Polycystic ovarian Syndrome


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Polycystic ovarian Syndrome

  1. 1. PCOS<br />Abdalmohsenababtain<br />October 2010<br />
  2. 2. Objectives<br />Definition<br />Epidemiology<br />Normal physiology<br />Pathophysiology<br />Diagnostic criteria<br />Presentation<br />Investigations<br />Management<br />
  3. 3. Definition<br />NIH (1990): chronic, unexplained hyperandrogenism and evidence of anovulation<br />It Is a Syndrome associated with a range of metabolic abnormalities which can lead to long term health problems <br />
  4. 4. Epidemiology<br />Prevalence: 6-10% females of reproductive age<br />the most common endocrine disorder among young women <br />
  5. 5. Normal physiology<br />
  6. 6. Normal physiology<br />
  7. 7. Pathogenesis<br />The Exact mechanism is not clear yet .<br />Intraovarian androgen excess appears to be responsible for both anovulation and formation of multiple ovarian cysts. This could be caused by DisturpedGnRH secretion OR ovarian or adrenal excess steroidogenesis<br />
  8. 8. Genetics and PCOS<br />PCOS is a familial disorder, but its genetic basis remains controversial.<br />A study reported that 46% of sister PCOS patients have some features of PCOS.<br />A study of 150 subjects with PCOS showed evidence of an autosomal dominant inheritance<br />
  9. 9. Abnormal gonadotropin secretion<br />Excess LH and low FSH<br />Hypersecretion of androgens<br />Disrupts follicle maturation<br />Substrate for peripheral aromatization  more estrogen<br />Negative feedback on pituitary <br />Decreased FSH secreation<br />Insulin resistance, Elevated insulin levels<br />High LH  high androgen level from thecal cell<br />
  10. 10. Final result :<br />arrested growth of the follicles at a diameter of 5–8mm i.e. well before a mature follicle would be expected to ovulate <br />
  11. 11.
  12. 12. Diagnostic criteria<br />Rotterdam criteria(2 out of 3) :<br />Unexplained hyperandrogenism<br />Oligo or anovulation<br />Polycystic ovaries (added 2003)<br />History-taking, specifically for menstrual pattern, obesity, hirsutism, and the absence of breast development, can diagnose PCOS with a sensitivity of 77.1% and a specificity of 93.8%<br />NIH 1990<br />
  13. 13. AES(Androgen Excess Society) criteria 2006<br />Hyperandrogenism, preferably confirmed by biochemical testing<br />Evidence of ovarian dysfunction(Oligo, anovulationor Polycystic ovaries )<br />
  14. 14.
  15. 15. presentation<br />Polycystic ovaries (80%)<br />Anovulatory bleeding (80%)<br />Anovulatory infertility (75%)<br />Hirsutism (70%)<br />Overweight or obesity (50%)<br />Premature pubarche, and/or precocious puberty<br />DUB<br />Acne<br />Male-pattern hair loss<br />Acanthosisnigricans<br />
  16. 16. PCOS Features<br />Cutaneous :<br />hirsutism, acne or acanthosisnigricans, male-pattern alopecia, seborrhea and hyperhidrosis<br />Anovulatory :<br /> include amenorrhea, oligomenorrhea, dysfunctional<br />uterine bleeding, ploycystic ovaries and infertility<br />General :<br />Obesity, Metabolic syndrome and Insulin Resistance<br />
  17. 17.
  18. 18. Hirsutism and PCOS<br />Acne vulgaris, pattern alopecia, seborrhea, hyperhidrosis, and hidradenitissuppurativa are considered to be hirsutism equivalents<br />Hirsutism defined as coarse terminal hair in a male distribution<br />do not confuse with lanugo hair<br />assessed by the Ferriman-Gallwey score if >8  excess androgen<br />does not always correlate with androgen levels<br />
  19. 19.
