Test Your Knowledge About Physiology! Trivia Quiz

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.
Distracter explanations:
1) NPY - which is released from the arcuate nucleus - may stimulate the release of prolactin, and
therefore levels would not be decreased.
2) Nitric oxide (NO), in normal levels, has been shown in animal models to inhibit prolactin release.
However, there has been no clear consensus on the role (if any) of changes in circulating NO and
changes in prolactin secretion.
3) PRH would increase, not decrease.
4) Acetycholine (Ach) can stimulate oxytocin release - and therefore could stimulate milk letdown.
However, the role of Ach on prolactin is unclear, and therefore this is not the best answer.

Follicular atresia is an ongoing process from fetal development until follicle depletion,
which most often occurs after 40 years of age. Oocyte number peaks at ~7-10 million follicles during
the second trimester (~28 weeks of fetal development), and these numbers then decline rapidly.
Distracter explanations:
1) Rates of atresia are high during toddler years and before puberty - at puberty most women have
~300,000 follicles. However, women have ~7-10 million follicles at ~28 weeks of development, and
therefore `6 million follicles undergo atresia before birth - which is a much greater loss.
2) Approximately 300,000 follicles are lost between puberty and menopause.
3) The majority of follicles are lost before the peri-menopause - and the loss of follicles is the cause of
premature ovarian failure or menopause.

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.
Distracter explanations:
1) 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.
2) The IGFs have no known role in the angiogenic process associated with CL development.
3) EGF acts in concert with VEGF to regulate vascular growth - but is not the best answer.

Inhibin B produced by the follicles, and Inhibin A produced by the corpus luteum, acts
primarily on the pituitary to suppress the production and secretion of FSH. The placenta
manufacturers and secretes both Inhibin A & B, which suppresses follicle recruitment/growth during
pregnancy.
Remember that Inhibin B produced in granulosa cells inhibits FSH during the proliferative
phase of the cycle. Levels of Inhibin B fall, and levels of Activin increase, during the ovulatory
window - collectively, these changes in Inhibin B and Activin modulate the FSH surge.
Distracter explanations:
1) Evidence(s) suggest hCG acts directly on the hypothalamus to block the production of GnRH,
thereby reducing production of both LH and FSH - but evidence is lacking to suggest hCG acts
directly on the pituitary.
2) Activin stimulates the production and/or release of the gonadotropins.
3) Testosterone and progesterone are not proteins (they are steroids). Both exert negative feedback
on the pituitary and regulate LH secretion - Inhibins/Activin exert greater regulatory control on FSH
secretion.

You recognized that LH and hCG exhibit a high degree of homology and both bind with
high affinity to the LH receptor. In a typical menstrual cycle, the peak of the LH surge occurs
approximately 10-12 hours before ovulation, which is considered the same day as ovulation (i.e.
within a 24 hr period). An acute release of hCG would mimic the LH surge, resulting in ovulation of
the dominant follicle.
You also remembered that the corpus luteum has a finite lifespan of 12-16 days, and therefore
to induce a 28 to 30 day menstrual cycle, ovulation must occur approximately 12-16 days before
menses. Thus, of the choices offered the optimal day to induce ovulation is Day 15, since this will
result in elevated progesterone for approximately 12-16 days resulting in a menstrual cycle length of
27-31 days.
Distracter explanations:
1) Day 10 would result in a likely 22 to 26 day cycle, which is a short cycle.
2) Day 20 would result in a cycle longer than 30 days.
3) Day 12 or Day 18 are possible choices. Giving the pill on day 12 could result in a menstrual cycle
of 24 to 28 days, and giving the pill on day 18 would likely result in a cycle length of 30-34 days.
However, the best choice is day 15, which covers the entire tight 3 day range (i.e. total length of 28 to
30 days).

Thinning of the cervical mucus, coupled with increased vaginal secretions during
intercourse, enhance sperm transport through the lower portion of the female reproductive tract.
Ferning of cervical mucus on a glass slide is indicative of a receptive cervix, and cervical mucus
typically exhibits ferning for approximately 10 days of the menstrual cycle (if menses is day 1, then
~day 5 to day 17). Slight contractility of the uterus aids in sperm transport through the endometrial
lumen. Cilia beat frequency becomes rhythmical and secretions increase in the fallopian tube, which
enhances both sperm and oocyte transport.
Distracter explanations:
Decreased vaginal secretions, increased uterine blood flow, decidualization of the endometrial stroma
and decreased uterine contractility are all effects induced by progesterone during the secretory phase
of the menstrual cycle, and are not associated with ovulation.

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, for 10 days or
longer, causes the endometrial stromal cells to undergo the decidual response (i.e. "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.).

