OVERVIEW OF THE RESPIRATORY SYSTEM

EMBRYOLOGY AND HISTOLOGY

Prof I. Edagha, PhD

FULBRIGHT FELLOW, NYU
Human Anatomy, MUSOM
• Outline
• THE RESPIRATORY PRIMODIUM
• LARYNX
• TRACHEA
• BRONCHI
• LUNGS
• Learning Objectives
QUICK REVISION
• Embryology Gk embryon – the unborn ; the
branch of biology that studies prenatal
development of gametes (sex cells), fertilization,
and development of embryos and fetuses

• Germinal stage – period of gestation from

fertilization or conception, when the egg meets the
sperm, to implantation of the embryo in the uterus

• Embryonic stage – period of gestation after

implantation during which all major organs and
structures within growing mammals are formed
• Development of the upper respiratory organs, the nasal
cavities.

• The lower respiratory organs (larynx, trachea, bronchi,

and lungs) begin to form during the fourth week of
development.
 RESPIRATORY PRIMORDIUM
• The respiratory primordium is indicated at approximately 28
days by a median outgrowth-the laryngotracheal groove-from
the caudal end of the ventral wall of the primordial pharynx.

• Primordium of the tracheobronchial tree develops caudal to the

fourth pair of pharyngeal pouches.

• Endoderm lining the laryngotracheal groove gives rise to the

pulmonary epithelium and glands of the larynx, trachea, and
bronchi.

• The connective tissue, cartilage, and smooth muscle in these

structures develop from the splanchnic mesoderm surrounding
the foregut.
A. Lateral view of a
4-week embryo
illustrating the
relationship of the
pharyngeal
apparatus to the
developing
respiratory system.
 B. Sagittal section
of the cranial half of
the embryo.
C. Horizontal section of
the embryo illustrating
the floor of the
primordial pharynx and
the location of the
laryngotracheal groove.
Successive stages in the
development of the
larynx. A, At 4 weeks.
B, At 5 weeks. C, At 6
weeks. D, At 10 weeks.

The epithelium lining the

larynx is of endodermal
origin.

The cartilages and

muscles of the larynx
arise from
mesenchyme in the
fourth and sixth pairs
of pharyngeal arches.

Note that the laryngeal

inlet changes in shape
from a slitlike opening
to a T-shaped inlet as
the mesenchyme
surrounding the
developing larynx
• By the end of the fourth week, the laryngotracheal
groove has evaginated to form a pouchlike
laryngotracheal diverticulum, which is located
ventral to the caudal part of the foregut.

• As this diverticulum elongates, it is invested with

splanchnic mesenchyme and its distal end enlarges
to form a globular respiratory bud.

• The laryngotracheal diverticulum soon separates from

the primordial pharynx; however, it maintains
communication with it through the primordial
laryngeal inlet.
• Successive stages in the
development of the
tracheoesophageal
septum during the fourth
and fifth weeks.

• A to C, Lateral views of
the caudal part of the
primordial pharynx
showing the
laryngotracheal
diverticulum and
partitioning of the
foregut into the
esophagus and
laryngotracheal tube.

• D to F, Transverse
sections illustrating
formation of the
tracheoesophageal
septum and showing how
it separates the foregut
into the laryngotracheal
tube and esophagus. The
arrows indicate cellular
changes resulting from
• Longitudinal tracheoesophageal folds develop in the
laryngotracheal diverticulum, approach each other, and
fuse to form a partition-the tracheoesophageal septum.

• This septum divides the cranial portion of the foregut into:

a ventral part, the laryngotracheal tube (primordium of
larynx, trachea, bronchi, and lungs), and
a dorsal part (primordium of oropharynx and esophagus.

• The opening of the laryngotracheal tube into the pharynx

becomes the primordial laryngeal inlet.
 DEVELOPMENT OF THE LARYNX
• Epithelial lining of the larynx develops from the
endoderm of the cranial end of the laryngotracheal tube.

• Cartilages of the larynx develop from those in the fourth

and sixth pairs of pharyngeal arches.

• Laryngeal cartilages develop from mesenchyme that is

derived from neural crest cells.

• The mesenchyme at the cranial end of the laryngotracheal

tube proliferates rapidly, producing paired arytenoid
swellings.
• Successive stages in
the development of the
larynx. A, At 4 weeks.
B, At 5 weeks. C, At 6
weeks. D, At 10 weeks.

• The epithelium lining

the larynx is of
endodermal origin. The
cartilages and muscles
of the larynx arise from
mesenchyme in the
fourth and sixth pairs of
pharyngeal arches.

• Note that the laryngeal

inlet changes in shape
from a slitlike opening
to a T-shaped inlet as
the mesenchyme
surrounding the
developing larynx
proliferates.
• These swellings grow toward the tongue, converting the slitlike
aperture-the primordial glottis-into a T-shaped laryngeal inlet
and reducing the developing laryngeal lumen to a narrow slit.

• The laryngeal epithelium proliferates rapidly, resulting in

temporary occlusion of the laryngeal lumen.

• Recanalization of the larynx normally occurs by the 10th week.

• The laryngeal ventricles form during this recanalization process.

• These recesses are bounded by folds of mucous membrane that

become the vocal folds (cords) and vestibular folds.
• The epiglottis develops from the caudal part of the
hypopharyngeal eminence, a prominence produced
by proliferation of mesenchyme in the ventral ends of
the third and fourth pharyngeal arches.

• The rostral part of this eminence forms the posterior

third or pharyngeal part of the tongue.
• Because the laryngeal muscles develop from
myoblasts in the fourth and sixth pairs of
pharyngeal arches, they are innervated by the
laryngeal branches of the vagus nerves (cranial nerve
X) that supply these arches.

• Growth of the larynx and epiglottis is rapid during the

first 3 years after birth.

• By this time, the epiglottis has reached its adult form.

 Laryngeal Atresia
• This rare anomaly results from failure of recanalization of the
larynx, which causes obstruction of the upper fetal airway-
congenital high airway obstruction syndrome.
• Distal to the region of atresia (blockage) or stenosis
(narrowing), the airways become dilated, the lungs are
enlarged and echogenic (capable of producing echoes during
ultrasound imaging studies because they are filled with fluid),
the diaphragm is either flattened or inverted, and there is fetal
ascites and/or hydrops (accumulation of serous fluid in the
intracellular spaces causing severe edema).
• Incomplete atresia (laryngeal web) results from incomplete
recanalization of the larynx during the 10th week.
• A membranous web forms at the level of the vocal folds,
partially obstructing the airway.
 DEVELOPMENT OF THE TRACHEA
• The endodermal lining of the laryngotracheal tube distal to
the larynx differentiates into the epithelium and glands of
the trachea and the pulmonary epithelium.
• The cartilage, connective tissue, and muscles of the trachea
are derived from the splanchnic mesenchyme surrounding
the laryngotracheal tube.