  20. 20. PCOS was the cause of hirsutism in (82%) of a study done to determine the clinical, biochemical and etiologic features of hirsutism in Saudi females<br />
  21. 21. Anovulation & PCOS<br />Found in 80% of PCOS<br />Anovulatory cycles are suggested by the lack of moliminal symptoms (eg, breast tenderness and dysmenorrhea) , and Not excluded by Normal menstrual cyclicity, as 50% regular menstrual cycles are anovulatory during the first two years after menarche<br />Presents as:<br /><ul><li>absence of periods
  22. 22. infrequent periods ( > 35 day cycle)
  23. 23. dysfunctional uterine bleeding</li></li></ul><li>DUB & PCOS<br />Dysfunctional uterine bleeding (DUB) is a common manifestation of PCOS and often is the initial presenting complaint.<br />
  24. 24. Metabolic syndrome & PCOS <br />PCOS is also associated with a characteristic metabolic syndrome that includes:<br />insulin resistance <br />dyslipidemia<br />hypertension<br />These features are linked with increased risks of type 2 diabetes and possibility of premature cardiovascular disease<br />
  25. 25. Hyperinsulinemia & PCOS<br />women with PCOS have a higher incidence of insulin resistance and hyperinsulinemia than age-matched controls<br />40% of women with PCOS have impaired glucose tolerance, and as many as 10% develop type 2 diabetes mellitus by the age of 40<br />hyperinsulinemia increases GnRH pulse frequency, LH over FSH dominance, decreased sex hormone binding protien<br />
  26. 26. DDx<br />
  27. 27. Investigations<br />Fasting insulin level or GTT (up to 38% of asymptomatic women with PCOS versus 8.5% in the general population had iGTT, 7.5% of those with frank diabetes) “according to ADA guidelines”<br />Hormonal study :<br />LH Level: Raised LH or LH:FSH ratio<br />Estradiol Level<br />Total and Free testosterone, androstendione(in the early morning, on days 4 through 10 of the menstrual cycle)<br />DHEAS (marker for adrenal hyperandrogenism)<br />Ultrasound pelvis<br />
  28. 28. remember to exclude secondary causes of PCOS :<br />Prolactin to rule out hyperprolactinemia<br />TSH to rule out hypothyroidism<br />17-hydroxyprogesterone to rule out 21-hydroxylase deficiency (CAH).<br />IGF-I to role out acromegaly<br />Random serum cortisol to role out cushing syndrome<br />Imaging For Tumors<br />
  29. 29. Polycystic ovary imaging<br />Imaging the ovaries is the Best by transvaginal route especially with obese patients<br />either excessive size or follicle number (or both), in the absence of a dominant-size follicle <br /><ul><li>Excessive ovarian size is defined as an ovary with a volume >10.8 cubic mL in adolescents
  30. 30. Excessive follicle number is defined as >12 follicles per ovary each follicle measures 2 to 9 mm in diameter</li></li></ul><li>Polycystic ovary<br />
  31. 31. Ultrasonographic appearance of a polycystic ovary in a 15-year-old with PCOS<br />Ovary containing more than10 follicles that are approximately 3 to 8 mm in diameter<br />
  32. 32. Managment<br />Medical treatment of PCOS is tailored to the patient's goals. <br />Broadly, these Goals may be considered under four categories:<br />Obesity and insulin resistance<br />Restoration of fertility<br />Treatment of hirsutism or acne<br />Restoration of regular menstruation<br />
  33. 33. Compined OCP<br />The first-line treatment for adolescents who suffer the menstrual and cutaneous symptoms of PCOS<br />The progestin component inhibits endometrial proliferation, preventing hyperplasia (control menses). The estrogen component reduces excess androgen, which improves menstrual irregularity, dysfunctional uterine bleeding, hirsutism, and acne.<br />As a general rule, OCPs should be continued until the patient is gynecologically mature (five years postmenarcheal)<br />
  34. 34. Obesity and insulin resistance<br />Diet & Exercise:<br />since PCOS is associated with overweight or obesity, successful weight loss and Low carb Diet is probably the most effective method of restoring normal ovulation/menstruation<br />Medication:<br />Metformin(recommended by NIH if BMI<25) “increases the frequency of ovulation 50%”<br />Thiazolidinediones <br />
  35. 35. Infertility<br />anovulation is a common cause for Infertility<br />clomiphene citrate and FSH are the principal treatments used to help infertility<br />metformin is not recommended for ovulation stimulation, as there was a large study comparing clomiphene with metformin, clomiphene alone was the most effective, 626 women were randomized to three groups: metformin alone, clomiphene alone, or both. The live-birth rates following 6 months of treatment were 7.2% (metformin), 22.5% (clomiphene), and 26.8% (both)<br />Glucocorticoid therapy to suppress adrenal source of androgen<br />
  36. 36. The most drastic increase in ovulation rate occurs with a combination of diet modification, weight loss, and treatment with metformin and clomiphene citrate<br />If previous measures failed we go to :<br />ovarian hyperstimulation with FSH + IVF <br />ovarian drilling (puncture of 4-10 small follicles with electrocautery)<br />
  37. 37. Hirsutism and acne<br />The goal of is to decrease the effect of excess androgens by:<br />Reducing their production : Cyproterone acetate (progestogen with anti-androgen effects) &Metformin(lowers testosterone 20%)<br />Reducing free plasma androgen levels by increasing androgen binding to plasma-binding proteins (OCP)<br />Blocking androgen action at the level of target organs (eg, hair follicle): Flutamide(Androgen receptor antagonist) &Spironolactone(antiandrogenic compound)<br />
  38. 38. Menstrual irregularity & DUB<br />contraceptive pills (often can be controlled with cyclic progestin alone)<br />The purpose of regulating menstruation is essentially for the woman's convenience and preventing DUB<br />If a regular menstrual cycle is not desired, then therapy for an irregular cycle is not necessarily required - most experts consider that if a menstrual bleed occurs at least every three months, then the endometrium is being shed sufficiently often to prevent an increased risk of endometrial abnormalities or cancer<br />
  39. 39. Some OCP limitations<br />OCP therapy may make weight loss more difficult to attain because they promote salt and water retention. <br />In perimenarcheal girls with short stature who have open epiphyses, OCPs are contraindicated because OCPs contain growth-inhibitory amounts of estrogen.<br />Risk of venous thromboembolism<br />