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7/30/2019 Pulmonary Alveolus - Copy
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Pulmonaryalveolus
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An alveolus (plural: alveoli, from Latin alveolus, "littlecavity") is an anatomical structure that has the form of ahollow cavity.
Found in the lung parenchyma, the pulmonary alveoli are
the terminal ends of the respiratory tree, which outcrop fromeither alveolar sacs or alveolar ducts, which are both sites ofgas exchange with the blood as well.
Alveoli are particular to mammalian lungs.
Different structures are involved in gas exchange in other
vertebrates.
The alveolar membrane is the gas-exchange surface.
Carbon dioxide rich blood is pumped from the rest of the bodyinto the alveolar blood vessels where, through diffusion, itreleases its carbon dioxide and absorbs oxygen.
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Alveolus diagram
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Location The alveoli are located in the
respiratory zone of the lungs, at thedistal termination of the alveolar ductsand atria.
These air sacs are the forming andtermination point of the respiratory
tract. They provide total surface area of about
100 m2.
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Anatomy The alveoli contain some collagen and elastic fibres.
The elastic fibers allow the alveoli to stretch as theyare filled with air during inhalation.
They then spring back during exhalation in order toexpel the carbon dioxide-rich air.
A typical pair of human lungs contain about 700million alveoli, producing 70m of surface area.
Each alveolus is wrapped in a fine mesh ofcapillariescovering about 70% of its area.
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An adult alveolus has an averagediameter of 200 micrometres, with anincrease in diameter during inhalation.
The alveoli consist of an epithelial layerand extracellular matrix surrounded bycapillaries.
In some alveolar walls there are poresbetween alveoli called Pores of Kohn.
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Pores of Kohn The Pores of Kohn (also known as interalveolar
connections) are discrete holes in walls of adjacentalveoli.[1] Cuboidal type II alveolar cell usually forms partof aperture
Etymology
The Pores of Kohn take their name from the Germanphysician Hans Kohn [1866-1935] who first describedthem in 1893
Development
They are absent in human newborns. They develop at 3-4years of age along with Canals of Lambert during processof thinning of alveolar septa
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Function They function as a means of collateral ventilation;
that is, if the lung is partially deflated, ventilationcan occur to some extent through these pores.
They equalize the pressure in adjacent alveoli andthus play important role in prevention of collapse oflung.[5]
The pores also allow the passage of other materials
such as fluid and bacteria, which is an importantmechanism of spread of infection in Lobarpneumonia and spread of fibrin in grey hepatisationphase of recovery from the same.
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Histology
There are three major cell types in the alveolar wall(pneumocytes):
Type I (Squamous Alveolar) cells that form the structureof an alveolar wall.
Type II (Great Alveolar) cells that secrete pulmonarysurfactant to lower the surface tension of water andallows the membrane to separate, therefore increasing itscapability to exchange gases.Surfactant is continuously released by exocytosis. It
forms an underlying aqueous protein-containinghypophase and an overlying phospholipid film composedprimarily of dipalmitoyl phosphatidylcholine.
Macrophages that destroy foreign material, such asbacteria.
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Reinflation of the alveoli following exhalation ismade easier bypulmonary surfactant, which is aphospholipid and protein mixture that reducessurface tension in the thin fluid coating within all
alveoli. The fluid coating is produced by the body in order
to facilitate the transfer of gases between blood andalveolar air.
The surfactant is produced by great alveolar cells(granular pneumonocytes, a cuboidal epithelia),which are the most numerous cells in the alveoli, yetdo not cover as much surface area as the squamousalveolar cells (a squamous epithelium).
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Great alveolar cells also repair the endotheilium ofthe alveolus when it becomes damaged.
Insufficient pulmonary surfactant in the alveoli can
contribute to atelectasis (collapse of part or all of thelung).
Without pulmonary surfactant, atelectasis is acertainty; however, there are other causes of lung
collapse such as trauma (pneumothorax), COPD,and pleuritis
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Regenerative ability of the humanpulmonary alveolus
The following small extracted statement is from a story (takenon Wednesday, November 2, 2011) from the Harvard Sciencewebsite,
"Guided by insights into how mice recover after H1N1 flu,researchers at Harvard Medical School and Brigham andWomens Hospital, together with researchers atA*STARofSingapore, have cloned three distinct stem cells from thehuman airways and demonstrated that one of these cells canform into the lung's alveoli air sac tissue. What's more, theresearchers showed that these same lung stem cellsare rapidlydeployed in a dynamic process oflung regeneration to combatdamage from infection or chronic disease.
"These findings suggest new cell- and factor-based strategiesfor enhancing lung regeneration following acute damage frominfection, and even in chronic conditions such as pulmonaryfibrosis," said Frank McKeon, professor ofcellular biologyatHarvard Medical School (HMS).
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Bronchial anatomy
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Surfactant
Surfactant is a complex substance containingphospholipids and a number of apoproteins.
This essential fluid is produced by the Type II
alveolar cells, and lines the alveoli and smallestbronchioles.
Surfactant reduces surface tension throughout thelung, thereby contributing to its general compliance.
It is also important because it stabilizes the alveoli.
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Laplaces Law tells us that the pressure within aspherical structure with surface tension, such as thealveolus, is inversely proportional to the radius ofthe sphere (P=4T/r for a sphere with two liquid-gasinterfaces, like a soap bubble, and P=2T/r for asphere with one liquid-gas interface, like analveolus: P=pressure, T=surface tension, andr=radius).
That is, at a constant surface tension, small alveoliwill generate bigger pressures within them than willlarge alveoli.
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Smaller alveoli would therefore be expected toempty into larger alveoli as lung volume decreases.
