pco by liuhongmei

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									In The Name
   Of God
    PCO AND
METABOLIC SYNDROM
Polycystic ovarian syndrome (PCOS) is an extremely

common disorder affecting 4% to 12% of women of

 reproductive age. Despite being heterogeneous in

      nature, the hallmarks of the disease are

    hyperandrogenism and chronic anovulation
   What's name?

    . Is it PCO or polycystic ovary disease (PCOD) or
    polycystic ovary syndrome (PCOS)? Since the
    name includes the word "polycystic" does that
    mean that all women with this problem have
    cysts in their ovaries?


    Not all women with polycystic ovary
    syndrome (PCOS) will present the same way or
    have the same symptoms or laboratory findings.
    Confused?
       The poly cystic ovary
   The characteristic polycystic ovary
    emerges when a state of anovulation
    persists for any length of time.

   Because there are many causes of
    anovulation there are many causes
    of polycystic ovaries.
       Ovarian hystologic
        characteristics
The surface area is doubled
average volume increases 2.8 times.
The number of growing and atretic follicles
doubled.
Each ovary may contain 20- 100 cystic
follicles(2-10mm)
The thickness of tunica is increased by
50%.
A 5-fold increase in stroma are noted.
  Ultrasonography Finding
Enlarged ovaries and necklace –like pattern

 Large number (>10) of tiny follicles (cysts) just
under the surface of the ovaries

The center of the ovaries is echogenic (highly
reflective on ultrasound) and with very few
follicles seen.

Women with ultrasound findings are said to have
polycystic appearing ovaries (PAO).
Ultrasonography as a diagnostic
 tool for PCOs is unnecessary.
   Frome %8 - %25 of normal women will
    demonstrate ultrasonographic picture.

   This woman are endocrinology normal and
    polyscystic ovaries observed with
    ulteasonography are associated with
    impaired fertility only when accompanied
    by symptoms of menstural irregularities
    and hyperandrogenism.
The cause of PCOS is most likely
  multiple factors, and genetic
 abnormalities may be involved

   PCOS as a heterogeneous disorder of
    unknown cause with various clinical
    features that can be divided into 3
    categories: clinical, endocrine, and
    metabolic.
   What signs and symptoms can be found in
    women with polycystic ovary syndrome
    (PCOS)?
    Ovulation problems
    Anovulation
   Oligo-ovulation
   Infrequent or irregular ovulation

   Irregular menstrual cycles (results from not
    ovulating regularly)
    Amenorrhea
   Oligomenorrhea        20%-50%
   Infrequent periods
   Hypermenorrhea
   Metorrhagia              30%
   Menometorrhagia
   Elevated androgen levels can
result in the development of some
  signs and symptoms in women

    Hirsutism:
   Unwanted hair growth. Usually on the lip-
    cheeks- chin neck-in between the
    breasts(70%).
   Acne
   Alopecia
         Endocrin abnormality
   Steady state of gonadotropins and sex stroids
   The higher mean concentrations of LH but low or
    low-normal levels of FSH.( LH/FSH )

   The average daily productin of Estrogen and
    Androgens is increased and dependent on LH
    stimulation

   50% reduction in circulating levels of SHBG
The higher concentration of
 Testestron
 Andrestendion
 DHA- DHEAS
 17OHP
 EStron.
   The circulating estron levels are due
    to peripheral conversion of the
    increased amounts of androstendion
    to estron.
 Etiology of increasing LH/FSH

Increased frequency of GNRH pulsatile
  secretion.
 Increase in LH pulse frequency and

  pituitary response to GNRH are
  characteristic of the anovulatory
  state and are independent of obesity.
   Because the FSH levels are not
    totally depressed ,new follicular
    growth is continuosly stimulated but
    not to the point of full maturation
    and ovulation.

   FSH                   new follicular
                           growth
                            and atresy
Theca cell       Cholestronl     testestron
   LH
                                   Andrestandion




Granolosa cell
                     Estron    Estradiol

   FSH
    Hyperandrogenism effect in ovary

   Androgens convertion to 5a-reduced
    metabolites that inhibit aromatase avtivity

   Preventing normal cycle and ovulation

   Preventing follicular development and
    indusing premature atresia of follicul
Hyperandrogenism effect in ovary

               Atresia

       degenerating granulosa
leaving the theca cells to the stromal



              Andrgens
   Increaseed free estradiol and estron



   FSH                      LH/FSH
      Genetic concideration
X- linked dominant transmission

Autosomal- dominant and
 Premature bladness in males

The stimulatory effect of insulin on
 ovarian androgen production is
 influenced by gegnetic predisposition
          Insulin Resistance and
            Hyperandrogenism



   The association between
    increased insulin resistance and
    PCO is now well – recognized.
            Questions
1- Which coms first , the
 hyperinsulinemia or the
 hyperandrogenism?