Tracheoesophageal Fistula (TEF)

• A fistula (abnormal passage) between the trachea and
esophagus occurs once in 3000 to 4500 live births; most
affected infants are males.
• In more than 85% of cases, the TEF is associated with
esophageal atresia.
• Transverse sections
through the
laryngotracheal tube
illustrating progressive
stages in the
development of the
trachea. A, At 4 weeks.
B, At 10 weeks. C, At 11
weeks (drawing of
micrograph in D).
• Note that endoderm of
the tube gives rise to the
epithelium and glands of
the trachea and that
mesenchyme surrounding
the tube forms the
connective tissue,
muscle, and cartilage.
• D, Photomicrograph of a
transverse section of the
developing trachea at 12
weeks. (D,

From Moore KL, Persaud TVN, Shiota K:

Color Atlas of Clinical Embryology,
2nd ed. Philadelphia, WB Saunders,
2000.)
• A TEF results from incomplete division of the cranial
part of the foregut into respiratory and esophageal
parts during the fourth week.
• Incomplete fusion of the tracheoesophageal folds
results in a defective tracheoesophageal septum and
a TEF, between the trachea and esophagus.
• TEF is the most common anomaly of the lower
respiratory tract. Four main varieties of TEF may
develop.
• The usual anomaly is for the superior part of the
esophagus to end blindly (esophageal atresia) and
for the inferior part to join the trachea near its
bifurcation.
• The four main varieties of tracheoesophageal fistula (TEF). Possible directions of the
flow of the contents are indicated by arrows. Esophageal atresia, as illustrated in
A - is associated with TEF in more than 85% of cases.
B - Fistula between the trachea and esophagus.
C - Air cannot enter the distal esophagus and stomach.
D - Air can enter the distal esophagus and stomach, and the esophageal and gastric contents may
enter the trachea and lungs.
Tracheoesophageal fistula (TEF) in a 17-week male fetus. The
upper esophageal segment ends blindly (pointer). B, Contrast
radiograph of a newborn infant with TEF. Note the communication
(arrow) between the esophagus (E) and trachea (T). (A, From Kalousek DK, Fitch
N, Paradice B: Pathology of the Human Embryo and Previable Fetus. New York, Springer-Verlag, 1990; B, Courtesy of
Dr. Prem S. Sahni, formerly of the Department of Radiology, Children's Hospital, Winnipeg, Manitoba, Canada.)
 Other varieties of this anomaly are illustrated
• Infants with the common type of TEF and esophageal atresia
cannot swallow so they frequently drool saliva at rest and
immediately regurgitate milk when fed.
• Gastric and intestinal contents may also reflux from the stomach
through the fistula into the trachea and lungs.
• This refluxed acid, and in some cases bile, can cause
pneumonitis (inflammation of the lungs) leading to respiratory
compromise.
• Polyhydramnios is often associated with esophageal atresia.
• The excess amniotic fluid develops because fluid cannot pass to
the stomach and intestines for absorption and subsequent
transfer through the placenta to the mother's blood for disposal.
 Laryngotracheoesophageal Cleft
• Uncommonly, the larynx and upper trachea may fail to
separate completely from the esophagus.
• This results in a persistent connection of variable
lengths between these normally separated structures.
• Symptoms of this congenital anomaly are similar to
those of tracheoesophageal fistula because of aspiration
into the lungs, but aphonia (absence of voice) is a
distinguishing feature.
 Tracheal Stenosis and Atresia
• Narrowing (stenosis) and obstruction (atresia) of the
trachea are uncommon anomalies that are usually
associated with one of the varieties of TEF.
• Stenoses and atresias probably result from unequal
partitioning of the foregut into the esophagus and trachea.
• Sometimes there is a web of tissue obstructing airflow
(incomplete tracheal atresia).
Tracheal Diverticulum
• This extremely rare anomaly consists of a blind, bronchus-
like projection from the trachea.
• The outgrowth may terminate in normal-appearing lung
tissue, forming a tracheal lobe of the lung
 DEVELOPMENT OF THE BRONCHI AND LUNGS
• The respiratory bud (lung bud) that developed at the
caudal end of the laryngotracheal diverticulum during the
fourth week soon divides into two outpouchings-the
primary bronchial buds.
• These buds grow laterally into the pericardioperitoneal
canals, the primordia of the pleural cavities.
• Secondary and tertiary bronchial buds soon develop.
• Together with the surrounding splanchnic mesenchyme, the
bronchial buds differentiate into the bronchi and their
ramifications in the lungs.
• Early in the fifth week, the connection of each bronchial
bud with the trachea enlarges to form the primordia of
main bronchi.
Illustrations of the growth of the developing lungs into the splanchnic
mesenchyme adjacent to the medial walls of the pericardioperitoneal
canals (primordial pleural cavities). Development of the layers of the
pleura is also shown. A, At 5 weeks. B, At 6 weeks.
• The embryonic right main bronchus is slightly larger than the left one
and is oriented more vertically.
• This embryonic relationship persists in the adult; consequently, a
foreign body is more liable to enter the right main bronchus than the
left one.
• The main bronchi subdivide into secondary bronchi that form lobar,
segmental, and intrasegmental branches.
• On the right, the superior lobar bronchus will supply the upper
(superior) lobe of the lung, whereas the inferior bronchus subdivides
into two bronchi, one to the middle lobe of the right lung and the other
to the lower (inferior) lobe.
• On the left, the two secondary bronchi supply the upper and lower
lobes of the lung. Each lobar bronchus undergoes progressive
branching.
• The segmental bronchi, 10 in the right lung and 8 or 9 in the
left lung, begin to form by the seventh week. As this occurs, the
surrounding mesenchyme also divides.
Successive stages in the development of the bronchial buds, bronchi, and lungs.
• Each segmental bronchus with its surrounding mass of mesenchyme
is the primordium of a bronchopulmonary segment.
• By 24 weeks, approximately 17 orders of branches have formed
and respiratory bronchioles have developed.
• An additional seven orders of airways develop after birth. As the
bronchi develop, cartilaginous plates develop from the surrounding
splanchnic mesenchyme.
• The bronchial smooth muscle and connective tissue and the
pulmonary connective tissue and capillaries are also derived from this
mesenchyme.
• As the lungs develop, they acquire a layer of visceral pleura from
the splanchnic mesenchyme .
• With expansion, the lungs and pleural cavities grow caudally into the
mesenchyme of the body wall and soon lie close to the heart.
• The thoracic body wall becomes lined by a layer of parietal pleura,
derived from the somatic mesoderm.
 MATURATION OF THE LUNGS
• Is divided into 4 stages: pseudoglandular,
canalicular, terminal sac, and alveolar.

Pseudoglandular Stage (6 to 16 Weeks)

• The developing lungs somewhat histologically resemble
exocrine glands during this stage.
• By 16 weeks, all major elements of the lung have
formed, except those involved with gas exchange.
• Respiration is not possible; hence, fetuses born during
this period are unable to survive.
• Photomicrographs
of sections of
developing human
lungs.
• A, Pseudoglandular
stage, 8 weeks.
• Note the
"glandular"
appearance of the
lung.
• B, Canalicular
stage, 16 weeks.
The lumina of the
bronchi and
terminal
bronchioles are
enlarging.
• (From Moore KL, Persaud TVN, Shiota
K: Color Atlas of Clinical Embryology,
2nd ed. Philadelphia, WB Saunders,
2000.)
• Sections of developing
human lungs.
• A, Pseudoglandular
stage, 8 weeks.
• Note the "glandular"
appearance of the lung.
• B, Canalicular stage, 16
weeks.
• The lumina of the bronchi
and terminal bronchioles
are enlarging.
• C, Canalicular stage, 18
weeks.
• D, Terminal sac stage, 24
weeks.
• Observe the thin-walled
terminal sacs (primordial
alveoli) that have
developed at the ends of
the respiratory bronchioles.
• Also observe that the
number of capillaries have
increased and that some of
them are closely
associated with the
developing alveoli.

