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Physiology & Science: Human Growth > Cardiorespiratory Adaptation At Birth I > Flashcards

Cardiorespiratory Adaptation At Birth I Flashcards

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1
Q

What are the 5 stages of lung development?

A
  1. Embryonic
  2. Pseudoglandular
  3. Canalicular
  4. Saccular
  5. Alveolar
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2
Q

Describe the embryonic phase

A
  • @ 3-6 weeks
  • Respiratory diverticulum develops off esophagotracheal ridge
  • Lung bud develops from foregut
  • This all turns into resp tract
  • Trachea develops with its 2 lung buds as bifurcation occurs
  • Further development of airways -> next stage
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3
Q

Describe the pseudoglandular phase

A
  • @ 6-17 weeks
  • Branching in lungs to form terminal bronchioles
  • Airways still closed however as no lumen
  • No respiratory bronchioles, no alveoli present (yet)
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4
Q

Describe the canalicular phase

A
  • @ 17-26 weeks
  • Each terminal bronchiole divides into 2+ respiratory bronchioles
  • “Canunlate” - open holes, to breathe through, tubes
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5
Q

Describe the saccular phase

A
  • @ 27 weeks -> term
  • Respiratory bronchioles divide into 2-3 alveolar ducts
  • These develop terminal sacs
  • Capillaries establish close association
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6
Q

Describe the alveolar phase

A
  • From term -> childhood
  • Mature alveoli w/ well-developed epithelial-endothelial association
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7
Q

Which growth factors are involved in lung development?

A
  • Hepatocyte nuclear factor 3beta - foregut
  • FGF-10, Sonic hedgehog, BMP4 - outgrowth of new end buds
  • Gli proteins - branching
  • Vascular endothelial growth factor (VEGF) - angiogenesis
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8
Q

When do the saccules start to develop?

A

Around 24 weeks

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9
Q

What develops around each saccule and what causes this?

A

Capillaries - caused by VEGF

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10
Q

Most alvolar development occurs post-term. By what age will there be adult numbers of alveoli?

A
  • 4 years
  • Mainly by growth in number
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11
Q

When are pneumocytes present?

A
  • Type 1 and type 2
  • Present at 22 weeks
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12
Q

What do lamellar bodies do and when are they present from?

A
  • From 24 weeks
  • Store surfactant
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13
Q

In terms of structural pathology, how does the time of onset impact alveoli?

A
  • < 16 weeks, branching irreversibly affected, potentially permanent reduction in number of alveoli
  • > 16 weks, branching complete, predominantly alveolar numbers affected
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14
Q

Give examples causing extrinsic restriction in terms of lung development

A
  • Congenital diaphgragmatic hernia
  • Effusions
  • Thoracic or vertebral abnormalities
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15
Q

Give an example causing intrinsic restriction of lung development

A
  • Lung cysts (cystic adenomatoid malformation)
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16
Q

Apart from time of onset and restriction, what other (lifestyle) factors affect lung development?

A
  • Malnutrition (vit A)
  • Smoking

Affect peak flow, alveolar number + lung size

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17
Q

Fetal lungs are filled with liquid, what is the content of lung liquid?

A
  • High sodium (150)
  • High chloride (157)
  • Low potassium (6.3)
  • Low bicarbonate (2.8)
  • Low protein (0.03)
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18
Q

Describe lung liquid secretion

A
  • Secondary active transport of Cl from interstitium to lumen
  • Sodium and water follow
  • Liquid production allows for positive pressure of 1cmH2O
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19
Q

Why is lung fluid required?

A
  • For lung growth
  • Not for branching
  • Interruption of lung liquid secretion -> abn dpmt
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20
Q

How is lung liquid absorbed?

A
  • Active sodium transport in apical membranes
  • Labour & delivery: adrenaline release -> reduced secretion + resorption begins
  • Thyroid hormone + cortisol required for maturation of fetal lung response to adrenaline
  • Exposure to postnatal oxygen increases sodium transport across pulmonary epithelium
21
Q

How does oligohydramnios result in abnormal lung development?

A
  • Reduced amniotic fluid surrounding fetus
  • Kidney abnormalities + early rupture
  • Abnormally developed lungs - die from lung problems
22
Q

Fetal breathing slows liquid loss - maintains expansion. What conditions can result in fetal breathing abnormalities?

A
  • Neuromuscular disorders
  • Phrenic nerve agenesis
  • Congenital diaphragmatic hernia
23
Q

What is TTN (transient tachypnoea newborn) and how does it come about?

A
  • Newborn presenting with abnormally rapid breathing + resp distress, should settle in 6-12 hours
  • Due to lack of lung liquid clearing
  • Due to delivery without labour - so by elective caesarean section - lack of adrenaline + cortisol, which is important for lung liquid absorption
24
Q

Pulmonary surfactant is key to sustaining life post-natally. Where is surfactant produced, stored and degraded?

A
  • Produced by type 2 pneumocytes: surfactant phosphatidylcholine prod in endoplasmic reticulum
  • Stored in lamellar bodies
  • Absorbed and recycled (>90%) by alveolar cells
  • Turnover time 10 hours
25
Q

How is surfactant release regulated?

A
  • Negative feedback
  • Also stretch receptors
  • B-adrenergic receptors on type 2 cells - increases w gestation
26
Q

Why do we need surfactant?

