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BIOL2018:Adaptive Physiology > Respiratory changes at Birth > Flashcards

Respiratory changes at Birth Flashcards

1
Q

What happens at birth?

A

Shunts are removed with major changes in heart due to altered resistance and demands in vascular system and a shift from a right to a left sided dominated system.

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2
Q

Neonate oxygen expenditure

A

Twice the rate of the adult/kg body mass.

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3
Q

Neonate ardiac output

A

4x of the adult.

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4
Q

Pressure change in heart

A

Right ventricular pressure halves while left ventricular pressure rises.

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5
Q

Heart muscle development before birth

A

Growth is hyperplasia, so number of cardiac cells increase.

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6
Q

Heart muscle development after birth

A

Growth shifts to entirely hypertrophic.

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7
Q

When does energy requirement increase stop in man?

A

At 18 years of age.

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8
Q

Myocardium in a 2 month old foetus

A

Lots of glycogen, no striation and many cells undergoing mitosis with immature RBCs in a nucleus.

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9
Q

Birth vs adult heart

A

Very similar other than cells are smaller in the baby, adult has more mitochondria but less mitochondrial DNA.

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10
Q

Foetal cardiomyocytes

A

Stop cell division at or shortly after birth.

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11
Q

What is phosphorylated in mitosis?

A

Histone H3.

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12
Q

Postnatal cardiomyocytes

A

Bi-nucleated and mature.

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13
Q

Ventricle differences in binucleation

A

Left ventricle peaks at around day 125 at 65% and then tails off while right ventricle peaks at day 140 at 70%.

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14
Q

What regulates cardiomyocyte proliferation in foetal life?

A

Both haemodynamic forces and circulating factors.

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15
Q

Factors that stimulate progression of cardiomyocyte proliferation

A

Increased arterial load, angiotensin II, cortisol and insulin-like growth factor-1, these all increase blood pressure.

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16
Q

Factors that suppress progression of cardiomyocyte proliferation

A

T3, reduced systolic load and ANP.

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17
Q

What do reduced systolic load and ANP lead to?

A

Decrease in blood pressure.

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18
Q

Effect of cyclin D1

A

Drives cell division.

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19
Q

Effect of p21

A

It blocks cyclin dependent kinases so inhibits cell division.

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20
Q

When does TSH peak?

A

After birth.

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21
Q

What does TSH do?

A

Up to birth it induces T3 and T4 production that are important for tissue maturation and driving change in cell divisions in the heart.

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22
Q

Critical window pre-birth

A

Where proliferative, hypertrophic and apoptotic responses determine cell population for ongoing hypertrophy.

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23
Q

What happens in critical window that reduces number of cells?

A

Poor nutrition, hypoxia and environmental stress, these limit number of cells and therefore limit population that can support myocardial growth trajectory.

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24
Q

What happens if maturity happens early?

A

A premature T3 surge so heart may be hypocellular with increased hypertrophy required to produce sufficient cardiac muscle strength, can lead to cardiac failure later in life.

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25
Q

Changes required for lung function at birth

A

Low surface tension, fluid removal, surface for gaseous exchange needed, need blood supply and protection from infective agents and oxygen radicals.

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26
Q

5 lung stages

A

Embryonic, pseudoglandular, canalicular, saccular and alveolar.

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27
Q

When does surfactant appear?

A

Week 25.

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28
Q

2 major development steps in the lungs

A

Organogenesis and differentiation.

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29
Q

Lung organogenesis

A

Up to week 16, includes development of bronchi, bronchioles and terminal bronchioles, with formation of major airways, bronchial trees and portions of respiratory parenchyma and birth of acinus.

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30
Q

Lung differentiation

A

Week 16 onwards, includes development of respiratory bronchioles, alveolar ducts and sacs, formation of the air-blood barrier, surfactant, lung periphery, air space expansion and secondary septation.

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31
Q

Earliest week that can survive birth

A

Week 24 as surfactant is present.

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32
Q

What does secondary septation form?

A

Alveolar sacs.

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33
Q

Saccular lung

A

24 weeks to 38 weeks, terminal air sacs form along with a thick septate and blood vessels develop.

