RRB Nsg. Superintendent-2026 (Shift -1st)
Child Health Nursing (Pediatrics)
Easy

Which of the following is a common cause of physiological jaundice in a newborn?

Appeared in: RRB Nsg. Superintendent-2026 (Shift -1st)

Explanation

  • Physiological jaundice is a common, transient condition in newborns, typically appearing after 24 hours of life.
  • It is caused by the combination of an increased breakdown of fetal red blood cells (higher bilirubin load) and the functional immaturity of the newborn's liver.
  • The liver's reduced ability to conjugate bilirubin, due to low levels of the enzyme UDP-glucuronyltransferase (UGT1A1), is the primary reason for the temporary buildup of unconjugated bilirubin.
  • This process is a normal part of neonatal adaptation and usually resolves without treatment as the liver matures.

Why Other Options Were Wrong

  • Option B: Liver infections, such as neonatal hepatitis or TORCH infections, cause pathological jaundice, which is a sign of disease, not a normal physiological process.
  • Option C: Genetic disorders like Crigler-Najjar syndrome or Gilbert syndrome are inherited conditions that impair bilirubin metabolism, leading to pathological, not physiological, jaundice.
  • Option D: Vitamin deficiency, specifically Vitamin K deficiency, is not related to jaundice. It causes impaired blood clotting, leading to Hemorrhagic Disease of the Newborn.

Related Visual

Visual explanation — Related Visual
  • Visual 1: Flowchart - Illustrating the pathway of bilirubin metabolism in a newborn, highlighting the increased production from RBC breakdown and the bottleneck at the immature liver (low UGT enzyme activity), leading to physiological jaundice.
  • Visual 2: Comparison Table - Differentiating the key features of physiological jaundice (e.g., onset after 24 hours, resolves in 1-2 weeks) versus pathological jaundice (e.g., onset within 24 hours, rapid rise in bilirubin, persists longer).
Clinical Relevance
  • Nursing practice connection: This is primarily an exam-oriented knowledge point with limited direct bedside application, so retain Pathophysiology of physiological neonatal jaundice as background academic context rather than a clinical decision trigger.
  • Nurses play a critical role in assessing newborns for jaundice. A key nursing responsibility is to note the time of onset. Jaundice appearing within the first 24 hours is always considered pathological and must be reported immediately.
  • Promoting adequate feeding (breast or formula) is an important nursing intervention. Frequent feeding helps stimulate bowel movements, which facilitates the excretion of bilirubin in the stool.
  • Patient education is vital. Nurses should educate parents about the nature of physiological jaundice, signs to watch for, and when to seek medical attention (e.g., if jaundice worsens, or the baby becomes lethargic or feeds poorly).
How to Approach the Question
  • First, identify the key terms in the question: 'common cause,' 'physiological jaundice,' and 'newborn.' This directs you to a normal, expected process in neonates.
  • Recall the definition of 'physiological.' It implies a normal body function, not a disease state. This helps you eliminate options related to pathology.
  • Evaluate each option. 'Liver infection' and 'genetic disorder' are clearly pathological conditions. 'Vitamin deficiency' is also a pathological state, but it's primarily linked to bleeding, not jaundice.
  • 'Immature liver function' aligns perfectly with the understanding that a newborn's organ systems are not fully developed at birth.
  • Connect the immature liver to bilirubin metabolism. The liver's job is to process bilirubin. An immature liver will be less efficient at this task, leading to a temporary buildup, which is the essence of physiological jaundice.
Concept Tested & Keywords
  • Concept Tested: Pathophysiology of physiological neonatal jaundice
  • Stem keywords: common cause, physiological jaundice, newborn
  • Lead-in keywords: Which of the following
  • Clinical cues: physiological jaundice

Question ID

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