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WEEK 4 SEM 4 > Cardiorespiratory adaptations at birth 1 > Flashcards

Cardiorespiratory adaptations at birth 1 Flashcards

1
Q

There are 4 stages of lung development. What are they?

A
  1. embryonic stage
  2. pseudoglandular phase
  3. cannalicular phase
  4. saccular phase
  5. alveolar phase
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2
Q

What happens in the embryonic stage?

A
  • resp bud comes off the oesophageal ridge

problems can arise= tracheooesophageal fistula

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3
Q

What is a tracheooesophageal fistula?

A

oesophagus and trachea abnormal combine

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4
Q

What happens in the pseudoglandular phase?

A
  • 5-16 weeks
  • resp tree branches into terminal bronchioles
  • now broncheoles are solid (not filled with air) ad has no lumen
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5
Q

What happens in the cannalicular phase?

A
  • 16-26 WEEKS
  • each bronchiole divides into 2+ resp bronchioles
  • tubes are cannulated and air can come in
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6
Q

What happens in the saccular phase?

A
  • between 24 weeks and term
  • further subdivisions of bronchioles into 3-6 alveolar ducts
  • ducts form terminal sacs
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7
Q

What happens in the alveolar phase?

A
  • just before term to 5-7y/o
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8
Q

What are the growth factors involved in the process of making the respiratory tract?

A

Sonic Hedgehog, FGF 10= bud formation
gli proteins= branching
VEGF (vascular endothelial growth factor)= angiogenesis

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9
Q

What is alveoli needed for?

A

gas exchange

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10
Q

Why is a preterm baby at risk of alveoli not forming?

A
  • because alveoli only form at 24 weeks

- 24 weeks, capillaries develop around saccules (precursors to alveoli)

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11
Q

At what stage does alveoli develop?

A
  • pneumocytes (type I and II) present= 22 weeks
  • capillaries around saccules= 24 weeks
  • shallow indents in saccules= 32 weeks
  • most alveoli develop post term
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12
Q

When does the number of alveoli increase?

A
  • fast growth till 5
  • slowed down growth in number till 10
  • after 10, stops increasing in number, just increases in size
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13
Q

What produces surfactant?

A

Type II pneumocytes

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14
Q

Where is surfactant stored?

A

in lamellar bodies in the lungs from 24 weeks

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15
Q

What happens if pathology occurs before 16 weeks?

A
  • affects number of branches in the lung
  • simple lung
  • permanent reduction in alveoli number
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16
Q

What happens if the pathology occurs after 16 weeks?

A
  • most branches already there

- affect alveoli number

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17
Q

What are the extrinsic restriction factors (restricting growth) on the lung?

A
  • congenital diaphragmatic hernia
  • effusion
  • thoracic or vertebral abnormalities
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18
Q

What is the problem with congenital diaphragmatic hernia?

A
  • diaphgragmatic structural defect
  • lungs have been squashed in early development
  • lungs not have chance to expand
  • less number of branches on that side
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19
Q

What causes effusions?

A
  • lymphatic abnormalities

- heart failure in foetus

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20
Q

What are the internal restriction factors affecting growth of the lung?

A
  • congenital malformation in lung= cysts
  • Malnutrition: vitamin A deficiency
  • Smoking
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21
Q

Inside the womb, what is the resp tree filled with?

A
  • fluid
  • lungs make this fluid
  • composition of fluid is very important
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22
Q

How much fluid is in the lungs?

A
  • mid gestationtation = 4-6mls/kg
  • term = 20ml/kg
  • fluid made at rate of 2-5ml/kg/hr
  • fluid need to be cleared by birth to take first breath
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23
Q

What is the composition of the fluid in the lungs?

A
  • Na in lung liquid= higher than Na in amniotic fluid
  • Na in lung liquid = EQUAL to Na in plasma
  • HCO3- and protein levels= lower than in amniotic fluid
  • HCO3- and protein levels= lower than in plasma
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24
Q

What is the process of manufacturing lung liquid?