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34
Q

Alveolar lung

A

Week 38 onwards, primitive then definitive alveoli form, loss of inter-septal connective tissue with 15% alveoli present at birth.

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35
Q

When do lungs mature?

A

7 years old.

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36
Q

What lung cells form first?

A

Type II.

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37
Q

Type II cells

A

Surfactant producing, as numerous as Type I but only cover 5% of surface.

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38
Q

Type I cells

A

Squamous epithelium cell that make up alveolar walls.

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39
Q

Type II cell function

A

Produce lamellar bodies that are secreted out, expand and sit on surface of a fine layer of fluid lining cells.

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40
Q

Pulmonary surfactant general structure

A

90% lipid, 10% protein.

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41
Q

Main lipid in surfactant

A

DPPC, makes up 40-70% of surfactant lipid at birth and is amphoteric.

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42
Q

Proteins in surfactant

A

SP-A (5%), SP-B (0.7%), SP-C (0.8%), SP-D (0.5%)and plasma proteins (3%).

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43
Q

Innate immunity proteins in surfactant

A

SP-A and SP-D.

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44
Q

Stabiliser proteins in surfactant

A

SP-B and SP-C.

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45
Q

Surface tension of air and water at 37C

A

70.4mN/m.

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46
Q

Surface tension of air, water and DPPC at 37C

A

5mN/m.

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47
Q

How much can surfactant lower tension?

A

5-10 fold.

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48
Q

What does high unsaturated DPPC proportion allow?

A

Semi-rigid packed surface to occur which becomes more dense on compression.

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49
Q

What does DPPC do?

A

It breaks up semi-crystalline structure of water molecules by sitting choline into it.

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50
Q

Laplace’s Law

A

Closing pressure is inversely proportional to alveolar size, no surfactant present will collapse bubble, if it is present as it closers further and further it inhibits collapse.

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51
Q

Biophysical properties of surfactant

A

Support lung expansion, prevent pulmonary oedema (balancing hydrostatic force) stabilise small airway structure and improves mucociliary function.

52
Q

Immunological properties of surfactant

A

Phospholipids inhibit proliferation, Ig production, lymphocyte cytotoxicity and cytokine (TNF, IL-1 and IL-6 release) from macrophages.

53
Q

SP-B and SP-C

A

Hydrophobic proteins that interact with lipids to enhance biophysical stability of surfactant and regulate response to compression and expansion.

54
Q

What does loss of SP-B and SP-C cause?

A

Unstable surfactant layers and lethal pulmonary distress.

55
Q

SP-B function

A

Provides mechanical stability to compressed films at aqueous interior, retained in rapid breathing.

56
Q

SP-C function

A

Facilitates compression-driven folding of surfactant interfacial films upon breathing.

57
Q

SP-A and SP-D

A

Hydrophilic surfactant collectins involved in innate immunity, they opsonise bacteria binding to sugar surfaces and enhance phagocytosis.

58
Q

SP-A and SP-D structure

A

An N-terminal non-collagenous domain, collagenous central, alpha helical coiled coil and a CRD.

59
Q

Bacteria opsonised by SP-A and SP-D

A

Haemophilus influenzae, P. aeruginosa and S. aureus.

60
Q

Where is SP-D expressed?

A

In lungs and other mucus membranes.

61
Q

When does surfactant spike?

A

Final fifth of gestation.

62
Q

What increases expression before birth?

A

SP-A, SP-B and SP-D.

63
Q

Pre-natal drivers of surfactant synthesis

A

Glucocorticoids increasing CCT and FAS in foetal lung, thyroid hormone and stress.

64
Q

Effect of CCT

A

Activates choline in formation of phosphatidylcholine.

65
Q

Effect of FAS

A

Needed for addition of Acetyl CoA in fatty acid chain elongation and steroids thought to stimulate mesenchymal cells to produce FGF7 altering activity of Type II epithelial cells.

66
Q

Post-natal drivers of surfactant synthesis

A

Labour and breathing.

67
Q

Lung fluid

A

Self-produced, expelled into amnion.

68
Q

How much lung fluid is produced towards end of gestation?

A

5ml/kg body mass/hour.

69
Q

How is lung fluid cleared?

