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Growth > cardiorespiratory adaptation at birth > Flashcards

cardiorespiratory adaptation at birth Flashcards

1
Q

What are the 5 stages of lung development?

A
  • Fairly predictable in time scale
  • Embryonic - lung buds start to develop. Respiratory diverticulum comes off of the esophageal ridge - An outpouching of the fore gut that will become the respiratory tract. Bifurcation into left and right
  • Pseudoglandular - multiple levels of branching, all airways are still closed (no lumen)
  • Canalicular - start to get holes and have open tubes. Start to see little alveol, but v small numbers. Develop terminal bronchioles
  • Saccular - more and more complex. Get surfactant formation about 24 weeks
  • Alveolar - sustainable airways ready for birth
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2
Q

What growth factors are required?

A
  • FOXA2 - branching
  • FGF-10, SHH, BMP4 - outgrowth of new buds
  • Gli proteins - branching
  • VEGF - angiogenesis
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3
Q

What are the time frames for alveolar development?

A
  • 24 weeks, saccules develop - VEGF causes capillaries to develop around each
  • 32 weeks, shallow indentations
  • Most development post term - mainly by growth in number. Adult numbers of alveoli by 4 years, also grow in size with age
  • Pneumocytes - type 1 and 2 present after 22 weeks. From 24 weeks lamellar bodies present (store surfactant)
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4
Q

What can cause structural pathologies?

A
  • Extrinsic restriction - congenital diaphragmatic hernia, effusions, thoracic or vertebral abnormalities
  • Intrinsic restriction - lung cysts (cystic adenomatoid malformation)
  • Malnutrition (vit A)
  • Smoking
  • Time of onset - <16 weeks, branching is irreversibly affected, potentially permanent reduction in alveolar number. >16 weeks, predominant alveolar numbers
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5
Q

What is lung liquid?

A
  • Foetal lungs are filled with liquid
  • 4-6mls/kg midgestation -> 20mls/kg term
  • Similar cations to plasma, with higher Cl- but much lower protein and bicarbonate
  • Composes some of amniotic fluid, however most is urine
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6
Q

How is lung fluid secreted?

A
  • Secondary active transport of Cl from interstitium to lumen - the Cl will move first, pulling Na and water with it
  • Get a very slight positive pressure in the lungs because of its production
  • Lung fluid is required for lung growth, but not branching
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7
Q

How is lung fluid absorbed?

A
  • Active sodium transport in apical membranes
  • Don’t want lungs full of liquid after delivery
  • Some comes out through coughing, but the adrenaline release of your birth itself will turn off lung fluid secretion
  • Thyroid hormone and cortisol are required for maturation of the foetal lung response to adrenaline
  • Exposure to postnatal oxygen increases sodium transport across pulmonary epithelium
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8
Q

What may cause lung liquid pathologies?

A
  • Oligohydramnios
  • Foetal breathing abnormalities
  • Delivery without labour
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9
Q

What is oligohydramnios?

A
  • Dont have enough fluid surrounding the foetus - leak or not enough produced
  • Kidneys dont work so cant produce urine
  • Lungs dont work properly
  • Usually die first due to lungs
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10
Q

What causes some foetal breathing difficulties?

A
  • Neuromuscular disorders
  • Phrenic nerve agenesis
  • Congenital diaphragmatic hernia
  • Foetal breathing slows lung liquid loss - maintains expansion
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11
Q

Why might there be lung liquid pathology from delivery without labour?

A
  • Can get transient tachypnoea newborn (TTN) from c-section

- Baby wont have surge in cortisol and adrenaline like in natural childbirth

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12
Q

How is surfactant produced and degraded?

A
  • Produced by type 2 pneumocytes
  • Stored in lamellar bodies
  • Degraded in alveoli - absorbed and recycled by alveolar cells. 10 hr turnover time
  • Negative feedback system to regulate release - also stretch receptors (b-adrenergic_
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13
Q

What is surfactant?

A
  • Mix of phospholipids, neutral lipids and protein
  • Phosphatidylcholine = 80%, P-glycerol = 10%
  • 60% PC desaturated, predominantly palmitic acid
  • So dipalmitoyl PC is the major component
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14
Q

Why do we have surfactant?

