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Nicu Brodsky+Pediatrix+NeoReview Questions > Respiratory > Flashcards

Respiratory Flashcards

1
Q

How to treat pneumomediastinum?

A

Observe. Usually resolves spontaneously

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2
Q

____ is actively transported across pulmonary epithelial cells to air spaces to create fetal lung fluid. Changes to ____ secreting to move fluid out of alveolar air spaces.

A

Chloride / Sodium. 30% of FLF is absorbed PTD

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3
Q

Diaphragm paralysis, the affected side has ____ movements compared to unaffected side. The _____ side is more common (_____ sign)

A

LESS movement on affected side. R side more common. Kienbock’s sign.

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4
Q

Which stages of lung development have which pathologies?

A

Embryonic: TEF, tracheal stenosis, laryngeal cleft:
Pseudoglandular: CDH, bronchogenic cyst, CCAM/CPAM, congenital lobar emphysema
Canalicular: pulmonary hypoplasia
Saccular: pulmonary hypoplasia

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5
Q

Difference between CCAM and bronchopulmonary sequestration?

A

CCAM: congenital cystic adenomatoid malformation. Cystic lesion occurs in developing lung. Supplied by PULMONARY circulation and connected to tracheobronchial tree

Bronchopulmonary sequestration: non-functioning lung tissue. NOT connected to tree. receives blood from systemic circulation.

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6
Q

By what principles does HFOV work?

A

PAM TB
Pendelluft effect: differential movement of gas as result of diff time constraints
Asymmetric velocity of gas
Molecular diffusion: across alveolar gradients all factor in gas exchange
Taylor dispersion: parabolic movement of inspired gas that allows for increased area for diffusion
Bulk Convection: bulk axial gas flow

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7
Q

How many types of surfactant are there? Which is NOT in exogenous surfactant?

A

A, B, C, D. SP-A is NOT in exogenous surfactant No clinical dz in deficiency of D. A is most abundant. B is “better” for you.

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8
Q

Type I vs Type II pneumocytes? Which comes first?

A

Type II –> Type 1 pneumocytes
Type II: cuboidal, 10% of alveolar surface. Greater # of cells in alveolar lining. Important role in SURFACTANT metabolism and secretion
Type I: fried egg, tight junctions. 90% of alveolar surface. Important role in gas exchange, no gene material for surfactant.

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9
Q

Surfactant is mostly comprised mainly of _____

A

Lipids. Phosphatidylcholine desaturated (50%), monosaturated (20%)

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10
Q

Most common organisms associated with chorioamnionitis?

A

ureaplasma and mycoplasma

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11
Q

Prenatal corticosteroids help mature fetal lung by ______? Postnatal corticosteroids help by ______?

A

Antenatal: Decreasing amount of mesenchymal tissue and increasing potential airspace volume. Arrest alveolar septation.

Postnatal: arrest alveolar septation and microvascular development

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12
Q

BPD Definition (2000 NIH)

A

Mild: O2 for 28 days, RA at 36 weeks
Moderate: O2 x 28 days plus <30% O2 at 36 weeks
Severe: same, but >30% O2 and/or PPV

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13
Q

New BPD pulmonary changes?

A

Consistent with ALTERED lung development. Arrest of alveolarization with increased alveolar diameters and fewer alveoli. Hyperinflation, minimal cystic emphysema. Less airway reactivity compared to “classical” BPD. Less pulmonary HTN, minimal fibrosis.

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14
Q

Factors that help distribute surfactant admnistration

A

Gravity, higher volume, faster rate of administration, positive pressure to distribute, higher volumes of fetal lung fluid/edema helps distribute

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15
Q

Central chemoreceptors that respond to CO2 are located on ____. Mechanoreceptors are located on ____ and respond to TV. Oxygen peripheral chemoreceptors are located on _____.

A

ventrolateral surface of medulla; airway smooth muscle; carotid and aortic bodies

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16
Q

Bohr equation and measuring dead space?

A

Volume of CO2 in expired air = volume of CO2 from dead space + volume of CO2 from alveoli that are V/Q

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17
Q

What is physiologic, alveolar, and anatomic dead space?

A

Anatomic: conducting airways (bronchoconsriction decreases dead space)
Alveolar: alveoli that are not involved in gas exchange with vasculature
Physiologic = anatomic + alveolar

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18
Q

Fetal breathing is interrupted by?

A

Prostaglandin

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19
Q

A-a gradient equation?

