Polycystic Ovary Syndrome

Functional Ovarian Hyperandrogenism

Stein Leventhal Syndrome

NOEL E. RAYMUNDO, MD, FPOGS

Obstetrics-Gynecology
Reproductive Endocrinology & Infertility
Gynecologic Endoscopy
Cosmetic Surgery
Diabetology
ESHRE / ASRM Criteria of Polycystic
Ovary Syndrome (2 out of 3)
l  Ovulatory dysfunction
l  Oligo-ovulation and/or anovulation
l  Clinical and/or biochemical signs of
hyperandrogenism
l  Hirsutism, acne, alopecia
l  Hyperandrogenemia (free T, DHEAS)
l  Elevated LH:FSH ratio
l  Polycystic ovaries
Exclusion of other androgen excess disorders
l  Non-classical adrenal hyperplasia
l  21-hydroxylase deficiency
l  Hypothyroidism
l  Cushing's syndrome
l  Hyperprolactinemia
l  Androgen-secreting tumors
PCOS Concensus Conference, Rotterdam 2003: European Society of Human Reproduction / American Society for
Reproductive Medicine (ESHRE/ASRM)
 PCOS

l High levels of androgens halt the

follicle's development, leaving a small
follicle containing the immature egg.
 Polycystic Ovary Syndrome

“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”

Guttmann-Bauman I, Journal of Pediatric Endocrinology &Metabolism, 2005.

 Initial diagnostic evaluation
of PCOS
Irregular bleeding

History of cyclic bleeding Irregular bleeding since menarche

Hirsutism
No Hirsutism
No hirsutism

17α-hydroxyprogesterone Testosterone
Increased Normal Normal
level level level
Prolactin and
Thyroid- Testosterone
Stimulating Normal Prolactin and
Increased
Hormone level level Congenital TSH level
level
Tests and adrenal Tests and
Further hyperplasia Further
evaluation evaluation
Polycystic ovary syndrome
 Polycystic ovary

l  Polycystic ovaries is diagnosed by

ultrasound
l  Criteria:
l  Presence of 12 or more follicles
l  Measuring 2-9 mm in diameter and/or
l  Increased ovarian volume greater than 10 cm
l  Increased stromal echogenicity and/or
stromal volume are specific to polycystic.
Palmert MR, Gordon CM, Kartashov AI, Legro RS, Emans SJ, Dunaif A. Screening for abnormal glucose
tolerance in adolescents with polycystic ovary syndrome. J ClinEndocrinolMetab. 2002 Mar; 87(3):1017–2
 Acanthosis nigricans

l  Dark, mucocutaneous eruption, raised

hyperpigmentation or papillomatosis of the skin,
found particularly on the nape of the neck, axilla
and skin flexures.
 Acanthosis Nigricans

l  A marker associated with insulin resistance and

compensatory increased insulin secretion
(Hyperinsulinemia)
Schwartz RA. Acanthosisnigricans. J Am
AcadDermatol. 1994 Jul;31(1):1-19.
 Metabolic syndrome

l  Criteria for metabolic syndrome in women with

PCOS (3/5 quality for the syndrome)
RISK factor Value
1.  Abdominal obesity > 88cm (>35inch)
(waist circumference)
2. Triglycerides (high) ≥ 150 mg/dl
3. HDL-Cholesterol (low) < 50 mg/dl
4. Blood Pressure (HPN) ≥ 130m/Hg systolic or ≥
5. Fasting and 2h glucose from OGTT 85mmHg diastolic
FBS: 110 - 126 mg/dl and/or
2h OGTT: 140 - 199 mg/dl
NCEP: National Cholesterol Education Program
Definitions of the Metabolic
Syndrome
 Manifestations of polycystic ovary
syndrome at different ages

In utero Peripuberty Adolescence and Ageing

adulthood
Small baby Exaggerated adrenarche Polycystic ovary Metabolic syndrome
syndrome syndrome
Intrauterine Increased adrenal Anovulation Diabetes
growth androgens and insulin
Hyperandrogenism Hypertension
retardation
Polycystic ovaries Dyslipidemia

Obesity Increased
plasminogen
activator inhibitor
-1
Leads to long- Leads to precocious puberty Leads to Leads to metabolic
term health reproductive effects
effects disorders
Hart R, Hickey M, Franks S. Definitions, prevalence and symptoms of polycystic ovaries and polycystic ovary syndrome. Best Pract Res ClinObstetGynaecol. 2004
Oct;18(5):671-83.
 Genetic Link

l  Familial clustering of PCOS common

l  1st degree relatives of patients with PCOS may be at
high risk for diabetes and glucose intolerance
l  Mothers and sisters of PCOS patients have higher
androgen levels
Yildiz BO et al, Journal of Clinical Endocrinology & Metabolism, 2003.

