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Respiratory > General Conditions > Flashcards

General Conditions Flashcards

1
Q

choanal atresia:
- how many occur with other associated conditions
- which condition most commonly

A
  • 70% associated with other conditions
  • 10-20% a/w CHARGE (CHD7)
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2
Q

close clinical mimic of choanal atresia?

A

pyriform aperture stenosis - narrowing caused by bony abnormality of anterior nasal aperture

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3
Q

congenital midline nasal masses: example in order of decreasing frequency

A

Dermoids (=60% of all), gliomas and encephaloceles

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4
Q

airway obstruction symptoms that are worse when awake vs asleep point to what location of airway?

A

worse when sleeping: pharyngeal airway (enlarged tonsils, adenoids, tongue, midface hypoplasia)

Obstruction worse when awake + exacerbated by exercise = laryngeal, tracheal, or bronchial

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5
Q

natural history of laryngomalacia

A

Symptoms usually appear within the first 2 weeks of life (usually by 6 weeks), and can increase in severity for up to 6 months – resolves by 12-18 months

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6
Q

what is the second most common congenital laryngeal anomaly cause of stridor?

A

congenital subglottic stenosis

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7
Q

DDx of laryngomalacia (give 6)

A

a. Subglottic stenosis
b. Vocal cord paralysis
c. Vascular ring
d. Laryngeal mass (cyst or haemangioma)
e. Subglottic haemangioma
f. Tracheomalacia

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8
Q

bilat vs unilateral VC paralysis

A

bilat: VC usually midline so normal cry and can be asymptomatic early on, stridor and obstructive symptoms more common, medial position means aspiration less likely

unilat: weak cry, stridor less common, aspiration more likely

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9
Q

which syndrome is most associated with congenital laryngeal webs?

A

22q11.2 deletion (Di George)

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10
Q

laryngocoele vs laryngeal saccular cyst

A

laryngocele: from dilatation of laryngeal ventricle. lumen communicates with larynx, so intermittently fills with air causing usually episodic hoarseness and dyspnoea

laryngeal saccule: more common in children. mucous containing cyst, not connected to laryngeal lumen. usually constant resp distress/stridor

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11
Q

Most common cause of secondary tracheomalacia?

A

aberrant innominate (or brachiocephalic) artery

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12
Q

most common type of symptomatic vascular ring? most common vascular ring anomaly?

A

double aortic arch most common symptomatic one
aberrant right subclavian artery most common overall

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13
Q

barium oesophagram: indentation where indicates what kind of abnormality?

A

anterior oesophageal indentation = aberrant pulmonary artery / innominate
posterior = aberrant subclavian
anterior and posterior = complete ring e.g. double aortic arch

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14
Q

symptoms of tracheomalacia

A
  1. Chronic brassy barking or seal-like cough
  2. Respiratory distress
  3. Wheezing and/or stridor
  4. ‘Dying’ spells
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15
Q

bronchomalacia:
- common symptom
- common presentation
- common complication

A
  • Low-pitched monophonic wheeze - predominantly during expiration, over central airways
  • persistent congestion despite no URTI
  • PBB
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16
Q

which lung agenesis has worse mortality: right or left?

A

right lung agenesis is worse

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17
Q

lung agenesis/aplasia: findings on CXR? which imaging modality is diagnostic?

A

CXR: unilateral lung likely with mediastinal shift -> would need to Ix for other cause e.g. FB/mass

CT is diagnostic

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18
Q

some examples of intra vs extra thoracic causes of lung hypoplasia

A

intrathoracic: CDH, masses, reduced pulmonary perfusion, CPAM
extrathoracic: oligohydramnios, skeletal dysaplsia causing narrow fetal thorax e.g. achondrogenesis / OI

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19
Q

CPAM: what is it?

A

congenital pulmonary airway malformation (previously CCM) = hamartomatous lung tissue formation

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20
Q

types of CPAM: incidence, origin, prognosis

A

type 0 = <3% least common, acinar dysplasia, microcystic in whole lung, poor prognosis
type 1 = 60% most common, bronchi/prox bronchioles, macrocystic usually only in one lobe, good prognosis
type 2 = 20%, terminal bronchioles, microcystic, poor prognosis - a/w other abnormalities inc renal agenesis, pulmonary sequestration and cardiac issues
type 3 = <10%, solid +/- cystic large lesions, poor prognosis
type 4 = 10%, acinar formation, can’t distinguish from type 1 radiologically

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21
Q

which type of CPAM is a/w cancer?