A

[FiO2(760-PH2O) - PaCO2/R] - PaO2
R = 0.8

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20
Q

3 observations about apnea of prematurity

A

1) decreased ventilatory response to hypercarbia
2) irritation of laryngeal mucosa induces inhibition of breathing (superior laryngeal nerve)
3) Hypoxic ventilatory depression is reaction to sustained hypoxia (mediated centrally in pons by inhibitory NT like adenosine). Caffeine is competitive antagonist of adenosine

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21
Q

Locations and names of sodium pumps to get fluid out of lungs

A

Apical surface: amiloride sensitive ENaC - actively transports Na from alveolar lumen into respiratory cell (dev. expressed, increase also after endogenous steroids/catecholamines of labor)

Basolateral cell membrane: Na-K-ATPase, transports Na from the respiratory cell into interstitial

Water follows via aquaporins

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22
Q

How long before echo shows improvement of PH on sildenafil?

A

2 weeks

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23
Q

Boyle’s Law
Charles’ Law
Dalton’s Law
Fick’s Law
Henry’s Law

A

BL: at constant temp, given V of gas varies inversely to P to which subjected
CL: warm gas expands, cool gas shrinks
DL: Total + by mixture of gases = sum of partial pressure of each gas
FL: transfer of solute by diffusion directly proportional to XS area available for diffusion
HL: at constant temp, any gas physically dissolves in liquid proportion to PP

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24
Q

Choanal atresia has problem b/w which weeks of development?

A

Failure of bucconasal membrane to rupture b/w 5-6th weeks of development. Unilateral more common. Can be bony or membranous obstruction or both. Most are sporadic, most have associated malformations. More common in females.

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25
Q

How many alveoli does term infant have at birth?

A

50-150 million alveoli (adults have 200-600 million)

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26
Q

When have chylothorax, switch to enfaport bc

A

lymphatic vessels not required for absorption of MCT

Chylothorax: transudative effusion; pH > 7.4, WBC < 1K, LDH < 200. >80% lymphocytes, TG > 110

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27
Q

Corticosteroid effects prenatally can be seen on US?

A

No! Less fetal breathing and movements, HR less variability. Fetal blood flow NOT affected.

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28
Q

Describe classic BPD (Pre surfactant era)

A

structural damage of normal pulmonary structures from mechanical ventilation and oxygen toxicity - airway squamous metaplasia, alveolar septal fibrosis, airway smooth muscle hypertrophy, marked inflammation

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29
Q

Describe new BPD

A

disruption of normal alveolar/vascular development; diffuse alveolar/capillary hypoplasia. Significant loss of surface area for gas exchange. Airway injury, inflammation, fibrosis are milder

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30
Q

What is the primary component of surfactant?

A

saturated phosphatidylcholine presents 50% of surfactant.

31
Q

Which surfactants are hydrophobic and hydrophilic? Which are more important to function

A

Surfactant B and C are hydrophobic, A/D are hydrophilic
B/C - critical to optimal dynamic behavior and function of surfactant and facilitate ABSORPTION AND SPREADING of phospholipid monolayer
A/D: collectins; part of host innate system
A: regulate surfactant expression and uptake
D: surfactant reuptake and recycling

32
Q

Describe function of surfactant B. What is the gene mutation associated?

A

critical to surfactant function, facilitates adsorption of surfactant lipids to air-liquid interface
SFTPB gene on chromosome 2
MC mutation in individuals of northern european descent = frameshift mutation (121ins2)

33
Q

Who in preterm neonates benefits from iNO

A

iNO in preterm neonates studied, no diff in incidence of death or BPD
Neonates BW > 1 kg, iNO decreased incidence of death or BPD from 60 to 30%

34
Q

How does caffeine act in the brain?

A

primary effects by antagonism of adenosine A1/A2 receptors in brain

35
Q

Mechanism of action of glucocorticoids

A

anti-inflammatory effect by annexin A1 synthesis —> decreased phospholipid A2 expression —> decreased production of prostaglandins, thrombaxnes, prostacyclins, leukotreienes

36
Q

What is primary reason why there is less MAS now?

A

fewer births > 41 weeks

37
Q

Incidence of intermittent hypoxia episodes during first few months of life

A

low incidence in first week —> progressive increase between 2-3 weeks, peaks at 4-5 weeks; plateau or decrease during weeks 6-10

38
Q

When does TTN resolve? When do X-ray findings show it?

A

TTN - resolves within 72 hrs
- Xray findings clear after 24 hrs

39
Q

When was surfactant approved for use bye FDA? When did NIH recommend antenatal steroids?