A
  1. secondary active transport of Cl- from interstitium to lumen of resp bronchiole
  2. this drives the fluid
  3. Na+ and H2O follow chloride passively
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25
Q

What is the pressure of the liquid in the lungs?

A
  • liquid production allows positive pressure (1cmH2O)

- important for lung growth not branching

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26
Q

What is done with babies with diaphragmatic hernias?

A
  • methods to block trachea (antenatally)
  • blocks exit of lung fluid
  • keeps exerting pressure on the lungs
  • expands the affected lungs
27
Q

How are the lungs cleared of fluid in utero?

A
  • Na+ active transport in apical membranes

- leads to absorption of lung fluids

28
Q

How are the lungs cleared of fluid quickly at birth?

A
  • adrenaline release= reduce liquid secretion and resorption of lung fluid promoted
  • thyroid hormone
  • cortisol
  • exposure to oxygen - increases sodium transport across the pulmonary epithelium to absorb the lung liquid
29
Q

Children born through C-Sections have the likelihood of developing what and why?

A

WHAT:
- develop small conditions like tachypnea

WHY:

  • they do not have stressful birth= so do not get adrenaline and cortisol release
  • these are needed for QUICK liquid absorption
30
Q

What pathologies can occur relating to lung liquid?

A
  • oligohydramnios
  • fetal breathing abnormalities
  • delivery without labour
31
Q

What is oligohydramnios?

A
  • less amniotic fluid
  • bc of early amniotic sac rupture or kidney abnormalities
  • potter’s syndrome
  • baby is squashed bc of less fluid= so not enough room to grow properly
  • get structural defects bc of the compression
  • lungs don’t grow properly
32
Q

WHAT PRODUCES AMNIOTIC FLUID?

A

KIDNEYS LOL

33
Q

How are fetal breathing abnormalities caused?

A
  • foetus breathe in utero= trains lung for postnatal life
  • neuromuscular disorders can affect breathing
  • foetal breathing slows down loss of fluid- so maintains pressure and expanded lungs
  • if foetus doesnt breathe, then pressure not maintaines and lungs fail to work
34
Q

What is the main component of surfactant?

A

phosphatydylcholine (PC)

- produced in ER of type II pneumocytes

35
Q

Where is surfactant degraded?

A
  • in the alveoli
  • it is absorbed and recycled by alveolar cells, more than 90% of PC is reprocessed
  • it has a turnover time of about 10 hours
36
Q

How is surfactant production regulated?

A

negative feedback

  • stretch receptors manage this
  • B adrenergic receptors on type II pneumocytes- regulate release of surfactant
37
Q

Why do we need surfactant?

A
  • preventing alveolar collapse at the end of expiration

- surfactant reduces surface tension (reduces surface area of water)

38
Q

What are the 2 stages of surfactants lining the alveolar lining?

A
  1. gel phase= surfactant spreads out in gel liquid phase

2. surfactant gets compressed- becomes solid in crystal phase

39
Q

What is the process of surfactant release?

A
  1. surfactant made in RER of type II pneumocyte through choline fatty acids
  2. stored in lamellar bodies
  3. release from cell membrane as tubular myelin (criss cross structure of surfactant which forms a solid strucutre if compressed)
  4. after release 10% of surfactant is lost from lungs though macrophages etc.
  5. some surfactant goes back into type II pneumocytes
40
Q

What is surfactant made of?

A
  • phospholipids
  • neutral lipids
  • proteins
    it has a water soluble end and a fat soluble end (hydrophobic and hydrophilic)
  • LIPIDS MOST IMPORTANT PART OF SURFACTANT
41
Q

What is the composition of lipids in surfactant?

A
  • 80% of the surfactant is phosphatidylcholine

- 10% of the surfactant is phosphatidylglycerol (important for mature surfactant)

42
Q

What is posphatidylcholine made of?

A

-60% of phosphatidylcholine is unsaturated and made of palmitic acid

43
Q

What other lipids are in surfactants?