A

type 4 a/w pleuropulmonary blastoma

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22
Q

median age of diagnosis of CPAM

A

at 21 week scan

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23
Q

antenatal clinical manifestations of CPAM (name 4)

A

i. Hydrops fetalis
ii. Mediastinal shift
iii. Pleural effusions
iv. Polyhydramnios

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24
Q

what is pulmonary sequestration?

A

Aberrant formation of segmental lung tissue that has NO connection with the bronchial tree or pulmonary arteries.

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25
Q

classify and differentiate types of pulmonary sequestration

A

intralobar (~80%): is in a lobe, doesn’t have its own pleura, more common in late childhood or adolescence
extralobar (20%): has its own pleura, more common in boys, almost always in left lung, more common in neonates

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26
Q

which type of pulmonary sequestration is more likely to be associated with other abnormalities?

A

50-60% extra-lobar a/w other things e.g. CDH, vertebral anomalies, CPAM / pulmonary hypoplasia

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27
Q

what is a bronchogenic cyst?

A

congenital malformation of bronchial tree (a foregut malformation)

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28
Q

most common location of a bronchogenic cyst?

A

middle mediastinum on right (~60-90%)

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29
Q

do bronchogenic cysts commonly communicate with the bronchial tree or not?

A

not commonly, therefore not usually air filled

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30
Q

congenital lobar emphysema: causes?

A

50% no cause identified
25% from air trapping via ball-valve:
1) intrinsic e.g. bronchial stenosis, intra-luminal e.g. mec granuloma
2) extrinsic e.g. vascular anomalies, intrathoracic masses
3) other e.g. bronchial atresia

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31
Q

most common lung site for congenital lobar emphysema?

A

i. Left upper lobe: most common, 40-45%
ii. Right middle lobe: 30%
iii. Right upper lobe: 20%
iv. May involve more than a single lobe: 5%
v. Much rarer in the lower lobes

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32
Q

CXR findings for congenital lobar emphysema

A
  • area of hyperlucency in the lung with a paucity of vessels
  • Mass effect with mediastinal shift and hemidiaphragmatic depression
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33
Q

congenital pulmonary lymphangectasia - 3) possible pathophysiologies

A

i. Pulmonary venous obstruction = produces an elevated trans vascular pressure and engorges pulmonary lymphatics
ii. Generalised lymphangiectasia = generalised disease of several organ systems e.g. in Noohna’s
iii. Primary lymphangiectasia = limited to the lung

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34
Q

cervical lung hernia: causes?

A

20% congenital from weakness in suprapleural membrane + neck msucles
80% acquired: pulmonary disease with lots of coughing e.g. asthma, cardiothoracic surgery

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35
Q

usual presenting complaint of a cervical lung hernia

A

usually a neck mass noticed while straining or coughing

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36
Q

how does congenital lobar pneumonia usually present?

A

Present in the 1st 2 weeks of life with tachypnoea

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37
Q

bronchogenic cysts - when to treat?

A

Always resect due to risk of infection (primarily), also rare risk of malignancy

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38
Q

what is scimitar syndrome?

A

partial or complete anomalous pulmonary venous drainage of a hypoplastic lung to the inferior vena cava. The term derives from the curvilinear shadow created by the anomalous pulmonary vein on the chest radiograph.

type of pulmonary venolobar syndrome

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39
Q

2 pathophysiologies explaining emphysema

A

1) compensatory hyperinflation (acute/chronic) e.g. pneumonia, empyema
2) obstructive overinflation: results from partial obstruction of a bronchus or bronchiole when it becomes MORE difficult for air to leave the alveoli than to enter

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40
Q

what is bronchiolitis obliterans? most common causes in kids?

A

bronchiolar inflammation with FIBROSIS associated with luminal stenosis and occlusions.
common causes in kids - post-infectious (ADENO), or post transplant

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41
Q

What is BO called when it occurs in transplant patients?

A

BOS - high mortality. 1/3 lung transplants get it.

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42
Q

BO vs BOOP

A

BOOP/ Cryptogenic Organising Pneumonia (COP):
- BO more fixed obstruction with PFTs, BOOP restrictive
- BO CXR hyperinflation/normal, BOOP ground glass interstitial
- BOOP more responsive to steroids

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43
Q

which age group is BOOP more common in?