• (From Moore KL, Persaud TVN, Shiota K:

Color Atlas of Clinical Embryology, 2nd
 Canalicular Stage (16 to 26 Weeks)
• Period overlaps the pseudoglandular stage because cranial
segments of the lungs mature faster than caudal ones.
• Lumina of the bronchi and terminal bronchioles become larger,
and the lung tissue becomes highly vascular .
• By 24 weeks, each terminal bronchiole has given rise to two or
more respiratory bronchioles, each of which then divides into
three to six passages-primordial alveolar ducts.
• Respiration is possible at the end of the canalicular stage
because some thin-walled terminal sacs (primordial alveoli)
have developed at the ends of the respiratory bronchioles, and
the lung tissue is well vascularized.
• Although a fetus born toward the end of this period may survive
if given intensive care, it often dies because its respiratory and
other systems are still relatively immature.
 Terminal Sac Stage (26 Weeks to Birth)
• During this period, many more terminal sacs or saccules develop,
and their epithelium becomes very thin. Capillaries begin to bulge
into these sacs (developing alveoli).
• Intimate contact between epithelial and endothelial cells
establishes the blood-air barrier, which permits adequate gas
exchange for survival of the fetus if it is born prematurely.
• By 26 weeks, the terminal sacs are lined mainly by squamous
epithelial cells of endodermal origin-type I pneumocytes-across
which gas exchange occurs. The capillary network proliferates
rapidly in the mesenchyme around the developing alveoli, and
there is concurrent active development of lymphatic capillaries.
• Scattered among the squamous epithelial cells are rounded
secretory epithelial cells-type II pneumocytes, which secrete
pulmonary surfactant, a complex mixture of phospholipids and
proteins.
• Surfactant forms as a monomolecular film over the internal
walls of the alveolar sacs and counteracts surface tension
forces at the air-alveolar interface.
• Facilitates expansion of the saccules (primordial alveoli) by
preventing atelectasis (collapse of saccules during exhalation).
• Maturation of type II pneumocytes and surfactant production
varies widely in fetuses of different gestational ages.
• Production of surfactant increases during the terminal stages of
pregnancy, particularly during the last 2 weeks.
• Surfactant production begins by 20 weeks, but it is present in
only small amounts in premature infants. It does not reach
adequate levels until the late fetal period.
• By 26 to 28 weeks after fertilization, the fetus usually weighs
approximately 1000 g and sufficient alveolar sacs and surfactant
are present to permit survival of a prematurely born infant.
• Before this, the lungs are usually incapable of providing
adequate gas exchange, partly because the alveolar surface
area is insufficient and the vascularity underdeveloped.
• It is not the presence of thin terminal sacs or a primordial
alveolar epithelium so much as the development of an
adequate pulmonary vasculature and sufficient surfactant that
is critical to the survival and neurodevelopmental outcome of
premature infants.
• Consequently, fetuses born prematurely at 24 to 26 weeks
after fertilization may survive if given intensive care; however,
they may suffer from respiratory distress because of surfactant
deficiency.
• Survival of these infants has improved with the use of antenatal
corticosteroids, which induces surfactant production, and also
with postnatal surfactant replacement therapy.
 Alveolar Stage (32 Weeks to 8 Years)
• Exactly when the terminal sac stage ends and the alveolar stage
begins depends on the definition of the term alveolus. Sacs
analogous to alveoli are present at 32 weeks.
• The epithelial lining of the terminal sacs attenuates to a thin
squamous epithelial layer.
• The type I pneumocytes become so thin that the adjacent
capillaries bulge into the alveolar saccules.
• By the late fetal period, the lungs are capable of respiration
because the alveolocapillary membrane (pulmonary diffusion
barrier or respiratory membrane) is sufficiently thin to allow gas
exchange.
• Although the lungs do not begin to perform this vital function
until birth, they are well developed so that they are capable of
functioning as soon as the baby is born.
• Diagrammatic sketches of histologic sections illustrating the stages of lung development.
• A and B, Early stages of lung development. C and D, Note that the alveolocapillary
membrane is thin and that some capillaries bulge into the terminal sacs and alveoli
• At the beginning of the alveolar stage, each respiratory
bronchiole terminates in a cluster of thin-walled
alveolar sacs, separated from one another by loose
connective tissue.
• These saccules represent future alveolar ducts.
• The transition from dependence on the placenta for gas
exchange to autonomous gas exchange requires the
following adaptive changes in the lungs:
- Production of surfactant in the alveolar sacs
- Transformation of the lungs from secretory into
gas exchanging organs
- Establishment of parallel pulmonary and
systemic circulations
• Characteristic mature alveoli do not form until after
birth; approximately 95% of mature alveoli develop
postnatally.
• Before birth, the primordial alveoli appear as small
bulges on the walls of respiratory bronchioles and
alveolar sacs.
• After birth, the primordial alveoli enlarge as the lungs
expand, but the greatest increase in the size of the
lungs results from an increase in the number of
respiratory bronchioles and primordial alveoli rather
than from an increase in the size of the alveoli.
• Alveolar development is largely completed by 3 years
of age, but new alveoli may be added until
approximately 8 years of age.
• Unlike mature alveoli, immature alveoli have the
potential for forming additional primordial alveoli.
• As these alveoli increase in size, they become mature
alveoli. The major mechanism for increasing the number
of alveoli is the formation of secondary connective tissue
septa that subdivide existing primordial alveoli.
• Initially, the septa are relatively thick, but they are soon
transformed into mature thin septa that are capable of
gas exchange.
• Lung development during the first few months after
birth is characterized by an exponential increase in the
surface area of the air-blood barrier through the
multiplication of alveoli and capillaries.
• Approximately 150 million primordial alveoli, one half of
the adult number, are present in the lungs of a full-term
newborn infant.
• On chest radiographs, therefore, the lungs of newborn
infants are denser than adult lungs.
• Between the third and the eighth years, the adult
complement of 300 million alveoli is achieved.
• At birth, the lungs are approximately half-filled with fluid derived
from the amniotic cavity, lungs, and tracheal glands.
• Aeration of the lungs at birth is not so much the inflation of empty
collapsed organs but rather the rapid replacement of intra-alveolar
fluid by air. The fluid in the lungs is cleared at birth by three routes:
• Through the mouth and nose by pressure on the fetal thorax during
vaginal delivery
• Into the pulmonary arteries, veins, and capillaries
• Into the lymphatics
• In the near term fetus, the pulmonary lymphatic vessels are
relatively larger and more numerous than in the adult. Lymph flow
is rapid during the first few hours after birth and then diminishes.
• Three factors are important for normal lung development:
adequate thoracic space for lung growth, FBMs, and an adequate
amniotic fluid volume.
 Oligohydramnios and Lung Development
• When oligohydramnios (insufficient amount of amniotic
fluid) is severe and chronic because of amniotic fluid
leakage or decreased production, lung development is
retarded and severe pulmonary hypoplasia results from
restriction of the fetal thorax.

