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Growth > Cardiorespiratory adaption at birth > Flashcards

Cardiorespiratory adaption at birth Flashcards

1
Q

what are the 5 phases of lung development

A
  • embryonic
  • pseudoglandular
  • canalicular
  • saccular
  • alveolar
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2
Q

what happens during the embryonic phase of lung development

A

The first thing that occurs is the embryonic growth of the lung buds from the foregut and this divides into the right and left bronchioles

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3
Q

what happens during the psuedoglandular phase of lung development

A

At about 6 weeks the lung buds are starting to branch to form terminal bronchioles and by around 16/17 weeks this branching has been completed

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4
Q

what happens during the canalicular phase of lung development

A

After 16/17 weeks there is no more branching rather there is development of the branches and this is called the canalicular phase where each bronchiole divides into 2+ respiratory bronchioles this occurs from 17-26 weeks.

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5
Q

what happens during the saccular phase of lung development

A

the respiratory bronchioles start to divide into the alveolar ducts and sacs. Capillaries also form around these

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6
Q

what happens during the alveolar phase of lung development

A 
By term alveoli are more established and these further mature into childhood. The adult no. of alveoli isn't reached until about 5yrs of age.
Surfactant production (and volume) starts at around 25 weeks and increases up to and after delivery.
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7
Q

after birth, there is simultaneous growth of vascular elements, the tubular airway elements and growth of the different cell types of the lung.
what growth factors are required for this

A

Hepatocyte nuclear factor 3β required for the lung buds to develop off the foregut
Fibroblast growth factor-10, sonic hedgehog, bone morphogenetic protein (BMP4) are all required for the outgrowth for new end buds
Gli proteins are required for the branching of the lungs
Vascular endothelial growth factor (VEGF) for angiogenesis around the alveol

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8
Q

how do alveoli develop

A
  • 24 weeks, saccules of alveoli start to develop. VEGF stimulates capillary development around saccules.
  • 32 weeks, shallow indentations in alveoli
  • post term, grow in number, by age 4/5 reach adult # of alveoli.
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9
Q

how does the tie of onset of a problem affect lung development

A

if insult occurs before 16 weeks, the branching is irreversibly affected
SO potential permanent reduction in number of alveoli.
before 16 weeks, branching would have already taken place so alveolar numbers and function affected

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10
Q

what is extrinsic restriction of the lung

A

outside factors that may squash and prevent the lung from developing

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11
Q

what is congenital diaphragmatic hernia (CGH)

A

a defect in the diaphragm where gut contents herniate up to the thorax. Usually occurring on left side and this pushes thoracic contents to the contralateral side. Squashing both aspects of the lung.

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12
Q

how may effusions affect lung development

A

fluid developing around the lung, tends to be bilateral. More of a problem later in gestation

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13
Q

what may be an intrinsic factor that affects lung development

A
  • Lung cysts (cystic adenomatoid malformation)

- Malnutrition, eg vitA

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14
Q

what does the foetal lung contain

A

lung liquid, which is produced by the foetal lung itself

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15
Q

what is the composition of lung liquid

A

unique in composition.

  • Na/K similiar to plasma concs
  • Cl much higher than plasma conc
  • HCO3- much lower
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16
Q

how is lung liquid produced

A
  1. active pumping of cl- from interstium->lumen of lung.

2. Cl- inc in lung (inc. -ve) so Na+ diffuses in. water follows.

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17
Q

what is the function of the lung liquid

A

liquid production allows for positive pressure in lung of 1cmH2O. this distending pressure keeps the lung open.
lung fluid required for lung growth but not branching; so problems with lung fluid will affect function rather than structure.

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18
Q

how does lung adapt its contents for extrauterine life

A

before birth, fluid is absorbed.
active Na pumping at the apical/luminal membrane. (into cell out of lumen)
and then secreted into interstium by Na/K transporter.
Cl- and h20 follow passively.

