Pcos management

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Polycystic Ovary Syndrome (PCOS) — Management

Diagnosis (Rotterdam 2003 Criteria — NIH 2012 endorsed)

Two of the following three must be present (after excluding other causes):
  1. Oligo-ovulation or anovulation (oligomenorrhea/amenorrhea)
  2. Hyperandrogenism — biochemical (elevated androgens) or clinical (hirsutism, acne, androgenic alopecia)
  3. Polycystic ovaries on ultrasound (≥12 antral follicles per ovary or ovarian volume >10 mL)
Exclude: hypothyroidism, hyperprolactinemia, non-classical congenital adrenal hyperplasia, androgen-secreting tumors, pregnancy.

Initial Workup

TestPurpose
Pregnancy testAlways exclude first
TSH, prolactinRule out thyroid disease, hyperprolactinemia
LH, FSHLH:FSH ratio classically >3:1 in PCOS
Testosterone, 17-OHPRule out CAH and androgen-secreting tumors
DHEASIf virilizing adrenal tumor suspected
Fasting glucose / OGTT, lipid panelMetabolic screening once PCOS confirmed
Transvaginal ultrasoundNot routine unless pelvic pain or mass suspected

Management by Clinical Goal

1. Lifestyle Modification (First-line for ALL patients)

  • Weight loss of even 5% improves menstrual regularity, hyperandrogenism, and pregnancy rates in overweight/obese patients.
  • Daily caloric reduction of ~500 kcal + regular physical exercise.
  • Weight-loss interventions should precede fertility treatment in patients with excess weight.
  • Berek & Novak's Gynecology

2. Menstrual Irregularity (No Fertility Desired)

  • Combined oral contraceptive pills (OCPs) — first-line; provide cycle control, reduce LH, suppress ovarian androgen production, and protect the endometrium from unopposed estrogen.
  • Cyclic progestins (e.g., medroxyprogesterone acetate 10 mg/day × 10 days) — to induce withdrawal bleeds at least every 3 months; prevents endometrial hyperplasia.
  • Depot medroxyprogesterone acetate or levonorgestrel IUD — if contraception is also desired.
Key point: All women with chronic anovulation need progesterone exposure at least 4×/year to protect against endometrial hyperplasia and carcinoma (unopposed estrogen state). — Textbook of Family Medicine 9e

3. Hyperandrogenism (Hirsutism, Acne)

  • OCPs — suppress ovarian androgen production; first-line.
  • Spironolactone — androgen receptor blocker; used as add-on or alternative when OCPs alone insufficient; requires contraception due to teratogenic risk.
  • Flutamide, finasteride — additional anti-androgen options.
  • Cosmetic measures (laser, electrolysis) as adjuncts.

4. Insulin Resistance / Metabolic Syndrome

  • Metformin — improves insulin sensitivity, may restore ovulation, reduces androgen levels; particularly useful in patients with glucose intolerance or frank T2DM.
  • Screen all PCOS patients for diabetes (fasting glucose or OGTT) and dyslipidemia.
  • Cardiovascular risk counseling is important — PCOS confers increased long-term risk for T2DM and CVD.

5. Infertility / Ovulation Induction

AgentMechanismNotes
Letrozole (aromatase inhibitor)Reduces estrogen → relieves hypothalamic feedback → ↑ FSHNow preferred first-line over clomiphene; shorter half-life (48h vs 2 weeks)
Clomiphene citrateBlocks estrogen receptors in hypothalamus → ↑ GnRH → ↑ FSH/LH60–85% of women ovulate; 15–20% pregnancy/cycle; 50% pregnant by 6 months
AnastrozoleAromatase inhibitor (off-label)Similar mechanism to letrozole
Gonadotropins (FSH/hMG)Direct ovarian stimulationHigh risk of ovarian hyperstimulation syndrome (OHSS) — careful monitoring required
IVFBypass ovulationFor those failing ovulation induction
60–85% of women with PCOS will ovulate with clomiphene or letrozole treatment. — Berek & Novak's Gynecology

6. Endometrial Protection

  • Chronic anovulation = unopposed estrogen = risk of endometrial hyperplasia → carcinoma.
  • All anovulatory PCOS patients not on OCPs must receive progestin withdrawal bleeds ≥4×/year.
  • Consider endometrial biopsy if prolonged amenorrhea or concerning symptoms.

Summary Algorithm

PCOS confirmed
     │
     ├─ Overweight? → Lifestyle modification (weight loss) FIRST
     │
     ├─ Fertility NOT desired
     │       ├─ Menstrual irregularity → OCP or cyclic progestin
     │       ├─ Hirsutism/acne → OCP ± spironolactone
     │       └─ Metabolic concerns → Metformin + screening
     │
     └─ Fertility desired
             ├─ Optimize weight first
             ├─ Letrozole or clomiphene (first-line)
             ├─ Add metformin if insulin resistant
             └─ Gonadotropins / IVF if above fails

Sources: Berek & Novak's Gynecology | Textbook of Family Medicine 9e | Swanson's Family Medicine Review

Menorrhagia

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Menorrhagia (Heavy Menstrual Bleeding / Abnormal Uterine Bleeding)

Terminology

The older term menorrhagia (heavy, prolonged bleeding at regular intervals) — along with menometrorrhagia and dysfunctional uterine bleeding — has been replaced by the FIGO 2011 framework: Abnormal Uterine Bleeding (AUB), classified by the PALM-COEIN system.
Normal menstrual parameters:
  • Cycle interval: 24–38 days
  • Duration of flow: 4–8 days
  • Bleeding <21-day cycles or >35-day cycles = abnormal