“PCOS is a genetically determined ovarian disorder… the

heterogeneity can be explained on the basis of interaction
of the disorder with other genes and with the environment.”
Franks S et al,International Journal of Andrology, 2006.
 Hirsutism

l  The presence of hirsutism without other signs of

virilization is associated with relatively mild
disorders of androgen production or increased
5-α-reductase activity
l  Circulating testosterone levels are either normal or
mildly to moderately elevated (less than 1.5 ng/mL).
 Hirsutism

l  The amount and location of the central hair

growth found in women with hirsutism vary.
l  In the milder forms hair is found only on the
upper lip and chin
l  In sever forms, it appears on the cheeks, chest
(intermammary), abdomen (superior to the
umbilicus), inner aspects of thighs, lower back,
and intergluteal areas
 Endocrine Metabolic
Manifestations Manifestations
Insulin resistance
Central Obesity

↑ Insulin

Liver Adrenal Glucose Intolerance

gland
Ovary Hypertension
↓ SHBG
Dyslipidemia
↑ Androgen activity
Clinical Long Term
Presentation Sequelae
Infertility
Menstrual disturbance Vascular Disease
Hirsutism
l  Schematic description
of various pathogenic
factors that manifest
PCOS in women of
reproductive age. Such
patients are at risk of
developing a spectrum
of disease phenotype
 Pregnancy Complications

l  Spontaneous Abortions
l  Increased in high BMI/PCOS patients
Wang JX et al, Human Reproduction, 2001.

l  Impaired Glucose Tolerance

Turhan NO et al, International Journal of Gynecology & Obstetrics, 2003.

l  Gestational Diabetes Bjercke S et al, Gynecologic and Obstetric Investigation, 2002.

l  Hypertension Weerakiet S et al, Gynecological Endocrinology, 2004.

l  Small for Gestational Age Sir-Petermann T et al, Human Reproduction, 2005.

 The Central Player
(Insulin Resistance & Vicious circle)

Pregnancy Aging Drugs Lifestyle

Insulin
Genetics Resistance Obesity

Hyperinsulinemia Increased lipid storage

PCOS
Altered lipoprotein &
Altered steroid cholesterol metabolism
hormone metabolism
 Hyperinsulinemia

Increased ovarian and Decreased SHBG

adrenal androgen synthesis
secretion

Increased free, biologically

active androgens

Premature ovarian Hirsutism &

atresia & Anovulation Acne
 PCOS: Facts to Know….

l  Many PCOS symptoms are the result of

high levels of androgens-"male hormones"
l  Androgens include:
l  Testosterone
l  DHT
l  Androstenedione.
l  Dehydroepiandrosterone(DHEA) and DHEA
sulfate (DHEAS) can be converted
intoàtestosterone or DHT.
 PCOS: Facts to Know….

l  PCOS is strongly linked to obesity and

insulin resistance (a precursor to type 2
diabetes).
l  For women with PCOS who are obese
l  treatment plan should incorporate a diet and
exercise program
l  45% of women with PCOS who are obese
have insulin resistance (35%) or type 2
diabetes (10%)
 PCOS: Facts to Know….

l  PCOS is associated with insulin resistance

and diabetes, but not all women who have
PCOS are insulin-resistant or diabetic.

l  Evaluated for diabetes with both a fasting

glucose test and a glucose challenge test with
insulin levels.
l  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.
 PCOS: Facts to Know….

l  Application of diabetes management

techniques aimed at reducing insulin
resistance and hyperinsulinaemia
l  reverse testosterone and luteinising
hormone abnormalities and infertility
l  improve glucose, insulin and lipid profiles
 PCOS: Facts to Know….

l  Insulin resistance leads to hyperinsulinaemia as

pancreatic insulin secretion rises to maintain
normoglycaemia.
 PCOS: Facts to Know….

