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DT3- EXAM 2 > Lung Embryo/ CD (6)-Melissa** > Flashcards

Lung Embryo/ CD (6)-Melissa** Flashcards

1
Q

Lung development stages + weeks they begin:

A

3-embryonic 5-pseudoglandular 16- canclicular 24-saccular 36- alveolar

3 executives caught

5 People

SIXTING (16) in the Canal

+saccular= time of Surfactant (24) Alveolar near birth= 36

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2
Q

When is the embryonic stage during lung development? What are three important events that occur during this stage?

A

3-7 weeks gestation

  • 28 days main stem BRONCHI form (+ branching to form 5 LOBES of the adult lung) *FIVE lobes by start of week FIVE*
  • 44 days pulm aa’s form from 6th aortic arch - Trachea and esophagus separate

*44- two fours; TWO ARTERIES FROM TWO ARCHES and T/E become TWO separate STRUCTURES!!!!!!

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3
Q

What happens if the trachea and esophagus fail to complete separation during the embryonic stage of lung development?

A

Formation of tracheoesophageal (TE) fistula

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4
Q

When is the pseudo glandular stage of lung development? Why is it called the pseudo glandular stage? What are three important events that happen during this stage?

A

5th-17th week (Looks like endocrine gland + GLANDS form)

  • 14th week = gland formation
  • 17-23 further branching events form terminal acinar units

*GLANDular = GLANDS + branching

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5
Q

When is the canalicular stage of lung development? What are the landmarks of this stage? (4)

A

16th-24th week (looks like a canal) -capillary bed expansion and thinning - endothelium thins enough to support extrauterine life

-23-24 weeks Gas XGE begins - ~23-24 weeks SURFACTANT + other chemicals are produced

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6
Q

What is one factor that will accelerate the production of surfactant?

A

Glucocorticoids– we give moms Betamethazone if they are expected to deliver before 28 weeks

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7
Q

What are three effects of Betamethazone on premature neonatal development?

A
  • ^surfactant production by Type II pneumocytes
  • DECREASE alveolar division and bronchial length
  • prevent hemorrhaging in premature brain

*Dose every 12 hours to prevent lung growth restriction *See positive results in 24 hours; will stop positive effects with multiple doses

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8
Q

What is alveolar capillary dysplasia?

A

This occurs if capillary beds fail to think and expand properly during the canalicular stage flung development= fatal but rare

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9
Q

When is the saccular stage during lung development? What are two hallmarks of this stage?***

A

24-38 weeks

  • cell proliferation slows–> decrease mesenchymal tissue
  • ^ Type II pneumocytes–> ^ surfactant + asstd. proteins
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10
Q

What is one external factor that might INHIBIT surfactant production in premature babies?

A

Maternal DM ^ blood glucose in mom–> ^ insulin, normal blood sugar in baby–> Insulin INHIBITS surfactant production

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11
Q

When is the alveolar stage of lung development? What are the hallmarks of this stage? What are two hallmarks of this stage?

A

36 weeks- 2 or 3 yoa

  • ^ epithelial cells - diffuse changes in pulm vasculature
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12
Q

Describe the distribution of type I and type II pneumocytes that ensues as a result of alveolar development?

A
  • 2/3 type II penumocyte - 1/2 type I pneumocytes (cover 93% alveolar surface!)
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13
Q

Describe the changes in vasculature that occur during alveolar development: What happens if these changes FAIL to occur?

A
  • DECREASE sm muscle
  • DECREASE pulm vascular resistance *Failure to occur will lead to PPHN (persistent pulm HTN of the newborn)
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14
Q

Describe the role VEGF plays in lung development;

What happens when it is blocked?***

What two pathological states can result from VEGF dysfunction?

A
  • Normally ^ angiogenesis
  • BLOCK VEGF–> ^ Alveolar size similar to emphysema
  • Dysfunction can result in Bronchopulm Dysplasia (BPD), Retinopathy of prematurity (ROP)
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15
Q

What is AVASTIN and what do we use it to treat?

A

AVASTIN–> Inhib VEGF–>

Inject directly into baby eyes to treat ROP

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16
Q

What role does Retanoic Acid play in lung development (2)?

Does it change pulm function test (PFT)?

A
  • ^ alveolarization
  • DECREASE BPD incidence
  • No change in PFT
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17
Q

How are estrogen and testosterone relevant to lung development? ***

A
  • estrogen required for surfactant production
  • too much testosterone can SLOW lung development (Wimpy White Boy Syndrome)
18
Q

What are three benefits to moderate maternal stress on a premature baby?

A

^ glucocorticoids–> facilitates structural development, fluid absorption, surfactant production

Does decrease birth weight though!

19
Q

What is the primary active agent in surfactant and what exactly does surfactant do?

A
  • (40%) Dipalmitoylphosphatidylcholine (DPPC)
  • 80% is generally phospholipids
  • Surfactant DECREASES surface tension to allow for inflation of alveoli
20
Q

How many surfactant proteins are there?

Which is the most abundant?

Which is the largest?

Which is recycled by Type II pneumocyte?***

Which is the most hydrophobic?

A deficiency in which is NOT compatible with life?

A

4 surfactant proteins: A, B, C, D

A- Most abundant; Recycled by type 2 pneumocyte

B- Deficiency NOT COMPATIBLE with life

C- Most hydrophobic

D- Largest

21
Q

Describe the structure of surfactant protein A: What is its role?

A

Surfactant A: Bouquet - **Recycled by type II pneumocyte**

  • Opsonin– plays role in immunodefence
  • Deficiency IS COMPATIBLE with life
  • Most abundant
22
Q

Describe the structure of surfactant protein B:

What is its role?

