9. The absence of what phenomenon would interfere with the
ability of sperm obtained by masturbation to fertilize an egg in
a test tube?
10. If a woman seven months pregnant is found to have a marked
decrease in plasma estrogen but a normal plasma progesterone
for that time of pregnancy, what would you conclude?
11. What types of drugs might you work on if you were trying to
develop one to stop premature labor?
12. If a genetic male failed to produce MIS during fetal life, what
would the result be?
13. Could the symptoms of menopause be treated by injections of
FSH and LH?
Chapter 17 Answers to Physiological Inquiries
Figure 17–3a
These drugs would be absorbed by the pregnant
woman and cross the placenta to enter the fetal circulation.
These drugs would block production of dihydrotestosterone in
target tissues with 5-alpha reductase activity, thereby interfering
with the development of normal sexual differentiation of the
penis, scrotum, and prostate in the male fetus.
Figure 17–11
Testosterone alone usually does not restore
spermatogenesis to normal. FSH is necessary to stimulate
spermatogenesis from the Sertoli cell independently of local
testosterone production. Furthermore, giving testosterone
as a drug is usually not suffi cient to replace the local
production of testosterone in the testes necessary to maintain
spermatogenesis. Therefore, gonadotropins with a mixture of
activity for receptors to LH (to stimulate local testosterone
production) and FSH (to stimulate the Sertoli cells) usually
must be given to restore spermatogenesis.
Figure 17–18
1. FSH increases because the corpus luteum is
degenerating. The loss of the negative feedback by progesterone
and estrogen from the corpus luteum relieves the pituitary
of this inhibitory effect and allows FSH to increase, thus
stimulating a group of follicles for the next menstrual cycle.
2. If conception occurs and the developing blastocyst implants
(pregnancy), the trophoblast cells of the implanted blastocyst
release a gonadotropin—human chorionic gonadotropin
(hCG)—into the maternal blood, thus rescuing the corpus
luteum in very early pregnancy. Production of progesterone
from the corpus luteum of pregnancy prevents menses and the
loss of the implanted embryo. The measurement of hCG in
maternal blood or urine is the basis of the pregnancy test.
Figure 17–20
The elevated pituitary gonadotropins suggest a
lack of estrogen and inhibin negative feedback, pointing to
premature ovarian failure as a diagnosis. One cause of premature
ovarian failure is autoimmune ovarian destruction. Like
Graves’ disease and Addison’s disease (see Chapters 11 and 19),
premature ovarian failure is a form of endocrine autoimmunity.
Figure 17–29
hCG stimulates progesterone and estrogen from
the corpus luteum early in pregnancy. The placenta takes over
this function during the second trimester of pregnancy such
that most of the maternal estrogen and progesterone later in
pregnancy is from the placenta. Placental production of these
steroids does not require gonadotropin stimulation.
Figure 17–31
The feet may not provide suffi cient cervical stretch
to maintain the positive feedback stimulation of oxytocin and
uterine contraction.
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