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LSS 1 - Thorax anatomy, Respiratory and Circulatory system > RS Lecture 15 and 16 - Lung Development and Pulmonary Circulation > Flashcards

RS Lecture 15 and 16 - Lung Development and Pulmonary Circulation Flashcards

1
Q

What are the 5 stages in the timeline of lung development?

A

Embryonic, pseudoglandular, canalicular, saccular/alveolar, postnatal

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2
Q

What is the embryonic phase of lung development?

A

Lasts 0-7wks -> lung buds form, main bronchi form

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3
Q

What is the pseudoglandular phase of lung development?

A

Lasts 5-7wks -> conducting airways, bronchi and bronchioli are formed

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4
Q

What is the canalicular phase of lung development?

A

Lasts 16-27 weeks -> respiratory airways and blood-gas barrier forms

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5
Q

What is the saccular/alveolar phase of lung development?

A

28-40wks -> alveoli appear

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6
Q

What is the postnatal phase?

A

Occurs until adolescence -> alveoli multiply and enlarge in size with chest cavity

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7
Q

In which lung development phases does vasculogenesis, branching and morphogenesis occur?

A

Embryonic and pseudoglandular

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8
Q

In which lung development phases does the blood gas barrier form?

A

Canalicular

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9
Q

In which lung development phases does alveo and angiogenesis occur?

A

Saccular/Alveolar

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10
Q

When does the majority of the complex airway and circulatory system grow?

A

During early foetal life -> alveoli appear before birth and continue to grow in early childhood

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11
Q

What is Scimitar syndrome?

A

Anomalous pulm venous drainage of right lung to the IVC, unusually close to the junction of the right atrium

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12
Q

What can scimitar syndrome lead to?

A

Associated right lung and right pulmonary artery hypoplasia; dextrocardia; anomalous systemic arterial supply (which can form heart disease)

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13
Q

What happens during embryogenesis?

A

Much of the airway is let down -> bifurcation occurs, and by 7wks you have the correct lobes of the lungs

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14
Q

What happens in the pseudoglandular phase?

A

Branching morphogenesis of airways into mesenchyme; preacinar airways all present by 17 weeks; development of cartilage, smooth muscle and glands continues into canalicular phase

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15
Q

What are bronchial cartilage and how do they change with age?

A

Incomplete rings posteiorly, with irregular plates -> calcify with age

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16
Q

How can bronchial cartilage become malacic?

A

Generalised: laryngotracheomalcia. Localised: malacic segment

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17
Q

What is laryngomalacia?

A

Floppy/collapsible larynx -> come together to close when swallowing but in laryngomalacia, the airway collapses on itself

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18
Q

How is branching morphogenesis driven?

A

Lung buds consistent i appearance during airway formation (5-17wks) -> epithelial cells at tips of buds (highly proliferative multipotent progenitor cells), so cells behind the tip divide and differentiate into the various cell types -> communication between epithelial cells in distal branching lung buds and surrounding mesenchyme

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19
Q

How is branching morphogenesis controlled?

A

Epithelial-mesenchymal interaction is essential for branching morphogenesis -> genetic and transcription factors are involved in early bud formation; after bifurcation a variety of growth factors are important

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20
Q

What are the growth factors in lung development?

A

Inductive: FGF (brnching morphogenesis), EGF (epithelial proliferation and differentiation). Inhibitory: TGF beta (matrix synthesis, surfactant production, inhibits proliferation of epithelium and blood vessels); Retinoic acid (inhibits branching)

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21
Q

What problems can occur when the pulmonary growth factors are not properly coordinated?

A

Primary ciliary dyskinesia

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22
Q

When does a circulation present in the foetus?

A

At 5 weeks gestation

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23
Q

What can go wrong during angio/vasculogenesis?

A

Congenital thoracic malformations

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24
Q

What is the prevalence of cystic pulmonary airway malformations?

A

1 per 8300-35000 -> diagnosed (mostly) on antenatal US screening

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25
Q

What is the pathogenesis of cystic pulmonary airway malformation?

A

Defect in pulmonary mesenchyma, abnormal differentiation 5-7th week; normal blood supply but can be associated with sequestration -> DOESN’T affect the whole lung

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26
Q

What are the signs of type 2 CPAM and what is the histology?

A

Multiple small cysts, may be associated with renal agenesis, CV defects, diaphragmatic hernia and syryngomyelia. Histology: bronchiolar epithelium with overgrowth, separated by alveolar tissue which was underdeveloped

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27
Q

What is congenital lobar emphysema/congenital large hyperlucent lobe?

