17. PCOS: diagnosis after exclusion

First principle: a syndrome of androgen excess + ovulatory dysfunction

Insulin resistance amplifies theca androgen output and lowers SHBG (raising free testosterone); disordered follicle selection causes anovulation. It is a reproductive–metabolic syndrome, not "cysts."

Diagnosis: Rotterdam — 2 of 3, after exclusion

1. Hyperandrogenism (clinical or biochemical).
2. Ovulatory dysfunction (oligo/anovulation).
3. Polycystic ovarian morphology on ultrasound — or raised AMH as an alternative in adults.

The pitfall that defines the concept 🚩

Discriminators

• Sudden, severe hyperandrogenism → tumour, not PCOS (Concept 16).
• Cushingoid features / very high DHEA‑S → adrenal work‑up.

Associations to screen for

Insulin resistance (± acanthosis nigricans), impaired glucose tolerance/T2DM, dyslipidaemia, OSA, mood disorder, and — long term — endometrial hyperplasia/carcinoma from chronic anovulation.

Pearls

• 🎯 2 of 3, after exclusion. AMH may substitute for ultrasound in adults; ultrasound is invalid in adolescents.
• 🩺 Screen every PCOS patient metabolically (OGTT/HbA1c, lipids, BP) — the diagnosis is a cardiometabolic flag, not just a fertility one.

Next → Once diagnosed, management is organised entirely around her goal (Concept 18).