GYNECOLOGY

Topic: Polycystic Ovary Syndrome (PCOS) / Hyperandrogenism

Lecturer: Dr. Raymundo (NER)

POLYCYSTIC OVARY SYNDROME  Polycystic ovaries is diagnosed by ultrasound

 Also known as:  Criteria:
o Functional Ovarian Hyperandrogenism o Presence of 12 or more follicles
Hyperandrogenism  means that testosterone or any o Measuring 2-9 mm in diameter and/or
androgen-like hormones are being secreted abnormally by o Increased ovarian volume greater than 10 cm
the ovaries o Increased stromal echogenicity and/or stromal volume are
specific to polycystic
o Stein Leventhal Syndrome
Named as such because this syndrome was discovered by ACANTHOSIS NIGRICANS
Stein Leventhal  Dark, mucocutaneous eruption, raised hyperpigmentation or
papillomatosis of the skin, found particularly on the nape of the neck,
ESHRE/ASRM CRITERIA OF POLYCYSTIC OVARY SYNDROME (2 OUT OF 3) axilla and skin flexures
 Ovulatory Dysfunction  A marker associated with insulin resistance and compensatory
o Oligo-ovulation and/or anovulation increased insulin secretion (Hyperinsulinemia)
 Clinical and/or biochemical signs of hyperandrogenism
o Hirsutism, acne, alopecia METABOLIC SYNDROME
o Hyperandrogenemia (free T, DHEAS)  Criteria for metabolic syndrome in women with PCOS (3/5 quality for
 Monitored by free testosterone & dihydroepiandrosterone
the syndrome)
o Elevated LH:FSH ratio
 If a patient was seen on ultrasound to have polycystic ovaries BUT did
 More LH than FSH
not have any manifestations of metabolic abnormalities  she will be
 Polycystic ovaries
known as a case of polycystic ovaries NOT polycystic ovary syndrome
o Use of ultrasound to check the ovaries
 So only with those with manifestations related to metabolic changes are
Exclusion of other Androgen Excess Disorders – rule this out known as a case of polycystic ovary syndrome
 Non-classical adrenal hyperplasia
o 21-hydroxylase deficiency Risk Factor Value
Abdominal obesity (waist circumference) > 88 cm (>35 inch)
 Hypothyroidism
Triglycerides (high) ≥ 150 mg/dl
 Cushing's syndrome
HDL-Cholesterol (low) < 50 mg/dl
 Hyperprolactinemia
≥ 130 mmHg systolic or
 Androgen-secreting tumors Blood Pressure (HPN)
≥ 85 mmHg diastolic
FBS: 110 - 126 mg/dl and/or
Diagnosis: Rule in first the clinical signs of hyperandrogenism and ultrasound Fasting and 2h glucose from OGTT
2h OGTT: 140 - 199 mg/dl
(see polycystic ovaries)  if we are able to confirm and diagnose that it is really
PCOS then no need to request for lab tests to rule out the other disorders

PCOS
 High levels of androgens halt the follicle's development, leaving a small
follicle containing the immature egg.
o There will be failure of follicles to rupture and ovulate therefore
they will be seen in the ovaries as cysts
 “Polycystic ovarian syndrome is the most common endocrinopathy in
adult women, and is emerging as a common cause of menstrual
disturbances in the adolescent population”

MANIFESTATIONS OF POLYCYSTIC OVARY SYNDROME AT DIFFERENT AGES

Adolescence &
In Utero Peripuberty Ageing
Adulthood
Small baby Exaggerated Polycystic ovary Metabolic
syndrome adrenarche syndrome syndrome
Intrauterine Increased adrenal Anovulation Diabetes
growth androgens and Hyperandrogenism Hypertension
retardation insulin Polycystic ovaries Dyslipidemia
Obesity Increased plasmin-
activator inhibitor
1
Leads to long- Leads to Leads to Leads to
term health precocious reproductive metabolic effects
Lecture Discussion: Initial diagnostic evaluation of PCOS effects puberty disorders
Majority of patient will come because of the irregular menstrual cycle or
abnormal uterine bleeding. From that we will be able to rule in or rule out
PCOS by just doing our P.E.  looking for signs of hyperandrogenemia (ex.
Hirsutism) will narrow down our differential diagnoses