l  Hyperinsulinaemia can then stimulate lipid

storage, altered lipoprotein and cholesterol
metabolism and altered steroid hormone
metabolism.
 PCOS: Facts to Know….

l  Hyperinsulinaemia increases ovarian androgen

production by stimulating an ovarian enzyme
complex cytochrome P450c17 , either directly
and/or by stimulating pituitary luteinising
hormone secretion.
 PCOS: Facts to Know….

l Insulin resistance is aggravated by

l  Physical inactivity
l  Upper abdominal obesity
l  Hyperandrogenism
l  Pregnancy
l  Ageing process
l  Medications:
l  thiazidediuretics, corticosteroids and
certain hormonal steroid preparations
 PCOS: Facts to Know….

l  Cigarette smoking should be vigorously

discouraged in all women with polycystic
ovary syndrome
l  Cigarette smoking has recently been shown to
aggravate insulin resistance in type 2
diabetes mellitus.

Targher G, Alberto M, Zenere M, et al.Cigarette smoking and insulin resistance in patients with noninsulin-dependent
diabetes mellitus. J ClinEndocrinolMetab 1997; 82: 3619-3624
 Hyperinsulinemia
Franks S. Polycystic ovary syndrome, a changing perspective. ClinEndocrinol
(Oxf). 1989 Jul; 31(1):87-120

l  Stimulates both ovarian and adrenal androgen

secretion directly and suppresses sex hormone
binding globulin (SHBG) synthesis from the liver
resulting in an àincrease in free, biologically
active androgens.
l  Excess in local ovarian androgen production
augmented by hyperinsulinaemia causes
premature follicular atresia and anovulation.
 Hyperinsulinemia

Increased ovarian and Decreased SHBG

adrenal androgen synthesis
secretion

Increased free, biologically

active androgens

Premature ovarian Hirsutism &

atresia & Anovulation Acne
Management of PCOS
 Treatment: PCOS

l  Lifestyle Modification
l  Physical exercise
l  Altered dietary composition
l  Weight loss
l  Low fat
l  Low carbohydrate
 Treatment: PCOS

l  Weight loss is important and will help in restoring

the hormonal milieu.
 Treatment: PCOS

l  Cigarette smoking raises DHEA and

androsteredione level and should be
avoided.
 Treatment: PCOS

l  Estrogen suppresses
androgen and adrenal
production.
l  It is best given with
progesterone cyclically as
oral contraceptives.
l  Norgestrel containing pill
should be avoided because
of its high androgenicity.
l  The desogestrel-containing
pill is best suited.
 Treatment: PCOS

l  Hyperinsulinemia, Insulin resistance ,

Glucose intolerance
l  Diet with exercise
l  There is no effective treatments that result in permanent
weight loss.
l  90% - 95% of obese patient who have a weight decrease later
gave a relapse.
l  Weight loss can improve the fundamental aspect of the :
- Endocrine syndrome of PCOS & result in lower circulatory
androgen level.
- Decrease level of circulating insulin.
- Decrease level of unbound testosterone by increasing
SHBG.
 Treatment

l  Spironolactone
l  An aldosterone antagonist / antihypertensive drug
l  Acts as an antiandrogen by binding to the peripheral
androgen receptor without inducing androgenic
activity.
l  It inhibits steroidogenesis
l  interfering with ovarian enzymatic activity
l  inhibiting 5-α-reductase activity in the pilosebaceous unit
 Treatment

l  Metformin
l  An oral antihyperglycemic agent that improves
glucose tolerance
l  decreasing hepatic glucose production
l  decreases serum insulin
l  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 Velazquez et al 1994
of Increased SHBG levels and reduced free T
studies levels Nestler&Jakubowicz 1996
Improved ovulation rates Velazquez et al. 1997
Improved response to clomiphene citrate Nestleret al.
1998b and exogenous gonadotropinsDe Leo et al. 1999

Increased follicular and luteal phase serum

glycodelin and IGFBP-1 levels and enhanced
luteal phase uterine vascularity and blood flow
Jakubowiczet al. 2001

No benefits Crave et al. 1995, Ehrmannet al. 1997a

 PCOS: Role of metformin for
treatment of infertility
Nestler JE, et al. N Engl

Current Monotherapy for induction of J Med 338:1879, 1998

and ovulation
Vandermolen DT, et al.