A

surfactant: 1989
Steroids: 1994

40
Q

What is most utilized finding to see if there is PH on echo?

A

TR Jet

41
Q

Dexamethasone is _____ times more potent than hydrocortisone. Name adverse effects.

A

25-50 times
adverse effects: hyperglycemia, hypertension, HOCM, growth failure, GI bleeding and perf, chronic suppression of hypothalamic-pituitary-adrenal axis, ND outcomes

42
Q

Name some mechanisms for lasix resistance

A
  • Distal tubule cell hypertrophy, altered furosemide oral absorption, concomitant NSAIDS that inhibit prostaglandins, blunt response to loop diuretics, decreased delivery to thick ascending loops
43
Q

How does chorio affect lung maturation?

A

can induce lung maturation and decrease RDS, but can lead to diffuse PNA presenting as respiratory distress

44
Q

What is the NAVA Break point

A

NAVA level is at a plateau phase, PIP and TV do not increase further as result of down regulation of Edi
Edi peak = measure of neural inspiratory effort or respiratory drive

Edi min: measure of tonic activity of diaphragm, or effort to prevent alveolar de-recruitment at end expiration
trigger: minimum increase in electrical activity from preceding baseline that will trigger ventilator
NAVA level: conversion factor that converts Eni signal into proportional pressure

45
Q

What is lucinactant (surfaxin)

A

third generation surfactants that are synthetic that contain proteins capable of mimicking properties of surfactant protein B and C

46
Q

What gram stain are tracheal aspirates?

A

94% are gram negative.
BAL –> 62% are pseudomonas

47
Q

Where and how is caffeine metabolized?

A

Liver via N7 demethylation process; matures with increasing GA and PMA

Caffeine metabolism higher in girls
In VLBW infants, caffeine clearance and Vd are lower, increasing linearly with increasing weight

48
Q

How many types of CPAM and describe them

A

5 types, typically in lower lobes. No L/R predilection. 40% of all congenital lung malformations.
0 rare: limited to upper tracheobronchial tree
1 70 %: macro-cystic (>2 cm), may have dominant single cyst or multiple cysts
2 (20%): multi cystic with size > 2 cm
3 (10%):: microcystic adenomatoid solid without cystic elements, can be associated with other anomalies and carries worse prognosis
4 (rare): hamartomatous malformation of distal acini with peripheral cysts.

49
Q

Intratracheal buesonide + surfactant compared to surfactant alone =

A

Prelim studies show intratracheal budesonide with surfactant compared with surfactant alone required lower MAP for ventilation, lower OI and PCO2 during first 24-48 hrs

50
Q

SpO2 in umbilical vein

A

Umbilical vein = O2 sat 70-75%; decreases to 60% prior to birth (same as NRP)

51
Q

Benefits of conventional lymphography, lymphoscintigraphy

A

Conventional lymphography – best anatomical details, but requires direct cannulation of lymphatic vessels

Lymphoscintigraphy – feasible in neonates but lower resolution than conventional. Performed by injecting radioisotope into webs b/w neonate’s fingers and toes and may provide information on lymph vessels aplasia, hypoplasia, or dysplasia
MR lymphangiography, noninvasive, is best at evaluating nodes, poor resolution for evaluation of lymph vessels

52
Q

What is inherited disorder of surfactant metabolism?

A

mutations in surfactant protein SP B, SP-C adenosine triphosphate-binding cassette member A3 (ABCA3) and NKX2-1 genes

ABCA3 – variable clinical presentation – acute resp distress vs interstitial lung dz in infancy or childhood. Lamellar bodies with eccentric dense inclusionsP

53
Q

What is inositol

A

essential nutrient shown to promote surfactant maturation. Meta-analysis = significantly decreases neonatal death

54
Q

What is risk for preterm neonates with BPD developing PH?

A

25-35%

55
Q

Incidence of congenital lung abnormalities

A

1 in 10k

56
Q

Describe lung development

A

Embryonic (0-7 weeks): formation of lung bud and conducting airways (trachea, lobar, segmental/subsegmental bronchi)
Pseudoglandular (7-17 weeks): branching morphogenesis with formation of 20 generations of conducting airways, terminal bronchioles, and closure of pleuroperitoneal folds. Type 22 pneumocystis are undifferentiated.
Canicular (16-27 weeks): terminal branching, respiratory bronchioles with establishment of early air-blood interface, alveolar ducts, PRIMITIVE ALVEOLI. Differentiation of type II pneumocytes with emergence of lamellar bodies
Saccular (26-36): Enlargement of peripheral airways, saccule formation with thinning of alveolar wall, SURFACTANT production in type II pneumocytes at 26 weeks.
Alveolar: 36 weeks-2 yrs: formation of terminal alveoli, secondary inter-saccular and inter-ductal septation with exponentional increase in lung SA for gas exchange. Further thinning of alveolar wall

