Describe microscopically, the cellular components of lungs. Add a note on fetal distress syndrome.

Microscopic Components of the Lungs

The lungs exhibit a complex microscopic architecture, broadly categorized into conducting and respiratory zones. The conducting zone filters, warms, and humidifies air, while the respiratory zone is where gas exchange occurs.

1. Conducting Zone

• Trachea & Bronchi: Lined by pseudostratified ciliated columnar epithelium with goblet cells. The epithelium rests on a basement membrane and is supported by cartilaginous rings.
• Bronchioles: Smaller airways lacking cartilage, composed of smooth muscle and cuboidal epithelium. Cilia are present but decrease in number as the bronchioles become smaller.
• Terminal Bronchioles: The final part of the conducting zone, transitioning to the respiratory zone.

2. Respiratory Zone

• Respiratory Bronchioles: Characterized by the presence of alveoli budding from their walls. The epithelium is cuboidal.
• Alveolar Ducts: Long, branching airways lined by squamous epithelium, connecting respiratory bronchioles to alveolar sacs.
• Alveolar Sacs: Clusters of alveoli, the primary site of gas exchange.
• Alveoli: Thin-walled, balloon-like structures.

3. Cellular Components of Alveoli

• Type I Pneumocytes: Thin, flattened cells covering ~95% of the alveolar surface. They are responsible for gas exchange.
• Type II Pneumocytes: Cuboidal cells comprising ~5% of the alveolar surface. They synthesize and secrete pulmonary surfactant. They also have the capacity to differentiate into Type I pneumocytes.
• Alveolar Macrophages: Phagocytic cells that remove debris and pathogens from the alveolar space.
• Capillary Endothelial Cells: Form the walls of the pulmonary capillaries, facilitating gas exchange.
• Interstitial Cells: Fibroblasts and immune cells present in the alveolar walls, providing structural support and immune defense.

Table: Comparison of Type I and Type II Pneumocytes

Feature	Type I Pneumocyte	Type II Pneumocyte
Shape	Flattened	Cuboidal
Surface Area Coverage	~95%	~5%
Function	Gas Exchange	Surfactant Production, Repair
Mitotic Activity	Low	High

Fetal Distress Syndrome (RDS)

Fetal Respiratory Distress Syndrome (FRDS) is a common respiratory illness in premature infants, primarily caused by a deficiency of pulmonary surfactant.

1. Etiology & Pathogenesis

The primary cause of RDS is prematurity, typically before 37 weeks of gestation. Surfactant production begins around 24-28 weeks of gestation, but its levels may be insufficient in premature infants. Surfactant, a complex mixture of phospholipids and proteins, reduces surface tension in the alveoli, preventing their collapse during exhalation. Without adequate surfactant, the alveoli collapse, leading to decreased lung compliance, increased work of breathing, and impaired gas exchange.

2. Clinical Features

• Respiratory Distress: Tachypnea (rapid breathing), grunting, nasal flaring, and retractions.
• Cyanosis: Bluish discoloration of the skin due to low blood oxygen levels.
• X-ray Findings: Diffuse granular opacities (“ground-glass appearance”) representing collapsed alveoli and hyaline membrane formation.
• Blood Gases: Hypoxemia (low blood oxygen) and hypercapnia (high blood carbon dioxide).

3. Management

• Surfactant Replacement Therapy: Exogenous surfactant is administered directly into the trachea to restore alveolar stability.
• Respiratory Support: Mechanical ventilation or continuous positive airway pressure (CPAP) to assist breathing.
• Monitoring: Close monitoring of blood gases, respiratory rate, and oxygen saturation.
• Supportive Care: Maintaining thermoregulation, hydration, and nutrition.

Advances in neonatal care, particularly surfactant replacement therapy, have significantly improved the prognosis of infants with RDS. However, long-term complications, such as bronchopulmonary dysplasia, can occur.