About This Page
This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.
The Bottom Line
- Diagnosis (Rotterdam): ≥2 of: (1) oligo/anovulation, (2) clinical/biochemical hyperandrogenism, (3) polycystic ovaries on USS or elevated AMH — after excluding other causes
- Clinical: irregular periods, hirsutism, acne, alopecia, weight gain, subfertility
- Metabolic: insulin resistance, T2DM risk (screen regularly), dyslipidaemia, NAFLD, cardiovascular risk
- First-line for cycle regulation + hyperandrogenism: combined oral contraceptive pill (COCP)
- Fertility: letrozole is first-line pharmacological ovulation induction. Clomifene ± metformin second-line
- Metformin: primarily for metabolic features (insulin resistance). Greater efficacy than inositol
Overview
Polycystic ovary syndrome (PCOS) is the most common endocrine disorder affecting women of reproductive age, characterised by a combination of hyperandrogenism, ovulatory dysfunction, and polycystic ovarian morphology. The Rotterdam criteria (2003, updated 2023) require at least two of these three features for diagnosis, after excluding other conditions that mimic PCOS (thyroid disease, congenital adrenal hyperplasia, Cushing syndrome, hyperprolactinaemia, androgen-secreting tumours). The pathophysiology involves insulin resistance and compensatory hyperinsulinaemia (even in lean women), which drives ovarian androgen production. The elevated androgens disrupt follicular development, leading to anovulation and the characteristic "string of pearls" appearance on USS. PCOS has significant metabolic, reproductive, dermatological, and psychological consequences.
Epidemiology
PCOS affects approximately 8–13% of women of reproductive age, making it the most common endocrine condition in this group. Up to 70% may be undiagnosed. Prevalence is higher in South Asian and Indigenous populations. Insulin resistance is present in 65–80% of women with PCOS, independent of BMI. Women with PCOS have a 5–10× increased risk of developing T2DM and earlier onset hyperglycaemia. Obesity worsens all features but ~30% of women with PCOS are lean. Psychological morbidity is high — depression and anxiety prevalence is 3–8× higher than in age-matched controls.
Clinical Features
Symptoms
Oligomenorrhoea (cycles >35 days) or amenorrhoea
Hirsutism (excess hair in male-pattern distribution — face, chest, abdomen, back)
Acne (often persistent beyond adolescence)
Androgenic alopecia (female-pattern hair loss — frontal thinning)
Weight gain (especially central/abdominal)
Subfertility (anovulation)
Low mood, anxiety, reduced self-esteem
Signs
Hirsutism scored by modified Ferriman-Gallwey scale (≥4–6 depending on ethnicity)
Acne (inflammatory, often jawline and chin)
Acanthosis nigricans (velvety hyperpigmentation in flexures — marker of insulin resistance)
Central obesity (waist circumference >80 cm in women)
BMI often ≥25 but lean PCOS exists (~30%)
Investigations
First-line
Total testosterone and SHBGCalculate free androgen index (FAI = total testosterone / SHBG × 100). Elevated FAI confirms biochemical hyperandrogenism
LH and FSHLH:FSH ratio often >2:1 (raised LH, normal/low FSH) — but not required for diagnosis. Not reliable if on COCP
Second-line
Pelvic USS (transvaginal preferred)Polycystic ovaries: ≥12 follicles per ovary (2–9 mm) or ovarian volume >10 mL. Not required if oligo/anovulation + hyperandrogenism both present
Anti-Müllerian hormone (AMH)Elevated in PCOS — can substitute for USS in diagnosis (2023 International Guideline)
17-hydroxyprogesteroneExclude non-classic congenital adrenal hyperplasia (21-hydroxylase deficiency) — elevated if present
TFTs and prolactinExclude hypothyroidism and hyperprolactinaemia
Oral glucose tolerance test (OGTT)Screen for impaired glucose tolerance / T2DM. Particularly if BMI >25 or other risk factors. Repeat every 1–3 years
Lipid profileDyslipidaemia common (raised triglycerides, low HDL)
Specialist
DHEAS and androstenedioneIf severe/rapid-onset hyperandrogenism — exclude adrenal tumour or ovarian androgen-secreting tumour
Cortisol/dexamethasone suppressionIf Cushing's suspected clinically
1
Lifestyle modification (ALL patients)
- Weight management: even 5–10% weight loss significantly improves hormonal and metabolic parameters
- Physical activity: ≥150 min/week moderate intensity, ≥75 min vigorous, or combination
- Healthy diet: no single "PCOS diet" is superior — general healthy eating principles, reduce refined carbohydrates
- Minimise weight stigma — healthcare professionals should seek permission to weigh and explain weight-related risks
2
Menstrual regulation + hyperandrogenism
- COCP (first-line): regulates cycles, reduces endometrial cancer risk, anti-androgen effect. No specific pill is superior — use lowest effective oestrogen dose
- Cyclical progestogens (if COCP contraindicated): medroxyprogesterone or norethisterone for 12–14 days each cycle — protects endometrium
- Anti-androgens (co-cyprindiol, spironolactone, finasteride): specialist-initiated, for persistent hirsutism/acne. Teratogenic — need effective contraception
- Topical eflornithine cream: facial hirsutism (adjunct to physical hair removal)
3
Metabolic management
- Metformin: recommended for metabolic features (insulin resistance, pre-diabetes). Greater efficacy than inositol (2023 guideline)
- Screen for T2DM (OGTT or HbA1c) every 1–3 years depending on risk
- Manage cardiovascular risk factors: dyslipidaemia, hypertension
4
Fertility (if desired)
- Letrozole: first-line pharmacological ovulation induction (2023 guideline — superior to clomifene)
- Clomifene: second-line, alone or combined with metformin
- Gonadotrophins: second-line if clomifene fails
- Ovarian drilling (laparoscopic): second-line if pharmacological failure
- IVF: third-line if above measures unsuccessful. Risk of OHSS with gonadotrophin stimulation in PCOS
Complications
- Type 2 diabetes: 5–10× increased risk. Screen regularly with OGTT
- Endometrial hyperplasia/cancer: Chronic anovulation → unopposed oestrogen. COCP or cyclical progestogens protect endometrium
- Cardiovascular disease: Increased risk from insulin resistance, dyslipidaemia, obesity, hypertension
- Obstructive sleep apnoea: Increased risk, especially with obesity
- NAFLD: Common association with insulin resistance
- Psychological: Depression, anxiety, body image issues, reduced quality of life — screen and manage
- Pregnancy complications: Gestational diabetes, pre-eclampsia, preterm birth — increased risk in PCOS
UKMLA Exam Tips
- 1Rotterdam criteria: ≥2 of 3 (oligo/anovulation, hyperandrogenism, polycystic ovaries). Must EXCLUDE other causes first
- 2LH:FSH ratio >2:1 is suggestive but NOT diagnostic. Testosterone/FAI is more useful for confirming hyperandrogenism
- 3Letrozole is now FIRST-LINE for ovulation induction (above clomifene) — 2023 international guideline
- 4Endometrial cancer risk: from chronic anovulation + unopposed oestrogen. Protect with COCP or cyclical progestogens
- 5Insulin resistance is present in 65–80% regardless of BMI — lean PCOS exists and still carries metabolic risk
- 6Metformin is for metabolic features, NOT first-line for cycle regulation (COCP is first-line for that)
- 7Screen for depression/anxiety routinely — 3–8× higher prevalence in PCOS
practicetest your knowledge on pcosApply what you've learnt with UKMLA-style questions from the iatroX Q-Bank — endocrine and beyond.
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