Thus intrauterine events that occur before 16 weeks of gestation will affect the number of airways. A condition known as congenital diaphragmatic hernia is an example of a congenital lung disease. It occurs at 6 to 8 weeks of gestation and is due to failure of the pleuroperitoneal canal to close and thereby separate the chest and abdominal cavities; the presence of the abdominal contents in the lung hemithorax results in abnormal lung growth with a decrease in the number of airways and alveoli. Before the birth of an affected infant, the alveolar epithelium is composed solely of type II epithelial cells, and it is not until birth that these cells differentiate into type I epithelial cells.
Growth of the lungs is similar and relatively proportional to growth in body length and stature. The rate of development is fastest in the neonatal and preadolescent periods (≈11 years of age), and girls’ lungs mature earlier than boys’. Although the growth rate of the lung slows after adolescence, the body and lung increase in size steadily until adulthood. Improvement in lung function occurs at all stages of growth development; however, once optimal size has been attained in early adulthood (20 to 25 years of age), lung function starts to decline with age. The decrease in lung function with age, estimated at less than 1% per year, appears to begin earlier and proceed faster in individuals who smoke or are exposed to toxic environmental factors. The major physiological insufficiencies caused by aging involve ventilatory capacity and responses, especially during exercise, and they result in abnormal ventilation with normal perfusion. In addition, gas diffusion decreases with age, probably as a result of a decrease in alveolar surface area. Age-related decreases in lung function and altered structure parallel biochemical observations of increased levels of elastin within the lung, which could explain some of the functional abnormalities.
TypeIcellslackfreeradicalscavengers(i.e.,superoxidedismutase)andaresusceptibletoinjuryanddeathinducedbytoxicO2compoundsandfreeradical(i.e.,H2O2,OH− ,andO2−).Invariousinflammatorylungdiseases,typeIcellsdie,andthealveolarepitheliumtherebybecomesdenuded,withincreasedvascularpermeabilityandensuingfluidaccumulation(impairedgasexchange).TypeIIcellshavesuperoxidedismutaseandarethusmoreresistanttothetoxicoxygenradicals.TheycansurvivetoproliferateanddifferentiateintotypeIcellstorestorethenormalalveolararchitecture.ThistypeofresponseisdependentonanintactbasementmembranetosupporttheproliferationoftypeIIcellsandisanexampleof“phylogenyrecapitulatingontogeny.”Ifthebasementmembranecannotberepopulated,thenthebody’srecourseforrepairiscollagendepositionandscarformation,whichisnotconducivetogas 1.
The lungs demonstrate anatomical and physiological unity; that is, each unit (bronchopulmonary segment) is structurally identical and functions just like every other unit.
2.
The upper airways (nose, sinuses, pharynx) condition inspired air for temperature, humidity, and atmospheric pressure, and they control, via the epiglottis, the flow of air into the lungs and food/fluids into the esophagus.
3.
Components of the lower airways (trachea, bronchi, bronchioles) are considered conducting airways in which air is transported to the gas-exchanging respiratory units composed of respiratory bronchioles, alveolar ducts, and alveoli.
4.