PHY2042 Chapter Notes - Chapter 17: Sertoli Cell, Leydig Cell, Seminiferous Tubule
13 Jun 2018
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Chapter 17
Quantitative and Thought Questions
17.1 Sterility due to lack of spermatogenesis would be the common finding. 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 deficiency.
17.2 The androgens act on the hypothalamus and anterior pituitary gland 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 deficient testosterone secretion,
and locally produced testosterone is required for spermatogenesis (i.e., the exogenous androgen cannot
do this job).
17.3 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 secretion.
17.4 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.
17.5 These findings are all due to testosterone deficiency. You would also expect to find that the testes
and penis were small if the deficiency occurred before puberty.
17.6 They will be eliminated or become very irregular. The androgens act on the hypothalamus to inhibit
the secretion of GnRH and on the pituitary gland 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
deficiency.
17.7 Such treatment may cause so much secretion of FSH that multiple follicles become dominant and
have their eggs ovulated during the LH surge.
17.8 An increased plasma LH. The other two are due to increased plasma progesterone and so do not
occur until after ovulation and formation of the corpus luteum.
17.9 The absence of sperm capacitation. When test-tube fertilization is performed, special techniques
are used to induce capacitation.
17.10 The fetus is in difficulty. The placenta produces progesterone entirely on its own, whereas estriol
secretion requires participation of the fetus, specifically, the fetal adrenal cortex.
17.11 Prostaglandin antagonists, oxytocin antagonists, and drugs that lower cytosolic Ca2+
concentration. You might not have thought of the last category because Ca2+ is not mentioned in this
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