An alveolus (plural: alveoli, from Latin alveolus, "little cavity") is an anatomical structure that has

the form of a hollow cavity.[1]Found in the lung parenchyma, the pulmonary alveoli are the
terminal ends of the respiratory tree, which outcrop from either alveolar sacs or alveolar ducts,
which are both sites of gas exchange with the blood as well.[2] Alveoli are particular to
mammalian lungs. Different structures are involved in gas exchange in other vertebrates.[3] The
alveolar membrane is the gas-exchange surface. Carbon dioxide rich blood is pumped from the
rest of the body into the alveolar blood vessels where, through diffusion, it releases its carbon
dioxide and absorbs oxygen.[4]
Contents
[hide]

1 Structure
o 1.1 Histology
2 Clinical significance
o 2.1 Diseases
3 References
4 External links

Structure[edit]
The alveoli are located in the respiratory zone of the lungs, at the distal termination of
the alveolar ducts and atria. These air sacs are the forming and termination point of
therespiratory tract. They provide total surface area of about 100 m2.[5]

Bronchial anatomy

A typical pair of human lungs contain about 700 million alveoli,[6] producing 70m2 of surface
area.[7] Each alveolus is wrapped in a fine mesh of capillaries covering about 70% of its area. An
adult alveolus has an average diameter of 200 micrometres, with an increase in diameter
during inhalation.[8]
The alveoli consist of an epithelial layer and extracellular matrix surrounded by capillaries. In
some alveolar walls there are pores between alveoli called Pores of Kohn. The alveoli contain
some collagen and elastic fibres. The elastic fibers allow the alveoli to stretch as they are filled
with air during inhalation. They then spring back during exhalation in order to expel the carbon
dioxide-rich air.

Histology[edit]

There are three major cell types in the alveolar wall (pneumocytes):

Type I (Squamous Alveolar) cells that form the structure of an alveolar wall

Type II (Great Alveolar) cells that secrete pulmonary surfactant to lower the surface tension
of water and allows the membrane to separate, therefore increasing its capability to
exchange gases. Surfactant is continuously released by exocytosis. It forms an underlying
aqueous protein-containing hypophase and an overlying phospholipid film composed
primarily of dipalmitoyl phosphatidylcholine.

Macrophages that destroy foreign material, such as bacteria.

Reinflation of the alveoli following exhalation is made easier by pulmonary surfactant, which is a
phospholipid and protein mixture that reduces surface 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 and alveolar air. The surfactant is produced by great alveolar cells (granular
pneumonocytes, a cuboidal epithelia), which are the most numerous cells in the alveoli, yet do
not cover as much surface area as the squamous alveolar cells (a squamous epithelium).
Great alveolar cells also repair the endotheilium of the alveolus when it becomes damaged.
Insufficient pulmonary surfactant in the alveoli can contribute to atelectasis (collapse of part or all
of the lung). Without pulmonary surfactant, atelectasis is a certainty; however, there are other
causes of lung collapse such as trauma (pneumothorax), COPD, and pleuritis.[9]

Clinical significance[edit]
Diseases[edit]
Main article: Respiratory disease

Acute respiratory distress syndrome (ARDS) is a severe inflammatory disease of the

lung. Usually triggered by other pulmonary pathology, the uncontrolled inflammation leads to
impaired gas exchange, alveolar flooding and/or collapse, and systemic inflammatory
response syndrome. It usually requires mechanical ventilation in an intensive care
unit setting.

Infant respiratory distress syndrome (IRDS) is a syndrome caused by lack of surfactant in

the lungs of premature infants.

In asthma, the bronchioles, or the "bottle-necks" into the sac are restricted, causing the
amount of air flow into the lungs to be greatly reduced. It can be triggered by irritants in the
air, photochemical smog for example, as well as substances that a person is allergic to.

Emphysema is another disease of the lungs, whereby the elastin in the walls of the alveoli is
broken down by an imbalance between the production of neutrophil elastase (elevated by
cigarette smoke) and alpha-1-antitrypsin (the activity varies due to genetics or reaction of a
critical methionine residue with toxins including cigarette smoke). The resulting loss of

elasticity in the lungs leads to prolonged times for exhalation, which occurs through passive
recoil of the expanded lung. This leads to a smaller volume of gas exchanged per breath.

