A Quiz On Reproductive Physiology

VEGF is an angiogenic growth factor secreted by the follicle just prior to
ovulation. VEGF is required to form the dense capillary bed in the corpus luteum. The dense capillary bed provides the
corpus luteum with a high rate of blood flow, and this high rate of blood flow is second only to the brain (on a per gram
tissue basis). This dense capillary bed also permits for the rapid secretion of progesterone into the maternal circulation.
PGF is also an angiogenic growth factor, but is secreted after formation of the corpus luteum is complete. PGF acts in
concert with VEGF to assist in the vascular remodeling of the uterine vessels and formation of the placental blood
vessels during early pregnancy.

Atresia is the process by which follicles/oocytes are depleted from the ovarian
germ cell reserve. The highest rate of atresia occurs during fetal development, and continues throughout a woman's lifespan until menopause, which signals complete follicle depletion. One could argue that atresia is a part of folliculogenesis, but we typically think of the two processes separately. The processes are considered separately because the primary outcome of folliculogenesis is the selection and ovulation of a dominant follicle, whereas the outcome of atresia is follicle death, regardless of follicle stage (i.e. preantral and antral follicles undergo atresia).

Testosterone is converted intracellarly by the 5 alpha‐reductase enzyme to
dihydrotestosterone (DHT) in the prostate gland, sebaceous glands, hair follicles and testis. Changes in the localized
levels of DHT are associated with adverse prostate function, and elevated levels of DHT in hair follicles are associated
with male pattern baldness.
DHT and testosterone both bind to the androgen receptor. However, DHT exhibits a greater affinity for the androgen
receptor, and therefore able to exert heightened effects at lower concentrations.

The endometrium expresses estrogen and progesterone receptors, and therefore the ovarian hormones directly influence endometrial changes. The endometrium proliferates rapidly under the influence of estradiol, and therefore this is termed the "proliferative phase". Progesterone induces glandular
sacculation and stimulates the production of secretory compounds, and therefore this phase is termed the "secretory phase". Extended exposure to progesterone cause the endometrial stromal cells to differentiate, a process termed "decidualization". In a normal menstrual cycle, the corpus luteum stops secreting progesterone after 12‐16 days, and the subsequent progesterone withdrawal induces sloughing of the endometrial functionalis zone during "menstruation". Regardless of which phase you list first, the sequence of events is always constant (i.e. proliferation always precedes secretion, which always precedes decidualization, etc.).

Follicular atresia is an ongoing process from fetal development until full‐blown
menopause. Oocyte number peaks during the second trimester of fetal development, and then these numbers decline rapidly. Rates of atresia are also high during early life, and the rate of atresia then gradually declines throughout a woman's reproductive years until menopause.

This woman is exhibiting a classic presentation of polycystic ovary syndrome
(PCOS), and this question tests your knowledge of the 2 cell theory of ovarian steroidogenesis. Women with PCOS typically exhibit elevated androgen levels, produced by the theca interna cells of the follicles. This excess androgen then exerts phenotypic changes associated with androgen action, such as increased facial hair. For reasons unknown, this overabundance of androgen is not aromatized into estradiol. A sufficient amount of androgen is aromatized, which leads to unopposed estradiol acting directly on the endometrium. The dysfunctional uterine bleeding is a direct effect of unopposed estradiol causing excessive endometrial proliferation. PCOS will be covered in detail in semester 4.

Dopamine is also referred to as "prolactin inhibiting factor". The vast majority
of hormones produced and secreted by the pituitary are stimulated by an associated releasing factor secreted by the hypothalamus. However, prolactin is under the tonic inhibition by dopamine. As levels of dopamine fall, the lactotrophs in the pituitary respond rapidly by actively secreting more prolactin. All of the currently prescribed galatagogues, such as Domperidone, are dopamine antagonists that act to increase prolactin secretion, resulting in increased breast milk production.
There is some evidence that TRH and a Prolactin Releasing Peptide (PrRP) may stimulate the secretion of prolactin. However, both of these compounds at physiological levels do not appear capable of overcoming the tonic inhibition of dopamine. Additionally, TRH stimulation of prolactin secretion is almost always accompanied by decreased levels of dopamine.

