Development of

Suprarenal Glands

 The cortex and medulla of the suprarenal

(adrenal) glands have different origins
The cortex develops from mesoderm and the
medulla differentiates from neural crest cells
The cortex is first indicated during the sixth
week by an aggregation for mesenchymal cells
on each side, between the root of the dorsal
mesentery and the developing gonad
The cells that form the fetal cortex are derived
from the mesothelium lining the posterior
abdominal wall

 The cells that form the medulla are derived

from an adjacent sympathetic ganglion,
which is derived from neural crest cells
Initially the neural crest cells form a mass on
the medial side of the fetal cortex
As they are surrounded by the fetal cortex,
these cells differentiate into the secretory
cells of the suprarenal medulla
Later more mesenchymal cells arise from the
mesothelium and enclose the fetal cortex

 These cells give rise to the permanent cortex

Differentiation of the characteristic suprarenal
cortical zones begins during the late fetal period
The zona glomerulosa and zona fasciculata are
present at birth , but the zona reticularis is not
recognizable until the end of the third year
The suprarenal glands of the human fetus are
10 to 20 times larger than the adult glands
relative to body weight, and are large compared
with the kidneys

 These large glands result from the extensive

size of the fetal cortex
The suprarenal medulla remains relatively small
until after birth
The suprarenal glands rapidly become smaller
as the fetal cortex regresses during the first
year
The glands lose about one-third of their weight
during the first 2 or 3 weeks after birth and do
not regain their original weight until the end of
the second year

Congenital Adrenal
Hyperplasia
An abnormal increase in the cells of the
suprarenal cortex results in excessive androgen
production during the fetal period
In females this usually causes masculinization of
the external genitalia and enlargment of the
clitoris
Affected male infants have normal external
genitalia and may go undetected in early infancy
Later in childhood in both sexes, androgen
excess leads to rapid growth and accelerated
skeletal maturation

 The androgenital syndrome associated with

congenital adrenal hyperplasia (CAH) manifests itself
in various clinical forms that can be correlated with
enzymatic deficiencies of cortisol biosynthesis
CAH is a group of autosomal recessive disorders that
result in virilization of female fetuses
CAH is caused by a genetically determined mutation
in the cytochrome p450c21-steroid 21-hydroxylase
gene, which causes a deficiency of suprarenal cortical
enzymes that are necessary for the biosynthesis of
various steroid hormones
The reduced hormone ouput results in an increased
release of adrenocorticotropic hormone (ACTH), which
causes adrenal hyperplasia and overproduction of
androgens by the hyperplastic suprarenal glands