Hyaline membrane disease of an infant is due to deficiency of surfactant and the source of pulmonary surfacta… - JIPMER Nursing Officer-2017

JIPMER Nursing Officer-2017

Child Health Nursing (Pediatrics)

Easy

Appeared in: JIPMER Nursing Officer-2017

Explanation

Pneumonocytes type 2, also known as type II alveolar cells, are cuboidal epithelial cells in the lungs that synthesize and secrete pulmonary surfactant.
Pulmonary surfactant is a complex mixture of lipids and proteins (primarily dipalmitoylphosphatidylcholine) that reduces surface tension at the air-liquid interface within the alveoli.
This reduction in surface tension is critical for preventing alveolar collapse (atelectasis) at the end of expiration, thereby reducing the work of breathing.
A deficiency of surfactant, common in premature infants, leads to Hyaline Membrane Disease, or Infant Respiratory Distress Syndrome (IRDS), characterized by progressive atelectasis and respiratory failure.

Option A: Alveolar macrophages are immune cells responsible for phagocytosis (engulfing debris and pathogens) within the alveoli. They play a role in lung defense, not surfactant production.
Option B: Capillary endothelium forms the walls of the blood vessels adjacent to the alveoli. Its function is to facilitate gas exchange between the blood and the alveolar air, not to produce surfactant.
Option C: Pneumonocytes type 1 are extremely thin, squamous cells that cover approximately 95% of the alveolar surface area. Their primary function is to provide a minimal barrier for efficient gas exchange. They lack the organelles necessary for synthesizing surfactant.

Clinical Relevance

Nursing practice connection: Use the key finding related to Source of Pulmonary Surfactant and Pathophysiology of Infant Respiratory Distress Syndrome (IRDS) to guide bedside assessment, documentation, and the next nursing action.
A key nursing intervention for premature infants with IRDS is the administration of exogenous surfactant directly into the lungs via an endotracheal tube to compensate for the deficiency.
Nurses must closely monitor infants at risk for IRDS for signs of respiratory distress, including tachypnea, nasal flaring, grunting, and intercostal retractions.
What if? If an infant with IRDS suddenly deteriorates despite surfactant therapy and ventilation, the nurse should suspect a complication like a pneumothorax (air leak) and immediately notify the medical team for urgent intervention.

How to Approach the Question

First, identify the key terms in the question: "Hyaline membrane disease," "deficiency of surfactant," and "source of pulmonary surfactant."
The question directly asks to identify the cell type responsible for producing surfactant.
Recall the histology of the pulmonary alveolus, which contains two main epithelial cell types: pneumocytes type 1 and pneumocytes type 2.
Differentiate their functions: Type 1 cells are thin and cover a large surface area for gas exchange, while Type 2 cells are cuboidal and metabolically active, known for producing surfactant.
Evaluate the other options. Alveolar macrophages are immune cells, and capillary endothelium forms blood vessels. Neither is involved in surfactant synthesis.
Based on this differentiation, conclude that Pneumonocytes type 2 are the correct answer.

Concept Tested & Keywords

Concept Tested: Source of Pulmonary Surfactant and Pathophysiology of Infant Respiratory Distress Syndrome (IRDS)
Stem keywords: Hyaline membrane disease, infant, deficiency of surfactant, pulmonary surfactant
Lead-in keywords: source of
Clinical cues: Age/sex group narrows the expected diagnosis, intervention, or normal reference range.

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E6 Pathology- ROBBINS & COTRAN PATHOLOGIC BASIS OF DISEASE 10TH Ed p. 465-467

E6 Nelson Textbook of Pediatrics(2024) — Volume 1 p. 1086-1088

E6 Pathology-Textbook of PATHOLOGYHarsh Mohan Part 2 (215-514) p. 38-40