Lungs of Newborn Infants

• Fresh healthy lungs always contain some air;
consequently, pulmonary tissue removed from them will
float in water. A diseased lung, partly filled with fluid, may
not float. Of medicolegal significance is the fact that the
lungs of a stillborn infant are firm and sink when placed in
water because they contain fluid, not air.
 Respiratory Distress Syndrome
• This disease (RDS) affects approximately 2% of live
newborn infants; those born prematurely are most
susceptible. These infants develop rapid, labored breathing
shortly after birth.
• RDS is also known as hyaline membrane disease (HMD). An
estimated 30% of all neonatal disease results from HMD or
its complications. Surfactant deficiency is a major cause of
RDS or HMD.
• The lungs are underinflated, and the alveoli contain a fluid
with a high protein content that resembles a glassy or
hyaline membrane.
• This membrane is believed to be derived from a
combination of substances in the circulation and from the
injured pulmonary epithelium.
• It has been suggested that prolonged intrauterine
asphyxia may produce irreversible changes in the type
II alveolar cells, making them incapable of producing
surfactant. There appear to be other causes for an
absence or deficiency of surfactant in premature and
full-term infants.
• All the growth factors and hormones controlling
surfactant production have not been identified, but
corticosteroids and thyroxine, which are involved in
fetal lung maturation, are potent stimulators of
surfactant production.
• Maternal glucocorticoid treatment during pregnancy
accelerates fetal lung development and surfactant
production.
• This finding has led to the routine clinical use of
corticosteroids (betamethasone) for the prevention of RDS in
preterm labor. In addition, administration of exogenous
surfactant (surfactant replacement therapy) reduces the
severity of RDS and neonatal mortality.

Lobe of Azygos Vein

• This lobe appears in the right lung in approximately 1% of
people.
• It develops when the apical bronchus grows superiorly, medial
to the arch of the azygos vein, instead of lateral to it.
• As a result, the vein lies at the bottom of a fissure in the
superior (upper) lobe, which produces a linear marking on a
radiograph of the lungs.
 Congenital Lung Cysts
• Cysts (filled with fluid or air) are thought to be formed
by the dilation of terminal bronchi.
• They probably result from a disturbance in bronchial
development during late fetal life.
• If several cysts are present, the lungs have a
honeycomb appearance on radiographs.
• Congenital lung cysts are usually located at the
periphery of the lung.
 Agenesis of Lungs
• Absence of the lungs results from failure of the
respiratory bud to develop.
• Agenesis of one lung is more common than bilateral
agenesis, but both conditions are rare.
• Unilateral pulmonary agenesis is compatible with life.
• The heart and other mediastinal structures are shifted
to the affected side, and the existing lung is
hyperexpanded.
• Congenital lung cysts.
• A, Chest radiograph (posteroanterior) of an infant showing a large left-sided congenital cystic
adenomatoid malformation (arrow). The heart (asterisk) has shifted to the right. Note the chest tube on
the left side, which was placed on the initial diagnosis of a pneumothorax (air in pleural cavity).
• B, Axial computed tomography image of the thorax in an infant with a large right-sided congenital
bronchogenic cyst (asterisk).
(Courtesy of Dr. Prem S. Sahni, formerly of the Department of Radiology, Children's Hospital, Winnipeg, Manitoba, Canada.)
 Lung Hypoplasia
• In infants with congenital diaphragmatic hernia (see Chapter
8), the lung is unable to develop normally because it is
compressed by the abnormally positioned abdominal viscera.
• Lung hypoplasia is characterized by a markedly reduced lung
volume and hypertrophy of the smooth muscle in the
pulmonary arteries.
• The pulmonary hypertension leads to decreased blood flow
through the pulmonary vascular system as the blood
continues to shunt through the ductus arteriosus.
• Many infants with congenital diaphragmatic hernia die of
pulmonary insufficiency, despite optimal postnatal care,
because their lungs are too hypoplastic for air exchange and
there is too much resistance for pulmonary blood flow to
support extrauterine life.
 Accessory Lung
• A small accessory lung (pulmonary sequestration) is very
uncommon. It is almost always located at the base of the
left lung.
• It does not communicate with the tracheobronchial tree,
and its blood supply is usually systemic rather than
pulmonary in origin.

