Pathophysiology of Polycystic Ovary Syndrome

The Rotterdam Consensus criteria defines PCOS as including at least two of the following characteristics: total testosterone level above 70 ng/dL, androstenedione above 245 ng/dL, or DHEA-S above 248 ug/dL, and/or clinical signs of hyperandrogenism including (hirsutism), anovulation, or polycystic ovaries on an ultrasound (Duijkers & Klipping, 2010). Research has shown that hyperandrogenism is the driving force in PCOS.
Hyperandrogenism causes hirsutism in which the “peach fuzz” females typically develop over their body and face transforms to coarser terminal hair in a male pattern (Panidis et al., 2013). Hirsutism may cause the follicles on the head to shrink, resulting in either a receding hairline, or excessive male pattern hair growth on the face, back, chest, abdomen, and inner thighs.
Since fat cells are metabolically active, more androgens are converted from estrogen when insufficient follicle stimulating hormone (FSH) releases in the presence of too much luteinizing hormone (LH). As a result, the ovary produces premature, small follicles that lack a corpus luteum with too little progesterone; thus, women have chronic anovulation (Sen, Baarad, & Gleicher, 2013).
According to the Rotterdam Consensus, women with PCOS may have polycystic ovaries that are greater than 12 follicles (2-9 mm diameter) in each ovary and/or an ovary volume of greater than 10cc (Duijkers & Klipping, 2010). In PCOS, a surplus of 5a-reduced androgens in the ovaries inhibits the action of aromatase (an adrenal enzyme that converts androstenedione and estrone to estrogen), which reduces estradiol synthesis, needed for further maturation (Goodarzi, Dumesic, Chazenbalk, & Azziz, 2011). As a result, a string of pearl appearance of non-functioning polycystic ovaries may appear on ultrasound and is clinically diagnostic of PCOS (Duijkers & Klipping, 2010).

References:

1) http://www.pathophys.org/pcos/; Alexandra Rotstein  Ragini Srinivasan, Sultan Chaudhry and Eric Wong
2) Goodarzi, M. O., Dumesic, D. A., Chazenbalk, G., & Azziz, R. (2011, January 25). Polycystic ovary syndrome: Etiology, pathogenesis and diagnosis. Nature Reviews Endocrinology, 7(4), 219-231. doi:10.1038/nrendo.2010.217
3) Duijkers, I. J., & Klipping, C. (2010). Polycystic ovaries, as defined by the 2003 Rotterdam consensus criteria, are found to be very common in young healthy women. Gynecological Endocrinology, 26(3), 152-160. doi:10.3109/09513590903247824
4) Panidis, D., Tziomalos, K., Papadakis, E., Chatzis, P., Kandaraki, E. A., Tsourdi, E. A., . . . Katsikis, I. (2013, April 04). The clinical significance and primary determinants of hirsutism in patients with polycystic ovary syndrome. European Journal of Endocrinology, 168(6), 871-877. doi:10.1530/eje-13-0039
5) Sen, A., Kushnir, V. A., Barad, D. H., & Gleicher, N. (2013). Endocrine autoimmune diseases and female infertility. Nature Reviews Endocrinology, 10(1), 37-50. doi:10.1038/nrendo.2013.212