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- Sep 23, 2007
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I'm having a terribly difficult time understanding the physiology of progesterone. As I understand it, progesterone acts to promote the endometrium to become more glandular thereby making the endometrium suitable for implantation.
BUT...in endometrial hyperplasia where there is nearly constant estrogenic stimulation of the endometrium, progestins are given to decidualize the endometrial stroma, in effect thinning the endometrium. Progestins are also given as contraceptive pills, where they act by the same mechanism to prevent implantation, among other effects.
Got it.
Now, Mifeprostone acts as a progesterone receptor antagonist and used in medical abortions to block progesterone from making the endothelium suitable to maintain the pregnancy.
I thought I had it, but now it's gone. Does anyone have a reasonable explanation as to how progesterone acts to both make the endometrium suitable for implantation, yet not in certain cases?
BUT...in endometrial hyperplasia where there is nearly constant estrogenic stimulation of the endometrium, progestins are given to decidualize the endometrial stroma, in effect thinning the endometrium. Progestins are also given as contraceptive pills, where they act by the same mechanism to prevent implantation, among other effects.
Got it.
Now, Mifeprostone acts as a progesterone receptor antagonist and used in medical abortions to block progesterone from making the endothelium suitable to maintain the pregnancy.
I thought I had it, but now it's gone. Does anyone have a reasonable explanation as to how progesterone acts to both make the endometrium suitable for implantation, yet not in certain cases?