Respiratory System

I. OVERVIEW (Figure 10 1)

A. The first sign of respiratory system development is the formation of a respiratory di^ verticulum in the ventral wall of the foregut.

B. The distal end of the respiratory diverticulum enlarges to form the lung bud.

C. The lung bud divides into two bronchial buds that branch into the primary, sec~ ondary, and tertiary bronchi.

D. The respiratory diverticulum is initially in open communication with the foregut, but eventually this communication is obliterated by the formation of the tracheoe^ sophageal septum, which separates the trachea from the esophagus.

E. The Hox complex, FGF-10 (fibroblast growth factor), BMP-4 (bone morphogenetic protein), N-myc (a proto-oncogene), syndecan (a proteoglycan), tenasin (an extracellular matrix protein), and epimorphin (a protein) appear to play a role in the development of the respiratory system.

II. DEVELOPMENT OF THE TRACHEA

A. Formation. The respiratory diverticulum elongates considerably before the bronchial buds appear. This elongated portion of the respiratory diverticulum forms the trachea.

B. Clinical correlation: tracheoesophageal fistula (Figure 10-2)

1. Definition. Tracheoesophageal fistula is an abnormal communication (fistula) between the trachea and the esophagus, which is caused by improper formation of the tracheoesophageal septum. It is generally associated with esophageal atresia and polyhydramnios. The most common type (90% of all cases) is esophageal atresia with a fistula between the esophagus and the distal one-third of the trachea.

2. Clinical features include excessive accumulation of saliva or mucus in the infant's nose and mouth; episodes of gagging and cyanosis after swallowing milk; abdominal distention after crying; and reflux of gastric contents into the lungs, causing pneumonitis.

3. Diagnostic features include the inability to pass a catheter into the stomach and radiographs demonstrating air in the infant's stomach.

III. DEVELOPMENT OF THE BRONCHI

A. Formation

1. The lung bud divides into two bronchial buds.

Bronchial Diverticula

Esophagus

5 Weeks

6 Weeks

Respiratory diverticulum

4 Weeks

Visceral mesoderm

Right lung

Left lung

Figure 10-1. Development of the respiratory system at weeks 4-6.

2. In week 5 of development, bronchial buds enlarge to form primary bronchi. The right primary bronchus is larger and more vertical than the left primary bronchus; this relationship persists throughout adult life and accounts for the greater likelihood of foreign bodies lodging on the right side than on the left.

3. Primary bronchi further subdivide into secondary bronchi (three on the right side and two on the left side, corresponding to the lobes of the adult lung).

Esophageal Fistula Adults
Figure 10-2. Tracheoesophageal fistula. In 90% of these cases, there is esophageal atresia with a fistula between the esophagus and the distal one-third of the trachea.

4. Secondary bronchi further subdivide into tertiary (or segmental) bronchi (10 on the right side and 8 or 9 on the left side). These are the primordia of the bronchopulmonary segments.

5. As the bronchi develop, they expand laterally and caudally into a space known as the primitive pleural cavity; visceral mesoderm covering the outside of the bronchi develops into visceral pleura, and somatic mesoderm covering the inside of the body wall develops into parietal pleura.

B. Clinical correlations

1. Bronchopulmonary segment. This segment of lung tissue is supplied by a tertiary (segmental) bronchus. Surgeons can resect diseased lung tissue along bronchopulmonary segments rather than removing the entire lobe.

2. Congenital neonatal emphysema is an overdistention with air of one or more lobes of the lung. Emphysema is caused by collapsed bronchi due to failure of bronchial cartilage to develop. Air can be inspired through collapsed bronchi, but cannot be expired.

3. Congenital bronchial cysts (bronchiectasis) are caused by dilatation of the bronchi. Cysts may be solitary or multiple and can be filled with air or fluid. Multiple cysts demonstrate a honeycomb appearance on a radiograph. The honeycomb appearance may be a useful diagnostic tool on a radiograph.

IV. DEVELOPMENT OF THE LUNGS (Figure 10-3 and Table 10-1)

A. Formation. The lungs undergo four periods of development: the glandular period, canalicular period, terminal sac period, and alveolar period.

B. Clinical correlations

1. Aeration at birth a. Aeration is the replacement of fluid by air in the newborn's lungs. At birth, the lungs are half-filled with fluid derived from the lungs (main source), amniotic cavity, and tracheal glands. The fluid is eliminated at birth through the nose and mouth during delivery, and later through resorption by pulmonary capillaries and lymphatics.

b. The lungs of a stillborn baby will sink when placed in water, because they contain fluid rather than air.