A

Pre-birth chest movement, labour squeezes it out and post birth absorption (majority).

70
Q

Fluid filled alveolus

A

Active Cl- secretion at alveolus transfers H2O and Na+ out of interstitial fluid, into the alveoli.

71
Q

Drying alveolus

A

Active Na+ absorption at alveolus drives H2O and Cl- transfer into interstitial fluid from alveolar lumen.

72
Q

How quick does absorption occur?

A

Within 2 hours.

73
Q

Hormone changes at birth that aid absorption

A

Adrenaline triggers cAMP and expression of amiloride sensitive Na channel, thyroid hormones and glucocorticoids act synergistically to increase Na pumps and reduce Cl pumps.

74
Q

Postnatal changes that aid absorption

A

High O2 tensions in lung inducing Redox sensitive nuclear factor NF-kB that maintains high expression of amiloride sensitive Na channel.

75
Q

Lumen channel

A

Chloride ion channel pre-natally is replaced by a Na+ channel and a basal surface 2Cl-/Na+/K+ co-transporter is lost, replaced by with a Na+/K+ ATPase that puts 3Na+ for 2 K+ into interstitial fluid.

76
Q

Amiloride channel

A

Opens so Na+ channels brought through from alveolar space to the interstitial space, dragging Cl- and water.

77
Q

Change in pulmonary resistance at birth

A

Change from low blood volume high resistance vascular bed to high blood volume low resistance vascular bed in 60-120 seconds.

78
Q

What reduces pulmonary resistance rapidly?

A

Fluid loss, ventilation & lung expansion, increase in eNOS activity driven partly by increased blood flow and oxygen levels, and local expression of PGI2 in lung endothelium.

79
Q

Pulmonary blood flow increase at birth

A

21% to 50%.

80
Q

Slower causes of reduced pulmonary resistance

A

Gradual post-natal loss of smooth muscle in wall of pulmonary vessels.

81
Q

What does NO do?

A

Increases vascular smooth muscle relaxation surrounding arterioles.

82
Q

What do PGI2 and PGE2 do?

A

Cause arterial small muscle relaxation.

83
Q

What does NO do to cause vasodilation?

A

NO is produced by L-Arg which diffuses into smooth muscle cell activating guanylate cyclase producing cGMP which is vasodilatory.

84
Q

What does PGI2 do to cause vasodilation?

A

It diffuses into smooth muscle cell and activates adenylate cyclase producing cAMP which is vasodilatory.

85
Q

Effect of NO and Prostacyclin signalling pathways in vascular tone regulation

A

It activates PKG and PKA which phosphates and inactivates MLCK which is required for actin-myosin interactions which doesn’t occur, so smooth muscle relaxes.

86
Q

What happens to smooth muscle walls post-natally?

A

They reduce with cells undergoing apoptosis.

87
Q

PPHN

A

Failure to achieve decrease in pulmonary vascular resistance with an altered pulmonary vascular tone, reactivity and/or structure causing severe hypoxaemia due to right to left blood shunting by DA and FO.

88
Q

Effects of PPHN

A

Common in infants requiring neonatal intensive care, 1-2 per 1000 births with a 10-20% mortality rate, long term sees pulmonary arteries appear thick walled and fail to relax normally upon vasodilator exposure with capillaries remodel to form protective muscles.

89
Q

Causes of Hyaline Disease

A

Caused by prematurity with development insufficiency of surfactant production and structural immaturity of the lungs OR a genetic problem in production of surfactant associated proteins/lipid metabolism.

90
Q

Incidence of Hyaline Disease

A

1% of newborns at 40 weeks, 25% at 30 weeks and 50% at 28 weeks, it is the leading cause of death in preterm infants.

91
Q

What happens in Hyaline Disease?

A

Smaller alveoli don’t expand, so they remain collapsed and causes thick-looking walls with a loss of a large surface area.

92
Q

Alveoli number and size at birth

A

15-30% of adult alveoli or 1 million.

93
Q

Alveoli formation rate

A

Maximal at birth, which gradually decreases and then stops at 18 months.

94
Q

When does septation begin?

A

30 weeks.

95
Q

Surfactant composition before birth

A

Very low phosphatidylinositol and SA proteins only seen in late gestation such as SP-B forming at 34 weeks.