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19
Q

how is absorption of lung liquid stimulated

A

during labour and delivery: alrenaline release stimulates Na+ transporters at the luminal/apical membrane.
postnatal exposure to o2 further increases Na+transort

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20
Q

what is oligohydramnios

A

occurs due to early rupture/kidney abnormalities of foetus.
as there is less amniotic fluid, get inc. pressure in lungs. so lung liquid is pushed out.
makes lung hypoplastic, and vasculature develops abnormally.
baby can also end up restricted and unable to move in the uterus.

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21
Q

how may foetal breathing abnormalities cause lung liquid pathology

A

neuromuscular tone of resp. system allows foetus to have normal breathing movements.
if this tone is lost it can cause liquid to be lost from the lung as pressure is lost.

May be due to:

  • Neuromuscular disorders
  • Phrenic nerve agenesis
  • CDH (diaphragmatic hernia)
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22
Q

what is ‘delivery without labour’

A

an elective c section

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23
Q

how may delivery without labour cause lung liquid patholofies

A

means mother doesnt produce adrenaline at same concs.
baby doesnt get the signal that it should stop secreting fluid and start reabsorbing.

called Transient Tachypnoea of the Newborn

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24
Q

what cells produce surfactant

A

type 2 pneumocytes

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25
Q

what is the main component of surfactant

A

phosphaidylcholine

26
Q

where is surfactant produced

A

in endoplasmic reticulum

27
Q

where is surfactant stored

A

in the type 2 pneumocytes in structures called lamellar bodies

28
Q

where is surfactant degraded

A

degraded in alveoli and then absorbed and recycled by the alveolar cells.
90% of the PC produced by the pneumocyte is reprocessed and turns over.

29
Q

how is surfactant release regulated

A
  • ve feedback system.

- stimulation of β adrenergic receptors on the type 2 pneumocytes cause surfactant release.

30
Q

how does the number of β adrenergic receptors on the type 2 pneumocytes change during gestation

A

increases with gestation.

this allows them to be more receptive to stimuli allowing them to produce more surfactant

31
Q

what does surfactant do?

A

reduces the surface tension of lung/alveoli .’. prevents the alveoli from collapsing
-prevents atelactasis and reduces work need to breathe

32
Q

what is atelactasis

A

incomplete inflation of the lung

33
Q

How is surfactant produced and recycled

A
  1. precursors ->t2 pneunocyte. combines with cellular components, surfactant is producted in ER.
  2. stored in lamellar bodies of t2 pneumocytes
  3. lamellar bodies secreted and form into a tubular framework that lines inside of alveolus.this keeps alveolus open.
  4. Surfactant is degraded by macrophages. The broken up particles ->back to type II cell degraded further while some is recycled.
  5. Some choline fatty acids are lost while phospholipids get reused.
34
Q

which component of surfactant is most important to relieve surface tension?

A

dipalmitoyl phosphatidylcholine (DPPC)

phosphatidyl glycerol (PG) promotes spreading of surfactant

35
Q

what is the breakdown of lipids in surfactant

A 
phosphatidylcholine 80%
phosphatidyl glycerol (PG) 10%
36
Q

what are the four main proteins in surfactant

A

SP-A
SP-B
SP-C
SP-D

37
Q

where is the gene for SP-A

A

chromosome 10

38
Q

how does the production of SP-A

A

from 28 weeks, foetus begins to produce SP-A more.

if born before 28wks both quanitity& composition of surfactant will be different .’. so will its function

39
Q

what is SP-A and function

A

is a large glycoprotein.
is essential in
-Determining the structure of the tubular myelin
-The stability and spreading of the phospholipids in surfactant

40
Q

how much SP-B is in surfactant

A

1-2% of surfactant by weight

41
Q

where is the gene for SP-B located

and how may its expression be changed

A

chromosome 2.