References
• Sadler, TW (2012). Langmans Medical Embroyology
• Moore K (2014). Clinical Oriented Embryology
 PRACTICE MCQ - EXAMPLE 3. The trachea is lined with
1. A young mother brings her recently born infant pseudostratified ciliated columnar
into your office and complains that the infant gags epithelium with goblet cells. This
and chokes after swallowing milk. A physical
examination indicates excessive saliva and mucus
epithelium is derived from
around the mouth and nose, abdominal distention, (A) Neuroectoderm
pneumonitis, and radiographs indicate air in the
infant's stomach. What is the most likely cause? (B) endoderm
(A) Hypertrophic pyloric stenosis (C) ectoderm
(B) Tracheoesophageal fistula (D) visceral mesoderm
(C) Congenital lobar emphysema
(E) mesoderm of fourth and sixth
(D) Respiratory distress syndrome pharyngeal arches
(E) Pulmonary hypoplasia
2. Within hours after birth, a baby, whose mother
is diabetic, had a rising respiratory rate and 4. Smooth muscle, connective tissue, and
labored breathing. The baby became cyanotic and cartilage of primary bronchi are derived
died. Postmortem histologic examination revealed from which one of the following sources?
collapsed alveoli lined with eosinophilic material.
What is the diagnosis? (A) Neuroectoderm
(A) Congenital emphysema (B) Endoderm
(B) Respiratory distress syndrome (C) Ectoderm
(C) Cystic fibrosis
(D) Visceral mesoderm
(D) Tracheoesophageal fistula
(E) Pulmonary carcinoma (E) Mesoderm of pharyngeal arches 4 and
 7. Collapsed bronchi caused by failure of
5. Components of the blood–air barrier in bronchial cartilage development is indicative
the lung are derived from which of the of which one of the following congenital
following sources? malformations?
(A) Congenital bronchial cysts
(A) Ectoderm only (B) Congenital neonatal emphysema
(B) Visceral mesoderm only (C) Tracheoesophageal fistula
(C) Visceral mesoderm and ectoderm (D) Hyaline membrane disease
(E) Pulmonary hypoplasia
(D) Endoderm and ectoderm
8. Pulmonary hypoplasia is commonly
(E) Visceral mesoderm and endoderm associated with which condition?
6. The respiratory diverticulum initially is (A) Hyaline membrane disease
in open communication with the primitive (B) Diaphragmatic hernia
foregut. Which of the following (C) Tracheoesophageal fistula
embryonic structures is responsible for (D) Congenital bronchial cysts
separating these two structures? (E) Congenital neonatal emphysema
(A) Laryngotracheal groove 9. Development of which one of the
following is the first sign of respiratory
(B) Posterior esophageal folds system development?
(C) Laryngotracheal diverticulum (A) Tracheoesophageal septum
(D) Tracheoesophageal septum (B) Hypobranchial eminence
HISTOLOGY OF THE RESPIRATORY SYSTEM
 Introduction
• A. The respiratory system includes the lungs and a series
of airways that connect the lungs to the external
environment.
• B. The respiratory system can be functionally classified
into two major subdivisions: a conducting portion,
consisting of airways that deliver air to the lungs, and a
respiratory portion, consisting of structures within the
lungs in which oxygen in the inspired air is exchanged for
carbon dioxide in the blood.
• C. The components of the respiratory system possess
characteristic lining epithelia, supporting structures,
glands, and other features, which are summarized in the
Table, below.
 Comparison of Respiratory System
Components
 II. Conducting Portion of the Respiratory System
• This portion of the respiratory system includes the nose,
nasopharynx, larynx, trachea, bronchi, and bronchioles of decreasing
diameters, including and ending at the terminal bronchioles. These
structures warm, moisten, and filter the air before it reaches the
respiratory components, where gas exchange occurs.
A. Nasal cavity
• The nasal cavity is subdivided by the median nasal septum into right
and left nasal cavities, each leading to the paranasal sinuses, thus
providing a large surface area for filtering, moistening, and warming
the inspired air.
• 1. The nares are the nostrils; their outer portions are lined by thin
skin. They open into the vestibule.
• 2. The vestibule is the first portion of the nasal cavity, where the
epithelial lining becomes nonkeratinized. Posteriorly, the lining
changes to respiratory epithelium (pseudostratified ciliated columnar
epithelium with goblet cells).
• a. The vestibule contains vibrissae (thick, short hairs), which
filter large particles from the inspired air.
• b. It has a richly vascularized lamina propria (many venous
plexuses) and contains seromucous glands.
• c. Each nasal cavity contains bony shelves that originate from
the lateral nasal wall and project into the nasal cavity. These are
the superior, middle, and inferior conchae(turbinate bones).
Their structure and placement within the nasal cavity divide it
into separate regions, thereby introducing turbulence to the air
flow. Since they are covered by respiratory epithelium, their
presence increases the surface area for warming, filtering, and
moistening the inspired air.
• d. Paranasal sinuses are air-filled, hollowed out portions of the
sphenoid, frontal, ethmoid, and maxillary bones. These air
sinuses are lined by a thin respiratory epithelium, but the
function of the paranasal sinuses is not known.
 3. Olfactory epithelium
• a. Overview
• (1) The olfactory epithelium is located in the roof of the nasal cavity, on
either side of the nasal septum and on the superior nasal conchae.
• (2) It is a tall, pseudostratified columnar epithelium consisting of olfactory
cells, supporting (sustentacular) cells, and basal cells (stem cells).
• (3) It has a lamina propria that contains many veins and unmyelinated
nerves, and houses Bowman glands.
• b. Olfactory cells are bipolar nerve cells characterized by a bulbous apical
projection (olfactory vesicle) from which several modified cilia extend.
• (1) Olfactory cilia (olfactory hairs)
• (a) are very long, nonmotile cilia that extend over the surface of the
olfactory epithelium. Their proximal third contains a typical 9  2 axoneme
pattern, but their distal two-thirds are composed of nine peripheral singlet
microtubules surrounding a central pair of microtubules.
• (b) act as receptors for odor.
• (2) Supporting (sustentacular) cells
• (a) possess nuclei that are more apically located than
those of the other two cell types. (b) have many
microvilli and a prominent terminal web of filaments.
• (3) Basal cells
• (a) rest on the basal lamina but do not extend to the
surface.
• (b) form an incomplete layer of cells.
• (c) are believed to be regenerative for all three cell
types.
• (4) Bowman glands (serous glands) produce a thin,
watery secretion that is released onto the olfactory
epithelial surface via narrow ducts. Odorous substances
dissolved in this watery material are detected by the
 B. Nasopharynx
• 1. The nasopharynx, the posterior continuation of the
nasal cavities, becomes continuous with the oropharynx
at the level of the soft palate.
• 2. It is lined by respiratory epithelium, whereas the
oropharynx and laryngopharynx are lined by stratified
squamous nonkeratinized epithelium.
• 3. The lamina propria of the nasopharynx, located
beneath the respiratory epithelium, contains mucous and
serous glands as well as an abundance of lymphoid
tissue known as Waldeyer ring, including the pharyngeal
tonsil. When the pharyngeal tonsil is inflamed, it is called
an adenoid.
• 4. Opening into the right and left lateral walls of the
nasopharynx are the auditory tubes (Eustachian tubes),
 C. Larynx
• 1. Overview
• a. The larynx connects the pharynx with the trachea. It functions to
produce sounds and close the air passage during swallowing.
• b. The wall of the larynx is supported by hyaline cartilages (thyroid,
cricoid, and lower part of arytenoids) and elastic cartilages (epiglottis,
corniculate, and tips of arytenoids). c. The laryngeal wall also possesses
skeletal muscle, connective tissue, and glands.
• 2. The vocal cords
• It consist of skeletal muscle (the vocalis muscle), the vocal ligament
(formed by a band of elastic fibers), and a covering of stratified squamous
nonkeratinized epithelium.
• a. Contraction of the laryngeal muscles changes the size of the opening
between the vocal cords, which affects the pitch of the sounds caused by
air passing through the larynx.
• b. Inferior to the vocal cords, the lining epithelium changes to respiratory
epithelium, which lines air passages down through the trachea and
intrapulmonary bronchi.
 3. Vestibular folds (false vocal cords)
• It lies superior to the vocal cords.
• a. These folds of loose connective tissue contain glands,
lymphoid aggregations, and fat cells.
• b. They are covered by stratified squamous
nonkeratinized epithelium.
 D. Trachea and Extrapulmonary (primary)
Bronchi
• 1. Overview
• The trachea, the largest conducting section of the
respiratory system, bifurcates into the right and left
primary bronchi, each of which enters the hilum of the
lung on its side.
• a. The walls of these structures are supported by C-
shaped hyaline cartilages (C-rings), whose open ends
face posteriorly.
• Smooth muscle (trachealis muscle in the trachea)
extends between the open ends of these cartilages.
• b. Dense fibroelastic connective tissue is located
between adjacent C-rings, permitting elongation of the
 2. Mucosa
• a. The respiratory epithelium in the trachea possesses
the following cell types.
• (1) Ciliated cells
• (a) have long, actively motile cilia that beat toward the
mouth.
• (b) move inhaled particulate matter trapped in mucus
toward the oropharynx, thus protecting the delicate
lung tissue from damage.
• (c) also possess microvilli.
• (2) Mature goblet cells are goblet shaped and are
filled with large secretory granules, containing
mucinogen droplets, which are secreted onto the
epithelial surface to trap inhaled particles.
 (3) Small granule-mucous cells (brush cells)
• (a) contain varying numbers of small mucous granules.
• (b) are sometimes called brush cells because of their many uniform
microvilli.
• (c) actively divide and often replace recently desquamated cells.
• (d) may represent goblet cells after they have secreted their
mucinogen.
(4) Diffuse neuroendocrine cells
• (a) are also known as small granule cells, amine precursor uptake
and decarboxylation (APUD cells), or enteroendocrine cells.
• (b) contain many small granules concentrated in their basal
cytoplasm.
• (c) synthesize different polypeptide hormones and serotonin, which
often exert a local effect on nearby cells and structures (paracrine
regulation). The peptide hormones may also enter the bloodstream
and have an endocrine effect on distant cells and structures.
• (5) Basal cells
• (a) are short cells that rest on the basal lamina, but do
not extend to the lumen; thus, this epithelium is
pseudostratified.
• (b) are stem cells that are able to divide and replace the
other cell types.
• b. The basement membrane is a very thick layer
underlying the epithelium.
• c. The lamina propria is a thin layer of connective tissue
that lies beneath the basement membrane. It contains
longitudinal elastic fibers separating the lamina propria
from the submucosa.
• 3. The submucosa is a connective tissue layer
containing many seromucous glands.
• E. Intrapulmonary bronchi (secondary bronchi)
• 1. Intrapulmonary bronchi arise from subdivisions of the
primary bronchi upon entering the hilum of the lung. It
is at this level that the cartilaginous rings of the bronchi
are replaced with plates of irregularly shaped hyaline
cartilage.
• 2. They divide many times and give rise to lobar and
segmental bronchi.
• 3. They are lined by respiratory epithelium.
• 4. Spiraling smooth muscle bundles separate the lamina
propria from the submucosa, which contains
seromucous glands
• F. Primary and terminal bronchioles lack glands in
their submucosa. Their walls contain smooth muscle
rather than cartilage plates (Figure 15.2).
• 1. Primary bronchioles
• a. Primary bronchioles have a diameter of 1 mm or less.
• b. They are lined by epithelium that varies from ciliated
columnar with goblet cells in the larger airways to
ciliated cuboidal with Clara cells in the smaller
passages.
• c. They divide to form several terminal bronchioles after
entering the pulmonary lobules.
• 2. Terminal bronchioles
• a. Terminal bronchioles are the most distal part of the
conducting portion of the respiratory system
• b. They have a diameter of less than 0.5 mm.
• c. They are lined by a simple cuboidal epithelium
that contains mostly club cells (formerly known as
Clara cells), some ciliated cells, and no goblet cells. d.
Function. Club cells have the following functions:
• (1) Club cells divide, and some of them differentiate
to form ciliated and nonciliated cells.
• (2) They secrete a surfactant-like material that reduces
alveolar surface tension, preventing the collapse of
alveoli. They also produce club cell secretory protein
whose function is assumed to be the protection of the
respiratory epithelium.
• (3) They metabolize airborne toxins, a process that is
carried out by cytochrome P450 enzymes in their
abundant smooth endoplasmic reticulum (SER).
 Clinical Considerations: Asthma
• 1. Asthma is marked by widespread constriction of smooth muscle
in the bronchioles, causing a decrease in their diameter.
• 2. It is associated with extremely difficult expiration of air,
accumulation of mucus in the passageways, and infiltration of
inflammatory cells.
• 3. It is often treated with drugs, such as albuterol, that act to relax
the bronchiolar smooth muscle cells and dilate the passageways
and/or with corticosteroids, which are anti-inflammatory.
• 4. Recent studies have demonstrated that there are taste receptors
on the smooth muscle cells of bronchioles of the lungs that respond
to bitter tastes, and when stimulated by a bitter tastant, they cause
bronchiolar smooth muscles to relax and the bronchioles to open to
90% of their normal volume.
• Current work is proceeding to develop aerosolized substances that
can be used to stimulate these receptors
 Respiratory Portion of the Respiratory System
• This portion of the respiratory system includes the
respiratory bronchioles, alveolar ducts, alveolar sacs,
and alveoli, all in the lung.

