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The alveolar type II epithelial cells are more resistant to damage, so after an insult to the alveoli, most of the damage will occur to the alveolar type I epithelial cells. [5] Left side demonstrate the structure of a normal alveolus including the difference between type I and type II alveolar epithelial cells.
The membrane between alveoli and capillaries is torn; damage to this capillary–alveolar membrane and small blood vessels causes blood and fluids to leak into the alveoli and the interstitial space (the space surrounding cells) of the lung. [11] With more severe trauma, there is a greater amount of edema, bleeding, and tearing of the alveoli. [17]
Mucociliary clearance (MCC), mucociliary transport, or the mucociliary escalator describes the self-clearing mechanism of the airways in the respiratory system. [1] It is one of the two protective processes for the lungs in removing inhaled particles including pathogens before they can reach the delicate tissue of the lungs.
Alveoli are the functional units of the lungs. Alveolar lung diseases are classified as processes that affect these units that ultimately lead to issues with ventilation. There are a number of different causes of insult to the alveoli including build up of fluid, hemorrhage, infection, malignancy and build up of protein and mineral deposits.
Atelectasis is the partial collapse or closure of a lung resulting in reduced or absence in gas exchange. It is usually unilateral, affecting part or all of one lung. [2] It is a condition where the alveoli are deflated down to little or no volume, as distinct from pulmonary consolidation, in which they are filled with liquid.
As the pulmonary venous pressure rises, these pressures overwhelm the barriers and fluid enters the alveoli when the pressure is above 25 mmHg. [14] Depending on whether the cause is acute or chronic determines how fast pulmonary edema develops and the severity of symptoms. [12] Some of the common causes of cardiogenic pulmonary edema include:
The actual number may be significantly higher due to misdiagnosis. Typically, patients are in their forties and fifties when diagnosed, while the incidence of idiopathic pulmonary fibrosis increases dramatically after age 50. But loss of pulmonary function is commonly ascribed to old age, heart disease, or more common lung diseases. [40]
Spontaneous subcutaneous emphysema is thought to result from increased pressures in the lung that cause alveoli to rupture. [5] In spontaneous subcutaneous emphysema, air travels from the ruptured alveoli into the interstitium and along the blood vessels of the lung, into the mediastinum and from there into the tissues of the neck or head. [5]