Chronic bronchitis occurs when an abundance of mucus is produced by the lungs. The
production of this substance occurs naturally when the lung tissue is exposed to irritants. In
chronic bronchitis, the air passages into the alveoli, the broncholiotes, become clogged with
mucus. This causes increased coughing in order to remove the mucus, and is often a result
of extended periods of exposure to cigarette smoke.

Cystic fibrosis is a genetic condition. A mutation of the cystic fibrosis transmembrane

conductance regulator gene causes defective CFTR proteins, which are transmembrane
proteins that function in Cl transport in wet epithelia. Because wet epithelium is such a
ubiquitous and multipurpose tissue type, CF has myriad deleterious effects, some of the
most serious of which are severe respiratory problems. Many of the mechanisms by which
CF causes damage or inadequate function in the wet epithelia of other tissues, such as the
digestive and reproductive tracts, are well-understood. CF's mechanisms in causing lung
disease, however, remain poorly elucidated. One popular hypothesis suggests increased
viscosity due to increased salinity of the mucous secreted by glands of the pseudostratified
respiratory epithelium, causing difficulty in maintaining normal respiratory tract mucociliary
clearance. The frequency of certain specific bacterial infections
(Pseudomonas, Haemophilus influenzae, Staphylococcus) has prompted two other popular
categories of hypotheses: that the high salt content may interfere with defensins and
lysosome, and/or may encourage the growth of the several bacterial species typically
infecting the ordinarily-sterile lower lungs of CF patients. Regular treatment is usually
requiredprimarily percussive therapy and antibiotics. Promising research into gene
therapies is taking place.

Diffuse interstitial fibrosis

Lung cancer is a common form of cancer causing the uncontrolled growth of cells in the
lung tissue. Due to the sensitivity of lung tissue, such malignant growth is often hard to treat
effectively.

Pneumonia is an infection of the lung parenchyma, which can be caused by

both viruses and bacteria. Cytokines and fluids are released into the alveolar cavity and/or
interstitium in response to infection, causing the effective surface area of gas exchange in
the lungs to be reduced. If this happens to such a degree that the patient cannot draw
enough oxygen from his or her environment to maintain cellular respiration, then the victim
may need supplemental oxygen.

Cavitary pneumonia is a process in which the alveoli are destroyed and produce a cavity.
As the alveoli are destroyed, the surface area for gas exchange to occur becomes reduced.
Further changes in blood flow can lead to decline in lung function.

Pulmonary contusion is a bruise of the lung tissue.

References[edit]
1. Jump up^ Weibel, E. R. (1963). Academic Press, ed. Morphometry of the human lung.
p. 151.ISBN 3-540-03073-5.
2. Jump up^ Hansen, J. E.; Ampaya, E. P.; Bryant, G. H. and Navin, J. J. (1975). "The
Branching Pattern of Airways and Air Spaces of a Single Human Terminal
Bronchiole". Journal of Applied Physiology 38 (6): 983989. PMID 1141138.
3. Jump up^ Daniels, Christopher B. and Orgeig, Sandra (2003). "Pulmonary Surfactant: The
Key to the Evolution of Air Breathing". News in Physiological Sciences 18 (4): 151
157.PMID 12869615.
4. Jump up^ C. Michael Hogan. 2011. "Respiration". Encyclopedia of Earth. Eds. Mark
McGinley & C. J. Cleveland. National council for Science and the Environment. Washington,
D.C.
5. Jump up^ "Alveoli: Gas Exchange and Host Defense". Functional Ultrastructure: An Atlas of
Tissue Biology and Pathology. Springer Vienna. 2005. pp. 224
225.doi:10.1007/b137527. ISBN 978-3-211-83564-7.
6. Jump up^ "Clinical Naturopathic Medicine" Leah,Hechtman. pg.420. 2012
7. Jump up^ Roberts, M., Reiss, M., Monger, G. (2000) "Gaseous exchange". Advanced
Biology. Surrey, Nelson. p. 167.
8. Jump up^ Ochs M., Nyengaard J. R., Jung A., Knudsen L., Voigt M., Wahlers T., Richter J.,
Gundersen H. J. G. (2004). "The number of alveoli in the human lung". American journal of
respiratory and critical care medicine 169 (1): 1204. doi:10.1164/rccm.2003081107oc.PMID 14512270.
9. Jump up^ Saladin, Kenneth S. (2007). Anatomy and Physiology: the unity of form and
function. New York: McGraw Hill. ISBN 0-07-322804-4.

