Report of Plenary Discussion

Block 15

Group 6 of Tutorial
FAKULTAS KEDOKTERAN DAN ILMU KESEHATAN
UNIVERSITAS MUHAMMADIYAH YOGYAKARTA
Jl. Lingkar Selatan, Tamantirto, Kasihan, Bantul, Yogyakarta
Telp. (0274) 387656, Fax (0274) 387646
Website:www.umy.ac.id
2018
 Group 6 of Tutorial
Member :
 Muhammad Syidqul Wafa Ismana (20160350003)
 Zulfa Sekar Dewinda (20160350008)
 Dea Muchcica Septioriny Putri (20160350033)
 Hendrawan (20160350034)
 Dyah Wikansih Sekarpertiwi (20160350040)
 Aldi Kurnianto (20160350057)
 Herdita Nugraheny Kusuma W (20160350064)
 Rafa Adinda Hapsari R (20160350065)
 Fadiah Widyaningsih (20160350073)
 Dita Ayu Lestari (20160350105)
 Naurah Nadhifah (20160350121)
 Muhammad Dhiki Wahyu S N (20160350123)
 PREFACE

Thank to Allah SWT who has given us His favor to the writers for completing the
English paper task entitle “Report of Plenary Discussion of Block 15” as a plenary discussion
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The writers realize this report is far from perfection. So, we apologize if there are some
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Yogyakarta, December 31st 2018

Writers,
 CHAPTER I
INTRODUCTION
1.1 Background
Polycystic ovary syndrome (PCOS) is the most common endocrinopathy of women of
reproductive age, affecting up to 10% of women. The clinical and biochemical features of the
syndrome are heterogeneous, including menstrual irregularity and fertility problems, excess
hair and acne. Women with PCOS are also more likely to be overweight and have an
increased risk of metabolic syndrome, type 2 diabetes and cardiovascular disease.

Although the exact aetiology of PCOS is unknown it involves a combination of

genetic and environmental factors). Insulin resistance, with compensatory hyperinsulinaemia
is considered a key factor in the development of symptoms. Hyperinsulinaemia is known to
stimulate ovarian androgen production and decrease hepatic sex hormone-binding globulin,
resulting in hyperandrogenism and the associated clinical features of PCOS .Treatment for
PCOS includes diet and lifestyle changes to promote a healthy body mass index (BMI) and
reduce hyperinsulinaemia. Specific medications, such as metformin, are used to manage the
presenting symptoms; at present there is no cure. Several authors have highlighted the
importance of weight management, through diet and lifestyle modifications, in the
management of PCOS .

To date, dietary management of PCOS has focused on weight loss in overweight

women, with research showing that weight loss of as little as 5% can reduce insulin levels,
improve menstrual function and reduce serum testosterone. Due to the increased prevalence
of obesity, insulin resistance and subsequent hyperinsulinaemia in women with PCOS,
dietary management should also focus on minimising the risk of diabetes and cardiovascular
disease. The Diabetes Prevention Program (2002) and Finnish Diabetes Prevention study
(2003) have both shown that positive changes to diet and lifestyle are successful in
preventing diabetes in both men and women . Lifestyle management is important in all
patients with PCOS, not just the overweight, however there is a paucity of research for the
appropriate lifestyle management of lean women with PCOS.

1.2 Aim
 a. Students can colaborate being a group discussion and any others can share idea or info
from jurnals.
b. Students know the problem of the scenario and they can solve the problem as a group
discussion.

CHAPTER II
DISCUSSION
2.1 Scenario
Ny R (25th) weight 85 kg height 165cm come to the doctor with complaints of irregular
menstruation. She said that often menstruating late even 3 months did not have menstruation.
After check up by a doctor it turns out that there is swelling of the ovaries and found several
cysts. results of blood pressure checks is 150/90 mmHg and blood checks show cholesterol
values 230 mg/dl and GD 2 hours PP 120 mg/dL. Diagnostic = Polycystic ovary syndrome
(PCOS) . After that doctor doctors then provide metformin 3x 500mg .
2.2 Seven Jumps
2.2.1 Clarifying unfamiliar terms
2.2.2 Problem Definition
a. Definition
b. Etiology Of PCOS
c. Epidemiology of PCOS
d. Pathophysiology of PCOS
e. Clinical manifestations of PCOS
f. Data diagnosis
g. Signs and symptoms
h. Therapeutic management
i. SOAP
j. Therapy Effect

