MICRO A 2.
8 – DEVELOPMENT OF RESPIRATORY SYSTEM
FEU-NRMF Institute of Medicine
Lecturer: Alvin B. Vibar, MD - 8.8.13
DEVELOPMENT OF THE RESPIRATORY SYSTEM
 Development of the larynx
 Development of the trachea
 Development of the bronchi
 Development of the lungs
 Clinical Considerations
EMBRYONIC PERIOD (wks 3-8): period of organogenesis
AT 4TH WEEK --respiratory system starts to develop
1st sign of Dev’t : Formation of the laryngotracheal
diverticulum in the ventral wall of the primitive foregut
 Diverticulum
- outpouching; open communication w/ foregut
- germ layer of origin:endoderm
Division of Forgut Into Laryngotracheal
Tube(respiratoty) & Esophagus(digestive)
1. Diverticulum expands in caudal direction
2. Median longitudibal groove develops along with
the tracheoesophageal folds
3. Tracheoesophageal folds fuse in the midline to
form the tracheoesophageal septum
4. Primitive foregut is now divisible into:
 laryngotracheal tube (ventral) (resp)
 esophagus (dorsal) (digestive)
What happens if tracheoesophageal septum did not
develop to separate respiratory & digestive systems?
- Open communication w/ the 2 systems & we call it
FISTULA(abnormal communication bet 2 structurs)
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DEVELOPMENT OF THE LARYNX
- Opening of the laryngotracheal diverticulum into
the primitive foregut becomes the laryngeal orifice
- Laryngeal tissues/cells derived from:
 epithelium & glands: endoderm
 muscles(skeletal) : somitomeric mesoderm of
pharyngeal arches 4 & 6
 connective tissue & cartilages: neural crest cells
Development of the Larynx
Review of pharyngeal arches
Pharyngeal arches 4&6 (develop at weeks 4-5)
- give rise to muscles of phonation
- supplied by vagus nerve
2 branches of vagus nerve
 superior laryngeal nerve: supply precothyroid
 inferior/recurrent laryngeal nerve: will supply
all muscles EXCEPT PRECOTHYROID
DEVELOPMENT OF THE TRACHEA
- Tracheal tissues/cells derived from:
 epithelium & glands: endoderm
 smooth muscle, connective tissue & C-shaped
cartilage rings: visceral/sphlancnic mesoderm
Clinical Consideration: TRACHEOESOPHAGEAL FISTULA
- Abnormal communication bet trachea & esophagus
- Results from improper division of the foregut by the
tracheoesophageal septum
- Assoc w/ Esophageal atresia (EA for this trans only)
MICRO A 2.8 – DEVELOPMENT OF RESPIRATORY SYSTEM
FEU-NRMF Institute of Medicine
Lecturer: Alvin B. Vibar, MD - 8.8.13 1B-Medicine

*Esophageal atresia: esophagus will end as a blind V – vertebral anomalies

puouch & will not continue to the stomach A – anal atrecia
C – cardiac defects
Types of TEF: T – TEF
A. EA + TEF at distal end E – esophageal atresia
(most common: 85-90%) R – renal agenesis
B. TEF only L – limb defects
C. EA + TEF at proximal end
DEVELOPMENT OF THE BRONCHI
D. EA + TEF at distal & proximal ends - Bronchial tissues/cells derived from:
 Epithelium & glands: endoderm
Clinical Manifetations:  smooth muscle, connective tissue & cartilage:
 Accumulation of milk in the mouth visceral mesoderm
 Excessive accum of saliva or  visceral pleura (covering outside bronchi):
visceral mesoderm
mucus in the nose & mouth
 parietal pleura (covering inside the body wall):
 Episodes of gagging & cyanosis somatic mesoderm
after swallowing milk
 Abdominal distention (because
the air in trachea will go to the
stomach) **not seen in TYPE C**
 Pulmonary distress
 Reflux of gastric contents into the lungs, causing
Pneumonitis (EXCEPT IN TYPE C)
*first feeding is normal healthy but fluid returns to Stages of Bronchial Development
1. Lung bud divides into two bronchial buds
nose & mouth and respiratory distress occurs in
2. Bronchial buds enlarge to form Primary bronchi
subsequent feedings
(Right is larger & more vertical than Left)(Week 5)
3. Primary further subdivide into Secondary/Lobar
CASE:
bronchi (3 on the right; 2 on the left)
A prenatal ultrasound revealed polyhydraminos & at
4. Secondary further subdivide into Tertiary/
birth, the baby had excessive fluid in its mouth. What
Segmental bronchi (10 on the right; 8-9 on left)
type of birth defect might be present & what is its
5. Bronchi expand laterally and caudally into a space:
embryological origin?
primitive pleural cavity that will become the
Birth defect: TEF w/ EA
pleural space
Clinical Manifestations:
 Excessive accum of saliva or mucus in the nose &
mouth
 Episodes of gagging & cyanosis after swallowing
milk
 Abdominal distention after crying
 Reflux of gastric contents into the lungs, causing
Pneumonitis (EXCEPT IN TYPE C)
Embryological Origin: improper division of the
tracheoesophageal septum
**TEF associated with POLYHYDRAMINOS
**TEF is associated with VACTREL

