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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,
&
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.
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NOTE:
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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