2.3.3. Analyzing the Problem

a. Definition

Polycystic ovary syndrome, or PCOS, is a hormonal condition. In women who have it, it
can affect your ability to have a child (fertility). It can also:

 Make your periods stop or become hard to predict

 Cause acne and unwanted hair
 Raise your chances for other health problems, including diabetes and high blood
pressure
 There are treatments for the symptoms, and if you want to get pregnant, that’s still
possible, though you may need to try different methods.
Many women who have PCOS don’t have cysts on their ovaries, so “polycystic” can be
misleading. You might have cysts, and you might not.

Hormones and PCOS

With PCOS, your reproductive hormones are out of balance. This can lead to problems
with your ovaries, such as not having your period on time, or missing it entirely.
Hormones are substances your body makes to help different processes happen. Some are
related to your ability to have a baby, and also affect your menstrual cycle. Those that are
involved in PCOS include.

 Androgens: Often called “male” hormones, women have them, too. Those with
PCOS tend to have higher levels, which can cause symptoms like hair loss, hair in
places you don’t want it (such as on your face), and trouble getting pregnant.
 Insulin: This hormone manages your blood sugar. If you have PCOS, your body
might not react to insulin the way that it should.
 Progesterone: With PCOS, your body may not have enough of this hormone. That
can make you to miss your periods for a long time, or to have periods that are hard to
predict.

b.Etiology Of PCOS
The 1990 NIH–National Institute of Child Health and Human Development
Conference of PCOS originally recommended that the major criteria for PCOS should
include (in order of importance): hyperandrogenism and/or hyperandrogenemia, oligo-
ovulation and the exclusion of other known disorders, making PCOS a
hyperandrogenic disorder of exclusion with an ovarian etiology and/or consequences.3
In 2003, the Rotterdam consensus expanded the diagnostic criteria to include at least
two of the following three features: clinical and/ or biochemical hyperandrogenism,
oligoanovulation, and PCO, excluding other endocrinopathies.4,5 These newer
Rotterdam criteria for PCOS include all patients defined by 1990 NIH criteria but also
women with either clinical and/or biochemical hyperandrogenism and PCO (namely,
ovulatory PCOS) or PCO with ovulatory dysfunction (but without signs of androgen
excess). In 2006, the Androgen Excess–PCOS Society recommended that PCOS be
defined by clinical and/or biochemical hyperandrogenism, with either
oligoanovulation and/ or PCO, excluding related disorders.6 The 1990 NIH and
Androgen Excess–PCOS Society criteria for PCOS emphasize hyperandrogenism,
which is closely interrelated with hyperinsulinism, which makes these definitions
 valuable in understanding metabolic dysfunction in PCOS. The Rotterdam criteria are
useful for the diagnosis of PCOS in ethnic groups who do not exhibit clinical
hyperandrogenism (for example, Asian patients).

c. Epidemiology of PCOS
Prevalence estimates for PCOS, as defined by the NIH/NICHD criteria,
indicate that PCOS is a common endocrinopathy affecting 4%–8% of women of
reproductive age. Recently, several groups have demonstrated that the prevalence of
PCOS varies depending on the diagnostic criteria used (see Table). These studies
consistently report that the prevalence estimates using the Rotterdam criteria are two
to three times greater than those obtained using the NIH/NICHD criteria.