The lungs are an essential part of the respiratory system (Fig. 1), consisting of both conducting and
respiratory portions. This wiki will describe the normal histology of the lung, as well as the changes
that occur with pneumonia.
Contents
[hide]

1 Histology of the Normal Lung

o

1.1 Conducting Zone

1.1.1 Bronchi

1.1.2 Primary and Terminal Bronchioles

1.2 Respiratory Zone

1.2.1 Respiratory Bronchioles

1.2.2 Alveolar Ducts and Sacs

1.2.3 Alveoli

1.3 Vasculature

1.3.1 Pulmonary Vascular System

1.3.2 Bronchial Vascular System

2 Changes in Pneumonia
o

2.1 Typical Bacterial Pneumonia (TBP)

2.1.1 Lobar Pneumonia

2.1.2 Bronchopneumonia

2.2 Atypical (Interstitial) Pneumonia

3 See also

4 References

Histology of the Normal Lung

Conducting Zone
Bronchi
As primary bronchi enter the lung hila, they branch into secondary (lobar) bronchi, one for each
lobe. These further divide into tertiary (segmental) bronchi that supply each bronchopulmonary
[2]
segment.
In a histological cross-section of intrapulmonary (secondary/tertiary) bronchi, four layers are seen:

Mucosa

Lumen is lined with respiratory epithelium (i.e. pseudostratified columnar ciliated

with goblet cells). Goblet cells produce mucous to trap airborne dust particles and
pathogens, which are then swept towards the oral cavity via the mucociliary escalator
[2]
to be coughed or swallowed. The lamina propria has a meshwork of reticular and
elastic fibres containing lymphocytes, which provide immunological defence against
[3]
invading pathogens.

Muscularis

External to the lamina propria, the lumen is encircled with criss-crossing bands
of smooth muscle, which constrict the lumen and shorten the airway via contraction,
[2][3][4]
thereby regulating bronchial airflow.
(Note: muscularis lies external to submucosa
[5]
in extrapulmonary (primary) bronchi)

Submucosa
with cartilage

Contains loose connective tissue (CT) and mixed glands, including light[2]
staining mucous glands , whose thick moist secretions coat and protect the luminal
surface, and dark-staining serous glands, whose watery proteinaceous secretions
[3]
flush out the lumen. Externally there are irregular hyaline cartilage plates that
provide structural support. (Note: extrapulmonary bronchi contain 8-10 C-shaped
[2]
hyaline cartilage rings per bronchus)

Adventitia

This is the thin outermost CT layer that connects the bronchial wall to its surrounding
[5]
[6]
lung tissue and conveys the nutritive bronchial vascular branches .

Fig. 2 Changes in the constituents of the respiratory airways and acini

[7]

Main changes that occur as large bronchi branch into small bronchi include:

Reduction of cartilage rings into irregular plates

Increase in elastic fibres, mucoid-associated lymphoid tissue and smooth muscle

Reduction of epithelial height, from pseudostratified columnar to simple columnar

Decline in goblet and ciliated cells (Fig. 2).

[2][3]

Primary and Terminal Bronchioles

Tertiary bronchi branch into primary bronchioles (<5mm diameter), which further bifurcate
[2]
into terminal bronchioles (0.5-1mm diameter) . These are the smallest airways of the pulmonary
[4]
conducting zone , with no cartilage or goblet cells and a thin lamina propria composed mainly of
longitudinal elastic fibres and smooth muscle (Fig. 3).

Fig. 3 Histological section and illustration of a bronchiole.

[8]

Changes with the transition from primary to terminal bronchioles (Fig. 2) include:

Proportional increase in size of smooth muscle in walls, however muscularis layer thins with
progressive branching

Epithelial reduction from ciliated columnar to ciliated/non-ciliated low cuboidal

Replacement of mucoserous glands (present in large bronchioles) by non-ciliated columnar Clara

[2]
[3]
cells , which constitute 75-80% of the bronchial epithelium . These cells:

[3]

Secrete component of surfactant,

Contain enzyme systems for detoxifying inhaled noxious substances e.g. NO2,

Act as progenitor (stem) cells to divide, differentiate and replace damaged bronchiolar
epithelial cells, especially after injury

[4]

Bronchioles may also contain pulmonary neuroendocrine cells: specialised airway epithelial cells
which occur solitarily or in groups of 80-100 forming neuroepithelial bodies. They secrete
serotonin/other peptides that regulate localised epithelial cell growth and regeneration, and smooth
[2]
muscle tone. They also function as chemoreceptors in monitoring air O 2 levels.