PALM-COEIN Classification

PALM — Structural Causes (diagnosed by imaging/histology)

Cause
PPolyp (AUB-P)
AAdenomyosis (AUB-A)
LLeiomyoma / Fibroids (AUB-L)
MMalignancy & hyperplasia (AUB-M)

COEIN — Non-structural Causes

Cause
CCoagulopathy (AUB-C) — up to 20% of HMB; Von Willebrand disease most common (up to 13%)
OOvulatory dysfunction (AUB-O) — PCOS, hypothyroidism, hyperprolactinemia, perimenopause
EEndometrial (AUB-E) — endometritis, endometrial inflammation
IIatrogenic (AUB-I) — anticoagulants, hormonal medications, copper IUD
NNot yet classified
"Dysfunctional uterine bleeding" is obsolete and should not be used. — Rosen's Emergency Medicine

Differential by Age

Age GroupKey Causes
AdolescentCoagulopathy (first presentation), HPO axis immaturity, PCOS, infection
Reproductive ageFibroids, polyps, endometrial hyperplasia, PCOS, anovulation
PerimenopausalAnovulatory bleeding (declining follicles), fibroids, hyperplasia/cancer
PostmenopausalAtrophy (most common), polyps, endometrial cancer (90% present with bleeding)

Workup

All Patients

  • Pregnancy test — always first
  • CBC — assess for anaemia
  • TSH — hypothyroidism causes AUB
  • Prolactin — hyperprolactinemia causes anovulation
  • Cervical cancer screening (if not up to date)
  • STI screening if indicated

Selective Testing

  • Coagulation screen (PT, aPTT, von Willebrand factor): if heavy bleeding since menarche, family history, or signs of systemic bleeding
  • Testosterone, 17-OHP, DHEAS: if PCOS or androgen excess suspected
  • Transvaginal ultrasound (TVUS): first-line imaging — detects fibroids, polyps, endometrial thickness
    • Endometrial stripe <4–5 mm in postmenopausal patient reliably excludes cancer

Endometrial Biopsy — Indicated If:

  • Age ≥45 with AUB
  • Any age with: obesity, unopposed estrogen exposure (anovulatory cycles), persistent or refractory AUB, elevated familial cancer risk

Management

Acute / Emergency Bleeding

Haemodynamically unstable → admit:
  • IV fluids, blood products
  • IV conjugated equine estrogen 25 mg IV every 4–6 hours (up to 24 h)
  • Intrauterine tamponade (26-French Foley catheter with 30 mL saline)
  • Urgent surgical options: D&C, uterine artery embolization, endometrial ablation, hysterectomy
Haemodynamically stable → outpatient medications:
DrugDoseNotes
Conjugated estrogen IV25 mg IV q4–6hFor acute emergent bleeding
Combined OCP1 pill TID × 7 days, or BID × 5 days then OD to finish pack (≤35 µg ethinyl estradiol)Contraindicated: smokers <35y, DVT/PE hx, breast cancer, liver disease
Progestin-only (MPA)20 mg TID × 7 daysUse when estrogen contraindicated
Tranexamic acid (antifibrinolytic)1.3 g PO q6–8h × 5 days OR 10 mg/kg IV (max 600 mg)Do NOT combine with OCP; contraindicated in thromboembolic disease
NSAIDsIbuprofen 200–400 mg TID/QID × 5 days; Mefenamic acid 500 mg TID × 4–5 days; Naproxen 500 mg then 250 mg TID × 5 daysReduce flow and dysmenorrhoea; less effective than tranexamic acid

Long-term / Outpatient Medical Management

GoalTreatment
Cycle regulationCombined OCP (also treats hyperandrogenism in PCOS)
Heavy flow reductionLevonorgestrel IUD (Mirena) — highly effective, long-term
Anovulatory AUBCyclic progestins (MPA 10 mg/day × 10 days/month) — protects endometrium
FibroidsGnRH agonists (pre-surgical shrinkage); ulipristal acetate; myomectomy
AdenomyosisNSAIDs, hormonal contraceptives → hysterectomy if refractory
Coagulopathy-relatedTranexamic acid, DDAVP (for VWD), OCP
PCOS-relatedOCP + metformin ± spironolactone (see PCOS management)

Surgical Management

ProcedureIndication
Endometrial ablationAUB refractory to medical therapy; completed childbearing
Hysteroscopic polypectomyUterine polyps
MyomectomyFibroids (fertility-sparing)
Uterine artery embolizationFibroids; fertility may be preserved
HysterectomyDefinitive; adenomyosis, intractable AUB, endometrial cancer, failed other treatments

Key Points to Remember

  • Endometrial protection with progestin is mandatory in all women with chronic anovulation (at least 4 withdrawal bleeds/year) — unopposed estrogen drives hyperplasia → carcinoma.
  • Von Willebrand disease is an underdiagnosed cause — screen all women with heavy bleeding since menarche.
  • Tranexamic acid and OCP are the two most evidence-based outpatient medical options for heavy flow.
  • Do not use tranexamic acid with combined OCPs (additive thrombotic risk).
  • Postmenopausal bleeding is always abnormal — exclude malignancy first.

Sources: Rosen's Emergency Medicine | Sabiston Textbook of Surgery | Berek & Novak's Gynecology | Textbook of Family Medicine 9e
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