Poly Cystic Ovarian Syndrome By Dr. Vidhi Agarwal

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Poly Cystic Ovarian Syndrome (PCOD)

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Poly Cystic Ovarian Syndrome By Dr. Vidhi Agarwal

  1. 1. Poly Cystic OvarianSyndrome Dr. Vidhi Agarwal
  2. 2. PCOS•PCOS IS ONE GYNAECOLOGICAL CONDITION IN WHICH KNOWLEDGE BASE IS RAPIDLY EVOLVING.•PCOS IS A CONDITION IN WHICH A WOMAN HAS AN IMBALANCE OF FEMALE SEX HORMONES.THIS MAY LEAD TO - 1. MENSTRUAL CYCLE CHANGES 2. CYSTS IN THE OVARIES 3. TROUBLE GETTING PREGNANT 4. OTHER HEALTH SYMPOTOMS
  3. 3. Rotterdam ESHRE/ASRM• Diagnosis of PCOS include two of the following three criteria: – Oligo- and/or anovulation – Clinical and/or biochemical hyperandrogenism, – Polycystic ovaries on ultrasound Rev Obstet Gynecol. 2011;4(2):45-51
  4. 4. Rev Obstet Gynecol. 2011;4(2):45-51
  5. 5. PATHOPHYSIOLOGY TRADITIONAL CONCEPTHYPERENDROGENISM & ANOVULATION ARE CAUSED BYABNORMALITIES IN 4 ENDOCRINOLOGICALLY ACTIVECOMPARTMENTS.1. OVARIES2. ADRENAL GLANDS3. THE PERIPHERY(FAT)4. HYPOTHALAMUS-PITITUTARY COMPARTMENT RECENT CONCEPTPATHOPHYSIOLOGY OF PCOS HAVE FOCUSED ON THE ROLE OF1. GENETICS2. INSULIN RESISTANCE3. INTERRELATIONSHIP BETWEEN OBESITY & GHRELIN
  6. 6. PATHOPHYSIOLOGY GENETICS RESULTS FROM SOME FAMILY STUDIES SUGGEST A POSSIBLE AUTOSOMAL DOMINANT PHENOTYPE INSULIN RESISTANCEPATIENTS WITH PCOS FREQUENTLY EXHIBIT IR& HYPERINSULINEMIA.
  7. 7. IRTHE MOST COMMON CAUSE OF IR & COMPENSATORY HYPERINSULINEMIA IS OBESITY.BUT IT ALONE DOES NOT EXPLAIN THIS IMPORTANT ASSOCIATION.THE OBSERVATIONS THAT PROVIDE EVIDENS THAT IR ASSOCIATED WITH PCOS IS NOT THE RESULT OF HYPERANDROGENISM ARE PCOS WITH OR HYPERANDROGENISM WITHOUT OBESITY # HYPERINSULINEMIA IS NOT A CHARACTERISTIC IN # UNIQUELY ASSOCIATED GENERAL # 30-45% HAVE GLUCOSE INTOLERANCE OR FRANK #NORMAL INSULIN LEVEL & GLUCOSE TOLERENCE DM # SUPPRESION WITH LONG ACTING GNRH ANALOG DOES NOT CHANGE INSULIN LEVEL OR IR # OOPHERECTOMY IN THESE PATIENTS DOES NOT CHANGE IR DESPITE A DECREASE IN ANDROGEN LEVEL
  8. 8. The Central Player (Insulin Resistance) Pregnancy Aging Drugs Lifestyle Insulin Upper abdominalGenetics Resistance obesity Hyperinsulinemia Increased lipid storage PCOS Altered lipoprotein & Altered steroid cholesterol metabolism hormone metabolism
  9. 9. Characteristics of PCOS Hyperinsulinemia, Insulin resistance Gestational Diabetes Hyperandrogenism Acne, hirsutism Menstrual PCOS Hormonal DysfunctionManifestations Imbalance Oligo/ Anovulation Metabolic Central Obesity, Syndrome Hypertriglycerides Anxiety, depression Psychological and poor self- problems esteem
  10. 10. Diagnosis Of PCOS
  11. 11. DIAGNOSIS• DIAGNOSIS IS BASED ON 2003 ROTTERDAM CRETERIA .TWO OUT OF THREE OF THE FOLLOWING WERE REQUIRED IN ORDER TO DIAGNOSE THE CONDITION AFTER EXCLUSION OF OTHER CAUSES OF ANDROGEN EXCESS.• 1- OLIGO OVULATION / ANOVULATION• 2- CLINICAL &/ BIOCHEMICAL SIGHNS OF HYPERANDROGENISM• 3- POLYCYSTIC OVARIES ON ULTRASOUND
  12. 12. PHYSICAL EXAMINATION• 1- PATIENTS USUALLY HAVE FEATURES OF HYPERANDROGENISM ie. HIRSUTISM, ACNE,DECREASED BREAST SIZE,DEEP VOICE• 2- CHRONIC ANOVULATION LEADING TO MENSTRUAL IRREGULARITY AND INFERTILITY• 3- INCREASED BMI AND WAIST HIP RATIO