This does not occur, however, because surfactant
differentially reduces surface tension, more at lowervolumes and less at higher volumes, leading toalveolar stability and reducing the likelihood ofalveolar collapse.
Surfactant is formed relatively late in fetal life; thuspremature infants born without adequate amountsexperience respiratory distress and may die.
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Alveolar Pressure This is the pressure, measured in cm H20, within
the alveoli, the smallest gas exchange units ofthelung.
Alveolar pressure is given with respect toatmospheric pressure, which is always set tozero.
Thus, when alveolar pressure exceeds atmosphericpressure, it is positive; when alveolarpressure is
below atmospheric pressure it is negative.
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Alveolar pressure determines whether air will flowinto or out of the lungs.
When alveolarpressure is negative, as is the case
during inspiration, air flows from the higherpressure at the mouth down the lungs into the lowerpressure in the alveoli.
When alveolar pressure is positive,which is the caseduring expiration, air flows out.
At end-inspiration or end-expiration, when flowtemporarily stops, the alveolar pressure is zero (i.e.,the same as the atmospheric pressure).
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Airway Resistance
Airway resistance is the opposition to flow caused by theforces of friction. It is defined as the ratio of drivingpressure to the rate of air flow. Resistance to flow in the
airways depends on whether the flow is laminar orturbulent, on the dimensions of the airway, and on theviscosity of the gas.
For laminar flow, resistance is quite low. That is, a
relatively small driving pressure is needed to produce acertain flow rate. Resistance during laminar f low may becalculated via a rearrangement of Poiseuille's Law :
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The most important variable here is the radius,which, by virtue of its elevation to the fourth power,has a tremendous impact on the resistance. Thus, ifthe diameter of a tube is doubled, resistance will
drop by a factor of sixteen. For turbulent f low, resistance is relatively large. That
is, compared with laminar flow, a much largerdriving pressure would be required to produce thesame flow rate. Because the pressure-flow
relationship ceases to be linear during turbulentflow, no neat equation exists to compute itsresistance.
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While a single small airway provides more resistancethan a single large airway, resistance to air flowdepends on the number of parallel pathwayspresent. For this reason, the large and particularly
the medium-sized airways actually provide greaterresistance to flow than do the more numerous smallairways.
Airway resistance decreases as lung volume
increases because the airways distend as the lungsinflate, and wider airways have lower resistance.
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Alveoli of the Lungs
The oxygen exchange in the lungs takes place acrossthe membranes of small balloon-like structurescalled alveoli attached to the branches of thebronchial passages. These alveoli inf late and deflate
with inhalation and exhalation. The behavior of thealveoli is largely dictated byLaPlace's law andsurface tension. It takes some effort to breathe inbecause these tiny balloons must be inflated, but
the elastic recoil of the tiny balloons assists us in theprocess ofexhalation. If the elastic recoil of thealveoli is compromised, as in the case ofemphysema, then it is difficult to exhale forcibly.
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Inflating the Alveoli
Inflating the alveoli in the process ofrespirationrequires an excess pressure inside the alveoli relativeto their surroundings. This is actually accomplishedby making the pressure in the thoracic cavitynegative with respect to atmospheric pressure. Theamount of net pressure required for inflation isdictated by the surface tension and radii of the tinyballoon-like alveoli. During inhalation the radii of
the alveoli increase from about 0.05 mm to 0.1 mm .The normal mucous tissue fluid surrounding thealveoli has a nominal surface tension of about 50dynes/cm so the required net outward pressure is:
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The remarkable property of the surfactant whichcoats the alveoli is that it reduces the surface tensionby a factor of about 15 so that the 1 mmHg pressuredifferential is sufficient to inflate the alveoli. Other
factors affecting the remarkable efficiency ofoxygentransport across the lung membranes ischaracterized in Fick's Law.
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Surfactant Role in Respiration
One of the remarkable phenomena in the process ofrespiration is the role of the f luid coating the walls of thealveoli of the lungs. This fluid, called a surfactant, lowers thesurface tension of the balloon-like alveoli by about a factor of 15
compared to the normal mucous tissue fluid in which they areimmersed. There appears to be a nearly constant amount ofthis surfactant per alveolus, so that when the alveoli aredeflated it is more concentrated on the surface. Since thesurface-tension-lowering effect of the surfactant depends onthis concentration, it diminishes the required pressure forinflation of the alveoli at their most critical phase. For a givensurface tension, the pressure to inflate a smaller bubble isgreater. It is the surfactant which makes possible the inflationof the alveoli with only about 1 mmHg of pressure excess overtheir surroundings. The baby's first breath depends upon thissurfactant and is made more difficult in premature infants bythe incomplete formation of the surfactant.
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Alveoli and Exhalation
The alveoli of the lungs act much like balloons in that there issome effort involved to inflate them, but when the inflatingpressure is released, the recoil of the elastic walls provides thepressure necessary to deflate them. The lungs are suspended in
the thoracic cavity which is normally at a slight negativepressure. When the diaphragm is lowered, that pressurebecomes more negative and the lungs expand into the cavity.Air from the atmosphere moves into the resulting partialvacuum and inflates the alveoli. One is aware of the effort, butit is not extreme as in the case of the baby's first breath . Oncethe alveoli are fully inflated, exhalation canbe accomplishedby merely relaxing the diaphragm, since thewall tension in allthe tiny alveoli will act to force the air out of them. By forcingthe diaphragm upward, we can exhale forcefully by adding thediaphragm effort to the recoil of the elastic alveoli. In diseaseslike emphysema, the elasticity of the alveoli is lost andexhalation becomes a laborious process.
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