Family history of PCOS is a risk factor for PCOS. Based on the clustering of
cases in families, PCOS is considered to be a heritable disorder. A high prevalence of
PCOS or its features among first-degree relatives is suggestive of genetic
influences. In addition, greater concordance has been reported in monozygotic twins
versus dizygotic twins. However, the mode of inheritance remains elusive. Issues that
hamper progress in this area include the heterogeneity of PCOS phenotypes, difficulty
in assigning a phenotype to men, postmenopausal women, and prepubertal girls, and
difficulties in obtaining large enough sample sizes to allow for adequate statistical
power. A genome wide association study conducted amongst Han Chinese has
identified loci on chromosomes 2p16.3, 2p21, and 9q33.3. Some of these results were
replicated in European cohorts, namely the chromosome 2p21 THADA and
chromosome 9p33.3 DENND1A susceptibility loci. The sharing of the same
susceptibility genes suggests that PCOS is an ancient disorder originating before
humans migrated out of Africa.
An increased prevalence of PCOS is associated with a number of conditions.
A history of weight gain often precedes the development of the clinical features of
PCOS, and following a healthy lifestyle has been shown to reduce body weight,
abdominal fat, reduce testosterone, improve insulin resistance, and decrease hirsutism
in women with PCOS. Obese women referred for assistance with weight loss had a
prevalence of PCOS of 28.3%.However, in an unselected population, prevalence of
PCOS did not vary significantly based on obesity class. PCOS prevalence rates for
underweight, normal-weight, overweight, mildly obese, moderately obese, and
severely obese women were 8.2%, 9.8%, 9.9%, 5.2%, 12.4%, and 11.5%, respectively.
The authors concluded that obesity may increase the risk of PCOS but that the effect
was modest.
An increased frequency of reproductive disorders, including PCOS, has been
reported in women with epilepsy. Using NIH criteria for diagnosis, Bilo et al identified
PCOS in 13 of 50 women (26%) with epilepsy. Among the 16 patients who were not
treated for epilepsy at presentation, five (31%) were diagnosed with PCOS, supporting
the contention that epilepsy, independent of antiepileptic drugs, increases the risk of
PCOS. Valproic acid, an antiepileptic drug widely used to treat epilepsy, bipolar
disorder, and migraine, is associated with features of polycystic ovary syndrome when
used to treat women with epilepsy. These features include menstrual disturbances,
polycystic ovarian morphology, and elevated serum testosterone. Substitution of
lamotrigine for valproic acid in women with epilepsy resulted in reductions in body
mass index, fasting serum insulin, and testosterone concentrations. Thus, the
confounding effects of medication must be considered when evaluating the literature
that probes the relationship between epilepsy, bipolar disorder, and PCOS.
Type 1, Type 2, and gestational diabetes have been associated with an
increased prevalence of PCOS. Escobar-Morreale et al screened 85 Caucasian women
with type 1 diabetes mellitus for PCOS using the NIH/NICHD criteria. PCOS was
diagnosed in 16 of these women (18.8%). Subsequently, Codner et al screened 42
women with type 1 diabetes mellitus and 38 age and body mass index (BMI) matched
controls for PCOS using the ESHRE/ASRM criteria. The prevalence of PCOS was
40.5% in the type 1 diabetes group and 2.6% in the control group, yielding a relative
risk of PCOS of 15.4 (95% confidence interval [CI] 2.2–110.2; P<0.0001) in the type
1 diabetes group. In type 2 diabetes, PCO are extremely common, occurring in 82% of
women. The prevalence of PCOS in type 2 diabetes using the NIH/NICHD criteria has
been estimated to be 26.7%.A diagnosis of PCOS was verified in 15 of 94 women
(16%) with gestational diabetes and in six of 94 (6.4%) of those without gestational
diabetes (P=0.03).
 A number of factors that are associated with an increased risk of PCOS have
been identified in children. Prenatal factors include high birth weight in girls born to
overweight mothers, congenital virilization, and low birth weight. Risk factors
apparent later in childhood include premature pubarche, atypical central precocious
puberty, obesity syndromes, acanthosis nigricans, and metabolic syndrome. A high
index of suspicion for the diagnosis of PCOS is warranted in adolescents with
persistently irregular menses and these risk factors.

d. Pathophysiology of PCOS

4 major disorders of PCOS

1. abnormal ovarian morphology
Causes of abnormalities this morphology is thought to be caused by excessive
androgens. Androgen stimulates the growth of primary follicles up to the stage of
pre-antral follicles and small antral, and this process is accelerated by the
presence of excessive androgens compared to a normal ovary.

