Neonatal Nurse Practitioner Practice Exam 2025 – Comprehensive All-in-One Guide to Exam Success!

The mechanism responsible for hypocalcemia in a neonate with birth asphyxia is primarily attributed to an increase in calcitonin levels. In the context of hypoxia commonly associated with birth asphyxia, there is a physiological response involving calcium regulation. Calcitonin, which is secreted by the thyroid gland, plays a role in reducing serum calcium levels by inhibiting osteoclast activity in the bones and increasing calcium excretion in the kidneys.

During birth asphyxia, the stress response can lead to alterations in the physiological balance of calcium. If there is significant stress on the body due to asphyxia, it is plausible that the production of calcitonin may increase to help modulate calcium levels, consequently leading to hypocalcemia.

In contrast, other mechanisms, such as parathyroid hormone, typically work to increase serum calcium levels in response to low calcium levels. Hypoparathyroidism, which refers to inadequate production of parathyroid hormone, would also lead to lowered calcium levels but is less directly linked to the acute stress response seen in birth asphyxia. Similarly, 1,25 dihydroxyvitamin D resistance primarily affects calcium absorption in the intestine and does not directly correlate with the immediate hormonal