Neonatal Lung Flashcards

1
Q

Stages of lung embryology

A
Embryonic (0-5)
Pseudogaldn 5-16
Canalicular 16-25*****
Saccular 25-36*****
ALveolar 36+
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2
Q

Preterm babies have problems because

A

Fewer alveoli and less SA relative to adults

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3
Q

Embryonic Period important hings

A

Day 26- primitive lung bud first appears as ventral outgrowth fro mthe foregut

PRoximal airways

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4
Q

Tracheal-esophageal fistual …what when, and most common

A

Occurs from incomplete sep of foregut into resp and digestive tracts (4th week)

Most common prox esoph atresia with distal tracheoesoph fistula

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5
Q

Congenital diaphrag hernia

A

Failure of pleuroperitoneal emmbrane to close

5-6 weeks

Herniation of intestinal contents into thorax at 10 weeks

Bochdalek defects (posterolateral) - 98%

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6
Q

Pseudogland stage

A

5-16 weeks

Conducting airways

Divisosn complete by 16 weeks
Glandular appearance on miccroscopic section

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7
Q

Canalicular period

A

16-24 weeks

Fromatiin of acini

Apposition of cap endothelial cells and alveolar lining cells (19-20)

Type 2 cells and lamellar bodies (20-22 weeks)

Type 1 flattened cells (24 weeks)

Produccing surfactant

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8
Q

Saccular period

A

24-36 weeks

Expansion of gas exchange sites

Secondary crests divide saccules into sub-saccules or primitive alveoli (27 weeks)

Major diff in survival

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9
Q

Alveolar stage

A

36 weeks to 3 years

Alveolarization

Exp of gas exchange SA

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10
Q

Pretemrm infants

A

Canalicular or saccular are before microvascular proliferation

24 - canalic
26 - saccular
Term - alcveolar

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11
Q

Term
Preterm
Post-term

A

37 0/7 to 41 6/7

Preterm less than 37

Late preterm is 34 and 0 to 36 6/7

Post is over 41 6/7

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12
Q

Normal fetus and pulmonary fluid

A

Pulmonary vascular resistance is high

Low alveolar oxygen and low pO2 tension

Vasoconstricted and most blood shunted from lungs via the ductus arteriossi

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13
Q

Fetal shunts

A

RV dominant

Pumps 90% across PDA and 10% to lungs

Low pul flow due t high pul vasc resistacne

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14
Q

Umbilical vein

A

Oxygenated from placenta…across DA to IVC…majority across the PFO, LA, LV, out

From SV, out through pulm artery and across DA

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15
Q

Fetal Lung

A

Active lung fluid secretion necessary for lung growth

Need normal neurolgic (phasic stretch)

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16
Q

Production of fetal lung fluid

A

Early on, from the placenta

Then comes from the lung**

In utero, type 2 cells produce surfactant and fetal lung fluid

Pump chloride actively into the alveolar air space and sodium and water follow

17
Q

Neonatal production**

A

Majority of lung fluid reabsorbed

Multiple triggers…most important is the onset of active labor via adrenaline

actively pump sodium out of the alveolar space and reabsorbing into interstitial

18
Q

Surfactant and composition

A

Type 2 pneumocytes produce

Capable at end of 2nd trimester

80% phospholipids

19
Q

Composition of surfactant

A

Major is dipalmitoylphosphatidylcholine

Phosphatidylinositol is majjor in premature

20
Q

SP-A and D

A

Non immune host defensive protein

Opsonin type

Immunologic

21
Q

SP-B and C

A

Hydrophonic

Lowers surface tension

Facilitates absorption of lipids

30% of term that die have SP-B def aused by 2 base insertion resulting in frame-shift and premature termination

Def causes decreased lamellar bodies

22
Q

Normal sufactant metabolism

A

Macrophages in the lung are important…lamellar are critical precursor from the type 2 cells

Defects result in accumulation of surfactant

23
Q

Synthesis and secretion compared to adults

A

Preterm have similar amount of surfactant to adults, but they NEED more

PReterm needs 3-4 days to produce levels comparable to term

Majority of exogenously given given surfactant is recycled within surfactant pool

24
Q

Surfactant function

A

P=2T/r

Amount of pressure needed to keep a bubble open

Results in collapse fo small alveoli to collapse and large to enlarge

25
Q

In inhalation

A

AMount of surfactant per millimeter will decrease becasue the lung has expanded

26
Q

Surfactant net effect

A

Prevents the small alveoli from collapsing and allows it to stay the same

27
Q

Lung compliance

A

Change is volume over change in pressure

28
Q

Benefits of surf

A

Decreased opening pressure

More uniform inflation with less collapse and hyperinflation

Increased FRC and complicance

29
Q

TTN risk and patho

A

Transient tachypnea of the newborwn
Risk - premature or C section without labor

Retained fetal lung fluid due to inadequate/delayed signaling for resorption to occur

30
Q

Clinical TTN

A

Soon after birth

Tachypnea, grunting, flaring, retractions

Hypoxemia and hypercapnia

Resolves in 48-72 hours

Diffuse haziness on X-ray

31
Q

Resp distress syndrome

A

Previously called hylaine membrance dz

Proteinaceous deposits lining alveoli in infants

Developmental insufficnecy of surfactant production and structural immaturit of the lungs

Clinical - resp distress

Radio - reticulogranular infiltrate and air bronchograms

32
Q

More preterm with RDS

A

THen takes longer

Born in canlicular stage
Need ventilator course

33
Q

RDS clinical

A

Grunting, flaring, retracting

Belly breathing - paradoxial resp

Tachypnea followed by low RR

Cyanosis and poor perfusion

34
Q

Pressurevolume curves with surfact def

A

Flattened becaasue more pressure needed to open up the lungs

35
Q

Comps from SD

A

Pneumothroax

Pulm hemorrhage

Acute lung injury

Increased mortality from other things

36
Q

COng diaphragmeatic hernia

A

Most common is posterolateral

Failure of sep of the pleuro-peritoneal canal durign embrylogic development which results in pulmonary hypoplasia and puml maldevelopment

37
Q

Clinical and management CDH

A

Cyanosis and resp failure due to pulm hypoplasia

Bowel decompression, sedation ,ventilation, NO

ECMO and reapir