  13. 13. PELVIC EXAMINATION• # SWOLLEN OVARIES• # SWOLLEN CLITORIS( OCCASIONALLY)
  14. 14. ULTRASONOGRAPHY ON USG POLYCYSTIC OVARIES WITH B/L ENLARGEMENT ARE SEEN.THESE ARE WITH –*HYPERECHOGENIC ENLARGED CENTRAL STROMA*WITH PERIPHERALLY ARRENGED MICROCYSTS MEASURING 2-9 mm IN DIAMETER*PRESENCE OF 12 OR MORE FOLLICLES IN EACH OVARY*INCREASED OVARIAN VOLUME(>10ml)
  15. 15. Laboratory TESTS• PTS WITH FEATURES OF HYPERANDROGENISM SHOULD BE INVESTIGATED FOR 1.SERUM PROLACTIN 2. TESTOSTERONE3. DHEAS 4.CORTICOTROPIN STIMULATED-17ALPHA HYDROXY PROGESTERON ; TO RULE OUT 1.LATE ONSET ANDROGEN SECRETING TUMORS OF OVARY OR ADRENAL GLAND 2. CONGENITAL ADRENAL HYPERPLASIA 3. HYPERPROLACTINAEMIA DUE TO PROLACTINOMAS• A LIPID PROFILE• FASTING BLOOD GLUCOSE
  16. 16. Treatment
  17. 17. TREATMENTTREATMENT SHOULD BE BASED ON# SYMPTOMS# AGE
  18. 18. ADOLESCENT GROUP• Prevalence of PCOS in Indian adolescents is 9.13%*• Adolescent Indian girls with PCOS were reported to have 4.26 times more chances of developing MS compared to those without^ *J Pediatr Adolesc Gynecol. 2011 Aug;24(4):223-7. ^J Obstet Gynaecol Res.2011 Oct;37(10):1303-7.
  19. 19. Nair MK, Pappachan P, Balakrishnan S, Leena ML, George B, Russell PS.Child Development Centre, Medical College, Thiruvananthapuram Kerala, India• 136 adolescent between 15 and 17 years of age with confirmed menstrual irregularity, with or without polycystic ovaries, were assessed in a gap of 2 years• 36% had PCOS & 63.9% were normal• Group with PCOS had higher %age of – irregular menses (59.9%), – hirsuitism (56.3%), – acne (17.8%), obesity (17.3%), – polycystic ovaries on ultrasound (47.8%) – clinical hyperandrogenism (56.1%) Indian J Pediatr. 2012 Jan;79 Suppl 1:S69-73
  20. 20. PATIENT EDUCATION1- LIFESTYLE MODIFICATION * DIET MODIFICATION * EXERCISE* WEIGHT LOSSDIET MODIFICATION __PT SHOULD BE ENCOURAGED FOR FREQUENT FEEDING TO AVOID HYPOGLYCAEMIA AND HENCE CRAVING AND POOR FOOD CHOICES.DIET SHOULD BE FOCUSED ON INTAKE OF CARBOHYDRATES WITH LOW GLYCEMIC INDEX , HIGH PROTEIN & LOW FATEXERCISE___ EXERCISE WILL BE HELPFUL IN RESUMING REGULAR CYCLESWEIGHT REDUCTION___ ONLY 5-10% OF WT LOSS IN OBESE PATIENTS LEADS TO A GOOD CONTROL OF MENSTRUATIONS AND IMPROVEMENT IN HIRSUTISM THROUGH DECREASING FREE TESTOSTERONE LEVEL
  21. 21. TREATMENT OF HIRSUTISM IF HIRSUTISM IS MODERATE & LOCALISED IT MAY BE TREATED WITH HAIR REMOVAL BY –1. SHAVING2. LASER3. ELECTROLYSIS4. DEPILATORY CREAMS. IN SEVERE & GENERALISEDHAIR GROWTH ANDROGENSSUPPRESING THERAPIESARE NEEDED.
  22. 22. MEDICAL TREATMENT OF HIRSUTISM
  23. 23. TREATMENT FOR MENSTRUAL IRREGULARATIES• LIFE STYLE MODIFICATION• INSULIN SENSITIZERS – METFORMIN,MYOINOSITOL,TROGLITAZONE, ROSIGLITAZONE & PYOGLITAZONE.• OCPs• ANTIANDROGENS
  24. 24. Clinical evidences with INSULIN SENSITISER in PCOS INSULIN Insulin Improves Sensitivity SENSITISER pregnancy rates Restores IR Menstruation & Improve Provides Good Normal Ovulation glucose quality utilization Oocytes Free & Serum Testosterone
  25. 25. TREATMENT IN CHILD BEARING AGEWHERE MAIN ISSUE IS INFERTILITY,TREATMENT IS MAINLY FOCUSEDON OVULATION INDUCTION AND PREVENTING MULTIPLE PREGNANCIES & ABORTIONS.
