Reproduction
641
decrease in cortisol in the fetal blood leads to an increase
in plasma ACTH, due to a loss of glucocorticoid negative
feedback. The increase in fetal ACTH stimulates the fetal
adrenal cortex to try to make more cortisol. Remember,
the adrenal cortex can synthesize androgens from the same
precursor as cortisol. ACTH stimulation results in an increase
in androgen production because the precursors cannot
be effi ciently converted to cortisol. This increase in fetal
androgen production results in
virilization
of an XX fetus
(masculinized external genitalia). If untreated in the fetus,
the XX baby is usually born with
ambiguous genitalia
—it
is not obvious whether the baby is a phenotypic boy or girl.
These babies require treatment with cortisol replacement.
We have already discussed amniocentesis and chorionic
villus sampling in the previous section. These techniques
can be used to obtain a sample of fetal cells. If a woman has
previously had a baby with congenital adrenal hyperplasia,
her subsequent pregnancies can be screened. If an XX fetus
is found to have one of the several possible mutations in the
enzymes of the pathway that synthesizes cortisol, the mother
can be given low doses of synthetic glucocorticoids, which
cross the placenta and suppress fetal ACTH release. This
lowers fetal adrenal androgen production and allows normal
development of the external genitalia.
Precocious Puberty
Precocious puberty
is defi ned as the premature appearance
of secondary sex characteristics. The age of the normal onset
of puberty is controversial, although it is generally thought
that pubertal onset before the age of 6 to 7 in girls and 8
to 9 in boys should be investigated. Precocious puberty is
usually caused by an increase in gonadal steroid production.
This leads to an early onset of the puberty growth spurt,
maturation of the skeleton, breast development (in girls), and
enlargement of the genitalia in boys. Therefore, these children
are usually taller at an early age. However, because gonadal
steroids also stop the pubertal growth spurt by inducing
epiphyseal closure, fi nal adult height is usually less than
predicted.
Although there are a variety of causes for the premature
increase in gonadal steroids,
true
(or complete) precocious
puberty is caused by the premature activation of GnRH
and LH/FSH secretion. This is often caused by tumors
or infections in the area of the central nervous system that
control GnRH release. Treatments that decrease LH and FSH
release are important to allow normal development.
Cholesterol
Cortisol
Adrenal gland
Hypothalamus–
Pituitary
+
Androgens
ACTH
Virilization
Enzyme
mutation
Negative
feedback
Figure 17–34
Mechanism of virilization in female fetuses with congenital adrenal
hyperplasia. An enzyme defect (usually partial) in the steroidogenic
pathway leads to decreased production of cortisol and a shift of
precursors into the adrenal androgen pathway. Because cortisol
negative feedback is decreased, ACTH release from the fetal
pituitary increases. Although cortisol can eventually be normalized,
it is at the expense of ACTH-stimulated adrenal hypertrophy and
excess fetal adrenal androgen production.
SECTION C SUMMARY
Anatomy
I. The female internal genitalia are the ovaries, fallopian tubes,
uterus, cervix, and vagina.
II. The female external genitalia include the mons pubis, labia,
clitoris, and vestibule of the vagina. These are also called the
vulva.
Ovarian Functions
I. The female gonads, the ovaries, produce eggs and secrete
estrogen, progesterone, and inhibin.
II. The two meiotic divisions of oogenesis result in each ovum
having 23 chromosomes, in contrast to the 46 of the original
oogonia.
III. The follicle consists of the egg, inner layers of granulosa cells
surrounding the egg, and outer layers of theca cells.
IV. At the beginning of each menstrual cycle, a group of preantral
and early antral follicles continues to develop, but soon
only the dominant follicle continues its development to full
maturity and ovulation.
V. Following ovulation, the remaining cells of that follicle
differentiate into the corpus luteum, which lasts about 10 to 14
days if pregnancy does not occur.
VI. The menstrual cycle can be divided, according to ovarian
events, into a follicular phase and a luteal phase, which last
approximately 14 days each and are separated by ovulation.
Control of Ovarian Function
I. The menstrual cycle results from a fi nely tuned interplay of
hormones secreted by the ovaries, the anterior pituitary, and
the hypothalamus.
II. During the early and middle follicular phases, FSH stimulates
the granulosa cells to proliferate and secrete estrogen, and
LH stimulates the theca cells to proliferate and produce the
androgens that the granulosa cells use to make estrogen.
a. During this time, estrogen exerts negative feedback
on the anterior pituitary to inhibit the secretion of the
gonadotropins. It probably also inhibits the secretion of
GnRH by the hypothalamus.
b. Inhibin preferentially inhibits FSH secretion.
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