Appendix A
17-2 c
Only females exhibit gonadal steroid (estrogen)
positive feedback on GnRH release.
17-3 d
The luteal phase of the ovary, when progesterone
production is maximal, occurs after ovulation but
before the end of the menstrual cycle.
17-4 c
Estrogen stimulates LH release (positive feedback)
just before the LH surge and ovulation (usually on
day 14).
17-5 b
One follicle becomes dominant early in the
menstrual cycle.
17-6 e
The death of the corpus luteum (in the absence of
pregnancy and hCG) results in a dramatic decrease
in ovarian progesterone and estrogen production.
17-7 a
The loss of ovarian steroid production with the
death of the corpus luteum releases the pituitary
from negative feedback and allows FSH to increase.
This stimulates the maturation of a small number of
follicles for the next menstrual cycle.
17-8 c
The primary function of the Leydig cell is
the production of testosterone in response to
stimulation with LH.
17-9 b
Prolactin is produced by the maternal pituitary.
It is homologous to but not the same peptide as
human placental lactogen, which is produced by the
17-10 a
The primary event in menopause is the loss of
ovarian function. The decrease in estrogen leads to
an increase in pituitary gonadotropin release (loss of
negative feedback).
Quantitative and Thought Questions
Sterility due to lack of spermatogenesis would
be the common symptom. The Sertoli cells are
essential for spermatogenesis, and so is testosterone
produced by the Leydig cells. The person with
Leydig cell destruction, but not the person with
Sertoli cell destruction, would also have other
symptoms of testosterone defi ciency.
The androgens act on the hypothalamus and
anterior pituitary to inhibit the secretion of the
gonadotropins. Therefore, spermatogenesis is
inhibited. Importantly, even if this man were given
FSH, the sterility would probably remain because
the lack of LH would cause defi cient testosterone
secretion, and
produced testosterone is
needed for spermatogenesis (i.e., the exogenous
androgen cannot do this job).
Impaired function of the seminiferous tubules,
notably of the Sertoli cells. The increased plasma
FSH concentration is due to the lack of negative
feedback inhibition of FSH secretion by inhibin,
itself secreted by the Sertoli cells. The Leydig cells
seem to be functioning normally in this person
because the lack of demasculinization and the
normal plasma LH indicate normal testosterone
FSH secretion. FSH acts on the Sertoli cells and
LH acts on the Leydig cells, so sterility would result
in either case, but the loss of LH would also cause
undesirable elimination of testosterone and its effects.
These fi ndings are all due to testosterone defi ciency.
You would also expect to fi nd that the testes and penis
were small if the defi ciency occurred before puberty.
They will be eliminated or become very irregular.
The androgens act on the hypothalamus to inhibit
the secretion of GnRH and on the pituitary
to inhibit the response to GnRH. The result is
inadequate secretion of gonadotropins and therefore
inadequate stimulation of the ovaries. In addition
to the loss of regular menstrual cycles, the woman
may suffer some degree of masculinization of the
secondary sex characteristics because of the combined
effects of androgen excess and estrogen defi ciency.
Such treatment may cause so much secretion of FSH
that multiple follicles become dominant and have
their eggs ovulated during the LH surge.
An increased plasma LH. The other two are due to
increased plasma progesterone and so do not occur
ovulation and formation of the corpus
The absence of sperm capacitation. When test-tube
fertilization is performed, special techniques are used
to induce capacitation.
The fetus is in diffi culty. The placenta produces
progesterone entirely on its own, whereas estriol
secretion requires participation of the fetus,
specifi cally, the fetal adrenal cortex.
Prostaglandin antagonists, oxytocin antagonists, and
drugs that lower cytosolic calcium concentration.
You may not have thought of the last category
because calcium is not mentioned in this context
in the chapter, but as in all muscle, calcium is the
immediate cause of contraction in the myometrium.
This person would have normal male external
genitals and testes, although the testes may not have
descended fully, but would also have some degree
of development of uterine tubes, a uterus, and a
vagina. These internal female structures would tend
to develop because no MIS was present to cause
degeneration of the Müllerian duct system.
No. These two hormones are already elevated in
menopause, and the problem is that the ovaries
are unable to respond to them with estrogen
secretion. Thus, the treatment must be with
estrogen itself.
Chapter 18
Test Questions
18-1 c
18-2 a
18-3 b
This is known as active immunity.
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