• The exchange of gases takes place in this portion of the

respiratory system.
Components of the
respiratory portion of the
respiratory system, including
a respiratory bronchiole,
alveolar duct, and alveolar
sac, are illustrated, as well as
the exchange of oxygen (O2)
and carbon dioxide (CO2)
across the blood– gas barrier.

(From Gartner LP, Hiatt JL. Color Atlas of

 A. Respiratory bronchioles
• 1. The respiratory bronchioles mark the transition from
the conducting to the respiratory portion of the
respiratory system.

• 2. They are lined by a simple cuboidal epithelium that

contains mostly club cells and some ciliated cells,
except where their walls are interrupted by alveoli, the
sites where gas exchange occurs and where the lining
abruptly changes to a simple epithelium composed of
highly attenuated squamous cells.
 B. Alveolar ducts
• 1. Alveolar ducts are linear passageways continuous
with the respiratory bronchioles.
• 2. Their walls consist of adjacent alveoli, which are
separated from one another only by an interalveolar
septum.
• 3. They are the most distal portion of the respiratory
system to contain smooth muscle cells, which rim the
openings of adjacent alveoli and which often appear as
knobs in histological sections.
• 4. Alveolar ducts are lined by type II pneumocytes and
the highly attenuated simple squamous epithelium of
type I pneumocytes
• D. Alveoli
• 1. Overview
• a. Alveoli are pouch-like evaginations about 200 μm in diameter
in the walls of respiratory bronchioles, in alveolar ducts, and in
alveolar sacs.
• b. They have thin walls, across which oxygen and carbon
dioxide diffuse between the air and the blood
• c. They are separated from each other by interalveolar septa
that may contain one or more alveolar pores (pores of Kohn).
These pores permit equalization of pressure between alveoli.
• d. They are rimmed by elastic fibers at their openings (except in
alveolar ducts, where they are rimmed by smooth muscle cells)
and are supported by many reticular fibers in their walls. e.
They are lined by a highly attenuated simple squamous
epithelium composed of type I and type II pneumocytes.
A low-magnification electron
micrograph showing part of a
terminal or respiratory bronchiole
lined by a simple cuboidal
epithelium composed of two cell
types: Clara cells (CL) and
ciliated cells (C).

In the wall of the bronchiole,

smooth muscle cells (M) and
elastic tissue (E) are present. A
venule (V) containing a white
blood cell, several capillaries
(arrowheads) cleared of blood
cells, and alveoli (A) lined by the
markedly thin cytoplasm of type I
pneumocytes (P1) are also
present (×1,500).
A light micrograph of an alveolar duct
(AD) leading from a respiratory
bronchiole into an alveolar sac (AS).

The alveolar duct consists of adjacent

alveoli, separated from one another only
by an interalveolar septum.

At the rims of the adjacent alveoli are a

few smooth muscle cells (arrow) that
appear as knobs in histological sections.

