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Understanding PCOS: Symptoms and Management

Polycystic Ovary Syndrome (PCOS) is a common endocrine-metabolic disorder affecting 6-15% of reproductive-age women, characterized by hyperandrogenism, ovulatory dysfunction, and polycystic ovarian morphology. It has multifactorial etiology, including genetic and environmental factors, leading to complications such as infertility, diabetes, and cardiovascular disease. Management involves lifestyle modifications, medications, and, in resistant cases, surgical options, with a focus on early treatment to prevent long-term complications.

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0% found this document useful (0 votes)
38 views2 pages

Understanding PCOS: Symptoms and Management

Polycystic Ovary Syndrome (PCOS) is a common endocrine-metabolic disorder affecting 6-15% of reproductive-age women, characterized by hyperandrogenism, ovulatory dysfunction, and polycystic ovarian morphology. It has multifactorial etiology, including genetic and environmental factors, leading to complications such as infertility, diabetes, and cardiovascular disease. Management involves lifestyle modifications, medications, and, in resistant cases, surgical options, with a focus on early treatment to prevent long-term complications.

Uploaded by

yraju326
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We take content rights seriously. If you suspect this is your content, claim it here.
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POLYCYSTIC OVARY SYNDROME (PCOS) – DETAILED NOTES

1. Definition
• PCOS is a common endocrine-metabolic disorder in women of reproductive age.

• Characterized by: (1) Hyperandrogenism, (2) Ovulatory dysfunction, (3) Polycystic ovarian
morphology.

2. Epidemiology
• Affects 6–15% of reproductive-age women.

• Common cause of anovulatory infertility.

• Begins during adolescence; strong familial/genetic predisposition.

3. Etiology
• Multifactorial – genetic + environmental.

• Factors: insulin resistance, obesity, HPO axis dysfunction, inflammation, ovarian enzyme
abnormality.

4. Pathophysiology
• Insulin resistance → hyperinsulinemia → ovarian androgen excess.

• Theca cells: ↑ P450c17 enzyme → ↑ androgen synthesis.

• Granulosa cells: ↓ aromatase activity → impaired follicle maturation.

• HPO axis: ↑ GnRH → ↑ LH > FSH → androgen excess and anovulation.

• Chronic inflammation (↑ CRP) worsens insulin resistance.

• Peripheral conversion of androgens to estrogens in adipose tissue → continuous estrogen


feedback.

5. Ovarian Morphology
• Ovarian volume >10 mL.

• Multiple small follicles (2–9 mm) arranged peripherally (“string of pearls”).

• Thickened capsule and theca cell hyperplasia.

6. Clinical Features
• Menstrual irregularities: Oligomenorrhea, amenorrhea, infertility.

• Hyperandrogenism: Hirsutism, acne, alopecia.

• Metabolic: Obesity, insulin resistance, dyslipidemia, diabetes.

• Others: Acanthosis nigricans, mood disorders, sleep apnea.


7. Complications
• Infertility, endometrial hyperplasia/cancer, diabetes, metabolic syndrome, cardiovascular disease.

8. Diagnostic Criteria (Rotterdam 2003)


• Any two of: (1) Oligo/anovulation, (2) Hyperandrogenism, (3) Polycystic ovaries on ultrasound.

9. Investigations
• ↑ LH/FSH ratio, ↑ Testosterone, ↓ SHBG, ↑ AMH.

• Fasting glucose, lipid profile, ultrasound findings.

• Exclude thyroid, prolactin, CAH, Cushing’s.

10. Management
• Lifestyle modification: weight loss, exercise, diet.

• Drugs: COCs, metformin, antiandrogens, letrozole/clomiphene for infertility.

• Surgery: Laparoscopic ovarian drilling for resistant cases.

11. Prognosis
• Chronic but manageable; early treatment prevents metabolic and reproductive complications.

Aspect Key Points


Core features Hyperandrogenism, oligo/anovulation, polycystic ovaries
Main hormones ↑ LH, ↑ androgens, ↓ FSH, ↓ SHBG
Main pathology Insulin resistance → hyperinsulinemia → androgen excess
Complications Infertility, diabetes, endometrial hyperplasia, obesity
First-line therapy Lifestyle modification
Fertility drug of choice Letrozole

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