ased on the textbook pages you provided, here are detailed, structured study notes on
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Polycystic Ovarian Disease (PCOD) / Syndrome (PCOS)andHirsutism.
hapter 6: Polycystic Ovarian Disease
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(PCOD) / Syndrome (PCOS)
1. Introduction & Definition
● W hat is it?It is the most common hormonal (endocrine)and multi-system abnormality in
women of reproductive age.
● History:First described by Stein and Leventhal in1935 (formerly calledStein-Leventhal
Syndrome).
● Incidence:Affects 6–10% of women worldwide (up to20% in infertility patients). It is
becoming more common due to lifestyle changes and stress.
2. Diagnostic Criteria (Rotterdam Criteria, 2003)
o diagnose PCOS, a woman must haveat least 2 outof the following 3criteria (after ruling
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out other causes):
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1 ligo-ovulation or Anovulation:Irregular or absentperiods.
2. Hyperandrogenism:Clinical signs (acne, excess hair)or Biochemical signs (high
testosterone in blood).
3. Polycystic Ovaries on Ultrasound:
○ $\ge$ 20 follicles measuring 2–9 mm in each ovary.
○ OROvarian volume $\ge$ 10 cm³.
3. Etiopathogenesis (Why does it happen?)
The exact cause is unknown, but several hypotheses exist:
● A . Insulin Resistance (The "Insulin Hypothesis"):
○ Most accepted theory.
○ Body tissues resist insulin $\rightarrow$ Pancreas pumps outmoreinsulin
(Hyperinsulinemia).
○ High insulin signals the ovaries to produceAndrogens(male hormones).
○ It also reducesSHBG(Sex Hormone Binding Globulin)in the liver, leaving more "free"
testosterone in the blood.
● B. Neuroendocrine Defects:
○ IncreasedGnRHpulses from the brain lead to highLH(Luteinizing Hormone)
production.
○ LH stimulates ovariesto make androgens.
○ FSH is relatively low, causing follicles to stop growing(arrest) and not release an
egg (anovulation).
● C. Ovarian Defect:
○ The ovaries themselves are genetically programmed to overproduce hormones.
● D. Low-Grade Inflammation:
○ PCOS patients often have slightly high inflammatory markers (CRP, TNF-$\alpha$).
This worsens insulin resistance.
● E. Genetics & Environment:
○ Runs in families.
○ Worsened by obesity, stress, and poor diet.
4. Clinical Features (Symptoms)
Symptoms vary but usually start around puberty, often accompanied by weight gain.
● M enstrual Disorders (Most Common):
○ Oligomenorrhea:Infrequent periods (cycle length >35 days).
○ Amenorrhea:Absence of periods (common in obesity).
○ Heavy bleeding:Can occur after a long period of nobleeding.
● Hyperandrogenism (Excess Male Hormones):
○ Hirsutism:Excess coarse hair in male patterns (face,chin, chest, abdomen).
○ Acne:Pimples on face and back.
○ Alopecia:Male-pattern hair thinning/balding.
● Obesity:
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○ een in ~50% of patients.
○ Central Obesity:"Apple shape." Waist circumference> 80 cm (Indian standards) or
> 35 inches.
● Acanthosis Nigricans:
○ Dark, velvety thickening of skin on the neck, armpits, and knuckles.
○ Sign of severe insulin resistance.
Infertility:
●
○ Difficulty getting pregnant due to lack of ovulation (anovulation).
● Psychological:Anxiety, depression, and body imageissues.
5. Diagnosis & Investigations
● U ltrasound (USG):
○ Necklace Appearance:Small follicles arranged aroundthe edge of the ovary.
○ Stromal Echogenicity:The center of the ovary looksbright/dense.
● Hormonal Tests (Blood work):
○ FSH & LH:High LH levels; LH/FSH ratio is often >2:1.
○ Testosterone:Levels are elevated.
○ SHBG:Low.
○ Glucose/Insulin:Oral Glucose Tolerance Test (OGTT)to check for insulin
resistance/diabetes.
6. Complications (Long-term Risks)
If untreated, PCOS can lead to:
● M etabolic Syndrome:Diabetes Type 2, Hypertension,High Cholesterol (Dyslipidemia),
Cardiovascular disease.
● Reproductive:Recurrent miscarriage, Gestational Diabetesduring pregnancy.
● Cancer:Increased risk ofEndometrial Cancer(dueto unopposed estrogen causing
lining thickening).
● Sleep Apnea.
7. Management (Treatment)
reatment depends on the patient's main complaint (e.g., does she want to get pregnantnow
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or just regulate periods?).
A. Lifestyle Modifications (First Line Treatment)
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● iet & Exercise:Crucial for all PCOS patients.
● Weight Loss:losing just5–10% of body weightcanrestore regular periods and
ovulation naturally.
● Avoid refined carbs and sugar.
B. Treatment for Menstrual Irregularities (If NOT trying to conceive)
● C ombined Oral Contraceptive Pills (OCPs):Mainstaytreatment.
○ Regulates periods.
○ Lowers androgen levels (treats acne/hirsutism).
○ Protects the endometrium from cancer.
● Cyclical Progestogens:Medroxyprogesterone acetategiven for 5-10 days a month to
induce a bleed (withdrawal bleeding).
C. Treatment for Hirsutism (Excess Hair)
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● echanical:Waxing, bleaching, laser, electrolysis.
● Medical:
○ Cyproterone Acetate:An anti-androgen usually combinedwith OCPs.
○ Spironolactone / Flutamide:Anti-androgens.
○ Eflornithine cream:Topical facial cream.
D. Treatment for Infertility (Trying to conceive)
. W
1 eight Loss:First step.
2. Letrozole:(Aromatase Inhibitor) Now considered thefirst-line drugfor ovulation
induction.
3. C lomiphene Citrate (CC):Stimulates ovulation. Used if Letrozole isn't available or
effective.
4. Metformin:An insulin sensitizer. Helps improve ovulationrates, especially in obese
patients.
5. Gonadotropins (FSH injections):If pills fail. (Risk:Multiple pregnancies).
6. IVF:Last resort.
E. Surgical Treatment
● L
aparoscopic Ovarian Drilling (LOD):
○ Used for cases resistant to Clomiphene.
○ Small holes are punctured in the ovary using electrocautery.
○ Goal:Destroy androgen-producing tissue $\rightarrow$lowers testosterone
$\rightarrow$ restores ovulation.
○ Advantage:One-time procedure, no risk of multiplepregnancy.
○ Risk:Adhesions or premature ovarian failure if donetoo aggressively.
8. Important Terminology
● H AIR-AN Syndrome:A specific severe subgroup of PCOScharacterized by
HyperAndrogenism,InsulinResistance, andAcanthosisNigricans.
● Metabolic Syndrome X:Cluster of conditions (BP, blood sugar, excess body fat around
the waist, and abnormal cholesterol levels) occurring together.