A

cholestrol- affect fluidity

44
Q

What are the proteins in surfactant?

A

SPA
SPB
SPC
SPD

45
Q

What does SPA do?

A

SP-A

  • large glycoprotein
  • gene on chromosome 10
  • only expressed in lung
  • production increase after 28 weeks
  • determines structure of tubular myelin
  • essential in stability and spreading of phospholipids-
  • involved in negative feedback
  • immune function
46
Q

What does SPB do?

A

SP-B

  • 1-2% of the weight of surfactant
  • its gene is on chromosome 2
  • its expression is increased through glucocorticoids-
  • spread surfactant evenly
  • tubular myelin formation
  • increases lung compliance
  • protects surfactant
47
Q

What does SPC do?

A

SP-C

  • on chromosome 8
  • small (35 amino acids)
  • it significantly enhances adsorption and spreading on phospholipids
48
Q

What does SPD do?

A

SP-D-

  • no structural function
  • expression increased with gestation
49
Q

What hormones are in surfactant?

A
  • glucocorticoids
  • thyroid hormone
  • insulin
50
Q

What happens to glucorticoid levels

A
  • increased production of glucocorticoids at the end of gestations
  • this increases expression of phosphatidylcholine
  • dexamethasone can be used to enhance B2 adrenoceptor gene expression, which leads to increased surfactant secretion
51
Q

What do thyroid hormones do to surfactant?

A
  • T4 increases surfactant production
  • T3 can cross the placenta
  • TRH increases the phospholipids in surfactant independent of T3 or T4
52
Q

What does insulin do to surfactant?

A
  • insulin delays maturation of type 2 cells
  • decreases percentage saturated phosphatidylcholine
  • this is imp for diabetic mothers, bc babies might develop resp distress after birth bc they dont have functional surfactant
53
Q

What pathologies are associated with surfactant?

A
  • prematurity

- surfactant protein deficiencies

54
Q

What happens to surfactant if a baby is born prematurely?

A
  • babies only make surfactant properly at 24 weeks bc they dont have enough type II cells
  • premature make surfactant which has:

= unsaturated phosphatidylcholine is unsaturated= makes monolayer unstable

55
Q

What do you need to give to premature babies?

A
  • artificial surfactant for the first 24 to 48 hours until they can produce some of their own
56
Q

What happens to the baby at birth?

A
  • lungs cut down fluid
  • fetal breathing stops
  • hypoxia detected by central chemoreceptors stimulate the baby to breathe
  • lungs open up (bc high pressure of 50cmH20 generated)
  • active expiration bc baby cries
57
Q

How does air replace fluid in the lungs?

A
  • some of the fluid is squeezed out due to the high pressure air
  • most of the fluid is absorbed into the lymphatics and capillaries within 1 to 24 hours
58
Q

Why do premature babies have trouble with controlled breathing?

A
  • bc resp centre is less well developed
  • cold babies dont have initial hyperventilation= so keep close to mothers
  • at normal oxygen levels, sometimes pre term babies stop breathing= give IV caffeine as resp stimulant
59
Q

What is the normal rhythm of breathing?

A
  • inspiration is done with inspiratory muscle contraction

- expiration is passively done due to elastic recoil

60
Q

Where do the signals that drive respiration come from?

A

ventrolateral brainstem (in the medulla)

61
Q

What happens if there is hypoxia in a feuts. What happens to the breathing?

A
  • stops breathing
  • bc loses energy if it tries to breathe
  • reduce all movements
62
Q

What happens if a preterm baby becomes hypoxic?

A
  • breathing rate goes up for a while
  • then switch to foetal response
  • stop breathing
    (SAME CAN HAPPEN TO BABIES BORN AT TERM)
63
Q

The adult’s main energy supply is glucose. What is used in a foetus?

A

utilize ketone bodies as an energy source for the brain and the heart

WEEK 4 SEM 4 (6 decks)

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