  26. 26. CLOMIPHENE CITRATE (ORAL ANTIESTROGENE)THIS IS THE 1ST LINE THERAPY FOR OVULATION INDUCTION IN PCOS PATIENTS.IT IS SUCCESSFUL IN INDUCING OVULATION IN 80 % PATIENTS HOWEVER PREGNANCIES OCCUR ONLY IN 40 % CASES.THERE IS ALSO RISK OF MULTIPLE PREGNANCIES.THEREFORE IT SHOULD BE PRESCRIBED UNDER ULTRASONIC GUIDANCE ONLY.
  27. 27. Metformin• Mainstay of managing insulin resistant PCOS is with insulin sensitizers.• Commonest drug used is Metformin.• Dose of 1500 – 1700mg/day in divided doses.• Other Insulin sensitizers in current practice.• Rosiglitazone• Pioglitazone• Troglitazone (withdrawn due to reports of hepatic infarcts and fatal liver failure)
  28. 28. Metformin for SubfertilityIndirect Effect Direct Effect Metformin Insulin levels OvarianAlters effect of Insulin on Gluconeogenesis Ovarian androgen production Theca cell growth Endometrial growth Ovarian androgen productionFasting Insulin / Glucose ratios do not predict ovulatory response tometformin
  29. 29. Other Insulin Sensitizers• Metformin - ↓ Insulin levels + ↑ Insulin sensitivity• Thiazolidinediones - ↑ insulin sensitivity.• Myoinositol - ↑ insulin sensitivity
  30. 30. MYOINOSITOL A NEWINSULIN SENSITISER
  31. 31. Pathway of Inositol deficiency & PCOS Hormonal imbalance Testosterone level
  32. 32. Mode of action for Myo-inositol Glucose I I R R Translocation IRS Of GLUT-4 Glut4 GLUT4 Myo-inositol helps in both Production & PI 3 Kinase Activation activationI = Insulin R = Insulin Receptor IRS = Insulin Receptor Substrates
  33. 33. Myo-inositol provides Good Quality Oocytes Provide good quality oocytesInositol infollicular fluids Follicular maturity Eur J Obstet Gynecol Reprod Biol. 2009,147(2):120-3
  34. 34. Superiority of Myo-inositol over Metformin Hyperinsulinemic PCOS womenMetformin N= 123 6 month therapy Inositol N=50 A significant improvement in the menstrual frequency and reduction in insulin levels Better tolerability Better patient compliance than Metformin Fertility and Sterility. 2006 September 86,( 3) Supplement 1,S461
  35. 35. SurgicalTreatment
  36. 36. Ovarian surgery for Ovulation Induction in PCOS• Laparoscopic Techniques of Ovarian Surgery {LOS} – Laparoscopic Ovarian Drilling (LOD) → diathermy / LASER.• Transvaginal Techniques of Ovarian Surgery {TVOS} – 1) Transvaginal mini-laparoscopy {Fertiloscopy} – 2) Transvaginal ultrasound (TVS)-guided ovarian drilling.
  37. 37. Mechanism of action of LOS• Drainage of atretic follicles with high {A+ Inhibin} content.• Destruction of ovarian stroma that produce A.• LOS → Postoperative ↑ of FSH →↑Intra-follicular aromatase activity↓Intra-follicular androgenic environment → remove intraovarian block to follicular maturation that precede ovulation.
  38. 38. Mechanism of action of LOS• Surgical trauma to the ovary : - Production of non steroidal factors → Restore hypothalamo-pitutary-ovarian function. - Production of ovarian growth factors {IGF-1}→ Sensitize ovary to circulating FSH.
  39. 39. Technique of LOS• Laparoscopy – Puncture technique
  40. 40. Utero-ovarianligament isgrasped byatrumaticforceps movingthe ovary{towardsanteriorabdominal wall&in front of theuterus}.
  41. 41. • Unipolar diathermy {hold perpendicular against antimesentric border away from the hilum}.
  42. 42. PCOS INPERIMENOPAUSAL AGE• THERE ARE LONGTERM RISK OF DEVELOPING DM & POSSIBLY CARDIOVASCULAR DISEAS.PATIENTS OF PCOS ARE LIKELY TO DEVELOP ENDOMETRIAL CARCINOMA , CA BREAST & OVARIAN CARCINOMAS DUE TO UNOPPOSED ACTION OF ESTROGENE & DRUGS OF INFERTILITY.
  43. 43. PCOS INPERIMENOPAUSAL AGE• THEREFORE CYCLE REGULATION IN THIS AGE GROUP SHOULD BE DONE WITH PROGESTOGENS.PROGESTOGENS SHOULD BE GIVEN FOR 12 DAYS EVERY 1-3 MONTHS FOR WITHDRAWL BLEEDING TO MAINTAIN ENDOMETRIUM IN SECRETORY PHASE.IF ON USG ENDOMETRIAL THICKNESS IS > 15 mm WITHDRAWL BLEEDING SHOULD BE INDUCED.IF ENDOMETRIUM FAILS TO SHED THEN EB SHOULD BE DONE FOR HISTOPATHOLOGICAL EXAMINATION.
  44. 44. Dr. Vidhi Agarwal

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