MENSTRUAL CYCLE

How long does the ovum stay in the ampulla for fertilization? Does it continuously move in the ampulla or does it stay
still? 

The part of the oviduct just after the ampulla has a narrower diameter, and fewer cilia, and this probably contributes to the slowing down of the ovum on its way down the oviduct.  It sort of stops at the end of the ampulla, and hangs out there for about 2 days.    If sperm find it during that time, it may get fertilized.  

The book says that estrogen is responsible for the uterine changes in the proliferative stage and progesterone is responsible during the secretory phase but your slides say both are responsible in the second stage. Just want to clarify which is true? 

Progesterone's actions on the uterus dominate in the secretory phase, but estrogen is also important, because it stimulates synthesis of progesterone receptors.  

In birth control pills, there are estrogen and progesterone whereas in the long acting "under the skin" implant, there is only progesterone. Both causes negative feedback, but is there a reason why estrogen is also made in the birth control pills? why is progesterone not sufficient, but is in the implant? 

When Gregory Pincus first hit on the idea of making a birth control pill, he was trying to mimic the hormonal situation that naturally exists at the one time when a woman can't get pregnant:  When she already is pregnant.  Since progesterone was known to be high then, he gave women huge doses of progesterone, which was sufficient to prevent ovulation.  But estrogen was later added to the Pill, because it better mimicked the normal menstrual cycle, although there are also some progesterone-only pills.  It seems that the dose of progesterone in the implant is often not enough to prevent the LH surge, and ovulation often happens in women with the implant.  However, the progesterone has another effect - making the cervical mucus less penetrable to sperm - and this second effect is important for the effectiveness of this contraceptive.  

During menstruation, does the entire functional layer slough off, and the entire basal layer remain? Don't the glands protrude into the functional layer? 

Yes, to both.  The glands, blood vessels, endometrial cells.... all is lost.  But don't worry, another layer will grow next month, from the basal layer that remains.

 

SEXUAL DIFFERENTIATION

What is the timing of the differentiation of internal and external genetalia during development? 

What you should know is 1. For the first 6 weeks, there is no obvious difference between males and females, and 2. Differentiation of the gonads has to begin before differentiation of the ducts and external genitals, since the later depend on gonadal secretions.  The testes begin to develop in week 7, and the ducts begin looking male-like in week 8, the external genitals begin looking male-like in week 9, but it takes a few more weeks for them to completely develop.

In the last example in lecture 8, how did the woman develop female secondary sex characteristics? In general what hormones are responsible for female secondary sex characteristics? 

In general, gonadal hormones at puberty are responsible for development of secondary sex characteristics.  So the broad muscles of men develop when the testes secrete testosterone at puberty, and the breasts of women develop in response to ovarian estrogen at puberty.  

I think this question refers to the last example in the slides, which I gave as a thought question, but didn't go over in class.  This woman has testes, which secrete testosterone, but she develops breasts that look like those of normal women, probably as a result of estrogen secreted by the testes or adrenal gland.  Usually men secrete some estrogen, but this has little effect because there is an overwhelmingly larger secretion of testosterone.  In the androgen-insensitive women, there is no testosterone to balance the estrogen, and the small amount of estrogen secreted seems to be enough to feminize the breasts.  

Do primordial germ cells move in response to TDF?  Do these cells to move after deciding that the gonad will differentiate male or female, or does the moving of the cells decide the differentiation? 

The chemical that induces the cells to move hasn't been identified yet, as far as I know.  Differentiation of the gonad depends on the presence of TDF, but the complete normal development of the gonad requires that the germ cells also be present.

In CAH,  in the absence of cortisol and the overproduction of ACTH, more testosterone is produced. But doesn't
testosterone have negative feedback on its own mechanism of production? Would there not be competing mechanisms to both produce and to prevent production of testosterone? How is it that testosterone production seems to "win"?

Testosterone does have negative feedback effects, acting on the hypo/pit to prevent GnRH and LH/FSH release.  But remember, these hormones act on the gonad, while the testosterone here is coming from the adrenal cortex, which isn't affected by the gonadotropins.

Do individuals with CAH develop other secondary male characteristics?

If CAH were untreated, there can be some masculine-like changes such as excessive hair growth.  But usually it is treated so that androgen levels decrease.

Are men with 5-alpha reductase deficiency ("Guevodoces") fertile?

Usually not.  During development, there may not be a connection between the vas deferens and the urethra, so there are anatomical problems, and the testes may develop inside the abdominal cavity, so there may be problems with sperm viability.

Would you classify someone as genetically male if they are XY or is it SRY that is the vital part of their classification?

How would you classify them?