potential Induction of ovulation in Fertil Steril 75:310, 2001

clomiphene-resistant cases
uses De Leo V, et al. Fertil
Adjuvant to gonadotropin ovulation Steril 72:282, 1999

induction
Stadtmauer LA, et al.
Adjuvant in in-vitro fertilization Abstract, ASRM, 72:S12,
1999

Jakubowics DJ, et al. J

Prevention of early pregnancy loss ClinEndocrinolMetab
87:524, 2002
 Treatment: PCOS

l  Surgery is reserved for those in whom

medical therapy fails or hyper stimulation
occurs.
l  Surgery comprises laparoscopic multiple
punctures of the cysts with electrocautery or
laser.
l  Wedge resection is now avoided on account of
postoperative ovarian adhesions and
continued infertility
 Ovarian Drilling

l  Reduction of the intra-ovarian androgen

production
l  Reduction of testosterone level by 40-50%

l  Pregnancy rates of 60-80% at 2 years

Consequences of polycystic
ovary syndrome
Thank you!
 GYNECOLOGY

POLYCYSTIC OVARIAN SYNDROME

DR. CCB (SEPT. 28, 2018)
GYNECOLOGY
SOURCE: PPT + RECORDING +
TH
COMPREHENSIVE GYNECOLOGY 6 EDITION

SAMPLE CASE
 39 year old
 Nulligravid
 Three years infertility
 Irregular menses
 Single sexual partner
 UTZ: PCOS

Study Criteria
National Institute of  Menstrual Irregularity
Child Health and  Hyperandrogenism
Human (clinical or
Development 1990 biochemical)
ESHRE-ASRM  Menstrual Irregularity
2003  Hyperandrogenism
“Rotterdam criteria” (clinical or
WE ONLY biochemical)
FOLLOW  Polycystic ovaries on
ROTTERDAM ultrasound (two of
CRITERIA three required)
AEPCOS 2006  Hyperandrogenism
(Androgen Excess (clinical or
and Polycystic biochemical) and
Ovary Syndrome menstrual irregularity
Society)  Polycystic ovaries on
ultrasound (either or
POLYCYSTIC OVARIAN SYNDROME
both of the latter two)
 aka Stein Leventhal syndrome NIH Workshop 2012  Endorsement of
 Originally described in 1935 by Stein and Rotterdam criteria,
Leventhal as a syndrome: amenorrhea, acknowledging its
hirsutism, obesity, enlarged PCO limitations and
 Most common hormonal disorder in suggesting the name
reproductive-aged women PCOS should be
 Classic definition: anovulatory, irregular changed
periods, hyperandrogenism (hirsutism or *All required the exclusion of other underlying hormonal
disorders or tumors
elevated blood levels of androgens,
testosterone and DHEA-S
 This should be in the absence of enzymatic
disorders (21-hydroxylase deficiency),
Cushing’s syndrome or tumors.

TOUGH TIMES NEVER LAST BUT TOUGH PEOPLE DO / KKE – OLFU MED 2020 1
 GYNECOLOGY

ROTTERDAM CRITERIA ULTRASOUND FINDINGS

2 out of 3 required
A. Menstrual irregularity due to anovulation
 includes oligomenorrhea where cycles
are more than 35 days (example: this
month your period is on the first week,
next month your period is on the last
week)
 menstrual frequency of every few
months (menstruation every 2 months
or 3 months etc) and frank amenorrhea
(more than 6 months missed)
 Menstrual irregularity is the most
important sign of infertility or
subinfertility
B. Hyperandrogenism/Androgen Excess
 Hirsutism – cardinal feature of PCOS,
but may be difficult to diagnose;
 Acne, Alopecia and Obesity
 Development of insulin resistance that PCOS PHENOTYPES
may lead to Acanthosis Nigricans
C. Polycystic ovary on ultrasound
TYPE CHARACTERISTICS RELATED
 enlarged ovaries (>10cm 3), any one PARAMETERS
ovary having 12 or more cystic
A Hyperandrogenism, Androgen levels,
structures (2 to 8mm) or an ovarian Chronic body weight,
volume >10cc
Anovulation, PCO insulin resistance
 This year (2018), the Ultrasound society on UTZ (Classical and CVD risk –
released that even though the cystic PCOS) – 90% of elevated
structures are not peripherally located cases
(which means it is centrally located) it is B Hyperandrogenism, Androgen levels,
considered PCOS already. Chronic body weight,
Anovulation, insulin resistance
Normal Ovaries and CVD risk –
(Clinical elevated
Presentation of
Type 1, relatively
uncommon)
C Hyperandrogenism, Androgen levels
Ovulatory cycles, and CVD risk –
PCO on UTZ elevated
Insulin resistance
- moderate
D No No
hyperandrogenism, hyperandrogenis
Chronic m or insulin
anovulation, PCO resistance
(Mild form of PCOs) Risk normal

