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Clinical Presentation
  1. average age 15-30 years
  2. anovulation
  3. hirsutism 
  4. infertility 
  5. obesity 
  6. virilization

  • most common pathologic finding: white, smooth, sclerotic ovary with a thick capsule, multiple follicular cysts in various stages of
    atresia, hyperplastic theca and stroma

  • but ovarian pathology varies and none is pathognomonic so  diagnosis is biochemical
  • fundamental defect = bad signals to hypothalamo pituitary axis:

high androgens + obesity = increased formation of estrone (acyclic estrogen) ---->acyclic positive feedback on LH + negative feedback on FSH ---->high LH with plasma LH/FSH > 2 -----> hyperplasia of ovarian stroma and theca cells ----> increased androgen production ----->more substrate for peripheral aromatization ---> chronic anovulation

  • increased incidence of endometrial cancer due to unopposed estrogen


  1. interrupt the self-perpetuating cycle by:
    • decreasing ovarian androgen secretion: BCP (wedge resections used in past)
    • decreasing peripheral estrone formation: weight reduction
    • enhancing FSH secretion: clomiphene, hMG (Pergonal),LHRH, purified FSH
  2. to prevent endometrial hyperplasia: progesterone (Provera), BCP
  3. for pregnancy
    • medical induction of ovulation
    • clomiphene citrate (Clomid)
    • human menopausal gonadotropin (Pergonal)
POLYCYSTIC OVARIAN DISEASE POLYCYSTIC OVARIAN DISEASE Reviewed by Radiology Madeeasy on August 23, 2010 Rating: 5
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