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 GYNECOLOGY
Topic: Polycystic Ovary Syndrome (PCOS) / Hyperandrogenism
Lecturer: Dr. Raymundo (NER)

GENETIC LINK PREGNANCY COMPLICATIONS

 Familial clustering of PCOS common  Spontaneous Abortions
 1st degree relatives of patients with PCOS may be at high risk for o Increased in high BMI/PCOS patients
diabetes and glucose intolerance  Impaired Glucose Tolerance
 Mothers and sisters of PCOS patients have higher androgen levels  Gestational Diabetes
 “PCOS is a genetically determined ovarian disorder… the heterogeneity  Hypertension
can be explained on the basis of interaction of the disorder with other  Small for Gestational Age
genes and with the environment.”
THE CENTRAL PLAYER
HIRSUTISM (INSULIN RESISTANCE & VICIOUS CIRCLE)
 The presence of hirsutism without other signs of virilization is
associated with relatively mild disorders of androgen production or
increased 5-α-reductase activity
o Circulating testosterone levels are either normal or mildly to
moderately elevated (less than 1.5 ng/mL)
 The amount and location of the central hair growth found in women
with hirsutism vary.
 In the milder forms hair is found only on the upper lip and chin
 In sever forms, it appears on the cheeks, chest (intermammary),
abdomen (superior to the umbilicus), inner aspects of thighs, lower
back, and intergluteal areas

FACTS TO KNOW ABOUT PCOS

 Many PCOS symptoms are the result of high levels of androgens -"male
hormones"
 Androgens include:
Any testosterone o Testosterone
secreted by the
adrenal glands
o DHT
will become free o Androstenedione.
testosterone due
to ↓ SHBG = ↑
o Dehydroepiandrosterone (DHEA) and DHEA sulfate (DHEAS)
androgen activity can be converted into  testosterone or DHT
 PCOS is strongly linked to obesity and insulin resistance (a precursor to
type 2 diabetes).
High chance
o For women with PCOS who are obese
of MI
 Treatment plan should incorporate a diet and exercise
**Insulin resistance is the central problem associated with PCOS** program
o 45% of women with PCOS who are obese have insulin
 Schematic description of various pathogenic factors that manifest PCOS resistance (35%) or type 2 diabetes (10%)
in women of reproductive age. Such patients are at risk of developing a  PCOS is associated with insulin resistance and diabetes, but not all
spectrum of disease phenotype women who have PCOS are insulin-resistant or diabetic.
o Evaluated for diabetes with both a fasting glucose test and a
glucose challenge test with insulin levels.
o The fasting glucose insulin test is the standard, but that test
alone misses about half the women with PCOS who have
diabetes or insulin resistance
 Application of diabetes management techniques aimed at reducing
insulin resistance and hyperinsulinaemia
o Reverse testosterone and luteinizing hormone abnormalities
and infertility
o Improve glucose, insulin and lipid profiles
 Insulin resistance leads to hyperinsulinaemia as pancreatic insulin
secretion rises to maintain normoglycaemia.
So at the end, the woman with PCOS will have hyperinsulinemia 
there will be some growth due to the effect of insulin-like growth
factor and hypoglycemia

 Hyperinsulinaemia can then stimulate lipid storage, altered lipoprotein

and cholesterol metabolism and altered steroid hormone metabolism.
 Hyperinsulinaemia increases ovarian androgen production by
stimulating an ovarian enzyme complex cytochrome P450c17, either
directly and/or by stimulating pituitary luteinizing hormone secretion.