2- How does hyperinsulinemia produce
 hyperandrogenism?

3- Are all women with PCOS have
 hyperinsulinemia?
1_ Hyper insulinemia is the primery
               factor
GNRH agonist and correction hyper
 androgenism
Administeration of insulin and glucose
Weight loss
Invitro , insulin stimulates theca cell
 androgen production
2_ How does hyperinsulinemia
 produce hyperandrogenism?
Insulin binds to IGF-1 reseptors



       increase androgen product
         in theca cells
    Are all women with PCOS have
           hyperinsulinemia?

Not every women with PCOS has
 hyperinsulinemia not even every
 overweigt.

   Hyperinsulinemia can be an
    underlying disorder.
    4 - why not all women who are insulin
        resistant are hyperandrogenic?

   The answer to this question is not
    known. But a logical speculation is
    that an ovarian genetic susceptibility
    is required or existence of long-term
    anovulation must be present and
    even preced huperinsulinemia.
              Obesity
Central body (android) obesity is
 associated with cardiovascular risk
 factors:
Waist/hip >0/85
Waist circumference >100cm
 (40inches) in men
 and>90cm(35 inches) in women.
    Obesity Prevalance: (35%-60%)

   Hyperinsulinemia and
    hyprandrogenism are not confined to
    anovulatory women who are
    overweight.
   The obes unovulatory women :
   Insulin - LH - SHBG -IGFBG-1
   In normal weight women:
   Insulin      - LH
Metabolic Syndrom
           Prevalence
Overall estimated: 24% higher in
 women( 40% by age 60)
In normal GTT : 10%
Imppaired GGT :40%
Type 2 diabet : 85%
Normal weight :5%
Obes             :60%
         Metabolic syndrom
   multiple studies indicate that women
    with PCO are at increased risk for the
    development of glucose intolerance
    or frank type 2 diabetes mellitus,
    hypertension, dyslipidemia, and
    atherosclerosis.
    In recent studies, the prevalence of
    MS in women with PCOS is
    approximately 43–47%.
    Hyperinsulinemia and coronary
               disease
   HT
   Triglycerides
   HDL
   PAI-1
     Clininical consequens
Infertility
AUB
Hirsutism-acne and alopecia
Endometrial cancer and perhaps
 breast cancer.
Cardiovascular disease
Diabetes melituse in patients with
 insulin resistant
    Cardiovascular disease

Advers lipid and lipoprotein profile
Subclinical atherosclerosis by corotid
ultra sonography in premenoppausal
women with PCO.
In women who undergoing cronary
angiography the prevalence of PCO is
increased.
Laboratory tests to exclude other
            problem
 TSH
 Prolactin
 Lipid and lipoprotein profile
 Screen for Cushing s
 Endometrial biopsy
 If presence of signs of exess androgens:
 Total testestron
 17-OHP
     Who should be tested for
        Hyperandrogenism
 In anovulatory women and their
 brother and sisters
Central obesity
                      How to test
   Measurement of 2- hours glucose and
    insulin level after a 75gr glucose.
   Glucose response
   Normal                          <140mg/dl
   Impaired                        140-199 mg/dl
   Diabet typ 2                    >200 mg/dl

   Insulin response
   Insulin resistant very likely   100-150 uU/ml
   Insulin resistant               151-300uU/ml
   Sever insulin resisrant          >300 uU/ml
   Treatment

                Hyperandrogenism
             Endometrium protect
            Hyperinsulinemia
          prevent of CVD
       Induced ovulation
    Endometrium protection
   Endometrial Biopsy

1- Duratin of exposure to unopposed
 estrogen is critical.
2- Endometrial Thickness is greater
 than 12mm
Medroxy progestron: 14 days every
 month
OCP

       1- Androgen suppression
       2- Improvement in lipid profile
       3 - protectin of endometrium
     Insulin Resistance
The best therapy is weight loss>5%
BMI<27
Lifestyle improvement with proper
diet and exercise
Druge agent : Metformin and
Glitazones
               Metformin
   Weight loss
   Ovulation
   Diabete risk reduction
   CVD risk reductin
    It is important component of
    health care of women with
    PCO.
           Cunclusion


In past we treated the specific
 problems of infertility-AUB and
 hirsutism but now we must
 effect on quality and quantity of
 life of this womens.
THE
  Best
     Wish
        For
              You

								
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