A
  • To prevent atelectasis (alveolar collapse) - reduces work to breathe
  • Achieved by reduced surface tension
  • Solid at body temp - becomes a solid monolayer, stabilises alveoli
27
Q

What is Laplace’s equation?

A

Internal pressure = 2 x surface tension / radius

Theory: 2 balloons, blow one up, easier to blow up as it gets bigger but hard to start.

If you put 2 balloons together, one full and one empty, the almost empty one will empty into the full one as there’s a lower surface tension/resistance than the bigger balloon. As radius gets bigger, the internal pressure drops.

28
Q

What is surfactant made of and which is the most important part?

A
  • Phospholipids
  • Neutral lipids (eg cholesterol)
  • Protein

Phospholipids most important

29
Q

What is the lipid part of surfactant made of?

A
  • Phosphatidylcholine comprises 80%
  • Phosphatidylglycerol comprises 10%
  • 60% PC disaturated, predominantly palmitic acid
  • Therefore dipalmitoyl phosphatidylcholine is the major component of surfactant
  • Hydrophillic head + hydrophobic tail
30
Q

List the composition of surfactant by mol weight (%)

A
  1. dipalmitoyl phosphatidylcholine 50%
  2. unsaturated phosphatidylcholine 17%
  3. serum proteins 8%
  4. phosphatidylglycerol 7%
  5. phosphatidylethanolamine 4%
  6. surfactant specific proteins 2%
31
Q

What is the difference between function of PC and PG?

A
  • PC reduces alveolar surface tension
  • PG promotes spreading of surfactant throughout lungs
32
Q

There are 4 types of surfactant proteins (SP A-D). How much of the surfactant do they make up by weight?

A

5-10%

33
Q

What is SP-A and why is it important?

A
  • Large glycoprotein
  • Gene on chromosome 10, only expressed in lung
  • Inc prod after 28 weeks
  • Essential in:
    • determining structure of tubular myelin
    • stability + spreading of phospholipids
    • negative feedback loop for surfactant
    • immune function
34
Q

What is SP-B and why is it important?

A
  • 1-2% of surfactant by weight, largest volume SP
  • Gene on chromosome 2
  • Glucocorticoids inc expression
  • Required for:
    • formation of tubular myelin
    • spreading
    • combined w lipid mixtures - most of surface activity in vitro + inc lung compliance in vivo
    • protects surfactant film from inactivation by serum proteins
35
Q

What is SP-C and why is it important?

A
  • Chromosome 8
  • 35 AA
  • Significantly enhances adsorption + spreading on phospholipids
36
Q

What is SP-D and why is it important?

A
  • Mol weight = 46,000
  • Inc expression w gestation
  • Expression is widely distributed in epithelial cells
  • No significant surfactant activity
  • Immune function
37
Q

How do glucocorticoids contribute to surfactant maturation?

A
  • Increased production of glucocorticoids at end of gestation
  • Increases DP PC
  • Dexamethasone enhances B2-adrenoreceptor gene expression -> leads to increased endogenous surfactant secretion
38
Q

How do thyroid hormones contribute to surfactant maturation?

A
  • T4 inc surfactant production
  • T3 crosses placenta
  • TRH increases phospholipid (independent of T3,4)
39
Q

How does insulin contribute to surfactant maturation?

A
  • Delays maturation of type 2 pneumocytes, decreases % saturated PC
  • Delayed PG
  • Inc sugar levels delay lung maturation
40
Q

What is the surfactant pathology of premature babies?

A
  • PC relatively unsaturated - unstable monolayer which buckles on expiration
  • PG replaces PI with increased gestation
  • Leaky capillary membranes - fibrin deposition in alveolus - inhibits reduction of surface tension - hyaline membranes
41
Q

What does a deficiency of SP-B lead to?

A
  • Absence leads to markedly reduced PG
  • No secretion of normal surfactant
  • Lethal ->> lung transplant possible for some
42
Q

What does a deficiency of SP-C cause?

A

Interstitial lung disease

43
Q

What events lead up to stimulate the baby’s first breath during birth?

A
  • Lung liquid prod ceases during labour
  • Fetal breathing ceases
  • Cooling stimulates breath along w other sense
  • Central chemoreceptor detection of hypoxia
  • First breath median time = 10 sec
  • High inspiratory pressure, active expiration with high pressure
44
Q

What happens to the lung liquid upon birth, where does it go?

A
  • Air replaces fluid within minutes
  • Some squeezed out, most absorbed into lymph + capillaries
  • Rapid fall in airway resistance, inc FRC
  • Slower inc in compliance ~ over 24 hours
45
Q

The normal rhythm for breathing is generated in the respiratory centre, where specifically?

A

Ventrolateral brainstem

46
Q

What would happen if the following breathed hypoxic gases for 5 mins?

  • Term infant
  • Older infant
  • Adult
A

Older infant and adult would be fine - their breathing efforts and RR would go up.

Breathing efforts will go up for 2 mins, then drop for term infant. Due to drive for respiration being immature still so breathing efforts decrease.

47
Q

What is the control of breathing like in preterm infants?

A
  • Resp centre less well developed
  • Very immature neonate responds like a fetus - apnoea
  • Cold babies don’t have initial hyperventilation
  • Sometimes, premies just stop breathing
48
Q

What happens with the blood flow when hypoxia occurs in the fetus?

A
  • Leads to redirection of blood flow in fetus
  • Blood directed to brain, heart + adrenals
  • Blood supply directed away from gut + other non-essential areas

Physiology & Science: Human Growth (9 decks)

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