A

Progressive lobar expansion -> underlying cause: weak cartilage, extrinsic compression, one way valve effect and alveoli expand

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28
Q

What is the prevalence of CLHL?

A

More common in LUL > RML > RUL; in males > females; CHD association

29
Q

What is intralobar sequestration?

A

75% of pulmonary sequestrations; abnormal segment shares visceral pleural covering of lung with aortic blood supply and with no communication to bronchial tree -> lower lobe predominance

30
Q

What can cause intralobar sequestration?

A

Chronic bronchial obstruction, chronic postobstructive pneumonia

31
Q

What are the types of lung growth anomalies?

A

Agenesis (complete absence of lung and vessel). Aplasia (blind ending bronchus, no lung/vessel). Hypoplasia (bronchus and rudimentary lung present, all elements reduced in size and number)

32
Q

What are the symptoms of agenesis of lung growth?

A

Caused by abnormal flow in 4th week -> associated with other pathology; causes mediastinal shift towards opaque hemithorax

33
Q

What is the cause of hypoplasia of the lung?

A

It is common (usually secondary) -> main cause is lack of space due to intra/extrathoracic complications like: Hernia, chest wall pathology, oligohydramnios, lymphatic or cardiac mass OR lack of growth -> congenital thoracic malformation

34
Q

How do the endothelial cells differentiate into blood vessels in the lungs?

A

VEGF is secreted by epithelial cells and stimulates endothelial differentiation, which occurs around the lung bud in the mesenchyme, coalescing to form capillaries (vasculogenesis); airways act as structural template

35
Q

What are some growth factors that control early blood vessel growth?

A

VEGF (prod: epithelial cells throughout gestation). Flk-1 (deficiency results in no blood vessel development). IGF/IGFR (from 4wks prevents capillary development). eNOS (stimulates proliferation and tube formation). Angiopoietin (important in wall differentiation)

36
Q

What happens when a new bifurcation occurs to the blood supply?

A

Newly formed endothelial tubes are added and the arteries and veins supplying these capillaries get longer

37
Q

What should be present at the end of the pseudoglandular period?

A

All airways and blood vessels at levels of terminal bronchiolus are present -> appearance of lung changes as it reaches canalicular stage

38
Q

What occurs during the canalicular stage?

A

Airspaces at periphery enlarge; thinning of epithelium by underlying capillaries allows gas exchange; epithelial differentiation into TI/II epithelial cells; surfactant first detectable at 24/25 weeks; blood gas barrier required for post-natal life

39
Q

When do alveoli appear?

A

28-40 weeks appear and multiply up to 3yrs

40
Q

How are the alveolar walls formed?

A

Saccule wall (epithelium on both sides with 2x capillary network, myofibroblast and elastin fibres along wall -> secondary septa develop from wall led by elastin produced by myofibroblast, capillary lines both sides with matrix in between -> capillaries have coalesced to form one sheet alveolar wall, thinner and longer with less matrix, with muscle and elastin still at the tip

41
Q

What is a future problem that could occur in preterm birth?

A

Becoming more common and effects can’t be ameliorated by surfactant; thought that maybe they could be a future risk group of COPD

42
Q

How can preterm births catch-up growth?

A

May be scope for airway catch-up growth under some circumstances (when baby is appropriate gestational age - so weighs what they are meant to weigh), alveolar growth continues much longer than we thought, may be scope for alveolar recovery after preterm birth

43
Q

What are the lungs like at birth in humans?

A

Volume small and related to body weight; all airways present and differentiated, 33-50% alveoli allow for normal gas exchange with blood-gas barrier same as in adults; most arteries and veins present

44
Q

What changes occur at birth in blood vessels?

A

Decrease in pulmonary vascular resistance and 10x rise in pulmonary blood flow -> arterial lumen increases and wall thins rapidly, change in cell shape and cytoskeletal organisation not loss of cells -> once thinning occurs, arteries grow and maintain a relatively thin wall -> LOW pressure and LOW resistance pulm vascular system

45
Q

What are the possible mechanisms to increase flow after birth?

A

Expansion of alveoli dilates arteries (direct physical effect); expansion stimulates release of vasodilator agents; inhibition of vasoconstrictors present during fetal like; direct effect of O2 on smooth muscle cells

46
Q

How do the airways grow in childhood and adolescence?

A

Lung volume increases 30x; airways increase in length and width by 2-3x (symmetrically); dysanaptic growth during the early period (alveoli growing more than airways); structural elements of wall increase

47
Q

How do the alveoli grow in childhood and adolescence?