TOUGH TIMES NEVER LAST BUT TOUGH PEOPLE DO / KKE – OLFU MED 2020 2
 GYNECOLOGY

PCOS IN ADOLESCENTS PATHOPHYSIOLOGY

 Not easily diagnosed and should be made
with caution
 Some are irregular because the HPA is still
immature and the body fat composition
varies individually
 Using Rotterdam criteria, all parameters for
the diagnosis change and evolve during the
postpubertal years
 Firm diagnosis should only be made if all
three Rotterdam criteria in the adolescent
patient are present 3 years after post
menarche (Ex. menarche around 13 years
old, at 16 years old if the patient is still
anovulatory, with PCO on UTZ and
hyperandrogenism – diagnosed as PCOS)
PHYSIOLOGY
(EARLY FOLLICULAR PHASE)

 In PCOS, there is abnormal GNRH secretion

(increase amplitude and frequency) leading
to increase LH secretion.
 Increase LH together with enhanced theca
cell responsiveness and sensitivity drives
the production of excess ovarian androgen.
 Increase androgen production will have
inhibitory effect on hypothalamic GNRH
pulse generation which further increases LH.
 Increase androgen may have direct effects
on the ovary to increase follicle size and
 Hypothalamus releases GnRH to number and possibly enhance granulosa cell
stimulate the anterior pituitary to release responsiveness to FSH and E2 (Estradiol).
FSH and LH to stimulate the ovary  In addition, increase androgen levels are
 FSH works particularly on Granulosa cells associated with android obesity, visceral fat
to produce Estrogen deposition and dyslipidemia, all of which
 LH works on Theca cells to produce may contribute to insulin resistance.
Androgens; these androgens can be  FSH is either decreased or normal leading to
converted to Estrogen by virtue of follicular arrest (undeveloped follicles =
Aromatization anovulation).
 Granulosa cells are needed for oocyte
 Independently, hyperandrogenism, obesity
development and estrogen production by
and hyperinsulinemia may decrease SHBG
the action of FSH
(sex hormone binding globulin) thereby
 Estrogen is going to send negative
increasing testosterone (thinning of hair, hair
feedback to the anterior pituitary and
hypothalamus to stop producing GNRH, on the upper lip, chest and abdomen).
LH and FSH. Book-based + Recording
TOUGH TIMES NEVER LAST BUT TOUGH PEOPLE DO / KKE – OLFU MED 2020 3
 GYNECOLOGY

 Normally, during early phase of MANAGEMENT

menstruation, there is increase in FSH and
increase in estrogen, on the latter part which 1. Hirsutism
is the secretory part LH surge increases
progesterone; progesterone will act on  Oral Contraceptive Pills
estrogen making the endometrium thin = (Cyproterone acetate)
MENSTRUATION Brand: Althea or Diane
 However in PCOS, there is low FSH and
high LH which causes increase estrogen  trial therapy for >6 months before
and decrease progesterone that’s why changing dose or medication
endometrium is still thickened – might be a because of the approximate growth
cause of endometrial cancer phase of a hair follicle. 60-100%
experience a significant reduction in
IMPORTANT IN PCOS (TAKE NOTE) hair growth
INCREASE LH
NORMAL OR DECREASE FSH  Combination therapy: OCP + Anti androgen
(Spironolactone)

 twice daily spironolactone >50mg or

cyproterone acetate 25mg/day, days
1-10 of OCP

 Anti – androgen
(Spironolactone or Cyproterone acetate)

 should not be used without adequate

contraception

2. Irregular bleeding
- risks of endometrial disease due to
unopposed estrogen stimulation from
anovulation
- Should be directed at supplying the
missing progesterone in anovulatory
IS THERE A CURE FOR PCOS? women