96
Q

What causes hyaline membrane formation?

A

Altered surfactant composition.

97
Q

Hyaline membrane

A

Raises alveolar surface tension, pulling out proteins, sit in fluid with staining as pink.

98
Q

Effect of birth on haemoglobin

A

Shift of subunits used.

99
Q

Haemoglobin structure

A

It is a heterotetramer of 2 chromosome 11 beta-like subunits and 2 chromosome 16 alpha-like subunits.

100
Q

What haemoglobin genes in chromosome 11?

A

1 epsilon, 2 gamma, 1 delta and 1beta.

101
Q

What haemoglobin genes in chromosome 16?

A

2 zeta and 2 alpha.

102
Q

Haemoglobins present in embryo

A

Gower 1 (zeta 2, epsilon 2), Gower 2 (alpha 2, epsilon 2), Hb Portland 1 (zeta 2, gamma 2) and Hb Portland 2 (zeta 2, beta 2).

103
Q

Haemoglobins present in foetus

A

Hb F (alpha 2, delta 2, 85% of foetal Hb) and Hb A (alpha 2, beta 2, 15%).

104
Q

Haemoglobins present after birth

A

Hb A (alpha 2, beta 2, >95% of Hb) and Hb 2 (alpha 2, delta 2, 1.5-3.5%).

105
Q

When does beta subunit overtake gamma subunit?

A

6 weeks after birth.

106
Q

Deoxy Hb

A

Inter-subunit salt bridges that resist movement, stabilising it in the tense state with low O2 affinity.

107
Q

Oxy Hb

A

Salt bridges broken with rotation of dimers and changed quaternary structure giving it a relaxed form with high O2 affinity.

108
Q

Subunits held in a salt bridge

A

Alpha 1 and beta 2, alpha 2 and beta 1 and alpha 1 and alpha 2.

109
Q

What do allosteric regulators do?

A

They bind Hb altering its affinity for oxygen.

110
Q

Examples of allosteric regulators

A

2,3-Bisphosphoglycerate (formed in glucose breakdown) and protons (captured when CO2 and lactic acid made).

111
Q

Effect of pH (and pCO2) on curve

A

It shifts it to the right as it increases, lowering Hb affinity.

112
Q

What can bind oxygen in the tense state?

A

Alpha.

113
Q

When can beta bind oxygen?

A

Only in relaxed state.

114
Q

2,3-BPG

A

Can bind to positive charged pocket between beta 1 and 2 subunits, forcing Hb toward the tense stage so will release more O2 in the presence of it.

115
Q

Effect of high CO2

A

Lowers pH so protons bind to beta 2 subunit, forming a charge bridge with Asp94 of the alpha 1 subunit causing increased tense stability .

116
Q

What effect do regulators have overall?

A

They have little effect on intake in lungs but a large change in oxygen release into tissues.

117
Q

Why is foetal haemoglobin needed?

A

Mother sends relatively deoxygenated blood into the placenta, so if adult Hb was used then it would not pick up oxygen, so uses high affinity foetal Hb.

118
Q

How does foetal Hb have higher affinity?

A

Beta subunit replaced with gamma for foetus.

119
Q

How do beta and gamma subunits differ?

A

Gamma has Ser143 instead of His143, this means that 2,3-BPG has no effect keeping curve to the left.

120
Q

Blood cell count in foetus

A

20% more RBCs in foetus.

121
Q

What vascular signals does embryo respond to?

A

CO2 and H+.

122
Q

Placental and foetal partial pressures

A

Placenta has 23ppO2 and foetal tissue is at 18ppO2, so delivers 2x as much oxygen as adult.

123
Q

Why do we change from foetal to adult Hb/

A

High affinity binding is fine at low oxygen tensions, but poor at high tensions so will not deliver to post natal tissues.

124
Q

Chronic hypoxia

A

Implicated in infant sudden death syndrome due to some evidence of increased/prolonged expression of Hb F.

125
Q

Hydroxyurea

A

Can induce Hb F expression in older children, can replace some HbA aswith treatment for HbA mutations like sickle cell.

BIOL2018:Adaptive Physiology (10 decks)

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