57
Q

How does iNO improve respiratory function

A
  • Decrease V/Q mismatch secondary to decrease in PVR and pulmonary vasodilation
  • Decrease in lung inflammation secondary to reduction in early neutrophil accumulation
  • Decreased oxidant stress
  • Protection against surfactant dysfunction
  • Restoration of normal angiogenesis and parenchymal growth
58
Q

How does lung injury affect surfactant function?

A

Inactivation by environmental exposure (oxidants), degradation by LIPASES, conversion to inactive structural forms, inhibition of function by plasma protein and lipids, altered synthesis by alveolar type 2 cell secondary to circulating cytokines

59
Q

Mechanisms of central apnea

A

Preterm neonates have enhanced sensitivity of respiratory control system to inhibitory neurotransmitters such as serotonin
Hypoxic ventilatory depression 2/2 increased peripheral chemoreceptor sensitivity in carotid bodies
Impaired hypercapnic ventilatory response and apnea threshold only slightly below eupnea threshold
Exaggerated laryngeal chemoreflex
Increased amount ofa ctive sleep associated with generalized inhibition of skeletal muscle activity

60
Q

Describe central and peripheral effects of caffeine

A

Stimulate medullary respiratory centers, increase co2 sensitivity, bronchodilation, enhanced diaphragmatic function, increased MV, reduced hypoxic respiratory depression, stimulate CNS and CV, increase catecholamine secretion, enhance diuresis, antagonize prostaglandin activity

61
Q

Describe congenital lobar emphysema. What stages of lung development do problems occur?

A

Congenital lobar emphysema - also known as CL hyperinflation; overdistension of one or more lobes, potentially causing severe respiratory compromise
Etiology: dysplastic cartilage formation in canalicular stage or endoluminal obstruction resulting in ball-valve effect in saccular and alveolar stages of lung development

62
Q

How does ACE activity get affected in BPD?

A

increased ACE activity —> fluid retention and increase risk of BPD

63
Q

What is CAP trial?

A

lower rates of severe retinopathy of prematurity among caffeine-treated group compared with placebo group
CAP trial - improved respiratory outcomes with caffeine, decreased need for intervention for PDA, decreases in death / disability at 18 months

64
Q

Cell count for Chylothorax

A

WBC > 1000 cells (80% monos, ie lymphocytes)
Protein count similar to plasma
TG > 100

65
Q

What factors help with surfactant administration?

A

larger volume, faster rate, ventilator assistance, lung fluid improves distribution, positional maneuvers help

66
Q

Mechanism for meconium aspiration syndrome

A

Airways obstruction is prominent early
PVR and PPHN - typically improve within 3-4 days
Surfactant dysfunction - subacute and late phases of dz
Chemical pneumonitis, secondary infection can occur

67
Q

the problem with INSURE

A

can alter cerebral perfusion and EEG activity

68
Q

When are trach-ed patients weaned off?

A

weaned off PPV by 5th Bday and median weaning time of 2 years

69
Q

How to dx VAP

A

dx is subjective
Radiographic - new or pgoressive infiltrate, consolidation
Clinically worsening gas exchange
At least 3 - temp instability, leukopenia, leukocytosis, left shift, change in secretion pattern, apnea or increase in work of breathing, abnormal lung auscultation, bradycardia or tachycardia

70
Q

Who is at risk for TTN? other than CS.

A

SGA/LGA are at increased risk for TTN. Males more susceptible. Maternal hx of asthma or GDM.

71
Q

Mechanism of bubble CPAP

A

variable distending pressure due to submerged expiratory limb in water. RCT showed bcpap support was decreased by 50% for preterm neonates 24-29 weeks compared to ventilator

72
Q

What long term risk do lung transplant patients face

A

susceptible to bronchiolitis obliterates as long term morbidity (short term = infections)

73
Q

What is primary component of surfactant?

A

lipids constitute 90% of surfactant; phosphatidylcholine (mainly desaturated form dipalmitoylphosphatidylcholine) is main phospholipid responsible for lowering surface tension; represents 50% of surfactant by weight

74
Q

percentage of variance in susceptibility for BPD attributable to genetic factor alone is

A

53%

Nicu Brodsky+Pediatrix+NeoReview Questions (14 decks)

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