A

55-60yo

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44
Q

common causes of hypersensitivity pneumonia in children

A

i. Exposure to pet birds (feathers in bedding)
ii. Humidifiers and hot tubs for thermophilic organisms and MAC
iii. Mould from prior flooding or damp condensation

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45
Q

histopathological findings of hypersensitivity pneumonia

A

lung biopsy needed to confirm Dx when critical elements not there:
Poorly formed, non-caseating granulomas

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46
Q

BAL findings in HP

A

Lymphocytosis stimulation by the offending antigen, with low CD4:CD8 ratio (Ie. CD8 higher than normal)

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47
Q

Granulomatosis with Polyangiitis (Wegner’s)
- what size vessel
- what kind of Ab is associated with it

A
  • small vessel (formally, but also medium)
  • ANCA vasculitis (cANCA in 90%)
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48
Q

most commonclinical manifestations of Wegner’s

A

ENT - rhinosinusitis + nosebleeds, septal perforation&raquo_space; saddle nose!
lungs - tracheobronchial stenosis, ILD, alveolar haemorrhage
kidneys - GN

then eyes, heart, joints, rash etc.

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49
Q

sarcoidosis in children vs adults

A
  • Skin rash, iridocyclitis, and arthritis seen most often WITHOUT pulmonary symptoms
  • pulmonary disease less progressive cf adults
  • ocular disease more likely to be progressive cf adults
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50
Q

most common lab findings with sarcoidosis

A

high Ca - produced by macrophages!
high ACE - produced by T cells!
hypergammaglobulinaemia
anaemia of chronic disease

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51
Q

sarcoidosis:
- lung BAL/biopsy results
- CXR

A
  • non-caseating granulomas ( or Langhan’s giant cells)
  • CXR: bilat hilar lymphadenopathies
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52
Q

pulmonary sarcoidosis - when to treat?

A

will resolve 75% without treatment
treat when stage III i.e. when reticular abnormalities predominate and hilar LN already regressing
treat with steroids

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53
Q

which of the eosinophilic lung diseases often presents seriously acutely?

A

AEP - acute eosinophilic pneumonia. often need mechanical ventilation for resp failure

54
Q

what is loeffler syndrome?

A

transient pulmonary eosinophilia 2nd to helminthic infections. self-limiting usually <1 month

55
Q

name the major pulmonary eosinophilias (mnemonic)

A

CC DHAAL:

CEP (chronic)
Churg-Strauss

Drugs - NSAIDs, phenytoin, anti-microbials - nitrofurantoin
AEP
allergic bronchopulmonary aspergillosis
hypereosinophilic syndrome
loeffler syndrome

56
Q

AEP vs CEP

A

AEP idiopathic but more likely to have environmental than CEP (which is entirely idiopathic) e.g. smoke, vape. more acute +++

CEP mostly in adults

57
Q

BAL diagnosis of AEP/CEP

A

> 25% or more of eosinophils

58
Q

EGPA/Churg-strauss:
- which antibody is associated
- common symptoms/systems affected / diagnostic criteria

A
  • one of the 3 ANCA vasculitides - MPO-ANCA (but also can be ANCA neg)
  • asthma (resp)
  • pulmonary opacities
  • mono/polyneuropathies
  • > 10% eosinophils peripherally
  • kdineys - GN
59
Q

ILDs - what do you see on PFT?

A

restrictive ventilatory deficit

60
Q

primary spontaneous PTX: associated mutation and conditions

A
  1. FLCN (folliculin) gene mutation: familial cases of spontaneous pneumothorax
  2. Collagen synthesis defects – Ehlers-Danlos, Marfan syndrome
61
Q

thoracocentesis - where to insert needle?

A
  1. Second intercostal space mid clavicular line on the side of the pneumothorax
  2. Insert vertically, above or below the rib
62
Q

pneumomediastinum in kids: suggestive signs

A

subcut emphysema is diagnostic
mediastinal crunch (hamman sign)
dyspnoea

63
Q

pneumomediastinum in kids: which age group and causes

A

peak in neonates (spontaneous) and
late infancy/early childhood due to LRTI.
adolescence (spont, thin males)

asthma also causes

64
Q

chylothorax - which side of the lung does it usually occur at?

A

rarely bilat - usually right

65
Q

what is chylothorax?

A

= pleural collection of fluid formed by the escape of chyle from the thoracic duct or lymphatics into the thoracic cavity

66
Q

some causes of chylothorax (and which is most common)

A

a. Thoracic duct injury as a complication of cardiac surgery = most common in children
b. Chest injury
c. ECMO
d. Primary or metastatic intrathoracic malignancy – particularly lymphoma
e. Newborns – during delivery
f. LESS COMMON = lymphangiomatosis, restrictive pulmonary disease, thrombosis of the duct, superior vena cava or subclavian vein, TB or histoplasmosis, congenital anomalies of lymphatic system

67
Q

what feeds do you choose to give in chylothorax, and why?

