Describe the diagnostic criteria, features, complications and management of polycystic Ovary Syndrome.
| Rotterdam criteria (any 2 of 3) | Detail |
|---|---|
| Oligo/anovulation | Irregular or absent cycles |
| Hyperandrogenism | Clinical (hirsutism, acne) or biochemical |
| Polycystic ovaries | ≥12 follicles 2–9 mm, or volume >10 mL |
KEY POINT
Exam question: diagnostic criteria, features, complications and management
Definition
Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine disorder of reproductive-age women characterised by hyperandrogenism, ovulatory dysfunction and polycystic ovaries. It is the commonest cause of anovulatory infertility.
Pcos - Rotterdam Criteria (2 of 3)
Diagnostic Criteria (rotterdam — Eshre/asrm)
Diagnosis requires any two of the following three (after excluding other causes):
- Oligo- or anovulation (oligomenorrhoea/amenorrhoea).
- Clinical and/or biochemical hyperandrogenism (hirsutism, acne; raised serum testosterone).
- Polycystic ovaries on ultrasound (≥ 12 small follicles per ovary and/or ovarian volume > 10 mL).
Pathophysiology
Central features are insulin resistance with compensatory hyperinsulinaemia, an increased LH:FSH ratio, and ovarian/adrenal hyperandrogenism, which together disturb folliculogenesis and ovulation.
Clinical Features
Menstrual irregularity (oligo-/amenorrhoea), hirsutism, acne and male-pattern hair loss, obesity (central), infertility, and acanthosis nigricans (a marker of insulin resistance).
Investigations
Serum testosterone, LH and FSH, prolactin and TSH (to exclude mimics); fasting glucose/insulin and an oral glucose-tolerance test, and a lipid profile; transvaginal ultrasound of the ovaries.
Differential Diagnosis
Other causes of hyperandrogenism/anovulation must be excluded — thyroid dysfunction, hyperprolactinaemia, congenital adrenal hyperplasia (late-onset), Cushing's syndrome and an androgen-secreting tumour (suggested by rapidly progressive virilisation).
Complications
Anovulatory infertility, type-2 diabetes and metabolic syndrome, dyslipidaemia, obstructive sleep apnoea, and — from chronic unopposed oestrogen — endometrial hyperplasia and carcinoma.
Management
- Lifestyle and weight reduction — the first-line measure; even modest weight loss restores ovulation and improves the metabolic profile.
- Menstrual regulation / endometrial protection — combined oral pills or cyclical progestins.
- Hirsutism — combined pills with anti-androgens (cyproterone, spironolactone), and cosmetic measures.
- Infertility — ovulation induction with letrozole (first line) or clomiphene, adding metformin, then gonadotrophins or laparoscopic ovarian drilling; IVF if these fail.
- Metabolic — metformin for insulin resistance and management of the cardiometabolic risk.
CLINICAL PEARL
Clinical pearl — Long-term surveillance: because of the lifelong cardiometabolic and endometrial risk, women with PCOS need periodic screening for diabetes, dyslipidaemia and hypertension, and endometrial protection (regular withdrawal bleeds) to prevent hyperplasia from chronic unopposed oestrogen.
PCOS is diagnosed by the Rotterdam criteria — any two of three: oligo- or anovulation, clinical or biochemical hyperandrogenism, and polycystic ovaries on ultrasound. Underlying it is insulin resistance: the resulting hyperinsulinaemia raises ovarian androgen production and lowers sex-hormone-binding globulin, causing hirsutism, follicular arrest and anovulation. The long-term consequences are metabolic (type 2 diabetes, metabolic syndrome) and endometrial (hyperplasia and carcinoma from unopposed oestrogen).
WHY Insulin Resistance Is the Engine of Pcos
The concept that unifies the whole syndrome is why insulin resistance drives the reproductive features of PCOS. The primary abnormality in most women is insulin resistance, so the pancreas compensates by secreting more insulin (hyperinsulinaemia). That excess insulin then acts on the ovary and liver in two ways. It directly stimulates the ovarian theca cells (acting with LH) to produce more androgens; and it suppresses hepatic production of sex-hormone-binding globulin, so a greater fraction of the circulating testosterone is free and biologically active. The result is hyperandrogenism — clinically, hirsutism and acne. The high intraovarian androgen also disrupts follicular development, so follicles are recruited but arrest before maturity, accumulating as the multiple small subcapsular follicles that give the ovary its polycystic appearance — and, since no dominant follicle emerges, ovulation fails: hence oligomenorrhoea and infertility. This single chain explains all three Rotterdam criteria at once. It also explains why weight loss is the single most effective treatment — by reducing insulin resistance it can restore ovulation, regularise cycles and lower androgens, and why metformin has a role.
WHY Pcos Is a Lifelong Metabolic Disorder, Not Just a Gynaecological One
A crucial point often missed is why the young woman treated for irregular periods or hirsutism must be followed for the rest of her life. PCOS is not merely an ovarian problem; the underlying insulin resistance carries major long-term metabolic consequences: impaired glucose tolerance and type 2 diabetes, dyslipidaemia, hypertension, metabolic syndrome, non-alcoholic fatty liver disease and an increased cardiovascular risk. Separately, the chronic anovulation means the endometrium is exposed to years of unopposed oestrogen with no progesterone — producing endometrial hyperplasia and a significantly increased risk of endometrial carcinoma, even in young women. Both consequences are preventable. Hence the management of PCOS must always include: screening for diabetes and lipids, blood-pressure monitoring, and vigorous encouragement of weight loss and exercise (the treatment that addresses the root cause); and endometrial protection — ensuring that a woman not on a combined pill has at least a withdrawal bleed every three months, with cyclical progestogen or an LNG-IUS. Understanding that PCOS is a metabolic disease with gynaecological manifestations — not the reverse — explains why its management extends far beyond restoring periods or fertility.
KEY POINT
Key points TO remember
- PCOS: diagnosed by any 2 of 3 Rotterdam criteria — oligo/anovulation, clinical or biochemical hyperandrogenism, polycystic ovaries on ultrasound.
- The engine is insulin resistance → hyperinsulinaemia → ↑ovarian androgens + ↓SHBG → hirsutism, acne, follicular arrest and anovulation.
- Long-term risks: type 2 diabetes, metabolic syndrome, dyslipidaemia, cardiovascular disease — and endometrial hyperplasia/carcinoma from unopposed oestrogen.
- Weight loss is the single most effective treatment — it can restore ovulation and regularise cycles.
- Treat by need: cycle control/endometrial protection (COC or cyclical progestogen); hirsutism (COC + anti-androgen); fertility (letrozole — first line — or clomiphene, ± metformin).
EXAM TIP
Sources: D.C. Dutta's Textbook of Gynaecology; Shaw's Textbook of Gynaecology.
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