Polycystic Ovary Syndrome Endocrinology!
1 - 12 of 12 Posts
Joined
·
753 Posts
PCOS hormonal changes
It is high LH and low FSH that is seen in PCOS.
The pathogenesis of PCOS is not yet completely understood but it is currently thought that the excess of fat promotes transformation of peripheral testosterone to estradiol and excess estradiol causes decreased FSH secretion via feedback inhibition and this leads to LH predominance over FSH making unovulatory cycles and arrested follicles (seen as cysts under U/S).
The set of hormonal changes that you must answer in USMLE with regard to PCOS is as follows:
It is high LH and low FSH that is seen in PCOS.
The pathogenesis of PCOS is not yet completely understood but it is currently thought that the excess of fat promotes transformation of peripheral testosterone to estradiol and excess estradiol causes decreased FSH secretion via feedback inhibition and this leads to LH predominance over FSH making unovulatory cycles and arrested follicles (seen as cysts under U/S).
The set of hormonal changes that you must answer in USMLE with regard to PCOS is as follows:
- Increased estrogen (causing FSH inhibition)
- Increased testosterone (hirsuitism)
- Increesed LH
- Decreased FSH
- Increased GnRH pulse frequency
- Increased insulin resistance
yes
generally patients with pcos are obese and cholesterol is the source of all the steroid pathways.. and thus the patients have excess of steroids including estrogen and androgens<androgens are produced frm adrenal medulla>// also peripheral conversion of these androgens to estrogens takes place,,, hence this excess estrogens causes feedback inhibition on FSH, and as v all know LH surge depends on an increased sustained estrogen level in a normal menstrual cycle..here ther estrogens are high..plus estrogen has a feedback inhibition on FSH but not as much on LH.. hence LH level is increased plus FSH/LH ratio is decreased
hirsutism is due to increased androgen production from adrenal medulla frm cholesterol or fat
generally patients with pcos are obese and cholesterol is the source of all the steroid pathways.. and thus the patients have excess of steroids including estrogen and androgens<androgens are produced frm adrenal medulla>// also peripheral conversion of these androgens to estrogens takes place,,, hence this excess estrogens causes feedback inhibition on FSH, and as v all know LH surge depends on an increased sustained estrogen level in a normal menstrual cycle..here ther estrogens are high..plus estrogen has a feedback inhibition on FSH but not as much on LH.. hence LH level is increased plus FSH/LH ratio is decreased
hirsutism is due to increased androgen production from adrenal medulla frm cholesterol or fat
regarding estrogen, specifically there will be increase in estrone (E1) and decrese in estradiol (e2), correct?
POS
occurs in 3% of adolescents and adults,increased risk of endometrial cancer.increased pituitary synthesis of LH and decreased synthesis of FSH.
increased LH increases androgen synthesis-hirsutism occurs more often than virilization.androgens are aromatized to estrogen in the adipose cells .increased estrogen increases risk for endometrial carcinoma .increased estrogen has positive feedback on LH and negative feedback on FSH.suppression of FSH causes follicle degeneration.
Oligomenorrhea is the most common compliant, POS manifest with hirsutism,infertility,obesity.LH:FSH ratio >2,increased serum testosterone and androstenedione ,increased serum estrogen
TREATMENT-weight reduction in obese women,low-dose OCPs or medroxyprogesterone (suppress ovarian steroidogenesis and LH),spironolactone if OCPs unacceptable (block androgen receptors on hair follicle),LH-releasing hormone analogues (inhibit ovarian androgen production),clomiphene- for womens who want to get pregnant
occurs in 3% of adolescents and adults,increased risk of endometrial cancer.increased pituitary synthesis of LH and decreased synthesis of FSH.
increased LH increases androgen synthesis-hirsutism occurs more often than virilization.androgens are aromatized to estrogen in the adipose cells .increased estrogen increases risk for endometrial carcinoma .increased estrogen has positive feedback on LH and negative feedback on FSH.suppression of FSH causes follicle degeneration.
