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14 Cards in this Set
- Front
- Back
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Lung Development
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Occurs in five periods (Embryonic, Pseudoglandular, Canalicular, Saccular, Alveolar). Initial development includes development of lung bud from distal end of respiratory diverticulum during week 4. Lung bud divides into two bronchial buds that branch off into bronchi |
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Embryonic period of lung development (weeks 4-7) |
Lung bud -> trachea -> mainstream bronchi -> secondary (lobar) bronchi -> tertiary (segmental) bronchi. Errors at this stage can lead to TE fistula |
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Pseudo glandular period of lung development (weeks 5-16) |
Endodermal tubules _> terminal bronchioles. Surrounded by modest capillary network. Respiration impossible, incompatible with life |
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Canalicular period of lung development (weeks 16-26) |
Terminal bronchioles -> respiratory bronchioles -> alveolar ducts. Surrounded by prominent capillary network. Airways increase in diameter. Respiration is capable at 25 weeks. |
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Saccular period of lung development (weeks 26-birth) |
Alveolar ducts -> terminal sacs. Terminal sacs separated by primary septa. Pneumocytes develop. |
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Alveolar period of lung development (week 32-8 years)
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Terminal sacs -> adult alveoli (due to secondary separation). In utero, "breathing" occurs via aspiration and expulsion of amniotic fluid causing increased vascular resistance through gestation. At birth, fluid gets replaced with air causing a decrease in pulmonary vascular resistance. At birth: 20-70 million alveoli. By 8 years: 300-400 million alveoli |
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Congenital lung malformations |
Pulmonary hypoplasia, bronchogenic cysts |
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Pulmonary hypoplasia |
Poorly developed bronchial tree with abnormal histology usually involving right lung. Associated with congenital diaphragmatic hernia, bilateral rena genesis (Potter sequence [syndrome]) |
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Bronchogenic cysts
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Caused by abnormal budding of the foregut and dilation of terminal or large bronchi. Discrete, round, sharply defined and air-filled densities on CXR. Drain poorly and cause chronic infecitons |
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Pneumocytes |
Type I cells, Type II cells, Club cells. Alveoli have increased tendency to collapse on expiration as radius decreases (law of Laplace). Pulmonary surfactant is a complex mix of lecithins, the most important of which is dipalmitoylphosphatidylcholine. Surfactant synthesis begins around week 26 of gestation, but mature levels are not achieved until around week 35 |
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Type I pneumocytes |
97% of alveolar surfaces. Line the alveoli. Squamous; thin for optimal gas diffusion. |
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Type II pneumocytes |
Secrete pulmonary surfactant causing decreased alveolar surface tension and prevention alveolar collapse, decreasing lung recoil and increasing compliance. Cuboidal and clustered. Also serve as precursors to type I cells and other type II cells. Type II cells proliferate during lung damage. |
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Club cells |
conciliated; low-columnar/cuboidal with secretory granules. Secrete component of surfactant; degrade toxins; act as reserve cells |
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Neonatal respiratory distress syndrome |
Surfactant deficiency causing increased surface tension, causing alveolar collapse ("ground-glass" appearance on lung fields). Screening tests for fetal lung maturity: lecithin-sphingomyelin (L/S) ratio in amniotic fluid (>2 is healthy; <1.5 predictive of NRDS), foam stability index test, surfactant-albumin ratio. Persistently low O2 tension leads to a risk of PDA. Risk factors: prematurity, maternal diabetes (due to increased fetal insulin), C-section delivery (decreased release of fetal glucocorticoids). Complications: metabolic acidosis, PDA, necrotizing enterocolitis. Treatment: maternal steroids before birth; artificial surfactant for infant. Therapeutic supplemental O2 can result in Retinopathy of prematurity, Intraventricular hemorrhage, Bronchopulmonary dysplasia (RIB) |
