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PH-RO02

Polycystic ovary syndrome

How androgen excess, an altered LH and FSH balance and insulin resistance stop follicles maturing, why that disrupts ovulation and periods, and why the condition looks different in different people.

By the end, you can

  • Describe follicle development and the hypothalamic–pituitary–ovarian axis, including the two-cell model of hormone production.
  • Explain how fast GnRH pulses, a high LH relative to FSH and theca-cell androgen excess arise and sustain each other.
  • Explain how insulin resistance and hyperinsulinaemia amplify androgen excess.
  • Relate follicle arrest and anovulation to irregular periods, subfertility and endometrial risk.
  • Explain why the condition varies between people and why diagnostic criteria differ.
  • Recognise the classic ovarian appearances, the diagnostic criteria and tests of PCOS, and explain how each main treatment acts on its mechanism.

What it is

Polycystic ovary syndrome (PCOS) is a common, lifelong hormonal and metabolic condition of people with ovaries, defined by combinations of androgen excess, ovulatory dysfunction and polycystic ovarian morphology, after other causes are excluded. In 2026 a global consensus renamed it polyendocrine metabolic ovarian syndrome (PMOS), because not everyone has polycystic ovaries and the old name hid its metabolic effects; both names are in use.

4 types to tell apart
Androgen excess, ovulatory dysfunction and polycystic ovaries
The full picture (often called phenotype A), usually with the most marked metabolic risk.
Androgen excess and ovulatory dysfunction
Ovaries look normal on ultrasound (phenotype B); metabolic risk is similar to the full picture.
Androgen excess and polycystic ovaries, ovulating
Cycles are regular or near regular (phenotype C); metabolic features tend to be milder.
Ovulatory dysfunction and polycystic ovaries, normal androgens
No clinical or biochemical androgen excess (phenotype D); usually the mildest metabolic profile.

US spelling: oestradiol → estradiol.

Normal function

Follicles and the ovarian axis

Each holds a reserve of follicles: an egg (oocyte) surrounded by granulosa cells, with an outer layer of theca cells. Each cycle, a group of small antral follicles grows under follicle-stimulating hormone (FSH); usually one becomes dominant and ovulates, while the rest regress.

Hormone production is shared between the two cell types (the two-cell, two-gonadotrophin model). Luteinising hormone (LH) drives theca cells to make androgens, such as androstenedione and testosterone, from cholesterol; FSH drives granulosa cells to convert them to oestradiol with the enzyme aromatase.

The hypothalamus releases gonadotrophin-releasing hormone (GnRH) in pulses, and the pituitary answers with LH and FSH. Rising oestradiol from the dominant follicle triggers the LH surge that releases the egg; the corpus luteum then makes progesterone, which slows the GnRH pulses and prepares the endometrium of the .

Point to it on the model
Two cells, two gonadotrophinsSchematic
Capillary bloodBrings LH, FSH and cholesterol
  • LH and cholesterol (from Capillary blood to Theca cell)
NormalTheca cellLH receptors; makes androgens
  • Androstenedione and testosterone (from Theca cell to Granulosa cell)
NormalGranulosa cellFSH receptors; aromatase
  • Oestradiol (FSH-driven aromatase) (from Granulosa cell to Follicle and circulation)
NormalFollicle and circulationOestradiol

In PCOS, theca androgen output rises while granulosa conversion lags, so androgen builds up in the follicle and the blood.