|Anatomy and Histology of
Normal Lung and Airways
The trachea is approximately 22 cm long, with a cross-sectional area of 2 cm.
At the tracheal carina it divides into two major bronchi.
The right bronchus diverges at a lesser angle from the trachea, which is why foreign material is more frequently aspirated on the right side.
On entering the lung the bronchus divide into lobar bronchi and then into segmental bronchi, which supply the 19 segments of the lung.
Because the segments are individual units with their own bronchovascular supply, they can be resected individually.
The number of further ramifications of the bronchi depends on the distance from the hilum.
Thus, there is a substantial number of ramifying bronchi in axial pathways that traverse the long distance to the periphery of the lung, such as the posterior basal segment, whereas there are far fewer in lateral pathways supplying the lung close to the hilum.
The tracheobronchial tree has cartilage and tracheobronchial mucous glands in the wall.
The glands are compound tubular glands that display both mucous (pale cells) and serous cells (granular, more basophilic cells).
Between them, both types of cell secrete most of the mucus that is found in the tracheobronchial tree.
The tracheobronchial tree is lined by a pseudostratified epithelium, which appears as layers, although all cells reach the basement membrane.
Most of the cells are ciliated, but mucus-secreting (goblet) cells also exist, as well as basal cells that do not reach the surface.
The basal cells are thought to be precursor cells that differentiate to form the more specialized cells of the tracheobronchial epithelium.
K (for Kulchitsky-like) cells which resemble the argentaffin and argyrophil cells found in the gut and elsewhere, are neuroendocrine cells that contain a variety of hormonally active polypeptides and vasoactive amines.
Although at one time these cells were thought to derive from the neural crest and migrate to the epithelium of the bronchus, it is now clear that they share a common stem cell with other cells of the bronchus and gut.
Succeeding the bronchi are the (membranous) bronchioles, which differ from bronchi in that they contain neither cartilage nor mucus-secreting glands.
As with bronchi, the number of branchings and their length depends on the pathway from the hilus to the periphery of the lung.
In axial pathways there may be up to 25 branchings of conducting airways and a length of approximately 23 cm, whereas in lateral pathways there are only seven generations and a total length of about 8 cm.
The epithelium of the bronchioles becomes thinner, until only one cell layer is apparent.
The last purely conducting structure is the terminal bronchiole, after which the airways have alveoli in their walls.
A major change then occurs as the gas-exchanging unit, the acinus, is encountered.
This unit consists of, in series:
1) Respiratory bronchioles, airways with both alveolated and nonalveolated epithelium in their walls,
2) Alveolar ducts, conducting structures with only alveoli in their walls, and
3) Alveolar sacs, terminal structures lined entirely by alveoli.
The acinus is the unit of gas exchange in the lung.
Understanding this structure is critical to understanding the very important condition known as emphysema.
Alveoli, the gas-exchanging structures of the lung, are lined by two types of epithelium.
- Type I cells cover 95% of the alveolar surface, although they comprise only 40% of all the epithelial cells of the alveolus.
They are thin and have a large surface area, a combination of that facilitates gas exchange.
- Type II cells comprise 60% of the alveolar lining cells, but because they are more cuboidal they contribute only a small part to the total alveolar surface area.
These cells secrete the surfactant material of the alveolar surface that maintains the patency of alveoli.
It should be noted that bronchioles are also line by surfactant and that displacement of surfactant by inflammatory exudates leads to the bronchiolar instability and thus impairs their function.
Type I cells are very vulnerable to injury, and when they die, type II cells multiply and differentiate to form type I cells, thereby reconstituting the alveolar surface area.
The alveolar epithelial cells are connected by tight junctions that prevent the passage of even small molecules through the epithelial surface.
The alveolar wall contains a dense network of capillaries, each alveolus having approximately 1000 capillary segments, about 15 micrometer long and 8 micrometer in diameter.
The capillaries are lined by endothelial cells that resemble type I epithelial cells in that they have abundant flat cytoplasm but differ in that their junctions are "leaky" or "semitight".
Because the junctions are tighter on the arterial side and looser in the small venules, molecules the size of albumin can pass through the capillary endothelium.
Both the endothelium and epithelium have basal laminae, and when they are adjacent they fuse into a single basal lamina that forms the thin side of the alveolar capillary membrane where gas exchange is most efficient.
On the opposite side (the thick side), the basal laminae are separate, and collagen, elastin, and proteoglycans are found there.
In addition, fibroblasts, some of which contain muscle filaments (myofibroblasts), are also found on the thick side of the alveolar capillary membrane.
This region, which constitutes the interstitial space of the alveolar wall, is where significant fluid and molecular exchange occurs and where edema begins.
The pulmonary arteries accompany the airways in a sheath of connective tissue known as the bronchovascular bundle.
The more proximal arteries are elastic and then become transitional (four or fewer elastic laminae in their walls).
They are succeeded by arteries whose walls have two elastic laminae with a layer of muscle between them.
In vessels about 100 micrometer in diameter or less, muscle extends in a spiral fashion between the elastic laminae, so that the arterial wall is partly muscular and partly non-muscular where the elastic laminae fuse.
The smallest arteries have no muscle.
The smallest veins, which resemble the smallest arteries, join with other veins and drain into the lobular septa, connective tissue partitions that subdivide the lung into small respiratory units.
The veins then continue in the lobular septa, joining other veins to form a network that is separate from the bronchovascular bundles.There are no lymphatics in most alveolar walls.
The lymphatics commence in alveoli at the periphery of the acinus, which lies along a lobular septum, the bronchovascular bundle, and the pleura.
The lymphatics of the lobular septa and bronchovascular bundle accompany these structures, and the pleural lymphatics drain toward the hilus via bronchovascular lymphatics.
A crucial concept in understanding the lung pathology is that of the interstitium of the lung.
This is composed of the connective tissue that surrounds the veins and bronchovascular bundle and the tissue on the thick side of the alveolar capillary membrane.
The proximal airways are lined by pseudostratified ciliated columnar epithelium and the distal airways by non-ciliated cuboidal epithelium.
Specialized cells found in the lining of the airways include Kulchitsky cells, Clara cells and goblet cell.
The proportion of goblet cells is lower in the distal airways than in the proximal airways, and there is a corresponding increase in the number of Clara cells after bronchial injury, they are recognized by PAS-positive, diastase-resistant granules in the apical part of their cytoplasm.
Kulchitsky cells form part of the diffuse neuroendocrine system and so contain cytoplasmic dense core granules.
Inflammatory changes such as active bronchitis, bronchiolitis, and areas of granulation tissue can be seen in biopsy or excision specimens as a result of previous instrumentation.
The trauma of biopsy or open surgery commonly causes fresh intra-alveolar hemorrhage, and so this feature should not be interpreted as a pathological process.
Age-related changes in the lung include calcification and ossification of cartilage in the large airways, intimal thickening in pulmonary vessels and oncocytic metaplasia of submucous glands.
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