Respiratory Zone
Respiratory Bronchioles
Each terminal bronchiole divides into 2-3 generations of respiratory bronchioles (0.2-0.5mm
[9]
diameter), which mark the transition between conducting and respiratory zones . Respiratory
bronchioles histologically resemble terminal bronchioles, except they are shorter and have thinner
[3]
walls interrupted by numerous alveoli between tags of smooth muscle . Their lumens are initially
[4]
lined with ciliated simple cuboidal epithelial cells and small numbers of non-ciliated Clara cells , while

[9]

distally they are lined with low cuboidal epithelium with abundant Clara cells . Bronchiolar epithelium
[2]
is continuous with type I alveolar cells at the rim of alveolar openings .
Alveolar Ducts and Sacs

Fig. 4 Histological sections showing alveolar duct, alveoli and alveolar wall.

[8]

Each respiratory bronchiole subdivides into 2-10 alveolar ducts (Fig. 4), whose walls consist entirely
of alveolar openings. Surrounding these openings are thin, sphincter-like bundles of smooth muscle,
which disappear as the alveolar ducts widen distally and terminate in alveolar sacs (clusters of
alveoli sharing a common chamber). Support is provided by networks of elastic and reticular fibres,
which enable alveolar expansion and passive contraction during the respiratory cycle. Reticular fibres
[2]
also prevent overdistension and damage to thin alveolar septa and its fragile capillaries.
Alveoli
Alveoli (200-250m diameter) are specialised sac-like structures that open into alveolar sacs and
[2]
constitute most of the lungs . Their walls consist of surface epithelium, blood vessels and supporting
[4]
tissue .
Alveolar epithelium has two cell types:
[2]

1. Type I pneumocytes squamous alveolar lining cells that constitute 40% of the epithelial
[3]
cell population but provide 95% of total alveolar SA . Function is to provide a barrier of large
SA and minimal thickness for efficient gas exchange between alveolar air and capillary
[4]
blood.
2. Type II pneumocytes rounded cuboidal cells that fill remainder of alveolar epithelium. They
[2]
occur in groups of 2-3 where alveolar walls unite , and have short microvilli on their free
[9]
surface (therefore protrude into lumen more than surrounding epithelium) . Their main role is
secretion of surfactant from lamellar bodies, which give the cells a characteristic vesicular
cytoplasm in histological sections. Surfactant coats the alveolar surface and, by lowering
surface tension, prevents the collapse of alveoli after each expiration. Partially-open alveoli
[2]
are expanded with less energy on inspiration. Type II pneumocytes also mitotically divide
[4]
and differentiate into type I pneumocytes in response to injury .

The wall between two adjacent alveoli is called an interalveolar septum. It contains an alveolar
pore of Kohn (8m diameter), which allows exchange of air and thus equalisation of air pressures in
alveoli. The pores also promote collateral circulation of air when there is bronchial obstruction, but
[2][3][4]
may permit spread of infections.
Within the septa, pulmonary capillaries (7-10m diameter)
form an extensive plexus around each alveolus and are supported by a meshwork of reticular and
[4]
elastic fibers . Additional cells of the septa include mast cells, fibroblasts andalveolar
[9]
macrophages (dust cells) . These macrophages are derived from circulating blood monocytes, and
have the role of phagocytosis and removal of inhaled particulate matter and bacteria in the alveoli.
After phagocytosing particles, most macrophages pass into the mucous in airways and are cleared
via the mucociliary escalator, while others enter the lymphatic system and drain into
[4]
bronchopulmonary (hilar) lymph nodes.
Note: Alveolar air and capillary blood are separated by a blood-air barrier (0.1-2m thick) composed
of type I pneumocytes, capillary endothelial cells and the fused basal laminae between these two
[2]
cells.

Vasculature
The lungs have a dual blood supply, consisting of pulmonary (major) and bronchial (minor) vascular
[3]
systems.
Pulmonary Vascular System

Fig. 5 Pulmonary vascular circuit.

