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MOD 1 Test > Neonatal Lung Disease and Development > Flashcards

Neonatal Lung Disease and Development Flashcards

1
Q

Pediatric airway compared to adults?

A

smaller, more anterior, epiglottis is floppier, larger tongue, larger occiput, narrowest point is the cricoid

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2
Q

Stomodeum?

A

the developing mouth, connected to gut tube

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3
Q

Nasal placode?

A

develops above the Stomodeum, connects back to the gut tube

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4
Q

What arch does upper airway develop from?

A

Pharyngeal arch I

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5
Q

Choana?

A

opening nasal cavity to nasopharnyx

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6
Q

What membrane breaksdown in development?

A

buccopharyngeal membrane

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7
Q

Choanal Atresia?

A

failure in reabsoption of buccopharyngeal membrane during embryonic development
can be membranous or bony, usually mixed
more common in females

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8
Q

Diagnose/manage Choanal Atresia?

A

endoscopy or CT
inital- oropharyngeal ariway
surgery is definitive

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9
Q

Pierre Robin Sequence?

A

multiple related developmental defects

  • Micrognathia
  • Glossoptosis
  • Celft palate
  • Macroglossia

Problem in development of the first pharyngeal arch

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10
Q

Treat Pierre Robin Sequence?

A

most cases- insert of nasopharyngeal airway, severe can require trachesostomy
other-forms of mandibular distraction, release of the floor of the mouth

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11
Q

Micrognathia?

A

small underveloped chini, cause airway obstruction

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12
Q

Congenital airway masses?

A

many causes:

cysts, vascular (hemangiomas), infectious (papillomas), other (Teratomas, Hetertopic brain)

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13
Q

Papillomas cause in newborn?

A

often caused by HPV, can be picked up during childbirth, cause airway obstuction on vocal cords, debreaded can come back

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14
Q

Forms the lining of the airway?

A

endoderm, blebs off from the gut tube

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15
Q

How is the respiratory diverticulum connected to the the foregut?

A

through the laryngeal orifice

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16
Q

How does the respiratory diverticulum seperate from the foregut?

A

tracheoesophageal ridges that partition the tubes

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17
Q

What happens when the epithelium in the area of the laryngeal orifice grows too quickly?

A

it recloses the laryngeal orfice, this is normal

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18
Q

The epithelium later does what to open and its evidence remaining is called what?

A

re-canalized (opens the laryngeal orifice)
leaving the false (vestibular) fold and laryngeal ventricle

the tongue develops on the floor of the mouth

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19
Q

The respiratory diverticulum forms?

A

the primary bronchi, secondary, tertiary

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20
Q

Laryngeal cleft?

A

developmental failure of the primitive tracheoesophageal septum
cause a split like opening between the posterior larynx and the esophagus

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21
Q

Laryngeal cleft presents?

A

recurrent aspiration or cyanotic spells with feeding

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22
Q

Traceheosophageal fistula?

A

always have a component of associated tracheomalacia
Rare H type can present with recurrent aspiration
asses with pressure barium esophogram

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23
Q

Laryngomalacia?

A

Floppiness of the larynx

Most common congetial anomaly of the upper airway

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24
Q

Laryngomalacia present?

A

supine worse than prone (positional)

inspiratory stridor and/or stertor (heavy snoring) within the first few weeks of life

