Presentation on theme: "Neonatal Endocrinology Prof Dr. Oya Ercan. Transition to extrauterine life -Hypothermia, hypoglycemia, hypocalcemia Adrenal cortex – autonomic nervous."— Presentation transcript:
Neonatal Endocrinology Prof Dr. Oya Ercan
Transition to extrauterine life -Hypothermia, hypoglycemia, hypocalcemia Adrenal cortex – autonomic nervous system including the paraaortic chromaffin system- essential!
Cortisol Surge: Occurs near term. a)Increased cortisol production by the fetal adrenal. b)Decreased rate of conversion of cortisol to cortisone.
Cortisol Surge 1.Augments surfactant synthesis in lung tissue. 2.Increases adrenomedullary phenylethanolamine N- methyl-transferase activity increases methylation of norepinephrine to epinephrine. 3.Increases hepatic iodothyronine outer ring MDI activity increases conversion of T4 to T3. 4.Decreases sensitivity of the ductus arteriosus to prostaglandins facilitates ductus closure. 5.Induces maturation of several enzymes and transport processes of the small intestine. 6.Stimulates maturation of hepatic enzymes.
Secondary effects of cortisol surge Increased T3 levels stimulate ß-adrenergic receptor binding and potentiate surfactant synthesis in lung tissue and increase the sensitivity of brown adipose tissue to norepinephrine.
Most of the chromaffin tissue in the fetus is represented by extramedullary paraganglia (derived from preaortic condensations of sympathetic neurons and chromaffin cells). The largest of these paraganglia; the organs of Zuckerkandl, near the origin of the inferior mesenteric arteries, enlarge to 10 to 15 mm in length at term. In paraaortic chromaffin tissue, PNMT activity is low.
Neonatal brown adipose tissue thermogenesis Brown adipose tissue is the major site for thermogenesis in the newborn. Largest masses: envelope the kidneys and adrenal glands. Smaller masses: surround the blood vessels of the mediastinum and neck. Norepinephrine, via ß-adrenergic receptors, stimulates brown adipose tissue thermogenesis and optimal responsiveness of this tissue to NE is thyroid hormone dependent.
Calcium homeostasis High concentrations of fetal calcium are maintained by active placental transport from maternal blood. Fetal parathyroid PTHRP acts in the placenta to stimulate maternal-fetal calcium transfer [1,25(OH) 2 D]. High total and ionized calcium in fetal blood PTH levels relatively low – CT concentrations high. 25-hydroxycholecalciferol and 1,25- dihydroxycholecalciferol are transported accross the placenta, and free vitamin D concentrations in the fetal circulation are similar to or higher than maternal values.
Adaptation High calcium environment regulated by PTHRP and CT Low calcium requiring regulation by PTH and vitamin D with removal of the placenta, plasma total calcium concentration falls and reaches a nadir of approximately 9 mg/dl in term infants by 24 hr of life. The ionized calcium concentration reaches a low level of about 1.2 mmol/L. Plasma PTH levels in the neonate are relatively low in the neonatal period and are minimally responsive to hypocalcemia during the first 2-3 days of life. (+CT increases)
Glomerular filtration is low for several days. Renal responsiveness to PTH is reduced for several days after birth limit phosphate excretion and predispose the neonate to hyperphosphatemia, particularly if the diet includes high phosphate milk such as unmodified cow’s milk.
Calcium homeostasis and PTH secretion usually normalize within 1-2 wk in full-term infants but normalization may require 2-3 wk in the small premature infants.
Glucose homeostasis The low glucose and high catecholamine levels stimulate glucagon secretion and a transient peak in plasma glucagon level occurs within 2h after birth. Plasma insulin levels are low at birth and tend to fall further secondary to hypoglycemia. The early glucagon and catecholamine surges rapidly deplete hepatic glycogen stores so that return of plasma glucose levels to normal after h and requires maturation of hepatic gluconeogenesis under the stimulus of a high plasma glucagon/insulin ratio. Glucagon secretion gradually increases during the early hours after birth, especially with protein feeding.
Premature infants have more severe and prolonged hypocalcemia because of relatively reduced glycogen stores and impaired hepatic gluconeogenesis. For the healthy term infant, glucose homeostasis is achieved within 5 to 7 d of life, in premature infants 1-2 wk may be required.