2. Excessive ovarian androgen production

Almost all enzymatic mechanisms in PCOS stimulate production androgen
increases. Increased insulin and LH, either alone or combination will increase
androgen production. There is a single gene with code cytochrome P450c17a, this
enzyme mediates the activity of 17a-hydroxylase and 17-20-desmolase at the
level of the ovary.
 3. Excessive serum LH levels
High levels of LH more is found in women with thin weight compared to with
obesity. Although the serum FSH level is within normal limits, however intrinsic
inhibition was found in FSH work. Prolactin levels are also possible slightly
increased.
4. Hiperinsulinemia
This is caused by abnormalities in post-receptors that have an effect on glucose
transport, and this is a unique disorder in women with PCOS.13 Insulin resistance
is significantly exacerbated by obesity, and is a major factor in the pathogenesis
of anovulation and hyperandrogenism.

e. Clinical Manifestasion of PCOS

1. Infertility
In polycystic ovary syndrome is related to two things. First because of
oligo-ovulation / anovulation. This situation is related to hyperinsulinemia in
which there is insulin resistance because peripheral tissue cells, especially muscle
and fat tissue, cannot use insulin and are often found in blood circulation. The
higher the insulin level of a woman, the less often she experiences menstruation.
The second cause is the presence of high LH levels which stimulates androgen
synthesis. Testosterone suppresses the secretion of SHBG by the liver so that free
testosterone and estradiol levels increase. An increase in estradiol levels provides
positive feedback on LH so that LH levels increase again while FSH levels remain
low. This causes obstructed follicle growth, never ripens especially ovulation.

2. Hypertension and coronary heart disease

It is known that obesity is often suffered by patients with polycystic ovary
syndrome. Excessive body fat gives a consequence of insulin resistance. Obesity
 and insulin resistance leads to changes in the response of fat cells to insulin, where
there is a disruption of suppression of fat free from fat tissue. The increase in free
fat that enters the portal circulation increases the production of triglycerides, in
addition there is also an increase in the activity of the lipase enzyme that is
responsible for transforming large lipoprotein particles into smaller ones. As a
result, it was found a decrease in the concentration of high density lipoprotein
(HDL) cholesterol and an increase in levels of low density lipoprotein (LDL)
cholesterol which is atherogenic, thereby accelerating the process of blood vessel
atherosclerosis due to reduced flexibility associated with hypertension. The
combination of high triglycerides and low HDL cholesterol is closely related to
cardiovascular disease, which in patients with polycystic ovary syndrome appears
at a relatively younger age.

3. Diabetes mellitus
Polycystic ovary syndrome is closely related to insulin problems. The
resistance of body cells to insulin causes organs to not store glucose in the form of
glycogen so that levels increase in the blood.

4. Endometrial cancer
Another risk faced by women with this syndrome is the increased incidence
of endometrial cancer. This is related to estrogen levels which are always high so
that the endometrium is always exposed to estrogen plus progesterone deficiency.
These cancers are usually well differentiated, the rate of cure for level I lesions is>
90%. High estrogen levels may also increase the occurrence of breast cancer.

f. Diagnosis
Based on Rotterdam criteria :
1. Oligo / anovulation
2. Hyperandrogenism (clinical and biochemical)
3. Ovarian polycystic on an ultrasound examination (≥ 10 - 12 follicles d = 2 - 9 mm
or increase ovarian volume> 10 cm3)

Additional criteria
- LH / FSH ratio> 2.5
- Hyperinsulinemia
g. Signs and symptoms

Early signs of PCOS are irregular ovulation or fertility, increased male

hormone levels (androgens) in a woman's body, and the emergence of many cysts
(fluid-filled bags) in the ovary. If a woman experiences at least two of the three initial
signs, then it is likely she has PCOS.

Symptoms of PCOS

Usually the symptoms of PCOS will become more apparent when women enter the
age of 16 to 24 years. Some of the common symptoms of PCOS are:

 Excessive hair growth, usually on the back, buttocks, face or chest.