2. Pulmonary agenesis involves the complete absence of lungs, bronchi, and vasculature. This rare condition is caused by failure of bronchial buds to develop. Unilateral pulmonary agenesis is compatible with life.

3. Pulmonary hypoplasia involves a poorly developed bronchial tree with abnormal histology. It may be partial (involving a small segment of lung) or total (involving the entire lung). It can be found in association with:

a. A congenital diaphragmatic hernia (i.e., a herniation of abdominal contents into the thorax compresses the developing lung; see Chapter 15).

b. Bilateral renal agenesis (see Chapter 8 V A), which causes an insufficient amount of amniotic fluid (oligohydramnios; see Chapter 5 111 C) to be produced, which in turn increases pressure on the fetal thorax.

4. Respiratory distress syndrome (RDS) is caused by a deficiency or absence of surfactant. This surface-active detergent consists of phosphatidylcholine (mainly di-palmitoyl lecithin) and proteins; it coats the inside of alveoli and maintains alveolar patency.

Type II

Type II

Canalicular Period

Glandular Canalicular Terminal sac Alveolar period period period period

Figure 10-3. Histologic appearance of lung tissue during the four time periods of lung development.

During the glandular period, the developing lung resembles the branching of a compound exocrine gland into a hush-like array of endodermal tubules, which comprise the air-conducting system. However, histologic structures involved in gas exchange are not yet formed, and respiration is not possible.

During the canalicular period, respiratory bronchioles and terminal sacs (primitive alveoli) develop. Vascularization increases owing to the formation of capillaries in visceral mesoderm that surround the respiratory bronchioles and terminal sacs.

During the terminal sac period, the number of terminal sacs and vascularization increases greatly. Differentiation of type 1 pneumocytes (thin, flat cells that make up part of the blood-air barrier) and type 11 pneumo-cytes (which produce surfactant) begins. Capillaries make contact with type I pneumocytes, which permits respiration and establishes the blood-air barrier.

The alveolar period begins at birth. The increase in size of the lung after birth is caused by the increased number of respiratory bronchioles and terminal sacs. Subsequently, terminal sacs develop into mature alveolar ducts and alveoli. By age 8, the adult complement of 300 million alveoli is reached.

(From Dudek RW, Fix JD: BRS Ejnbryology, 2nd ed. Baltimore, Williams & Wilkins, 1998, p 142.)

Table 10-1

Stages of Lung Development

Table 10-1

Stages of Lung Development

Stage

Time Period

Characteristics

Glandular

Weeks 5-17

Respiration is not possible. Premature fetuses cannot survive.

Canalicular

Weeks 16-25

Respiratory bronchioles and terminal sacs form. Vascularization increases.

Premature fetuses born before week 20 rarely survive.

Terminal sac

Week 24-birth

Types 1 and II pneumocytes are present. Respiration is possible.

Premature fetuses born between weeks 25 and 28 can survive with intensive care.

Alveolar

Birth-year 8

Respiratory bronchioles, terminal sacs, alveolar ducts, and alveoli increase in number. On chest radiograph, the lungs of a newborn infant are denser than are those of an adult because there are fewer alveoli.

Adult Infant Alveoli

Figure 10-4. Photomicrograph of hyaline membrane disease. The air-filled bronchioles and alveolar ducts are widely dilated. In addition, they are lined by a homogeneous hyaline material (arrows) that consists of fibrin and necrotic cells. Note the presence of atelectasis (i.e., the collapse of distal alveoli).

Figure 10-4. Photomicrograph of hyaline membrane disease. The air-filled bronchioles and alveolar ducts are widely dilated. In addition, they are lined by a homogeneous hyaline material (arrows) that consists of fibrin and necrotic cells. Note the presence of atelectasis (i.e., the collapse of distal alveoli).

a. Thyroxine and Cortisol increase the production of surfactant.

b. Prolonged intrauterine asphyxia decreases the production of surfactant by permanently damaging type II pneumocytes.

C. RDS is common in premature infants and in the infants of diabetic mothers.

d. RDS accounts for 50%-70% of deaths in premature infants.

e. Not only does RDS threaten the infant with immediate asphyxiation, bur it can also bring about hyaline membrane disease (Figure 10-4). Repeated gasping inhalations can damage the alveolar lining and cause hyaline membrane disease. Hyaline membrane disease is characterized histologically by collapsed alveoli (atelectasis) that contain an eosinophilic fluid that resembles a hyaline or glassy membrane.

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Responses

  • FEARNE
    Is rds caused by agenesis of hyaline catilage?
    2 years ago
  • Semhar
    What are the clinical correlate of the respiratory system?
    1 year ago
  • antonio
    What are the clinical correlates of respiration?
    1 year ago

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