[10]

[4]

Main left and right pulmonary arteries enter the lungs with primary bronchi and follow the airways .
The more proximal elastic arteries gradually change into muscular arteries beyond the junction of
[3]
bronchi and bronchioles . Muscular arteries have a pronounced elastic inner membrane and a tunica
media predominantly composed of smooth muscle, as opposed to elastic tissue in elastic arteries.
Distal pulmonary arteries continue to follow bronchioles and become progressively smaller. The
tunica media thins and becomes discontinuous as the pulmonary arteries narrow into pulmonary
[4]
arterioles .
Function of pulmonary arteries and arterioles is to transport deoxygenated blood, at low pressures,
[3]
from the right ventricle of the heart topulmonary capillaries in alveolar walls . After oxygenation at
these sites, blood is passed through pulmonary venules (indistinguishable from arterioles) into a
[4]
series of gradually enlarging venules and veins in the fibrocollagenous lung septa. (See pic) These
eventually drain into large, thin-walled pulmonary veins that leave the lung hila and, at low
[3]
pressures, deliver oxygenated blood to the left atrium of the heart . (Fig. 5)

Bronchial Vascular System

Bronchial arteries (lateral branches of the thoracic aorta) follow the bronchial tree and, under high
[4]
pressures, supply oxygenated blood to :

Tissue in the walls of larger airways up to respiratory bronchioles, at which point they
anastomose with the pulmonary vascular system

Major pulmonary vessels

Parts of the visceral pleura (covering the lungs)

[3]

Blood is returned to the heart via pulmonary veins, which drain smaller bronchial
[4]
veins and venules.

Changes in Pneumonia

Fig. 6 Schematic illustration of lobar pneumonia and bronchopneumonia [11]

Pneumonia refers to microbial invasion of the lung parenchyma and the associated host response. Its
occurrence signifies impairment and failure of host defence mechanisms, i.e. cough reflex,
mucociliary clearance, reclosure of vocal cords, macrophage activity and immune competence, to
[12]
prevent entry and colonisation of pathogens in the lung.

Typical Bacterial Pneumonia (TBP)

Pneumonia is most commonly bacterial in causation. TBP can be divided into lobar pneumonia and
bronchopneumonia based on pathological/anatomical patterns (Fig. 6).
Lobar Pneumonia
Lobar pneumonia (95% cases caused by Streptococcus pneumoniae) is characterised by
[12]
fibrinosuppurative consolidation throughout entire lobe(s) of the lung . It involves four stages:

Stage

Key Features

Congestion

Red
hepatisation

[13]

Vascular engorgement/congestion

Intra-alveolar fluid

Small numbers of neutrophils

Numerous bacteria

[12]

[13]

Massive confluent exudation

Alveolar spaces are filled with exudate, composed of RBCs, fibrin and
leukocytes (especially neutrophils)

Grey
hepatisation

[12]

[13]

Progressive RBC disintegration

Persistence of neutrophilic and fibrinous exudate

[12]

Resolution
[13]

Digestion of consolidated exudate by enzymatic activity

Resulting debris is cleared by macrophages or by cough mechanism

[12]

Bronchopneumonia

Fig. 7 Typical presentation of bronchopneumonia[14]

Bronchopneumonia involves patchy, often bilateral distribution of consolidation, resulting from

[15]
fibrinosuppurative exudate filling the airways and alveolar spaces . Inflammatory progression may
vary between different foci of involvement and, in advanced bronchopneumonia, multiple patches of
[12]
consolidation may merge (i.e. become confluent) to resemble the pattern of lobar pneumonia . As in
[14]
typical acute inflammation, bronchopneumonia also exhibits localised vasodilation and congestion .
(Fig. 7)

Atypical (Interstitial) Pneumonia

Fig. 8 Acute interstitial pneumonia [16]

Acute interstitial pneumonia is generally caused by atypical bacteria and some viruses e.g. HIV. It
differs histologically to the patterns of TBP, in that the damage is restricted to alveolar walls and there
is no consolidation or significant exudation and leukocytosis (increase in WBC count).
Typically, the alveolar septa become:
[15]

diffusely thickened , due to major interstitial fibroblastic proliferation and fibrosis, and lining of
walls by hyaline membranes (fibrous layers produced by combination of fibrin and alveolar cell
debris)

oedematous, with an inflammatory infiltrate of mostly lymphocytes, some plasma cells, mast cells
[17]
and eosinophils.
(Fig. 8)

The result is significantly reduced capacity for gas exchange.