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 GYNECOLOGY
Topic: Polycystic Ovary Syndrome (PCOS) / Hyperandrogenism
Lecturer: Dr. Raymundo (NER)

 Insulin resistance is aggravated by Spironolactone

o Physical inactivity
o Upper abdominal obesity
o Hyperandrogenism
o Pregnancy
o Ageing process
o Medications: Thiazide diuretics, corticosteroids and certain
hormonal steroid preparations
 Cigarette smoking should be vigorously discouraged in all women with
polycystic ovary syndrome
o Cigarette smoking has recently been shown to aggravate
insulin resistance in type 2 diabetes mellitus.
HYPERINSULINEMIA
 Hyperinsulinemia causes hyperandrogenemia  can lead to PCOS
 Stimulates both ovarian and adrenal androgen secretion directly and
suppresses sex hormone binding globulin (SHBG) synthesis from the
liver resulting in an  increase in free, biologically active androgens
o Excess in local ovarian androgen production augmented by
hyperinsulinaemia causes premature follicular atresia and
anovulation  Polycystic ovaries
PATHOGENESIS OF PCOS
 Use this if the concern is hirsutism
 An aldosterone antagonist / antihypertensive drug
 Acts as an antiandrogen by binding to the peripheral androgen receptor
without inducing androgenic activity.
 It inhibits steroidogenesis
o Interfering with ovarian enzymatic activity
o Inhibiting 5-α-reductase activity in the pilosebaceous unit
Metformin
 Considered a wonder drug for PCOS
 An oral antihyperglycemic agent that improves glucose tolerance
o decreasing hepatic glucose production
o decreases serum insulin
 Induces ovulation whether or not a woman is glucose-intolerant,
probably through a direct ovarian effect
Metformin: Studies in PCOS Results
 Decreased T and free T levels
 Increased SHBG levels and reduced free T levels
 Improved ovulation rates
 Improved response to clomiphene citrate and exogenous gonadotropins
 Increased follicular and luteal phase serum glycodelin and IGFBP-1 levels
and enhanced luteal phase uterine vascularity and blood flow
 No benefits

Metformin: Role for Treatment of Infertility

 Monotherapy for induction of ovulation
 Induction of ovulation in clomiphene resistant cases
 Adjuvant to gonadotropin ovulation induction
 Adjuvant in in-vitro fertilization
 Prevention of early pregnancy loss

Surgery
 Surgery is reserved for those in whom medical therapy fails (along with
failed lifestyle modification) or hyper stimulation occurs
MANAGEMENT OF PCOS o Surgery (Ovarian drilling) comprises laparoscopic multiple
Treatment of PCOS punctures of the cysts with electrocautery or laser.
 Lifestyle Modification o Ovarian Wedge resection is now avoided on account of
o Physical exercise postoperative ovarian adhesions and continued infertility
o Altered dietary composition  Removing a part of the ovary will decrease the number
 Weight loss of follicles
o Low fat
o Low carbohydrate Ovarian Drilling
 Weight loss is important and will help in restoring the hormonal milieu.  Not advocated nowadays
 Cigarette smoking raises DHEA and androsteredione level and should  Reduction of the intra-ovarian androgen production
be avoided  Reduction of testosterone level by 40-50%
 Estrogen suppresses androgen and adrenal production.  Pregnancy rates of 60-80% at 2 years
o It is best given with progesterone cyclically as oral
contraceptives. CONSEQUENCES OF POLYCYSTIC OVARY SYNDROME
o Norgestrel containing pill should be avoided because of its high
androgenicity.
o The desogestrel-containing pill is best suited.
 Hyperinsulinemia, Insulin resistance , Glucose intolerance are
addressed by Diet with exercise
o There is no effective treatments that result in permanent
weight loss.
o 90% - 95% of obese patient who have a weight decrease later
gave a relapse.
o Weight loss can improve the fundamental aspect of the :
 Endocrine syndrome of PCOS & result in lower
circulatory androgen level. We see here what we are afraid of if we do not treat the PCOS 
 Decrease level of circulating insulin. Endometrial Ca, Ovarian Ca, DM, Hypertension and CVD
 Decrease level of unbound testosterone by increasing
SHBG

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