Notice that the rims of alveoli (A) in the

alveolar sac do not contain smooth
muscle
• 2. Alveolar cells
• a. Type I pneumocytes (type I alveolar cells)
• (1) cover about 95% of the alveolar surface and form
part of the blood–gas barrier where exchange of oxygen
and carbon dioxide occurs.
• (2) have an extremely thin cytoplasm that may be less
than 80 nm thick (see Figure 15.4).
• (3) form tight junctions with adjacent cells.
• (4) may have phagocytic capabilities.
• (5) are not able to divide.
• b. Type II pneumocytes (type II alveolar cells; great alveolar
cells; granular pneumocytes; septal cells)
• (1) are cuboidal and are most often found near septal intersections.
• (2) bulge into the alveolus and have a free surface that contains short
microvilli around their peripheral borders.
• (3) are able to divide and regenerate both types of alveolar
pneumocytes.
• (4) form tight junctions with adjacent cells.
• (5) synthesize pulmonary surfactant, which is stored in cytoplasmic
lamellar bodies. (a) Structure—Pulmonary surfactant.
• Pulmonary surfactant consists of dipalmitoylphosphatidylcholine,
phospholipids, the four apolipoproteins, surfactant-associated
proteins (known as SP-A, SP-B, SP-C, and SP-D), and cholesterol. It
forms tubular myelin (a network configuration) when it is first
released from lamellar bodies; it then spreads to produce a
monomolecular film over the alveolar surface, forming a lower
aqueous phase and a superficial lipid phase.
Electron micrograph of a type
II pneumocyte that
synthesizes surfactant and
stores it in lamellar bodies
(LB) in its cytoplasm.

Type II pneumocytes are

present mainly near the
septal intersections and line
only small portions of the
alveoli (A).

They possess microvilli

 (b) Function—Pulmonary surfactant.

• Pulmonary surfactant reduces the surface tension at the air–

liquid interface of the alveolar surface, permitting the alveoli to
expand easily during inspiration and preventing alveolar collapse
during expiration.

• Additionally, surfactant reduces fluid accumulation in the alveoli.

• Moreover, SP-A and SP-D, apolipoproteins of the surfactant,

participate in innate immunity by binding to bacterial and viral
surfaces, and in that fashion opsonizing them.

• The opsonized microorganisms are recognized and phagocytosed

by macrophages (dust cells) of the lung.
 Hyaline membrane disease; infant respiratory
distress syndrome
• 1. Hyaline membrane disease is frequently observed in
premature infants (28 weeks’ gestational age) who lack
adequate amounts of pulmonary surfactant.

• 2. It is characterized by labored breathing, which results

from difficulty expanding the alveoli because of a high
alveolar surface tension.

• 3. If detected before birth, hyaline membrane disease

can often be prevented by prolonging pregnancy and
sometimes by administering glucocorticoids to the
expectant mother a few days prior to delivery to help
 Spontaneous pneumothorax
• A spontaneous pneumothorax is the collection of gas in
the pleural cavity, the potential space between the
visceral and parietal pleurae.
• It causes sudden sharp, severe chest pain on the same
side as the affected lung and leads to shortness of
breath.
• The condition occurs most often in young people who
have no known underlying pulmonary disease. But
computed tomography scans typically reveal blebs near
the lung surface that rupture, allowing gas to invade the
pleural space and causing the lung to collapse (either
partially or completely).
• A minor lung collapse will often resolve on its own, but
when the pneumothorax is larger, a needle or tube is
 c. Alveolar macrophages (alveolar phagocytes;
dust cells)
• (1) are the principal mononuclear phagocytes of the
alveolar surface.

• (2) remove inhaled dust, bacteria, and other particulate

matter trapped in the pulmonary surfactant, thus
providing a vital line of defense in the lungs.

• (3) migrate to the bronchioles after filling with debris.

From there, they are carried via ciliary action to the
upper airways, eventually reaching the oropharynx,
where they are either swallowed or expectorated.
 Asbestosis
• 1. Asbestosis is a pulmonary disease caused by inhaling
asbestos fibers (used in insulation materials, tiles, etc.).
• 2. The fibers deposit in the alveolar ducts and alveoli.
The smaller fibers are phagocytosed by macrophages,
but the larger ones penetrate the lung interstitium.

• 3. Activated macrophages release inflammatory

mediators, which lead to interstitial pulmonary fibrosis
in the walls of respiratory bronchioles, alveolar ducts,
and alveoli.

• 4. Asbestos bodies, fibers 10 to 50 µm long encrusted

with beads of protein, form in the interstitium and
 Emphysema
• 1. Emphysema results from destruction of alveolar walls and
formation of large cyst-like sacs, reducing the surface area
available for gas exchange.
• 2. It is marked by decreased elasticity of the lungs, which are
unable to recoil adequately during expiration. In time, the lungs
expand and enlarge the thoracic cavity (barrel chest).
• 3. Emphysema is associated with exposure to cigarette smoke
and other substances that inhibit `1-antitrypsin, a protein that
normally protects the lungs from the action of elastase produced
by alveolar macrophages.
• 4. It can be a hereditary condition resulting from a defective α1-
antitrypsin. In such cases, gene therapy with recombinant α1-
antitrypsin is being used in an effort to correct the problem, and
it has recently been successful in boosting the availability of this
protective protein.
• E. Interalveolar septum

• 1. The interalveolar septum is the wall, or partition,

between two adjacent alveoli.
• 2. It is bounded on its outer surfaces by the extremely
thin, simple, squamous epithelium lining the alveoli.
• 3. It contains many elastic and reticular fibers in its
thicker regions.
• 4. It houses continuous capillaries in its central (interior)
region.
• 5. It accommodates the blood–gas barrier, which
separates the alveolar airspace from the capillary
lumen. a. Structure—Blood–gas barrier.
• (1) The thinnest regions of the barrier are 0.2 μm
or less in thickness and consist of the following
layers:
• (a) Type I pneumocytes and layer of surfactant lining
the alveolar airspace
• (b) Fused basal laminae of type I pneumocytes and
capillary endothelial cells
• (c) Endothelium of the continuous capillaries within the
interalveolar septum
• (2) Thicker regions of the barrier measure as much as
0.5 μm across and have an interstitial area interposed
Electron micrograph
showing the blood–gas
barrier in the lung, which
permits the exchange of
gases between the
alveolar airspace and the
blood.

Oxygen diffused from the

alveolus (A) into the
capillary containing
erythrocytes (RBC) and
carbon dioxide diffused
from the capillary blood
into the alveolus.

The barrier shown here

consists of the following
 Carbon monoxide poisoning
• 1. Carbon monoxide is an odorless, tasteless gas that
binds to hemoglobin in red blood cells with a greater
affinity than does oxygen. It is produced whenever fuel-
burning appliances are used, which explains the
importance of using carbon monoxide detectors.

• 2. Individuals exposed to carbon monoxide are often

unaware of the symptoms it may cause (such as
nausea, headache, and sleepiness). Death may occur as
the gas replaces oxygen in red blood cells of the lung
and blocks the delivery of oxygen to tissues of the body.

• 3. Treatment consists of exposing the patient to 100%

 Lung Lobules
• A. Lung lobules vary greatly in size and shape, but each
has an apex directed toward the pulmonary hilum and a
wider base directed outward.

• B. Each lobule contains a single primary bronchiole,

which enters at the apex and branches to form five to
seven terminal bronchioles.