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

Atresia is the process by which follicles/oocytes are depleted from the ovarian pool. The
highest rate of atresia occurs during fetal development, and continues throughout a woman's lifespan
until menopause, which signals complete follicle depletion.
Distracter explanations:
1) 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).
2) Ovulation is the temporospatial and hormonally-regulated release of the ovum from the follicle.
The ovulatory process has not been correlated with oocyte quality.
3) Fertilization is the union of an egg with sperm - this does not have any effect on egg quality.
However - it has been argued for ages that only high-quality oocytes can get fertilized by semen.
4) Oogenesis is the development of ova - which occurs during fetal development.

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. Prolonged exposure to
low levels of testosterone can also lead to systemic effects, such as decreased muscle mass,
lethargy and/or libido. 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.
Distracter explanations:
1) DHT is not associated with decreased muscle mass or lethargy. Effects on libido are unclear.
2) FSH does not regulate testosterone production. FSH is required by the Sertoli cells during the
process of spermatogenesis, but has no known effects on libido.
3) If given alone, prolactin could be a possible answer. Hyperprolactinemia causes reduced GnRH
secretion, leading to reduced (or low normal) levels of LH and FSH. In men, this can result in low
testosterone. However, for this question, prolactin was paired with DHT, and therefore this is not the
correct answer.

This man is suffering from a condition termed anejaculation. This man is experiencing a
problem with the ejaculatory process and you recognized that emission is the transport of semen from
the testis into the urethra.
Distracter explanations:
1) History reveals this patient is exhibiting no difficulties in achieving an erection, and therefore this
suggests that he has a sufficient release of nitric oxide and adequate blood flow to the penis.
2) He has no problems with arousal or erection, therefore there is most likely no problems with his
penile nervous system.
3) This man may be depressed, but men experiencing psychological sexual problems typically
experience erectile dysfunction or do not experience an emotional "orgasm".

All of these events are associated with changes in intracellular calcium, and in some
instances (such as GVBD) the changes in calcium are classic hallmark indicators of the event.
In some events, such as hyperactivation and the acrosome reaction, intracellular changes
occur rapidly and therefore it has been difficult for scientists to determine if the changes in calcium
directly cause the event or are a direct result of the event. Regardless, changes in calcium are
associated with the events occurring.

Testosterone is converted intracellularly by the 5 alpha-reductase (5ARD) 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 DHT is able to exert heightened effects at lower
concentrations.
Distracter explanations:
1) Androstenedione, Androstenediol, and DHEA are weaker androgens, and are not associated with
male pattern baldness.
2) Levels of testosterone may affect circulating levels of DHT - but localized/intracellular
concentrations of DHT are more dependent on the level and activity of 5ARD.

This woman is exhibiting a classic presentation of polycystic ovary syndrome (PCOS).
Hyperandrogenemia is one of the diagnostic markers used to diagnose women with PCOS.
Increased amounts of androgen are produced by the theca cells of the follicles - the ovarian cortex
and the adrenal are also sources of increased androgens. Collectively, the excess androgen exerts
phenotypic changes associated with androgen action - many women exhibit hirsutism.
For reasons unknown, the overabundance of ovarian androgen does not cross the basement
membrane and get aromatized into estradiol in the granulosa cells - instead, the majority of this
excess androgen escapes into the systemic circulation. However, some androgen is aromatized to
estradiol in the follicle, and additionally some of the systemic androgen is metabolized to estrone in
the peripheral adipose tissue. Collectively, women with PCOS typically have elevated androgens,
and normal to high-normal levels of estrogen (estradiol PLUS estrone).
Most women with PCOS exhibit anovulatory menstrual cycles, and because most women do
not ovulate this leads to unopposed estrogen acting directly on the endometrium. The effect of this
unopposed estrogen is excessive endometrial proliferation, which eventually causes estrogen
breakthrough bleeding.
Distracter explanations:
1) Progesterone would not cause these effects - this woman likely has very low (or undetectable)
levels of progesterone.
2) Estradiol and Estrone - are likely not elevated. Total estrogen (estrone plus estradiol) may be
elevated. Recognize that it is the unopposed estrogen and lack of progesterone that is most likely
causing the menstrual problems - not the level of estrogen.
3) Cortisol levels may be elevated, may cause irregular cycles, and may cause hirsutism. Cortisol is
a possible answer - but not the best answer.

