
Q

A 4 wk old healthy-appearing term infant is evaluated in the office for stridor, which has persisted since birth. The noisy breathing is accompanied by moderate signs of inspiratory obstruction including suprasternal and subcostal retractions. He feeds adequately and is gaining weight but frequently spits up. The most likely cause of his symptoms is:

Bronchomalacia

Vascular ring

Laryngomalacia

Tonsil and adenoid hypertrophy

Bronchiolitis

A

Laryngomalacia

77
Q

A 4 yr old boy presents with sore throat and fever of sudden onset. He has difficulty swallowing and his breathing is labored. He is drooling and sitting upright and leaning forward in a tripod position. What is the appropriate next step in patient management?

Complete blood cell count and blood culture followed by immediate prophylactic intravenous antibiotics

Lateral radiograph of the neck

Dose of oral dexamethasone

Direct laryngoscopy in the operating room

Complete physical examination including inspection of the oral cavity

A

Direct laryngoscopy in the operating room

78
Q

A 2 yr old boy is presented to the emergency department at 3 AM with a chief complaint of fever and cough. His respiratory rate is 36 breaths/min, his temperature is 39°C, and his pulse oximetry reading is 96%. On physical examination he has a barky cough and stridor only with crying. He is well hydrated, able to drink, and consolable. What is the appropriate next step in patient management?

Nasal washing for influenza virus and respiratory syncytial virus

Lateral radiograph of the neck

Nebulized racemic epinephrine

Complete blood cell count and blood culture

Dose of dexamethasone

A

Dose of dexamethasone

The effectiveness of oral corticosteroids in viral croup is well established. Corticosteroids decrease the edema in the laryngeal mucosa through their anti-inflammatory action. Oral steroids are beneficial, even in mild croup, as measured by reduced hospitalization, shorter duration of hospitalization, and reduced need for subsequent interventions such as epinephrine administration. Most studies that demonstrated the efficacy of oral dexamethasone used a single dose of 0.6 mg/kg; a dose as low as 0.15 mg/ kg may be just as effective. Intramuscular dexamethasone and nebulized budesonide have an equivalent clinical effect; oral dosing of dexamethasone is as effective as intramuscular administration. A single dose of oral prednisolone is less effective. There are no controlled studies examining the effectiveness of multiple doses of corticosteroids.

Paediatrics (23 decks)

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