Internal Diseases and Therapy · MU Sofia

89. Polycystic ovarian syndrome

Covers polycystic ovary syndrome as the most common endocrine disorder in women of reproductive age, then the Rotterdam diagnostic criteria and when ultrasound is not used. It goes on to the pathophysiology, clinical features, and a table of conditions to exclude with their tests, followed by investigations, long-term risks, and a goal-based management table covering contraception, hirsutism, ovulation induction and metabolic risk. It closes with a list of key points.

Inside: 1 section · 2 tables · 1 min

Topic 90 of 139 in the MU Sofia syllabus for Internal Diseases and Therapy (Medicine, Years 4 and 5). The free AceMed note covers it in 1 section, about 633 words (1 min of reading).

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  1. Polycystic ovarian syndrome

Polycystic ovarian syndrome

Polycystic ovary syndrome (PCOS) is the most common endocrine disorder of women of reproductive age, affecting about 8–13%. It combines ovulatory dysfunction, androgen excess and a metabolic disorder based on insulin resistance. It is the leading cause of anovulatory infertility and of hirsutism. The "cysts" are not true cysts but many small antral follicles whose development has stopped.

Diagnosis: Rotterdam criteria

PCOS is diagnosed when 2 of the following 3 criteria are present, after other causes have been excluded:

  • Oligo- or anovulation – cycles longer than 35 days or fewer than 8 periods a year, or amenorrhoea
  • Hyperandrogenism – clinical (hirsutism, acne, androgenic alopecia) or biochemical (raised total or free testosterone)
  • Polycystic ovarian morphology on ultrasound – 20 or more follicles of 2–9 mm in at least one ovary, or ovarian volume of 10 mL or more (raised AMH can replace ultrasound in adults)

Ultrasound is not used in adolescents (less than 8 years after menarche), because multifollicular ovaries are normal at that age; they need both irregular cycles and hyperandrogenism.

Pathophysiology

  • LH excess – increased GnRH pulse frequency raises LH relative to FSH; LH drives androgen production by ovarian theca cells
  • Relative FSH deficiency – too little aromatase activity in granulosa cells, so androgens are not converted to oestrogen; follicles stop growing and no dominant follicle forms → anovulation
  • Insulin resistance with compensatory hyperinsulinaemia – present in most women, including many who are lean; insulin acts with LH on theca cells and lowers hepatic SHBG, increasing free testosterone
  • Hyperandrogenism – further impairs follicle development; obesity worsens all of these steps
  • Anovulation – no corpus luteum and no progesterone, so the endometrium is exposed to unopposed oestrogen
  • Genetic predisposition (polygenic, familial clustering)

Clinical features

  • Irregular or absent periods, subfertility
  • Hirsutism (modified Ferriman–Gallwey score), acne, female-pattern hair loss
  • Overweight and central obesity are common but not universal; acanthosis nigricans (a sign of insulin resistance)
  • Depression, anxiety, poor body image; obstructive sleep apnoea
  • Rapidly progressive hirsutism or virilisation (clitoromegaly, deep voice, temporal balding) is not PCOS – exclude an androgen-secreting ovarian or adrenal tumour

Investigations

  • Androgens – total testosterone (normal or mildly raised), low SHBG, free androgen index; very high testosterone or DHEAS suggests a tumour
  • LH and FSH – LH often raised with normal FSH (high LH/FSH ratio); supportive, not diagnostic
  • Pelvic ultrasound (transvaginal) – ovarian morphology and endometrial thickness

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