• The terminal bronchioles in turn divide, ultimately giving

rise to alveoli at the base of the lobule
 Pulmonary Vascular Supply
A. Pulmonary artery
• 1. The pulmonary artery carries blood to the lungs to be
oxygenated.
• 2. It enters the root of each lung and extends branches along
the divisions of the bronchial tree. 3. It enters lung lobules,
where its branches follow the bronchioles (see Figure 15.2).
B. Pulmonary veins
• 1. In lung lobules, pulmonary veins run in the intersegmental
connective tissue, separated from the arteries.
• 2. After leaving the lobules, the pulmonary veins come close
to divisions of the bronchial tree and run parallel to branches
of the pulmonary artery as they accompany bronchi to the
root of the lung
 C. Bronchial arteries and veins
• 1. Bronchial arteries and veins provide nutrients to and remove
wastes from the nonrespiratory portions of the lung (bronchi,
bronchioles, interstitium, and pleura).
• 2. They follow the branching pattern of the bronchial tree and form
anastomoses with the pulmonary vessels near capillary beds.

Pulmonary Nerve Supply

• The pulmonary nerve supply consists primarily of autonomic fibers
to the smooth muscle of bronchi and bronchioles. Axons are also
present in the thicker parts of the interalveolar septa.
• A. Parasympathetic stimulation causes contraction of pulmonary
smooth muscle.
• B. Sympathetic stimulation causes relaxation of pulmonary smooth
muscle and can be mimicked by certain drugs that cause dilation of
bronchi and bronchioles.
QUESTIONS & ANSWERS 3. The trachea possesses which one of the
• Directions: Each of the numbered items or following components?
incomplete statements in this section is followed
by answers or completions of the statement. (A) Irregular cartilage plates in its wall
Select the ONE lettered answer that is BEST in (B) Skeletal muscle in its wall
each case.
1. Characteristics of olfactory epithelium include
(C) An epithelium containing only two cell
which one of the following? types
(A) It is located in the inferior region of the nasal (D) A thick basement membrane
cavity. underlying its epithelium
(B) It is classified as simple columnar. (E) Bowman glands in its lamina propria
(C) It has an underlying lamina propria containing
mucous glands. 4. Which of the following statements
(D) It has modified cilia, which act as receptors for concerning respiratory bronchioles is true?
odor. (F) No gas exchange occurs in them.
(E) It is unable to regenerate. (G)They do not have alveoli forming part of
2. Which of the following statements concerning their wall.
terminal bronchioles is true?
(A) They are part of the conducting portion of the (H) They contain goblet cells in their lining
respiratory system. epithelium.
(B) They function in gas exchange. (I) They are included in the conducting
(C) They do not contain ciliated cells. portion of the respiratory system.
(D) They have cartilage plates present in their walls. (J) Ciliated cells comprise a portion of their
(E) They do not contain secretory cells. lining epithelium.
5. True statements about asthma include which one of 8. Which one of the following is characterized
the following?
by interstitial pulmonary fibrosis?
(A) It is due to a loss of lung elasticity.
(A) Asbestosis
(B) It eventually causes the lungs to expand and leads to
a barrel chest. (B) Asthma
(C) It is associated with difficulty expiring air from the (C) Carbon monoxide poisoning
lungs.
(D) Emphysema
(D) It may be helped by gene therapy using recombinant
α1-antitrypsin. (E) Hyaline membrane disease.
(E) It is usually not associated with inflammation. 9. Which one of the following is associated with
6. Which of the following statements concerning alveolar a barrel chest?
macrophages is true?
(F) Asbestosis
(F) They secrete α1-antitrypsin.
(G) They secrete elastase. (G) Asthma
(H) They originate from blood neutrophils. (H) Carbon monoxide poisoning
(I) They may play a role in causing hyaline membrane (I) Emphysema
disease.
(J) Hyaline membrane disease
(J) They secrete small amounts of surfactant.
7. Which one of the following disorders may in some
10. Which one of the following is frequently
cases be successfully treated with antielastase (α1- treated successfully with glucocorticoids?
antitrypsin)? (K) Asbestosis
(K) Asbestosis
(L) Asthma
(L) Asthma
(M) Carbon monoxide poisoning
(M) Carbon monoxide poisoning
(N) Emphysema (N) Emphysema
 Answers & Explanations
• 1. D. The olfactory epithelium possesses nonmotile cilia, which act as
receptors for odor. They are extensions of the bipolar nerve cells that
form part of this tall, pseudostratified epithelium located in the roof of
the nasal cavity. Bowman glands, which lie in the lamina propria
beneath this epithelium, produce a watery secretion, which moistens
the olfactory surface.
• 2. A. Terminal bronchioles are the most distal components of the
conducting portion of the respiratory system. They lack alveoli and
thus do not function in gas exchange. They are lined by an epithelium
composed of two cell types: secretory (Clara) cells and ciliated cells.
Cartilage is not present in bronchioles.
• 3. D. The pseudostratified ciliated columnar epithelium lining the
trachea rests on a thick basement membrane and contains five cell
types. The trachea possesses C-shaped cartilages with smooth muscle
(the trachealis) extending between their ends. Bowman glands are
found only in the nasal cavity and produce a thin watery secretion.
• 4. E. Respiratory bronchioles have alveoli interrupting their walls,
so some gas exchange takes place at this level. Their remaining
walls are lined by a simple cuboidal epithelium consisting of
Clara cells and ciliated cells. Respiratory bronchioles are
categorized as part of the respiratory portion of the system.
• 5. C. Asthma results from the constriction of smooth muscle in
the bronchioles, which decreases their diameter and makes the
expiration of air very difficult. Mucus accumulates in the airways,
and inflammatory cells invade the bronchiolar walls.
• 6. B. Alveolar macrophages secrete elastase. Normally, α1-
antitrypsin, a serum protein, interacts with elastase, thereby
protecting the lung against damage that may lead to
emphysema. Alveolar macrophages, like all macrophages, arise
from blood monocytes; they do not secrete surfactant; and they
are unrelated to the pathogenesis of hyaline membrane diseases.
• 7. D. Hereditary forms of emphysema are now being treated
with recombinant α1-antitrypsin, which has antielastase
activity.
• 8. A. Inhaling asbestos fibers causes interstitial pulmonary
fibrosis in the walls of respiratory bronchioles, alveolar ducts,
and alveoli. Asbestos bodies are a classic feature of
asbestosis. After prolonged heavy exposure to asbestos, this
disease may progress to mesothelioma (a malignant tumor).
• 9. D. A loss of lung elasticity in emphysema makes it difficult
for the lungs to recoil normally during expiration. The lungs
and thoracic cavity enlarge, producing a barrel chest.
• 10. E. Glucocorticoids, which stimulate synthesis of
pulmonary surfactant, are often administered to the
expectant mother a few days prior to delivery to prevent or
alleviate hyaline membrane disease in the premature infant.
References
• Gartner, LP and Hiatt JL . Cell Biology & Histology Board
Review Series 7th Edn
• Gray's Anatomy The Anatomical Basis of Clinical
Practice, 41e
• Larsen's Human Embryology
• Langman's Medical Embryology, 12th Edition
• Mescher A. Junqueira's Basic Histology. Text and Atlas
16ed 2021