Daisy Baker Flashcards

1
Q

What occurs in the 6-17 week period of lung development

A

Pseudoglandular - branching to form terminal bronchioles

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2
Q

What occurs in the 17-26 week period of lung development

A

Canalicular - each bronchiole divides into 2+ respiratory bronchioles

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3
Q

What occurs in the 27 week to term period of lung development

A

Saccular - respiratory bronchioles divide into 3-6 alveolar ducts which then develop terminal sacs and capillaries establish close association

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4
Q

What occurs in the term to childhood period of lung development

A

Alveoli mature with well developed epithelial-endothelial association

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5
Q

Which growth factors are required for lung development?

A
Hepatocyte nuclear factor 3beta 
Fibroblast growth factor-10 
Sonic hedgehog
Bone morphogenetic protein 4 (BMP4)
Gil proteins 
Vascular endothelial growth factor
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6
Q

What’s the function of hepatocyte nuclear factor 3beta in lung development?

A

Growth of the foregut

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7
Q

What’s the function of Gli proteins in lung development?

A

Branching of bronchioles

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8
Q

What’s the function of VEGF in lung development?

A

Angiogenesis

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9
Q

Which growth factors promote the outgrowth of new end buds in lung development?

A

Fibroblast growth factor-10, sonic hedgehog and BMP4

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10
Q

When does the majority of alveolar development occur?

A

Post term, reaching adult numbers by 4 years

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11
Q

When do type I and type II pneumocytes first develop?

A

22 weeks

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12
Q

What structural pathologies are most likely to occur <16 weeks gestation?

A

Branching irreversibly affected and potential permanent reduction in the number of alveoli

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13
Q

What structural pathologies are most likely to occur >16 weeks of gestation?

A

Issues with alveolar numbers

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14
Q

What could cause respiratory structural pathology in the foetus?

A

Extrinsic restriction
Intrinsic restriction
Malnutrition due to vitamin A deficiency
Smoking

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15
Q

What can cause extrinsic restriction of the lungs in the foetus?

A

Congenital diaphragmatic hernia (CDH), effusions, thoracic or vertebral abnormalities e.g. scoliosis

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16
Q

What could cause an intrinsic restriction of the lungs in the foetus?

A

Lung cysts due to cystic adenomatoid malformation

17
Q

How does the ionic composition of foetal lung liquid compare to amniotic fluid?

A

More sodium and chloride ions

Few potassium and bicarbonate ions, and protein

18
Q

How is lung liquid secreted into the lumen of the lungs?

A

Secondary active transport of chloride ions from interstitial fluid, followed by passive transport of sodium ions and water

19
Q

What does the secretion of lung liquid into the lumen do?

A

Allows for a positive pressure of 1cmH2O

20
Q

When does reabsorption of lung liquid occur?

A

During labour and delivery, catelochamines are released reducing secretion and stimulating reabsorption. This involves active transport of sodium into the interstitium where it is followed by chloride ions and water. Exposure to postnatal oxygen also increases sodium transport across the pulmonary epithelium, where lung liquid is reabsorbed by the lymphatic system.

21
Q

Give examples of lung liquid pathologies

A

Oligohydramnios due to early rupture of the amniotic sac or kidney abnormalities
Foetal breathing abnormalities due to NMD, phrenic nerve agenesis or CDH
Delivery without labour due to an elective Caesarean section - causes transient tachypnoea in the newborn (TTN)

22
Q

Define oligohydramnios

A

Low amniotic fluid levels

23
Q

Which cell is surfactant produced by?

A

Surfactant phosphatidylcholine (PC) is produced in the endoplasmic reticulum of type II pneumocytes and stored in lamellar bodies

24
Q

What is the function of surfactant?

A

Prevents atelectasis by reducing the surface tension of alveoli, therefore reducing the work required to breathe

25
Q

What percentage of surfactant is recycled by type II pneumocytes?

A

90%

26
Q

What are the major components of surfactant and what are their functions?

A

DPPC (50%)
PG - phosphatidylglycerol (7%)
Proteins SP-A, SP-B, SP-C and SP-D
Other lipids such as cholesterol

27
Q

What is the function of DPPC (dipalmitoylphosphatidylcholine) in surfactant?

A

Reduces alveolar surface tension

28
Q

What is the function of PG (phosphatidylglycerol) in surfactant?

A

Promotes the spreading of surfactant throughout the lungs

29
Q

What is the protein SP-A essential for in the function of surfactant?

A

Determining the structure of tubular myelin, stability and spreading of phospholipids and the negative feedback loop

30
Q

What is SP-B required for in the function of surfactant?

A

Formation of tubular myelin, spreading, increasing lung compliance and protecting the surfactant film from inactivation by serum proteins

31
Q

What is the role of SP-C in surfactant?

A

Significantly enhances adsorption and spreading on phospholipids

32
Q

What stimulates the production and maturation of surfactant?

A

Glucocorticoids e.g. dexamethasone enhance beta2-adrenoceptor gene expression leading to increased surfactant secretion

Thyroid hormone T3 crosses the placenta and is converted to T4 to increase surfactant production

TRH also increases phospholipid independent of T3/4

33
Q

How does gestational diabetes affect surfactant maturation in the foetus?

A

Increased sugar levels in the mother which aren’t dealt with by an appropriate increase in her insulin crosses the placenta into the foetus where it over produces insulin

Insulin delays maturation of type II pneumocytes, decreases % saturated PC and delays PG production, overall delaying lung maturation and the production of surfactant

34
Q

What are the 2 main causes of surfactant deficiency?

A

Prematurity and genetic SP deficiencies

35
Q

Where is the respiratory centre for the regulation of breathing located?

A

Ventrolateral brainstem

36
Q

How does the control of breathing in hypoxia differ between infants and term/preterm babies?

A

When exposed to hypoxic gases, infants will keep increasing their breathing efforts until reaching a plateau

However, term and preterm babies will increase their breathing efforts only temporarily (for 1-2 minutes) before exhausting and paradoxically decreasing their breathing efforts, sometimes to a point of apnoea in preterm infants

37
Q

What happens to foetal lung liquid at birth?

A

Thyroid hormones and corticosteroids promote the synthesis of sodium channels, beta adrenoceptors and sodium-potassium ion pumps

A surge of adrenaline in response to the stress of birth acts on b-adrenoceptors to increase adenylate cyclase activity and increase levels of cAMP

This leads to incorporation of pre-formed sodium channels into the apical membrane and adsorption of the foetal lung liquid from the lung lumen and into the lymphatic system