Glucocorticoids increase its expression

42
Q

what is SP-B required for

A

is required for

  • Formation of tubular myelin
  • Spreading of phospholipids across the alveolar membrane
  • When combined with lipid mixtures, increased lung compliance
  • protects the surfactant film from inactivation by serum proteins (this is important once baby is born)
43
Q

where is gene for SP-C

A

located on chromosome 8

44
Q

what is the role of SP-C

A

enhances absorption and spreading of the phospholipids

45
Q

what is the SP-D

A

NOT STRUCTURAL function
has an immune function -
protects the surfactant from external pathogens

46
Q

where is SP-D distributed

A

expression is widely distributed in epithelial cells and its expression is increased with gestation.

47
Q

what factors are involved in the maturation of surfactant

A
  • glucocorticoids
  • thyroid hormones
  • insulin
48
Q

what is the role of glucocorticoids in maturation of surfactant?

A

increased production of glucocorticoids in gestation

dexamethasone increased expression of β2-adrenoceptor gene and thus leads to inc. surfactant production

49
Q

what is the role of thyroid hormones in maturation of surfactant

A

T4 increases surfactant production (T3 crosses placenta?) and TRH

50
Q

what is the role of insulin in maturation of surfactant

A

insulin has a -ve impact.
delays maturation of t2 pneumocytes and decreases amount of phosphatidylcholine (PC)
delays production of PG

51
Q

effect of maternal diabetes on the foetus

A

leads to poor glucose control .’. high fetal glucose. As a result it will increase insulin release and this will make the baby fat and they have delayed lung maturation.

52
Q

how does prematurity (before 23 weeks) affect the lungs ability to function outside the uterus

A

Before 23 weeks there are very few type II pneumocytes and the alveoli are very poorly formed. This is why the threshold of viability hasn’t moved beyond about 23/24 weeks

53
Q

how does prematurity (before 28 weeks) affect the lungs ability to function outside the ute

A

Before 28wks there little surfactant & surfactant produced is relatively unsaturated
SO means it is stiff and unstable and more likely to buckle on expiration.

PG also replaces PI with gestation and PG is important for the spreading of the phospholipids, so an earlier delivery means less PG.

54
Q

how does prematurity affect capillaries in the lungs

A

leaky capillary membranes so there is leakage of serum proteins in the lungs.
Also fibrin deposition.
Formation of hyaline membranes across alveolar membrane that reduces diffusion of gases into capillaries

55
Q

how does prematurity affect SP in the lungs

A

SP deficiencies
SP-B absence leads to markedly reduced PG .’.no secretion of normal surfactant and is lethal.
Luckily lung transplants are possible for some if they have reduced SP-B.
SP-C deficiency is often seen in interstitial lung disease.

56
Q

How does birth stimulate breathing of the baby

A

foetal lung is exposed to edrenaline .’. reabsoption of lung liquid
cooling during labour along with other stimuli (chemoreceptors) stimulate breathing.

57
Q

what happens to the lungs after birth

A

Air replaces fluid in the lungs within minutes after delivery

  • most fluid is reabsrbed by lymphatics (takes 1hr) and capillaries (6-24hrs)
  • removal of fluid results in a rapid fall in airway resistance and an increase in FRC
58
Q

how does the baby regulate breathing

A
  • done by the VRG and DRG and pneumotaxic areas
    These are in venterolateral brainstem and is stimulated by CO2

-

59
Q

what happens when a preterm baby is hypoxic

A

has a small ability to breathe faster but starts to hypoventilate.
This is bc:
- Have less developed respiratory centres and can’t breathe very well
- Very premature babies respond like a foetus and can go into apnoea when hypoxic during or after labour when in an incubator.
- We try stop this by giving babies caffeine so that once delivered they breathe better and do not become hypoxic or respond to hypoxia by apnoea.

60
Q

how are babies adapted to the hypoxic environment in labour/delivery

A

Newborn brains utilise non-oxidative glycolysis and utilise ketone bodies, thus allows the brain to continue to obtain energy and function up until oxygen is present again
Hypoxia also leads to redirection of blood flow in the foetus towards the vital organs like brain, heart etc.

Growth (6 decks)

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