It is estimated that 50% of all zygotes are lost to spontaneous abortion before
implantation, and that another 20-30% of all pregnancies are lost during the implantation process.
Thus, the slightly extended menstrual cycle is most likely due to a spontaneous abortion during very
early pregnancy.
Distracter explanations:
1) The secretory phase is 12-16 days, because the corpus luteum has a finite lifespan of 12-16 days
in a non-pregnant cycle. Extending the secretory phase indicates the woman was pregnant - but this
is not the best answer.
2) There is no evidence to suggest that elevated levels of estradiol during the secretory phase affect
menstrual cycle length.
3) Elevated levels of progesterone would not extend the phase - in actuality, very high levels of
progesterone of the secretory phase have been correlated (in some studies) with heavy menstrual
bleeding.
4) An extended proliferative phase, which is the primary cause for variations in the menstrual cycle
(remember the secretory/luteal phase is 12-16 days and dependent on the lifespan of the CL), is a
possible answer. However, because this woman experienced 10/11 menstrual cycles of exactly 29
days (3 prior to trying to get pregnant and 7/8 while trying), this suggests her proliferative phase is
tightly controlled. This woman was having unprotected intercourse for 8 months, and therefore the
lone deviation in menstrual cycle length in this woman's specific situation is more likely due to a
spontaneous abortion than a result of an extended proliferative phase.

Granulosa-lutein cells (GLC) and theca-lutein cells (TLC) both express functional LH
receptors, and the GLC secrete progesterone and estrogen whereas the TLC secrete androgen
(predominantly androstenedione) and progesterone. The GLC then aromatize the androgen into
estrogen. These cells types can also be distinguished histologically, since the TLC express high
levels of CYP17 (the enzyme required to convert progesterone into androgen) whereas the GLC
express CYP19 (aromatase, required to convert androgen into estrogen).
Remember that the primary function of the CL is to secrete progesterone.
Steroidogenesis Summary:
Granulosa cells = estrogen during the follicular phase
Granulosa cells = estrogens and progesterone during the pre-ovulatory window (after they acquire the
LH receptor)
Granulosa-lutein cells = progesterone and estrogen during the luteal phase
Theca cells = androgens
Theca-lutein cells = androgens and subsidiary amounts of progesterone
hCG = binds to the LH receptor and therefore maintains luteal steroidogenesis resulting in continued
progesterone production
The CL predominantly secretes progesterone. Follicles predominantly secrete estrogen.

The luteal-placental shift occurs between 7-9 weeks of gestation. A fully functional
placenta begins secreting hormones, including estriol, during the luteal-placental shift. A rise in
estriol, the estrogen of pregnancy, indicates that the maternal-fetal-placental unit is fully functional.
Distracter explanations:
1) Blastocyst invasion and formation of the placenta are complete by the end of the first month of
gestation.
2) Spiral artery remodeling and hCG production are ongoing events during the first trimester, but
these events are not specific to 8 weeks of gestation.
3) hCG levels start to decline during/after the luteal-placenta shift - the placenta starts producing the
large amounts of progesterone necessary to maintain pregnancy, and these high levels of placental
progesterone are thought to suppress the production of placental hCG.

A rise in intra-ovarian progesterone just prior to ovulation is associated with ovulation and
the subsequent formation of a functional corpus luteum. Cohorts of granulosa cells express a
functional LH receptor prior to ovulation, and during the pre-ovulatory period these cohorts of
granulosa cells bind LH and actively start secreting progesterone into the follicular fluid and systemic
circulation.
This rise in progesterone prior to ovulation, especially as measured in a single blood draw,
may be below the threshold of assay detection in a single serum sample. Measurable increases in
serum progesterone, secreted by the newly formed corpus luteum, are detectable (above baseline)
typically within 24-hrs following ovulation, (and most of the time much sooner, within 6 -12 hrs).
Further, increases in progesterone above baseline are always indicative of a successful ovulation and
associated with the formation of a corpus luteum.
Distracter explanations:
1) Estradiol and estrone levels rise in pre-ovulatory follicles, but that high intraovarian estrogen levels
typically persist for 48 to 96 hours prior to ovulation. Estrogen is measurable throughout the entire
menstrual cycle, with concentrations highest just before ovulation.
2) Inhibin B levels fall during the pre-ovulatory period, and coupled with a rise in Activin, stimulate the
FSH surge associated with ovulation.
3) Inhibin A is produced predominantly by the corpus luteum - levels of Inhibin A do not typically rise
until AFTER ovulation.

