Hello guys. So just looking to make sure I've got my mind wrapped around PCOD and the general Repro phys concepts happening in the background.
So I understand there is excessive desmolase activity d/t elevated LH secretion, causing excessive cholesterol conversion to Progesterone and Androgens. Obesity being a common presentation; the excess androgens are being converted to estrone in adipose tissue, which causes negative feedback on FSH release, thus the LH:FSH >2.
Now this is my confusion...Is the root cause of the issue excessive LH secretion? Or is that a side effect of some other pathology? Why does the excessive estrone level not cause negative feedback on LH secretion as it does for FSH? (Or is that the pathology again?). My Kaplan text on pg 356 indicates *Estrogen* ought to have an inhibitory feedback effect on the LH AND FSH release, however I believe estrogen is just a broad term, so I am wondering if the products of what Ive listed below have different feedback mechanisms for LH vs FSH? Will Estrone inhibit FSH more than it does LH if at all?
Lastly...Because I know with my luck Ill get a question like this on Step...
"A woman has PCOD... Which direction will the arrows point for the following items?
Inhibin --> Down d/t very little/nothing being released from the granulosa cells
Estrone --> Up d/t elevated peripheral conversion in adipose tissue
Estradiol --> Down d/t low/no FSH stimulation
Estriol --> No change (made from placental tissue)
Testosterone --> High? I dont even know how I would explain this one. Just my assumption d/t elevated androgens
Any help or clarification will be very appreciated. Thanks!
So I understand there is excessive desmolase activity d/t elevated LH secretion, causing excessive cholesterol conversion to Progesterone and Androgens. Obesity being a common presentation; the excess androgens are being converted to estrone in adipose tissue, which causes negative feedback on FSH release, thus the LH:FSH >2.
Now this is my confusion...Is the root cause of the issue excessive LH secretion? Or is that a side effect of some other pathology? Why does the excessive estrone level not cause negative feedback on LH secretion as it does for FSH? (Or is that the pathology again?). My Kaplan text on pg 356 indicates *Estrogen* ought to have an inhibitory feedback effect on the LH AND FSH release, however I believe estrogen is just a broad term, so I am wondering if the products of what Ive listed below have different feedback mechanisms for LH vs FSH? Will Estrone inhibit FSH more than it does LH if at all?
Lastly...Because I know with my luck Ill get a question like this on Step...
"A woman has PCOD... Which direction will the arrows point for the following items?
Inhibin --> Down d/t very little/nothing being released from the granulosa cells
Estrone --> Up d/t elevated peripheral conversion in adipose tissue
Estradiol --> Down d/t low/no FSH stimulation
Estriol --> No change (made from placental tissue)
Testosterone --> High? I dont even know how I would explain this one. Just my assumption d/t elevated androgens
Any help or clarification will be very appreciated. Thanks!