See also
Virginia Tech: Respiratory System Histology

Summary of Alveoli & Diagram of Alveolar Wall

Vanderbilt University Medical Center: Respiratory System

References
1. Wikipedia (n.d.) Respiratory System (2008), Retrieved 12 March, 2012,
from http://en.wikipedia.org/wiki/Respiratory_system
2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 2.14 2.15 2.16

2.
Mescher, A.L. (2009).
Junqueiras Basic Histology: Text & Atlas. (12th ed.). New York, USA: McGraw-Hill Medical.
3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 3.11 3.12 3.13

3.
Ovalle, W.K. & Nahirney, P.C. (2007).
Netters Essential Histology. (1st ed.). Philadelphia, USA: Saunders.
4.00 4.01 4.02 4.03 4.04 4.05 4.06 4.07 4.08 4.09 4.10 4.11 4.12 4.13 4.14

4.
Young, B., Lowe, J.S., Stevens, A. &
Heath, J.W. (2006). Wheaters Functional Histology: A Text and Colour Atlas. (5th ed.). U.K.:
Churchill Livingstone, Elsevier.
5.0 5.1

5.
Vanderbilt University Medical Center: (2002) Histology Lab Manual: Respiratory
System. Retrieved 24 March, 2012,
fromhttp://www.mc.vanderbilt.edu/histology/labmanual2002/labsection2/Respiratory03.htm
6. Fritsch, H. & Khnel, W. (2008). Color Atlas of Human Anatomy: Internal Organs (Vol. 2).
(5th ed.). Wemding, Germany: Thieme Medical. Retrieved 24 March, 2012,
fromhttp://books.google.com.au/books?id=SlubDooAJNoC&pg=PA126&lpg=PA126&dq=laye
rs+of+intrapulmonary+bronchial+wall&source=bl&ots=ftgPrYyBxn&sig=qMZCGHf5wK6Onr_
w37aGcwU5eRs&hl=en&sa=X&ei=rAltTzyJsGSiQeN2qjrBQ&ved=0CC0Q6AEwAw#v=onepage&q=layers%20of%20intrapulmonary
%20bronchial%20wall&f=false
7. University of Michigan: Histology and Virtual Microscopy Learning Resources. Respiratory
System, Retrieved 14 March, 2012,
fromhttp://histology.med.umich.edu/sites/default/files/respTissueDistribution.jpg
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8.
Slomianka, L. (2006) Blue Histology: Respiratory System. Retrieved 25 March, 2012,
from http://www.lab.anhb.uwa.edu.au/mb140/CorePages/Respiratory/respir.htm
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Kierszenbaum, A. L. & Tres, L. L. (2011). Histology and Cell Biology: An
Introduction to Pathology. (3rd ed.). Philadelphia, USA: Mosby, Inc.
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from http://upload.wikimedia.org/wikipedia/commons/5/53/Illu_pulmonary_circuit.jpg
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Retrieved and adapted 24 March, 2012,
fromhttp://commons.wikimedia.org/wiki/File:Lobar_Pneumonia_and_bronchopneumonia_illus
trated.jpg
12.0 12.1 12.2 12.3 12.4 12.5 12.6

12.
Grimes, M. M. Pathology of Bacterial Pneumonia and Abscess,
Tuberculosis, & Chronic Obstructive Pulmonary Disease. (22 June 2011). Virginia, USA:
VCU Department of Pathology. Retrieved 14 March, 2012,
from http://www.pathology.vcu.edu/education/dental2/pneumonia.html
13.0 13.1 13.2 13.3

13.
Viney, K., Abul K, A. and Nelson F. (2004). Robbins and Cotran Pathologic
Basis of Disease (7th ed). New York, USA: McGraw-Hill Medical. Files retrieved 16 March,
2012,
from http://php.med.unsw.edu.au/medwiki/index.php?title=File:Congestion.jpg*/ http://php.me

d.unsw.edu.au/medwiki/index.php?title=File:Red_hepatization.jpghttp://php.med.unsw.edu.a
u/medwiki/index.php?title=File:Grey_in_table.jpg http://php.med.unsw.edu.au/medwiki/index.
php?title=File:Resolution.jpg
14.0 14.1

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from www.adaptiveelearning.com/aelp/portal/unsw/pathology/bronchopneumonia
15.0 15.1

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Kamangar, N., Harrington, A., Rager, C., Stearns, D.A. & Stephen, J.M. Bacterial
Pneumonia: Background. (3 January 2012). Medscape Reference. Retrieved 15 March,
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from http://commons.wikimedia.org/wiki/File:Acute_interstitial_pneumonia_(AIP)_Idiopathic_
DAD_2.jpg
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ed.). Philadelphia, USA: Saunders, Elsevier.