A

Enteral feeds with low fat or medium-chain TG, high protein diet, or TPN

  • Dietary exclusion of long chain fatty acids – this avoids their conversion into monoglycerides and free fatty acids (FFA) which are transported as chylomicrons to the intestinal lyph ducts
  • Medium chain triglycerides (MCTs) can be provided – absorbed directly into intestinal cells and transported directly to the liver via the portal vein – BYPASSING the thoracic duct
68
Q

most common viral cause of bronch

A

RSV 50%

69
Q

what mab can you give for RSV bronch, and which patient groups would you consider it in?

A

palivizumab - reduces risk of hospitalisation:

  • Preterm infants with or without chronic lung disease of prematurity or congenital heart disease
  • Infants with haemodynamically significant congenital heart disease
  • Children with anatomic pulmonary abnormalities or neuromuscular disorder
  • Immunocompromised children assessed on an individual basis
70
Q

what is the evidence for HFNC in bronch?

A

HFNC doesn’t shorted O2 therapy, but does avoid ICU admissions

71
Q

bronchodilation and constriction is mediated by which receptors and nervous systems?

A

PNS: bronchoconstriction (M3 receptors)
SNS: bronchodilation (B2 receptors)

72
Q

bronchodilator reversibility is defined as what change of FEV?

A

improvement of FEV1 of 12% in absolute values

73
Q

transient hypoxemia post salbutamol: explain

A

-usually in first 30mins after ventolin
- Beta 2 effects also include pulmonary vasodilation, thereby countering the normal protective hypoxic pulmonary vasoconstriction that occurs, thereby leading to increased intrapulmonary shunt and hypoxemia
- need supplemental O2 for a short while

74
Q

options for preventative asthma medication

A

i. Inhaled corticosteroids
ii. Montelukast
iii. Cromone
iv. Inhaled corticosteorids + LABA

75
Q

examples of inhaled steroids for asthma (and most common)

A

beclomethasone, budesonide, ciclesonide, fluticasone propionate

76
Q

what is montelukast’s MOA, and when would we trial it first in place of ICS?

A
  1. The child is unable to use inhaled therapy
  2. The child also has significant allergic rhinitis
  3. The parents have strong concerns about adverse effects of ICS
77
Q

how long do we give for a trial of ICS vs montelukast?

A

ICS: 2-3 months
montelukast: 4 weeks

78
Q

why are cromones (cromoglycate / nedocromil) more complex?

A

more frequent dosing and meticulous daily care to prevent clogging of inhaler device

79
Q

Why are LABAs never first line in children?

A

LABA also results in phosphorylation and internalisation of beta 2 receptor – results in increased mortality

80
Q

what age can symbicort be used?

A

formoterol + salmeterol (symbicort) >/= 6yo
LABAs have no evidence in 5 or under

81
Q

what mabs can be used in asthma? how do they work and how often do they have to be taken?

A

Omalizumab (anti-IgE)
- Prevents binding of free IgE to high affinity receptors on basophils and mast cells
- Approved for moderate to severe allergic asthma in children 12 years or older
- Delivered by SC every 2-4 weeks

Mepolizumab
- An add-on maintenance therapy for severe asthma with an eosinophilic phenotype in patients age 12 years and older
i- Anti-IL-5 Mab injected SC every 4 weeks
- Decreases the production an survival of eosinophils, a major inflammatory cell involved in asthma pathogenesis

82
Q

classify asthma by frequency of symptoms

A

infrequent episodic: flares >6weeks apart
frequent episodic: flares <6 weeks apart, but fine in between
persistent: daytime Sx >2x/week. nocturnal once/week.

83
Q

what is plastic bronchitis?