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MICRO A 2.8 – DEVELOPMENT OF RESPIRATORY SYSTEM
FEU-NRMF Institute of Medicine
Lecturer: Alvin B. Vibar, MD - 8.8.13
DEVELOPMENT OF THE LUNGS
- Lung matures in proximal-distal direction
Periods of development:
 Pseudoglandular Period
 Canalicular Period
 Terminal sac Period
 Alveolar sac Period
Conducting part
- passageway of air
- nose to terminal bronchioles
Respiratory part
- exchange of gas
- resp bronchiole, alveolar duct, alveolar sac, alveolus
PSEUDOGLANDULAR PERIOD (Weeks 5- 16)
- Developing lung resembles branching of a
compound exocrine gland
- Histologic structures involved in gas exchange are
not yet formed: respiration is NOT possible
- Branching continued to form terminal bronchioles,
but no respiratory bronchioles present yet
- Premature fetuses born during this period cannot
survive
CANALICULAR PERIOD (Weeks 16 - 26)
- Respiratory bronchioles & terminal sacs develop
(primitive alveoli but lining is still cuboidal
respiratory epithelium)
- Vascularization increases due to capillaries forming
in visceral mesoderm
- Premature fetuses born at less than 20 weeks
gestation rarely survive
Note: Respiration becomes possible when cells of
the cuboidal respiratory bronchioles change into
flat/squamous lining
TERMINAL SAC PHASE (Week 26 – Birth)
- # of terminal sacs and vascularization increases
- Differentiation of Type I pneumocytes and Type II
pneumocytes begins
 Type I pneumocytes : forms lining (simple
squamous so respiration is possible) that
contacts with the capillaries
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 Type II pneumocytes: secrete surfactants to
prevent collapse of alveoli
- Premature fetuses born between week 25 to 28 can
survive with intensive care
* 7th month: gas exchange between blood & air in
the primitive alveoli is possible
ALVEOLAR SAC PERIOD (Birth – Age 8 y/o)
- Lung dev’t continues after birth until about 8 y/o
(300 million alveoli is reached)
- Terminal sacs develop into mature alveolar ducts
and alveoli
- Mature blood: air barrier is established
CLINICAL CONSIDERATIONS:
1. AERATION AT BIRTH (not a defect)
- Before birth: Lungs are half- filled w/ fluid derived
from lungs, amniotic cavity & tracheal gland
- At birth:
 Replacement of fluid w/ air in the newborn’s
lung
 fluid is eliminated through nose & mouth, and
through resorption by pulmonary capillaries &
lymphatics
*Fresh healthy lung always contain some air &
pulmonary tissue removed from them will float in
water; a diseased lung however, partly filled with
water will not float
- Medicolegal significance: lungs of stillborn (dead)
infant are firm & will sink in water
MICRO A 2.8 – DEVELOPMENT OF RESPIRATORY SYSTEM
FEU-NRMF Institute of Medicine
Lecturer: Alvin B. Vibar, MD - 8.8.13 1B-Medicine

2. RESPIRATORY DISTRESS SYNDROME/ HYALINE

MEMBRANE DISEASE
- Caused by deficiency or absence of surfactant w/c
coats the inside of alveoli & maintain alveolar
patency
- Collapsed alveoli will contain a high protein fluid &
hyaline membrane
- Very common in premature infants & infants of
diabetic mothers
- Mothers in premature labor is given with
corticosteroid (betamethasone) injection to
accelerate fetal lung development & production of
lung surfactant

3. PULMONARY AGENESIS
- No formation of parts respiratory system
- Complete absence of lungs, bronchi & alveoli
- Failure of lung buds to develop

*agenesis: no formation at all

* hypoplasia: there is formation but they are
underdeveloped

4. PULMONARY HYPOPLASIA
- Poorly developed bronchial tree w/ abnormal
histology
- Associated w/ renal agenesis
Renal agenesis= no development of kidney, no
urine & will lead to oligohydraminos
**Oligohydraminos: insufficient amt of amniotic
fluid
- Fluid in lungs is an important stimulus for lung
development

At prenatal screening:
- Oligohydraminos = pulmonary hypoplasia
- Polyhydraminos = esophageal atrecia w/
tracheoesophageal fistula

Happy Studying!!