Little help with PCOD Pathophys

[Kboy2]

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!

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[EazyE1907]

The main problem is a Hypothalamic-pituitary- ovarian axis problem

Where you just have alot of LH being secreted. The increased in LH leads to increase production of androgens via stimulation of theca cells. Some of those androgens get peripherally converted to estrone in adipose tissue and that is what results in the increased estrogen. Also some of the androgens are peripherally converted to testosterone via aromatase giving the symptoms of hirsutism and acne.

The increase in estrogen has a negative feedback on FSH. The reason why estrogen DOES NOT have a negative feedback on LH Is because estrogen cannot overcome the high levels LH being secreted from the HPA defect to elicit a negative feedback response. Thats why you have a 3:1 LH:FSH ratio. The decrease in FSH = decrease stimulation of follicles which then leads to cystic spaces in the follicles.

I would watch pathoma, it helped me nail this down. However since PCOS has such a debatable pathophys i doubt they are going to test the pathophys itself but then again i guess you never know what the NBME will do. I think it's key to know 3:1 LH:FSH, the increase in estrogen and testosterone and the presenting signs and symps. Knowing that clomiphene is the tx for the associated infertility is pretty high-yield and also that these pts can get DM2 later in life due to insulin resistance. But not sure about the exact mechanism on that.

good luck!

 

[Kboy2]

Thanks for the response.

So the take home point and ROOT OF THE WHOLE PROBLEM starts with excessive LH secretion? I did use Pathoma, and he explained it well, but I just want to take it to the "nbme level" where Im ready to answer or explain just about anything about the process. I feel like this condition has a lot of steps/points making it quite HY.