Oligomenorrhea is the most common compliant, POS manifest with hirsutism,infertility,obesity.LH:FSH ratio >2,increased serum testosterone and androstenedione ,increased serum estrogen
TREATMENT-weight reduction in obese women,low-dose OCPs or medroxyprogesterone (suppress ovarian steroidogenesis and LH),spironolactone if OCPs unacceptable (block androgen receptors on hair follicle),LH-releasing hormone analogues (inhibit ovarian androgen production),clomiphene- for womens who want to get pregnant
Yes, increase estrone & decrease estradiol.
Increased LH hits the theca cells & induces excess androgen production. Androgens will go into the blood will lead to resulting in hirsutism (excess hair in a male distribution; heavy facial hair. Androgens also go into adipose tissue & the androgens will convert to estrone (recall that estrone is the estrogen made from adipose tissue). The excess estrone will go back to the pituitary & feedback & shut down production of FSH. A low FSH will not allow granulosa cells to do its job. So, the granulosa cells will not be able to convert androgens into estradiol, thus a decrease in estradiol.
Subsequently, there will be a degeneration of this follicles bc they’re not able to produce the estrogen necessary to be able to maintain the follicle. The follicle will degenerate & become cystic…also…high levels of circulating estrone increase risk for endometrial carcinoma (recall that the risk for endometrial carcinoma is an increase exposure of estrogen) will lead to polycystic ovarian syndrome.
Increased LH hits the theca cells & induces excess androgen production. Androgens will go into the blood will lead to resulting in hirsutism (excess hair in a male distribution; heavy facial hair. Androgens also go into adipose tissue & the androgens will convert to estrone (recall that estrone is the estrogen made from adipose tissue). The excess estrone will go back to the pituitary & feedback & shut down production of FSH. A low FSH will not allow granulosa cells to do its job. So, the granulosa cells will not be able to convert androgens into estradiol, thus a decrease in estradiol.
Subsequently, there will be a degeneration of this follicles bc they’re not able to produce the estrogen necessary to be able to maintain the follicle. The follicle will degenerate & become cystic…also…high levels of circulating estrone increase risk for endometrial carcinoma (recall that the risk for endometrial carcinoma is an increase exposure of estrogen) will lead to polycystic ovarian syndrome.
Joined
·
1 Posts
Why distal ileal resection lead to cholesterol gallstones
Joined
·
83 Posts
removal of the ileum disrupts the bodys ability to reabsorb bile. enterohepatic recycling of bile is vital for body's normal processing. now the liver gets upset and has to start making more bile acids. in order to make bile acids you need to make more cholesterol. this increases the cholesterol content of bile = supersaturation = stone formation. another way to think about this is the effect of bile acid binding resins which effectively bind bile acids and prevent them from being reabsorbed. this is exact same situation, less bile acids = upregulation of cholesterol and bile synthesis = supersaturation and stone formation.
hope this helps
hope this helps
Hi, I just want to point out that the LH:FSH ratio is high, but FSH is not low.
LH and FSH are the hormones that encourage ovulation. Both LH and FSH are secreted by the pituitary gland in the brain. At the beginning of the cycle, LH and FSH levels usually range between about 5-20 mlU/ml. Most women have about equal amounts of LH and FSH during the early part of their cycle. However, there is a LH surge in which the amount of LH increases to about 25-40 mlU/ml 24 hours before ovulation occurs. Once the egg is released by the ovary, the LH levels goes back down.
While many women with PCOS still have LH and FSH still within the 5-20 mlU/ml range, their LH level is often two or three times that of the FSH level. For example, it is typical for women with PCOS to have an LH level of about 18 mlU/ml and a FSH level of about 6 mlU/ml (notice that both levels fall within the normal range of 5-20 mlU/ml). This situation is called an elevated LH to FSH ratio or a ratio of 3:1. This change in the LH to FSH ratio is enough to disrupt ovulation. While this used to be considered an important aspect in diagnosing PCOS, it is now considered less useful in diagnosing PCOS, but is still helpful when looking at the overall picture.
http://www.obgyn.net/infertility/hormone-levels-and-pcos#sthash.Ncq8b5Gc.dpuf
Note that BOTH LH and FSH are actually usually within the normal range, but within the normal range, the ratio can still be increased in favor of LH!
Hope that helps anyone as confused as I was.
1 - 12 of 12 Posts
Join the discussion