 OCP – most logical and effective treatment

 Currently, no cure for PCOS. It does not go
 Progesterone therapy alone for 2 to 3 month
away on its own.
intervals
 Medications are given to treat the patient
 Medroxyprogesterone acetate
symptomatically.
(Provera) - 5 to 10mg
 Even after menopause, women with PCOS
 Norethindrone acetate (Micronized
often continue to have high levels of
Progesterone) - 2.5mg to 10mg
androgen as well as insulin resistance.
 Health risks associated with PCOS are
ACTION OF OCPs
lifelong.
 Regulation of menstrual cycle
 Increase SHBG (estrogen component)
 Reduction of LH and FSH, suppressing
levels of free testosterone and ovarian
androgen production
TOUGH TIMES NEVER LAST BUT TOUGH PEOPLE DO / KKE – OLFU MED 2020 4
 GYNECOLOGY

 Follow up at 6 months to assess adherence PROCEDURE:

or compliance and satisfaction  Insert foley catheter into the uterus through
 Withdraw OCPs for 3 months to facilitate the vagina injecting the indigo blue to see if
appropriate hormonal assessment for the the fallopian tubes are patent
androgens (LH:FSH ratio) and SHBG (sex  If the color is blue after injection that means
hormone-binding globulin) levels to return to the tubes are patent and the cause of
basal levels infertility is not obstruction
 Uncertainty remains regarding the best  Then perform the drilling
OCPs and the duration of use in adolescents  Electric current is used to destroy small
with PCOs areas of ovarian tissue where testosterone
is produced
3. Fertility concerns and subfertility  Overtime, testosterone is diminished,
ovalution then occurs
 Normalize overt abnormalities in glucose  After which, suction the indigo blue
tolerance before pregnancy
 Encourage weight loss for overweight 4. Obesity
women
 Rule out other fertility factors (male factors –  Diet and exercise
erectile dysfunction, azoospermia)  Metformin
 Ovulation induction: First line drugs –  Bariatric surgery
Metformin (control DM, regulate  Flutamide – anti androgen
menstruation, cause weight loss) and
Clomiphene citrate
 Letrozole, Gonadotropins (given by
reproductive endocrinologist – entails close FOLLOW UP
monitoring because of the fear of
hyperstimulation syndrome of hormones)  OGTT should be performed every 2 years
 Side effect – cardiovascular and annually to those who have additional
dysfunction, pulmonary edema risk factor: DM Type 2, High blood glucose
 Pulsatile GnRH level, physician inactivity, Hypertension,
 Ovarian diathermy or laparoscopic Ovarian increase waist circumference
drilling (purpose: to decrease the follicles)  Lipid profile every 2 years
 Monthly monitoring if on ovulatory agents
(Clomiphene) given day 2-6 day of
menstruation;
LAPAROSCOPIC OVARIAN DRILLING  Side effect – hyperstimulation
syndrome
 6 months when on hormonal therapy to
manage menstrual cycle and hirsutism –
assess compliance and satisfaction
 1-2 months when on Metformin – assess for
adverse effects and tolerance
 Side effect: diarrhea; give in
increments on the 1st week
(once a day), on the 2nd week (2
x a day), on the 3rd week (3 x a
day etc)

TOUGH TIMES NEVER LAST BUT TOUGH PEOPLE DO / KKE – OLFU MED 2020 5
 GYNECOLOGY

TREATMENT SUMMARY

Infertility 1. Letrozole, Clomiphene citrate

(day 2-6 of cycle) with or
without Metformin
 request for Ultrasound day
11-12 of cycle – if there is
a dominant follicle, it
responded to Clomiphene
citrate (that means there is
ovulation)
 advice the patient every
other day – sexual
contact; if there is
cessation of menses then
positive for pregnancy
 if she doesn’t want
pregnancy – give OCP
2. Ovarian drilling

Skin 1. OCP (cyproterone acetate) or

manifesta- 2. Anti-Androgens
tions (spironolactone)
(acne,
hirsutism)

Abnormal 1. OCP or
bleeding 2. Progesterone (given at day
16-25 of cycle)

Supplementary YouTube Video

(5 minutes) - Title: PCOS Nucleus Health

Black – PPT
Blue – Recording
Red – Book

TOUGH TIMES NEVER LAST BUT TOUGH PEOPLE DO / KKE – OLFU MED 2020 6