 Oily or pimpled skin.
 Depression.
 Difficulty getting pregnant.
 Head hair falls out or thinning.
 Increased weight.
 Irregular menstruation. In a year the frequency of menstruation is less, or the
amount of blood released during menstruation is more.
h. Therapeutic management

Effectiveness of lifestyle interventions

- Lifestyle intervention (preferably multicomponent including diet, exercise and

behavioural strategies) should be recommended in all those with PCOS and
excess weight, for reductions in weight, central obesity and insulin resistance.
- A variety of balanced dietary approaches could be recommended to reduce dietary
energy intake and induce weight loss in women with PCOS and overweight and
obesity.
- General healthy eating principles should be followed for all women with PCOS
across the life course.
1. Letrozole
- Letrozole should be considered first line pharmacological treatment for
ovulation induction in women with PCOS with anovulatory infertility and
no other infertility factors to improve ovulation, pregnancy and live birth
rates.
- Where letrozole is not available or use is not permitted or cost is
prohibitive, health professionals should use other ovulation induction
agents.
- Health professionals and women should be aware that the risk of multiple
pregnancy appears to be less with letrozole, compared to clomiphene citrate

2. Clomiphene citrate and metformin

- Clomiphene citrate could be used alone in women with PCOS with
anovulatory infertility and no other infertility factors to improve ovulation
and pregnancy rates.
- Metformin could be used alone in women with PCOS, with anovulatory
infertility and no other infertility factors, to improve ovulation, pregnancy
and live birth rates, although women should be informed that there are more
effective ovulation induction agents.
- Clomiphene citrate could be used in preference, when considering
clomiphene citrate or metformin for ovulation induction in women with
PCOS who are obese (BMI is ≥ 30 kg/m2) with anovulatory infertility and no
other infertility factors.
- If metformin is being used for ovulation induction in women with PCOS who
are obese (BMI ≥ 30kg/m2) with anovulatory infertility and no other
infertility factors, clomiphene citrate could be added to improve ovulation,
pregnancy and live birth rates.
- Clomiphene citrate could be combined with metformin, rather than persisting
with clomiphene citrate alone, in women with PCOS who are clomiphene
 citrate-resistant, with anovulatory infertility and no other infertility factors, to
improve ovulation and pregnancy rates.
- The risk of multiple pregnancy is increased with clomiphene citrate use and
therefore monitoring needs to be considered.

3. Gonadotrophins
- Gonadotrophins could be used as second line pharmacological agents in
women with PCOS who have failed first line oral ovulation induction
therapy and are anovulatory and infertile, with no other infertility factors.
*Gonadotrophins could be considered as first line treatment, in the presence
of ultrasound monitoring, following counselling on cost and potential risk of
multiple pregnancy, in women with PCOS with anovulatory infertility and
no other infertility factors.
- Gonadotrophins, where available and affordable, should be used in
preference to clomiphene citrate combined with metformin therapy for
ovulation induction, in women with PCOS with anovulatory infertility,
clomiphene citrate-resistance and no other infertility factors, to improve
ovulation, pregnancy and live birth rates.
- Where gonadotrophins are prescribed, the following should be considered:
 cost and availability
 expertise required for use in ovulation induction
 degree of intensive ultrasound monitoring required
 lack of difference in clinical efficacy of available gonadotrophin
preparations
 low dose gonadotrophin protocols optimise monofollicular development
 risk and implications of potential multiple pregnancy

4. Laparoscopic ovarian surgery

- Laparoscopic ovarian surgery could be second line therapy for women with
PCOS, who are clomiphene citrate resistant, with anovulatory infertility and
no other infertility factors.
 - Laparoscopic ovarian surgery could potentially be offered as first line
treatment if laparoscopy is indicated for another reason in women with
PCOS with anovulatory infertility and no other infertility factors.
- Risks should be explained to all women with PCOS considering
laparoscopic ovarian surgery.
- Where laparoscopic ovarian surgery is to be recommended, the following
should be considered:
 comparative cost
 expertise required for use in ovulation induction
 intra-operative and post-operative risks are higher in women who are
overweight and obese
 there may be a small associated risk of lower ovarian reserve or loss of
ovarian function
 periadnexal adhesion formation may be an associated risk