A

recurrent episodes of airway obstruction secondary to large proteinaceous branching casts – take the shape of and obstruct the tracheobronchial tree

84
Q

plastic bronchitis - associated conditions (4)

A

a. Lymphangitic disorders
b. Pulmonary infections
c. Acute chest syndrome of sickle cell disease
d. Congenital cardiac disease – Fontan: occurs in 14%

85
Q

what is the most important predictor of a specific cause of cough in children

A

wet vs dry

86
Q

3 most common causes of persistent cough in kids

A
  1. Protracted bacterial bronchitis (most common 0-2 years)
  2. Asthma
  3. Bronchiectasis
87
Q

chronic cough duration

A

> 4 weeks

88
Q

Suggest some aetiologies with the following types of cough:
i. Onset in infancy (and barking)
ii. Dry (worse at night)
iii. Dry (paroxysmal)
iv. Wet (productive)
v. Onset in older childhood (honking)

A

i. Onset in infancy (and barking): tracheomalacia
ii. Dry (worse at night): post-viral cough, chronic non-specific cough of childhood, asthma
iii. Dry (paroxysmal) : pertussis
iv. Wet (productive) : suppurative lung disease = chronic suppurative bronchitis, CF, immunodeficiency, primary ciliary dyskinesia, inhaled FB
v. Onset in older childhood (honking): psychogenic

89
Q

Suggest some lung aetiologies with the following types of exam findings with cough:
- dextrocardia
- organomegaly
- digital clubbing
- pectus carinatum

A
  • dextrocardia: PCD
  • organomegaly: CF, storage disorders, malignancy, haemaglobinopathy
  • digital clubbing: suppurative lung disease
  • pectus carinatum: chronic airway obstruction
90
Q

dry staccato cough in infancy =

A

chlamydia

91
Q

most common causes dry cough in kids (4)

A

o Asthma
o Allergic rhinitis
o GORD
o TB

92
Q

most common cause of chronic wet cough in kids

A

PBB

93
Q

3 most common causative organisms of PBB

A

H. influenzae, Streptococcus pneumoniae, and Moraxella catarrhalis

94
Q

current diagnostic criteria for PBB

A

■ Wet cough lasting at least 4 weeks
■ Absence of other findings to identify another cause of
the cough
■ Resolution of the cough with at least 2 weeks of an
antibiotic (usually augmentin)

95
Q

classic cxr findings of PBB

A

bilat peribronchial accentuation or ‘cuffing’ or ‘doughnut’ sign

96
Q

what is the narrowest part of the trachea?

A

subglottis - surrounded by cricoid cartilage

97
Q

inspiratory stridor = ?
expiratory stridor = ?
biphasic stridor = ?

A

Inspiratory stridor = stridor originating from obstruction in the extrathoracic region
Expiratory stridor = stridor originating from obstruction in the intrathoracic region
Biphasic stridor = fixed (rather than dynamic) central airway obstruction

98
Q

at what age do bronchogenic cysts and laryngeal clefts usually manifest?

A

infancy-toddler (not neonatal)

99
Q

vascular rings - usually insp/exp stridor?

A

exp - its intra-thoracic usually

100
Q

Recurrent respiratory papillomatosis (RRP) usually caused by which HPV valents?

A

6 and 11 (covered by gardasil)

101
Q

Recurrent respiratory papillomatosis (RRP) - age groups affected?

A

bimodal age distribution and manifests most commonly in children younger than five years (juvenile-onset) or in persons in the fourth decade of life (adult-onset)

102
Q

what does vit d have to do with stridor?!

A

hypocalcaemia reported to cause laryngeal spasm (e.g. vit d def or rickets)

103
Q

common 3 causative organisms retropharyngeal abscesses

A

group A Streptococcus
S. aureus
anaerobic organisms, e.g. Bacteroides, Peptostreptococcus, and Fusobacterium

occasionally hib.

103
Q

cxr findings:
- epiglotittis
- croup
- bacterial tracheitis
- retropharyngeal abscess

A
  • epiglotittis - thumb sign
  • croup - steeple sign
  • bacterial tracheitis - steeple sign (but older kid)
  • retropharyngeal abscess - widening of pre-vertebral tissue (but indistinguishable from vertebral asbcess on plain xr)
104
Q

compare bacterial tracheitis to epiglottits

A

-drooling uncommon in bacterial tracheitis; epiglottitis 3 D’s (drooling, dysphagia, distress)
-bacterial tracheitis - poor response to steroids
-epiglottitis classically younger

105
Q

vocal cord dysfunction - more common in which gender

A

females 3:1

106
Q

some causes of wheeze

A
  1. asthma / bronch
  2. FB
  3. structural e.g. vascular rings
  4. tracheobronchomalacia
  5. VC dysfunction
  6. mucociliary clearance issue e.g. CF, bronchiectasis
107
Q

what findings might you find in a cxr for FB

A
  • opaque FB only in 20%
  • hyperinflation
  • atelectasis
  • infection
  • mediastinal shift
108
Q

aspirated FB - where is it most likely to lodge?