This woman's history and age suggest early menopause is possible (two of her sisters
experienced menopause before age 50), but nausea is not a typical symptom associated with
menopause. The history of no menstrual period for 3 months and onset of nausea is indicative of
pregnancy, likely near the beginning of the 2nd trimester. An hCG test will quickly determine
pregnancy status.
Distracter explanations:
1) Measuring progesterone will help determine if the patient is ovulating - but elevated progesterone
is not associated with nausea or amenorrhea.
2) Elevated levels of FSH and estrone are associated with depletion of the ovarian follicles, and are
markers for premature ovarian failure and menopause. However, nausea is not a symptom typically
associated with menopause - therefore, measuring hCG and determining pregnancy status is the first
(and easiest) hormone assay. IF the pregnancy test is negative, then measuring the levels of FSH
would be the next best answer.
3) GnRH is released into the portal system, and therefore GnRH can not be measured in women.
The relative levels of GnRH are estimated based on the levels of FSH and LH.

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 - however, some
studies have shown that viable sperm can be recovered 5 days after a single ejaculation during
intercourse.

All three estrogens are secreted in large amounts and (estrone, estradiol, estriol) act as
vasodilators to increase blood flow to the uterus and growing placenta. Estriol is synthesized by the
fully functional placenta after the luteal-placental steroidogenic shift, and is considered the estrogen
of pregnancy.
Remember that you can associate each estrogen with significant events in a woman's reproductive
years:
 Estrone (E1): Estrogen of menopause; increased due to peripheral metabolism of androgens
to estrone (especially in adipose tissues).
 Estradiol (E2): Estrogen of reproductive years and primary estrogen produced during the
menstrual cycle; associated with follicle growth & development and reproductive tract changes
during the proliferative phase of the menstrual cycle.
 Estriol (E3): Estrogen of pregnancy; produced by the placenta.
Also remember that all three estrogens bind to the same nuclear estrogen receptors (ER). The order
of binding affinity/specificity is as follows: E2 > E1 > E3
 E2 binding affinity to the ER is 5 to 10-fold greater than E1, and E2 binding affinity to the ER is
at least 20-fold (and likely 100-fold or more) greater than E3.
Distracter explanations:
1) Estrogens are not associated with blastocyst invasion.
2) Progesterone, not estrogen, stimulates hypertrophy of the spiral arteries.
3) LH and hCG stimulate luteal progesterone production - the role of estrogen is unclear.
4) Exposure to progesterone for ~10 days stimulates decidualization of the endometrial stromal cells -
the endometrial epithelia do not decidualize.

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 ( estradiol and estrone). By blocking the LH
receptor, this pathway will be inhibited and estradiol levels will decline.
Distracter explanations:
1) Progesterone levels will decline - recall that progesterone is an immediate precursor required for
androgen production.
2) Androstenedione is an androgen and will decrease, not increase.
3) LH levels will increase (think about the HPO axis) - but will be unable to act on cells, due on the
receptor antagonist blocking the LH receptor pathway.
4) 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.

An adequate functionalis layer is required to support an invading blastocyst during the
process of implantation. In women experiencing infertility, ultrasound is often used to measure
endometrial thickness - progesterone supplementation may be prescribed to those women exhibiting
an abnormally thin endometrium. Remember that implantation requires progestational differentiation
of the endometrium - progesterone induces sacculation of the endometrial glands, stimulates
epithelial cell secretion, stromal cell expansion and hypertrophy of the spiral arteries.
Distracter explanations:
1) The processes of decidualization and menstruation will occur in a normal manner, there will just be
less tissue to undergo differentiation and enzymatic breakdown during those processes, respectively.
2) An underdeveloped endometrium is not capable of supporting implantation, but to date there is no
evidence to suggest an inadequate functionalis zone will inhibit gamete transport or subsequent
fertilization of an egg and sperm.

Cohorts of granulosa cells begin expressing functional LH receptors prior to ovulation,
and these cells then respond to LH by secreting progesterone. LH also acts to stimulate the
increased production of prostaglandins and the matrix metalloproteinases (MMPs), two components
that are required for the temporospatial breakdown of the follicular wall.
Distracter explanations:
1) Estradiol is produced by the granulosa cells in response to FSH - not LH. The granulosa-lutein
cells (of the CL) secrete estrogens in response to LH - but the granulosa cells of the dominant follicle
still require FSH stimulation.
2) Androstenedione is secreted by the theca cells, not granulosa cells.
3) Serine proteases are released by the granulosa cells during ovulation, but this is an FSH mediated
event.
4) Fibronectin is a component of the basal lamina of ovarian follicles. Levels of fibronectin do not
increase due to the effects of LH - levels of fibronectin increase as a result of MMP degradation.

Blocking the GnRH receptor will result in decreased production of LH and FSH, which will
subsequently inhibit growth of the dominant follicle.
Distracter explanations:
1) 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.
2) Blocking the ER or PR will have variable effects on different systems - and therefore although also
pausible, either of these are not the best answer.