What happens if there is a deficiency?

A

Surfactant B: Cruciform - Small but fusogenic

–spreads and stabilizes surfactant

–DEFICIENCY NOT COMPATIBLE WITH LIFE (RDS will ensue within hours after birth)

23
Q

Describe the properties of surfactant protein C:

  • What is required for it to function?
  • What is its role?
  • What is the inheritance pattern of a deficiency?
  • Is deficiency compatible with life?
A

Most hydrophobic

  • must be activated by SP-B
  • recruits phospholipids to lipid layer
  • Deficiency is AD and compatible with life (results in late interstitial pneumonitis and emphysema)
24
Q

Describe the properties of surfactant protein D:

  • What is its role
  • Where is it found?
A

Largest

  • Plays role in innate immunity against bacteria, fungi, virus
  • Found in GI tract, pancreas, bile duct, cervical glands

(other slimy glandy organs)

25
Q

When does surfactant production begin?

A

23-24 weeks *Prognosis for pre-term births prior to this point are not favorable :(

26
Q

3 Factors that INCREASE and 1 factor that DECREASES surfactant production:

A

INCREASE: 1. glucocorticoids (stress) 2. estrogen 3. thyroid hormone DECREASE: 1. HIGH CIRCULATING INSULIN

27
Q

What are 4 examples of how AVAILABLE surfactant might be INACTIVATED after birth?

A
  1. Aspiration: formula, sterile H2O, BM
  2. meconium– sterile and DIRECTLY deactivates surfactant
  3. Swallowed blood
  4. Pneumonia (Infection)
28
Q

What types of exogenous surfactant are available and which are preferred in clinical practice?

A

Curosurf (porcine)>>> Bovine>> Artificial

*Porcine and bovine admin every 12 vs. 6 hours and possess all functional proteins

29
Q

How do we dose betamethasone when delivered to mom?

A

Dose sparingly in order to prevent decrease in fetal lung growth;

this side effect will worsen with higher # doses

30
Q

How should we evaluate a neonatal CXR?

A

RIPS Rotation- head aligned with clavicles and spine;

Rotation may make heart look enlarged

Inspiration- should see 8-9 ribs

Penetration- see all vertebral bodies behind heart

Size of the heart- base looks bigger because of thymus!

31
Q

What should a starburst neonatal CXR tell you?

A

fluid in lymphatics; sometimes minor fissure is visible

32
Q

When you hear “elective c section”…

A

Think mom didn’t go into labor–less glucocorticoids (trigger Na/K pump action and surfactant into lung) = cause of TTN

33
Q

Describe Transient Tachypnea of the Newborn (TTN): Who gets this?

A
  • Na/K pumps didn’t get working and surfactant wasn’t pumped into baby lungs -

More common in wimpy white boys, *c-sections*, perinatal asphyxia, umbilical cord prolapse, and depressed newborns (mom w/ anesthesia)

34
Q

By when does TTN resolve? How do we treat it?

A
  • resolves in 12-48 hours
  • DIURETICS and SURFACTANT DO NOT HELP
  • Treat with O2 and nasal CPAP
35
Q

Neonatal Respiratory Distress Syndrome (NRDS): Describe the CXR. What else do we look for when making diagnosis?

A
  • CXR: Ground glass appearance (frosty beer mug)
  • premature baby (good surfactant after 35wks)
  • mom with DM
  • wimpy white boys, multiples, and kiddos with PDA at higher risk
36
Q

Describe the pathogenesis of NRDS:

A

No surfactant–> alveolar collapse–> protein accumulate in alveoli (hyaline membrane)–> NO GAS XGE

37
Q

What element of maternal history should be a red flag neonatal infection?

A

Membrane rupture LONGER than 12 hours (little guy should have come out by then!); especially if coupled with fever and uterine tenderness

38
Q

Congenital Pneumonia: How does this happen? What is its time to onset? What should we check for? How do we treat it? Prognosis?

A
  • Baby swallowed infected maternal fluid
  • Onset 3-4 hours after admission to nursery
  • Check for foul smelling amniotic fluid
  • Treat with Amp/Gent 7-12 days +/- CPAP if necessary
  • Most improve within 5-7 days

*Note: check to see if baby aspirated fluid because aspiration of virtually any fluid will deactivate surfactant and this is even worse than pneumonia!

39
Q

Neonatal Pneumothorax: How common is it?

What are some risk factors?

How serious are they?

How is it treated?

Are these guys at risk for future pneumothorax?

A
  • 1/100 births
  • Associated with alveolar malformation, shoulder distotia, big babies
  • Typically small and asx.
  • If large and problematic use pigtail cath and let it run until the bubbles stop; leave in for 3-4 days
  • Typically NOT at risk for further pneumothorax UNLESS associated with CT disorder (EDS, Marfan)
40
Q

Congenital Diaphragmatic Hernia: What is it? How severe are they? Which side is more common? Prognosis?

A
  • Failure of diaphragm development–> intestines in chest–> pulm hypoplasia
  • Spectrum of severity; can be small and asx until incidental finding on CXR later in life
  • More common on the left
  • Difficult to manage in NICU (give EGMO, run heart for them, admin O2)
  • Surgery necessary and typically curative

**NOTE: I HAVE NOW HAD THREE RX QUESTIONS ON THIS!!!!!

Know it!! failure of pleuroperitoneal folds = congenital diaphragmatic hernia (usually LEFT) –> pulm hypoplasia. HEAR BOWEL SOUNDS IN THORAX ON NEWBORN EXAM!!!!!!!!

41
Q

When might TE fistula occur?

A

-occurs during EMBRYONIC phase (weeks 3-7)

DT3- EXAM 2 (19 decks)

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