Tanner Stage 2 is typically defined by thelarche, which is the development of
breast buds. Adrenarche is a primary characteristic associated with Stage 1, peak growth occurs during Stage 3,
Menarche occurs during Stage 4, and adult features and menstrual cyclicity define Tanner Stage 5.

This man is experiencing a problem with the ejaculatory process and you must recognize that emission is the transport of semen from the testis into the urethra. The history reveals that this 54 yo man is exhibiting no difficulty in achieving an erection, and therefore this suggests that he has a sufficient release of nitric oxide and adequate blood flow to the penis.
He has no problems with arousal or erection, therefore there is most likely no problems with his penile nervous system.
This man may be depressed, but men experiencing psychological sexual problems typically experience erectile dysfunction or do not experience an emotional "orgasm".
This man is suffering from a condition termed anejaculation. Pathophysiological and anatomical disorders of the male reproductive tract will be covered in detail during Semester 4.

This question pertains directly to the 2‐cell theory of steroidogenesis. Theca
interna cells express LH receptors and, in response to LH, primarily produce androgens. These androgens then cross the
basement membrane and enter the granulosa cells, where these androgens are then converted (by the aromatase
enzyme) into estrogen (predominantly estradiol). By blocking the LH receptor, this pathway will be inhibited and
estradiol levels will decline. It is possible that the follicle will undergo atresia and die, but many follicles persist on low
levels of FSH and LH, which is why the proliferative phase can exhibit such extended variations in length.

Mature sperm survive in the epididymis for approximately 4 to 6 weeks before
being ejaculated or being catabolized and resorbed. A man is informed that he can father a child for up to 6 weeks
following a vasectomy. Most urologists and or vasectomy clinics will test a man's sperm count after 20 ejaculations or 6
weeks following a vasectomy.
Sperm are able to survive for this extended duration due to the lower temperatures within the scrotum. In the female
reproductive tract, most sperm die within 24‐48 after ejaculation, although viable sperm can be recovered up to 5 days
after a single ejaculation during intercourse.

Inhibin acts primarily on the pituitary to suppress the production and secretion
of FSH, and can also suppress the secretion of LH. Levels of inhibin fall during the ovulatory window, leading to the LH and FSH surges, respectively. Evidences suggest hCG acts directly on the hypothalamus to block the production of GnRH, thereby reducing production of both LH and FSH. Activin stimulates the production and/or release of the gonadotropins. Testosterone and progesterone can both block the production and release of FSH and LH, but these are steroids, not proteins.

Luteinizing hormone (LH) works directly on the interstitial cells of Leydig (i.e.
Leydig cells) to stimulate the production of testosterone. Low levels of LH can result in decreased levels of testosterone,
which can subsequently lead to decreased sperm production. Remember that LH acts directly on the Leydig cells, and
then the testosterone generated within the Leydig cells acts on the Sertoli cells to regulate spermatogenesis Prolonged
exposure to low levels of testosterone can also lead to systemic effects, such as decreased muscle mass and/or lethargy.
Evaluating the levels of DHT and FSH would also be beneficial, since levels of DHT are directly correlated with levels of
testosterone and FSH is also required by the Sertoli cells during the process of spermatogenesis. Additionally, checking
the levels of prolactin could be informative, since prolactin helps stimulate the expression of the LH receptors.
However, in this particular case the PCP suspects a problem with testosterone production and/or secretion, and
therefore the first step is to directly measure serum levels of testosterone and LH.

Blocking the GnRH receptor will result in decreased production of LH and FSH,
which will subsequently inhibit growth of the dominant follicle.
Interestingly, you could also suppress follicle growth and development by administering receptor antagonists designed
to inhibit FSH receptor pathway or the LH receptor pathway, but the best answer is a GnRH antagonist that blocks both
LH and FSH activity. Recall the 2‐cell theory of steroidogenesis, and how LH and FSH action on the theca and granulosa
cells is a complementary system that results in estradiol production.