Polycystic Ovary Syndrome Pathophysiology Flashcards
PCOS
Hyperandrogenism, ovarian dysfunction (oligo-anovulation and/or polycystic ovaries), exclusion of other conditions
Oligo-ovulation or anovulation
fewer than 6-9 menses/yr, low mid luteal progesterone levels // rule out hypothyroidism and hyperprolactinemia
T/F PCOS is the most common cause of anovulation
T
Clinical features of hyperandrogenism
hirsutism, acne, male pattern balding
T/F PCOS female androgen levels are in the male range.
F –> less than normal male range
T/F PCOS prevalence is the same world wide
T
T/F PCOS testosterone levels are the same across ethnicities
F –> higher in AA
T/F obesity is part of the PCOS diagnosis.
F
Pathophysiology of PCOS
persistent rapid frequency gnRH release –> increased LH pulse amplitude and frequency –> LH > FSH + decreased sensitivity to progesterone/estrogen feedback on GnRH + change in LH responsiveness to gnrh
T/F Granulosa cells from PCOS ovaries have increased response to FSH
T –> but not as much of a surge as LH
Is it possible women with PCOS were born with increased density of small pre-antral follicles –> i.e. different starting point?
Yes it is possible
T/F Insulin resistance may increase hormone production at the level of the ovary contributing to PCOS risk.
T –> thecal cells
Clinical signs of insulin resistance
acnthosis nigricans (raised velvety hyperpigmentation of skin)
Tissue selective insulin resistance
ir in muscle, adipose, liver but not ovary
PCOS tx
oral contraceptives, cyclic progesterone, anti-androgens, weight loss & insulin sensitizing agents