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25
Laryngeal webs or atresias result from?
failure of recanalization of the larynx during embryogenesis
26
where do most lesions occur?
the glottic area and extend into subglottic
27
Subglottic stenosis?
can be congenital or aquired | 3rd most common congenital laryngeal anomaly
28
Congential Subglottic stenosis?
result from incomplete recanalization of the laryngotracheal tube during the 3rd month of gestation
29
Risk factors for aquired Subglottic stenosis?
prolong intubation, aspiration, prolonged or severe infections, previous airway surgery
30
Tracheomalasia?
weakness (floppiness) of the tracheal wall | segmental/generalized, congenital/aquired
31
Tracheomalasia preset?
recurrent wheezing or barky cough with illness or activity tends to impair cough efficiency coarse, low pitch, monophonic wheeze on exam
32
Thing to watch with Tracheomalasia?
Beta agonist can worsen | important because asthma is very common and presents with monophonic wheeze
33
Bronchogenic cysts?
single cyst arising anywhere in bronchial tree, variable in size, abnormal budding of the ventral foregut endoderm 85% mediastinal, most cases located in right parathracheal or canial region malignant transformation has been reported
34
Clinical presentation of Bronchogenic cysts?
often aymptomatic noted incidentally on chest imaging depends on location- airway compression, wheeze, respiratory distress hemorrhage or peptic ulceration in cysts containing gastric mucosa
35
Bronchogenic cysts management?
resected due to risk of malignant transformation removed thoracoscopically does not result in loss of any functional lung tissue
36
Primary bronchial lesions?
Bronchomalacia | Bronchial stenosis/atresia
37
Bronchomalacia?
monophonic wheezing symptoms may persist past age 2, not symptomatic past school age impair clearance of mucous clearance can lead to recurrent pneumonias beta agonists worsen associated with other anatomic anomalies
38
Bronchial stenosis/atresia?
can both cause and result from recurrent infection
39
Congenitcal Cystic Adenomatoid Malformation (CCAM)?
discrete intrapulmonary mass that contains cysts of variable size defect in dev of terminal bronchioles leading to structures that resemble a cystic collection bronchioles malignant transformation known to occur
40
CCAM clinical presentation?
Antenatally -polyhyraminos if lesion compresses the esophagus or hydrops fetalis if it compresses the heart or great vessels neonatal -may cause respiratory distress as a result of mediastinal shift and atalectasis (mass effect), or even pneumothorax often noted incidentally on CXR
41
CCAM management?
large antenatal lesions are candidates for surgery, EXIT procedure,etc most favor resection resection can be delayed until child reaches appropriate size
42
Bronchopulmonary sequestration?
Tissue mass with abnormal communication with tracheobronchial treet anomalous arterial supply intrapulmonary, meaning within the normal lunch pleural, extrapulmonary
43
Bronchopulmonary sequestration (BPS) clinical presentation?
``` neonatal -usually asymptomatic childhood -recurrent pneumonias in same location present even late, noted incidentally on imaging ```
44
BPS management?
managed expectantly if asymptomatic followed with full PFTs and instructed in airway clearance techniques Surgical resection recommended for symptomatic cases
45
Congenital large hyperlucent lobe (CLHL)?
massive overinflation of one or more lobes -postnasally following intiation of respiration abnormal developed bronchus almost half are located in upper left lobe right middle and right upper lobe next most common assoc with congenital heart disease
46
CLHL clincal presentation?
neonatal: -mild to moderate respiratory distress mediastinal shift may be preent with hyperresonace and decreased breath sounds on involved side child: - recurrent pneumonia, respiratory inection - chronic cough, wheez, dyspnea - incidental noted on chest imaging
47
CLHL management?
observe asymptomatic gradual resolution historical- resected due to concern for hyperinflation compressing surrounding lung tissue
48
Development of smallest airways?
endorermal cells of the bronchi associate with the vessels of the presumptive lung and flatten
49
flat cells lining the respiratory pathway?
become type I pneumocytes | allows for normal gas exchange
50
Type II pneumocytes?
begin secreting surfactant, not reach sufficient level until near term released into the amnion as the fetus, "breathes" fluid
51
Purpose of surfactant?
``` after birth, the amnion is expelled and leaves surfactant to decrease surface tension on the alveoli prevents atelactasis (collapse of alveoli) and allow easy expansion of lungs ```
52
Respiratory distress syndrome (RDS)?
most common cause of respiratory failure in newborns | lack of mature surfactant production
53
Complications from deficient surfactant?
``` increased surface tension in the alveoli increased atelectasis decreased lung compliance V/Q mismatch hypoxia respiratory distress ```
54
Respiratory distress (inspection)?