A

Alveoli increase in no. up to 2-3yrs (maybe adolescence), with adult alveolar no.=300-600million; alveoli increase in size and complexity to increase SA until body growth complete after adolescence (20x); arteries, veins and capillaries increase alongside the alveoli (35x)

48
Q

How is the pulmonary circulation different from the systemic one?

A

Systemic arteries are a lot thicker, with a smaller lumen; left ventricle has thicker walls as it needs to pump a longer distance -> right side of the heart, is thin because it doesn’t need to pump far or against gravity; systemic=high pressure circuit

49
Q

How does the circuit pressure differ between systemic and pulmonary circuits?

A
50
Q

How does these variables differ between systemic and pulmonary circuits?

A
51
Q

What are the 3 functions of the pulmonary circulation?

A

1) Gas exchange (O2/CO2). 2) Metabolism of vasoactive substances (ACE -> AngII [vasoconstrictor], Bradykinin). 3) Filtration of blood -> pulm. circulation filters emboli before the systemic arteries

52
Q

What is an embolus?

A

Mass within the circulation capable of causing obstruction

53
Q

What is an embolism?

A

Event characterised by obstruction of major artery

54
Q

How does the pulmonary circulation filter the blood?

A

x

55
Q

What are the pulmonary shunts and what are they used for?

A

Circumstances associated with bypassing the respiratory exchange surface -> Save the blood passing through the pulmonary circulation

56
Q

What are some examples of pulmonary shunts?

A

Bronchial circulation (LA, LV, Aorta, PA, BA, BV, PV, LA then RHS -> pass through LHS of heart 2x). Foetal circulation (foramen ovalae, ductus arteriosus). Congenital defect (septal defect, which mixes arterial and venous blood)

57
Q

What should and does happen to the pulmonary vascular resistance when Cardiac output is increased?

A

Pulm circulation is low resistance, high capacity circuit at Q of 5L/min -> instead of increasing the pressure, the blood vessels stretch so there isn’t a change is MAP

58
Q

How does perfusion of the lungs change with increasing CO?

A

Pulmonary arteries are more compliant that systemic arteries -> hence more perfusion when greater CO

59
Q

What happens to vascular resistance when ventilation increases?

A

Inspiration compresses alveolar vessels and expiration compresses extra-alveolar vessels

60
Q

What happens to vascular resistance when hypoxaemia occurs?

A

Systemic vascular response is vasodilation and pulmonary vascular response is vasoconstriction

61
Q

When is the hypoxic response in pulmonary circulation beneficial?

A

During foetal development -> blood follows path of least resistance, high-resistance pulmonary circuit means increased flow through shunts, with first breath increasing alveolar PO2, dilating pulmonary vessels

62
Q

When is the hypoxic response in pulmonary circulation detrimental?

A

Chronic obstructive lung disease -> Reduced alveolar ventilation and air trapping, so increases resistance in pulmonary circuit > leading to pulmonary hypertension, right ventricular hypertrophy and congestive heart failure

63
Q

How does the pulmonary fluid keep balanced?

A

Plasma hydrostatic is the main force in the vessel pushing fluid into the interstitial space; interstitial hydrostatic pressure is basically 0, as no fluid builds up in a healthy individual; Plasma oncotic is a main sucking force of proteins in the blood, to move water into the capillary; Interstitial oncotic is a sucking force of proteins in the interstitial space, to move water into the interstitium -> net movement out of the capillary which is easily controlled by the lymphatic system

64
Q

What happens if the lymphatic drainage in the lungs fail?

A

Fluid accumulates, causing oedema (can also be due to production exceeding maximum rate of clearance)

65
Q

What does a mitral valve stenosis cause to the fluid balance in the lungs?

A

Increased plasma hydrostatic pressure, more fluid forced into interstitium -> lymph clearance is exceeded, so oedema occurs

66
Q

What does hypoproteinaemia cause to the fluid balance in the lungs?

A

Plasma oncotic pressure reduced, less fluid drawn into capillary, so fluid accumulates in interstitium -> lymph clearance exceeded, so oedema

67
Q

What does an infection cause to the fluid balance in the lungs?

A

Increases interstitial oncotic pressure, more fluid drawn out of capillaries , large net fluid movement out of capillary -> so lymphatic clearance exceeded, so oedema

68
Q

What does cancer cause to the fluid balance in the lungs?

A

Blocked lymph vessels -> oedema

LSS 1 - Thorax anatomy, Respiratory and Circulatory system (27 decks)

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