A
  • Prevents atelectasis - reduces work to breathe
  • Achieved by reduced surface tension
  • Solid at body temp; stabilises alveoli. Can phase shift between liquid gel and solid very quickly
  • When alveoli are open, very low internal pressure, lower ST, but gaps between PL molecules in surfactant
  • Areas exposed to water will be pulled on to try and close it.
  • AS it shrinks down, molecules become compressed, eventually like a solid
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15
Q

What are the 4 types of proteins in Surfactant?

A

SP-A,B,C,D

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16
Q

What is SP-A?

A
  • Large glycoprotein
  • Gene on chr10, only expressed in lung
  • Increased production after 28 weeks
  • Essential in determining structure of tubular myelin; stability and spreading of PLs; negative feedback loop
17
Q

What is SP-B?

A
  • 1-2% of surfactant by weight
  • Gene on Chr2
  • Glucocorticoids increase expression
  • required for tubular myelin and spreading
  • In vivo has greatest activity in terms of lung compliance
  • Protects surfactant film from inactivation and degradation by serum proteins
18
Q

What is SP-C?

A
  • Gene on Chr 8
  • 35AA long - smaller
  • Significantly enhances absorption and spreading on PLs
19
Q

What is SP-D?

A
  • MW 46000
  • Increases expression with gestation
  • Expression is widely distributed in epithelial cells
  • No significant surfactant activity
  • Immune function
20
Q

What are 3 things that affect surfactant production?

A
  • Glucocorticoids
  • Thyroid hormones
  • Insulin
21
Q

How do glucocorticoids affect surfactant production?

A
  • Increased production at end of gestation - increases DPPC

- Dexamethasone increases b2-adrenoceptor gene expression -> increased surfactant secretion

22
Q

How do Thyroid hormones affect surfactant production?

A
  • T4 increases production of surfactant
  • T3 crosses placenta
  • TRH increases PL independent of T3/4
23
Q

How does insulin affect surfactant?

A
  • Delays maturation of type 2 cells, decreases % saturated PC
  • Delayed PG (phosphatidylglycerol)
  • Increased sugar levels delay lung maturation
24
Q

What surfactant pathologies are there?

A
  • In prematurity - PC relatively unsaturated (unstable monolayer buckles on expiration); PG replaces PI with increased gestation; leaky capillary membranes > fibrin deosition, inhibits reduction of ST
  • SP deficiencies - SP-B absence leads to reduced PG; no secretion of normal surfactant and so lethal
  • SP-C -> interstitial lung disease
25
Q

What happens to the lungs at birth?

A
  • Lung liquid production ceases during labour
  • Foetal breathing ceases
  • Cooling stimulates breath along with other senses
  • Air replaces fluid in minutes
  • Some squeezed out, most absorbed into lymphatics and capillaries
  • Rapid fall in airway resistance, increases FRC
  • Slower increase in compliance over 24 hrs
26
Q

What is the regulation of breathing?

A
  • Normal rhythm - inspiration (inspiratory muscle contraction), Passive with a bit of active expiration
  • Generated in respiratory centre in ventrolateral brainstem
27
Q

How is the breathing controlled?

A
  • Foetus tries to stop all nonessential activity if hypoxic
  • Hypoxic gas mixture will cause breathing rates and effort to go up in children
  • Term babies will revert to more intermittent breathing patterns
  • preterm babies it is much more marked - may even do it at low altitude - may not restart
28
Q

How does prematurity affect breathing/lungs?

A
  • Respiratory centres less well developed
  • Very immature neonate responds lika a foetus - apnoea
  • Cold babies dont have initial hyperventilation
  • Sometimes, premature babies just stop breathing
  • Caffiene is a respiratory stimulant - iv caffiene reduces apnoeic prematurity
29
Q

What neurological adaptations are there?

A
  • Built to withstand labour - fewer synapses and reduced O2 requirement. Newborn babies utilise non-oxidative glycolysis and ketone bodies
  • Hypoxia leads to redirection of blood flow in foetus - will send blood to brain, heart and adrenals, turn off blood supply to nonessential areas like gut

Growth (7 decks)

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