tachpnea nasal flaring, head bobbing, grunting retractions cyanosis
55
Respiratory distress (ascultation)?
decreased air movement | crackles, wheezing, stridor
56
RDS radiographic?
reticular granular or ground glass appearances air bronchograms poor lung expansion
57
Treat RDS?
direct delivery of exogenous surfactant and ventilatory support long term- bronchopulmonary dysplasia (BPD) and chronic lung disease
58
Meconium Aspiration Syndome?
under stress meconium happens in the womb, gets into airway, cause aspiration
59
Meconium?
first intestinal discharge from newborns composed of intestinal epithelial cellls, lanugo, mucus, and intestinal secretions (bile)
60
Aspiration leads to disruption of normal lung function?
airway obstruction, surfactant dysfunction, direct chemical pneumonitis, resultant presistant pulmonary hypertension
61
Mortality for Meconium Aspiration Syndome?
still hight 20%, incidence decreasing
62
Spaces (intraembryonic coelom) develop?
in lateral plate mesoderm
63
Intraembryonic coelom then?
fuse and expand, eventually they enlarge and seperate the lateral plate mesoderm into a somatic layer and a visceral layer
64
The visceral and the pariental layers?
seperate and fold anteriorly | fold to form the gut tube and mesentary
65
The parietal layer, ectoderm, and amniotic cavity fold to?
completely surround the gut tube
66
Forms the intraembryonic cavity?
somatic layers of the lateral plate mesoderm approach each other anteriorly, they fuse and form this cavity will produce the pericardial, pleural, and peritoneal cavities
67
Intraembryonic vaity then splits?
pleural and the pericardial cavities by the developing diaphragm they communicate through the left and right pericardioperitoneal canals
68
Pericardioperitoneal canals close as?
two pleuroperitoneal folds extend from lateral body to fuse with the septum transversum and esophageal mesentary
69
Create remainder of diaphragm?
muscle from the body wall
70
Congential diaphragmatic hernia?
abdominal viscera herniating into thorax faulty development of the septum transversum, should seperate the body cavities during early gestation typically left sided ipsilateral lung is hypoplastic contralateral lung may also be hypoplastic lesion with significant lung hypoplasia are usually fatal, associated congenital abnromalities common
71
Common weakness of diaphragm?
50% Hiatal 36% Posterolateral 7% Eventration Left side more common
72
Congential diaphragmatic hernia CXR?
air in gut tube in throax
73
Clincal presentation Congential diaphragmatic hernia?
antenatally: large CDH often now Dx on prenatal U/S Neonatal: babies with significant lung hypoplasia present with severe respiratory distress/failure on DOL1 Infancy/Childhood: Chronic respiratory symptoms or decreased pulmonary reserve, feeding difficulty or GI symptoms may be asymptomatic
74
Congential diaphragmatic hernia management?
Antenatally fetal surgery Neonatal: supportive care to maintain oxygenation, ECMO Childhood Surgical closure of diaphragmatic defect
75
Pulmonary hypoplasia?
spectrum- incomplete development of lung tissure to complete lung aplasia direct compression, low amnitoic fluid volume, fetal respiratory muscle failure
76
diagnose Pulmonary hypoplasia?
lung biopsy clincial suspicion raised by small or absent lung tissue on imagin in the setting of respiratory distress severe- not compliable with life
77
Eventration of the diaphragm?
manifests similarily to a mild congenital disphragmtaic hernia but pushes weakened diaphragm into the thoracic cavity
78
Parasternal and esophageal hernias?
result in gut herniation from the abdomen into the thorax
79
formation of the pleural cavity?
lungs take up space, push two pleuropericardial folds (phrenic nerves) ahead of them
80
Heart enter embryonic pericardial cavity?
before the lungs
81
What happens when the pleuropericardial folds fuse?
with each other to seperate the pleuarl cavity from the pericardial cavity anterior to it
82
Extrapleural lesions?
Pneumothorax Chylothorax (milk liquid from lymph) Hemothorax
83
Number of alveoli present at infancy?
as few as half the number of adult
84
infant bronchi?
more collapsible, decreased elastin and collagen content
85
Pores of Kohn?
Internalveolar canals, not well developed | decreased collateral ventilation, propensity for atelaectasis
86
Ribs orientated horizontal in infants?
much more compliant chest wall than adults, much less outward recoil
87
Glottic bakeing?
creates PEEP to balance inward elastic recoil, don't breath out all the way
88
Poiseuille's law and edema?
resistance equals 1 over radius to the 4th which means a smaller radius in an infant with the same amount of edema will dramatically affect infant more than an adults resistance
89
How to infants breath?
nose breathers (inflammatory process causing nasal congestion lead to apnea)
90
Compliance infant?
increased airway and chest wall compliance, increase propensity for atelectasis/collapse
91
Airways of babies, size?
smaller, exponentially easier to obstruct

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