5. Bariatric Surgery
- Bariatric surgery should be considered an experimental therapy in women
with PCOS, for the purpose of having healthy baby, with risk to benefit
ratios currently too uncertain to advocate this as fertility therapy.
- If bariatric surgery is to be prescribed, the following should be considered:
 comparative cost
 the need for a structured weight management program involving diet,
physical activity and interventions to improve psychological,
musculoskeletal and cardiovascular health to continue post-operatively
perinatal risks such as small for gestational age, premature delivery,
possibly increased infant mortality
 potential benefits such as reduced incidence of large for gestational age
fetus and gestational diabetes
 recommendations for pregnancy avoidance during periods of rapid
weight loss and for at least 12 months after bariatric surgery with
appropriate contraception
 - If pregnancy occurs, the following should be considered:
 awareness and preventative management of pre- and post-operative
nutritional deficiencies is important, ideally in a specialist
interdisciplinary care setting
 monitoring of fetal growth during pregnancy

i. SOAP

SUBJEKTIVE OBJEKTIVE
 Weight = 85 kg.  Swelling of the ovaries and the
number of cysts.
 Height = 165 cm.  Blood pressure = 150/990 mmHg.
 Irregular menstrual complaints.  Cholesterol values of 230 mg/dl.
 Late period of 3 months.  GD 2 hours PP = 120 mg/dl.
 Polyscistic Ovary
Syndrome(PCOS).

DRUG ANALYSIS

Medicine Dose
No. Indication Mechanism Dose ESO
name rek.

1 Metformin 3 - DM type 2 - Inhibit the 2-3 x 2250 Gastroint

x 500 mg - Polyscistic production of 500 mg estinal
Ovary glucose in the mg per disorders.
Syndrome(PC liver and day
OS) increasing
sensitivity Insulin
in peripheral
tissues.
- Lowering the
levels of Insulin,
Insulin effect
change on the
ovary in androgen
formation,
proliferation of
theca cells and the
formation of
endometrial.
 ASSESMENT

PM S/O Therapy analysis DRP Guideline

Polyscistic Ovary Subjektive Metformin 3 - - International

Syndrome(PCOS) x 500 mg evidence-based
 BB = 85 kg
guidelines for
 TB = 165 cm
the assessment
 Irregular
and
menstrual
management of
complaints
Polyscistic
 Late period of 3
ovary
months
syndrome
(PCOS) 2018

Objektive
 Swelling of the
ovaries and the
number of cysts
 BP = 150/90
mmHg
 Cholesterol
values of 230 ng /
dl
 GD 2 hours PP =
120 mg / dl
 Polyscistic Ovary
Syndrome(PCOS)

Planning
It can be recommended to use metformin xr because many complaints in patients such as
discomfort and side effects

KIE
- blood pressure control,
- cholesterol,
- weight,
- monitoring the menstrual cycle
- Healthy lifestyles,
- physical exercise,
- well organized drug consumption (metformin xr 500mg/day) after eating

Monitoring
- side effects of metformin, which is nausea,
- indigestion menstrual fluency
- usg,
- control the level of LH / FH,
- control androgen levels,
- control prolactin levels
- development of cysts in the ova
- blood sugar levels

j. Therapy Effect
 CHAPTER III
CONCLUTION
In this case, the patient Ny R (25th) weight 85 kg height 165cm experienced Polycystic
ovary syndrome (PCOS), irregular menstruation,Overweight, high blood pressure and the
cholesterol is high . Patients go to the doctor, then the doctor provide metformin 3x 500mg.
Metformin is recommended to improve menstruation and improve insulin receptors. the
mechanism of metformin also overcomes obesity so that it can lower blood pressure. By
improving lifestyle cholesterol can decrease.
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Hershlag A, Peterson CM. Endocrine disorders. In: Berek JS, Adashi EY, Hillard PA, editors.
Novak’s gynecology. 12th ed. Baltimore: Williams & Wilkins; 1996. p 837-45.
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