A

right lung (60%): RMB (52%), middle lobe bronchus <1%, lower lobe bronchus 6%

109
Q

aside from trauma / friable tissue, what are some other causes of epistaxis in children?

A
  • FB, nasal polyps, bleeding diatheses, vascular malformations, and nasopharyngeal tumours
  • Hereditary haemorrhagic telangiectasia, varicosities, haemangiomas, bleeding diatheses (particularly vWD), HTN, renal failure
  • Juvenile nasal angiofibroma – seen in adolescent males, resulting in recurrent often severe nosebleeds
110
Q

what is the most common childhood cause of nasal polyposis?

A

50% CF patients have polyps and it is RARE for non-CF children to have it

111
Q

what meds can you give for nasal polyps?

A

IN steroids
doxycycline, very good for size and symptoms

112
Q

what is the most common cause of chronic hoarseness in kids?

A

vocal nodules

113
Q

what can cause vocal nodules in kids? how to distinguish between these causes?

A

a. Chronic vocal abuse or misuse > voice is worse in the evening
b. Laryngopharyngeal reflux > hoarseness worse in the morning

114
Q

association between cutaneous and subglottic haemangiomas

A

1% of children with cutaneous haemangioma have subglottic haemangioma
50% of those with subglottic haemangioma will have cutaneous haemangioma

115
Q

what kind of cutaneous haemangiomas are associated with airway ones?

A

those in beard distribution: including pre-auricular skin, chin, anterior neck and/or lower lip

116
Q

what syndrome do you need to think about when there are large plaque-type haemangiomas?

A

up to 1/3 will have PHACE:
posterior fossa malformations
haemangiomas
arterial anomalies
cardiac anomalies
eye abnormalities and endocrine
sternal cleft

117
Q

DDx for anterior mediastinal mass (mnemonic)

A

4Ts:
• Thymus – thymic cyst
• Teratoma – germ cell
• Thyroid
• Terrible lymphoma (T lymphoma, T ALL)

118
Q

pulmonary haemosiderosis - how does it happen, and common presenting issues?

A
  • recurrent episodes of DAH (diffuse alveolar haemorrhage)
  • IDA, haemoptysis, cxr alveolar infiltrates
119
Q

where in the lungs is atelectasis most common in children?

A

In 90% of children involves upper lobe; 63% involves right upper lobe

120
Q

what can cause pectus excavatum?

A

a. Associated with CT disorder (Marfan, Ehler’s Danlos)
b. Acquired secondarily to chronic lung disease, neuromuscular disease, or trauma

121
Q

Two conditions associated with pectus CARInatum

A

a. Mitral valve disease
b. Coarctation of aorta

122
Q

what are some pregnancy effects of maternal smoking?

A

• Spontaneous miscarriage
• Placental abruption
• PPROM
• Placenta praevia
• Pre-term delivery
• Low birth weight
• Ectopic pregnancy

123
Q

what are some post-natal effects of maternal smoking?

A

• SIDS
• Respiratory infections – bronchitis, pneumonia
• Asthma, atopy, otitis media
• Infantile colic
• Bronchiolitis
• Short stature
• Lower reading and spelling scores, reduced school performance
• Shorter attention spans, hyperactivity
• Childhood obesity

124
Q

differentiate between severe and late onset CCHS

A

i. Severe CHHS = hypoventilation manifests during wakefulness sand sleep
ii. Late onset CCHS (LO-CCHS) = symptoms manifest after 1 month of age but hypoventilation is typically during sleep only

125
Q

gene most associated with congenital hypoventilation syndromes, and:
- most common mutation in that gene
- de novo/inherited?

A

paired-like homeobox 2b (PHOX2B)
Polyalanine repeat expansion mutation (PARM) in 90%
most de novo, 25% inherited

126
Q

CHS with ANSD - two most common associated conditions

A

a. Hirschsprung’s disease – 20%
b. Neural crest cell origin tumours

127
Q

what is ROHHAD?

A

Rapid-onset obesity with hypothalamic dysfunction, hypoventilation, and autonomic dysregulation. Starting after 1.5 years of age, and also hypothalamic dysfunction and absence of a CCHS-related PHOX2B mutation

128
Q

nocturnal hypoventilation occurs in REM/non-REM for A) neuromuscular disorders B) CCHS

A

neuromuscular - in REM
CCHS - in non-REM

129
Q

with what FVC in NMD is NIV indicated?

A

BIPAP / CPAP – indicated when FVC< 50% predicted

Respiratory (5 decks)

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