2. TABLE OF CONTENTS
1. Definition
2. Prevalence
3. Causes
4. Pathophysiology
5. Symptoms
6. Long term risks
7. Treatment
8. Conclusion
3. HISTORY
1721 1844 1902 1915 1990 1935
In 1721 Vallisneri, an Italian
scientist, described a
married, infertile women
with shiny ovaries with a
white surface, and the size
of pigeon eggs.
Chereau and Rokitansky
described fibrous and
sclerotic lesions in the
ovaries of a degenerative
character with hydrops
follicle.
In 1902 von Kahlden
published a review on the
pathology and clinical
implications of these
ovaries.
Because of many critical
voices regarding ovarian
resection, John A. McGlinn
in 1915 suggested
puncturing “those cysts
which are upon the surface”
rather than resorting to
ovarian resection.
Until early 1990s at NIH
sponsored conference on
PCOS that formal
diagnostic criteria were
proposed and afterwards
largely utilized.
PCOS was first described in
1935 by Stein and
Leventhal.
4. 8-20%
• PCOSisonethem
ostcom
m
onhorm
onalendocrinedisorde
rsaffe
cting ofadultw
om
en.
5m
illionw
om
en
• AccordingtoNIH,PCOSaffe
ctsappro
xim
ate
ly ofchildbe
aringageinU.S.
• PCOSislinkedtodevelopmentofothermedicalconditions,suchasinsulinresistance,type2diabetes,highcholesterol,HBP
,
andheartdise
ase
.
• M
orethanhalfofw
o
m
e
nwithPCOSdeveloptype2diabetesbeforetheageof40years.
• Around70%ofovulatoryfertilityissuesarerelatedtoPCOS.
5. DIAGNOSTIC TOOLS FOR
PCOS
• According to these criteria, POCS is defined as unexplained hyperandrogenic
anovulation.
• PCOS can be diagnosed in women if the following criteria are found:
symptoms of excess of androgens (clinical or biochemical), rare ovulations.
6. PREVALENCE OF
PCOS
• PCOS is highly variable ranging from 2.2% to 26% globally.
• In fewAsian country prevalence figures are ranging from 2-7.5% (China) & 6.3% (Sri Lanka)
(byAndrogen Excess Society criteria) respectively.
Epidemiology of PCOS in India Indian Journal of
Medical
Research
7. INTRODUCTION
PCOS, a hormonal disorder causing enlarged ovaries with small cysts, or fluid-filled
sacs.
Experience menstrual cycle abnormalities, increased androgen levels, excess hair
growth, acne, and obesity.
Women who can conceive with PCOS have a higher incidence of miscarriage,
gestational diabetes, pregnancy-induced high blood pressure, preeclampsia, and
premature delivery.
8. PCOS is usually characterized by:
1) Oligomenorrhea= Menstrual intervals >35 days
2) Hyperandrogenism= ↑ testosterone or hirsutism/acne
3) Amenorrhea= Absence of menses (more than 3 months)
PCOS
Amenorrh
ea
Oligomen
orrhea
Infertility
Hirsutism
The new criteria include 2 of the following
three signs:
1> Ovulation dysfunction
2> excessive hair growth/ acne
3> polycystic appearing ovaries
9. PHENOTYPES
Since PCOS tends to present as a spectrum of diseases, the Rotterdam criteria
divided the disease into four phenotypes (Rotterdam, 2004):
Frank or classic polycystic ovary PCOS (chronic anovulation,
hyperandrogenism, and polycystic ovaries)
Classic non-polycystic ovary PCOS (chronic anovulation,
hyperandrogenism, and normal ovaries)
Non-classic ovulatory PCOS (regular menstrual cycles,
hyperandrogenism, and polycystic ovaries)
Non-classic mild or normoandrogenic PCOS (chronic
anovulation, normal androgens, and polycystic ovaries)
10. CAUSES
EXCESS INSULIN:
EXCESSIVE INSULIN
MIGHT INCREASE
ANDROGEN
PRODUCTION,
CAUSING
DIFFICULTY WITH
OVULATION
Low-grade
inflammation: PCOS
women have low-grade
inflammation that
stimulates polycystic
ovaries to produce
androgen, which can
lead to heart& blood
vessel problems
Heredity
20. FUNCTIONAL CYSTS
Follicular cyst
• Forms before ovulation.
• Dominant follicle fails to
rupture & keeps growing
(happen when normal LH
surge doesn’t happen
• Condition where multiple
follicular cyst (PCOS).
Corpus luteal cyst
• If dominant follicle
ruptures & closes after
ovulation
• Corpus luteum doesn’t
grow
• Arteries nourishing it can
rupture & hemorrhage
into the cyst.
Theca Lutein cyst
• Caused by over
stimulation by hCG.
• Only seen in pregnancy
• hCG stimulates growth of
theca cells (bilateral)
• Found on both ovaries.
• Both are around 2-3 cm. but can be as big as 10 cm diameter.
• They contain clear serous liquid & have smooth internal lining.
21. NEOPLASTIC CYSTS
ENDOMETRIOSIS CYST
- Endometrial tissue grows on ovary.
- Also called “chocolate cysts”.
-Release proinflammatory factors that causes inflammation, leads
to cyst growth.
- They are complex i.e. 10 cm, have regular borders.
•- They contain heterogenous fluid.
22. Excessiv
e body
hair
growth Weight
changes
& trouble
loosing it
Ovarian
cysts
Irregular
or
missed
periods
Acanthos
is
nigricans
High
testoster
one
levels
Insulin
resistanc
e
Fatigue
Acne
Trouble
conceivi
ng/
infertility
24. PCOD PCOS
• Polycystic ovary disease.
• Condition where ovaries release a lot of immature/
partially-mature eggs which turns into cysts.
• Not considered to be a disease with right diet & exercise,
it can be managed.
• Does not lead to infertility & shouldn't be considered an
obstacle towards pregnancy.
• Symptoms include wt gain, irregular periods & male
pattern hair loss.
• More common, almost a third of the women around
world suffer.
• Polycystic ovary syndrome.
• The ovaries produce higher levels of androgens
than usual, which interferes with development &
release of the eggs. Some of the eggs develop into
little sacs filled with liquid.
• Is a serious condition. Is a metabolic disorder and
more apparent from a younger age.
hormonal
• Conception can be challenge due to
irregularities (disrupts ovulation process).
• Symptoms include hair loss and infertility.
25. • No single test can determine the presence of PCOS, but a doctor can diagnose
the condition through medical history, a physical exam that includes a pelvic
exam, and blood tests to measure hormone, cholesterol, and glucose levels.
• An ultrasound may be used to look at the uterus and ovaries.
26. Criteria for diagnosis of polycystic ovary syndrome (PCOS)
Major criteria
• Chronic anovulation
• Clinical signs of androgen excess
• Hirsutism
• Acne
• Alopecia
• Menstrual disturbance
• Infertility
• Virilization
Minor criteria
• Insulin resistance
• Onset at puberty
• Elevated LH:FSH ratio (> 2.5–3)
• Ultrasonographic evidence of polycystic ovaries
27. LABORATORY
EVALUATION
• NIH in1990 proposed a criteria for diagnosis which should feature hyperandrogenism with chronic anovulation.
• The patient should undergo laboratory evaluation to exclude hyperprolactinemia, late-onset congenital adrenal
hyperplasia, and androgensecreting tumors of the ovary or adrenal gland.
• Normal serum levels of following hormones can be done:
Prolactin, Testosterone, DHEAS, Corticotropin-stimulated 17-alpha-hydroxyprogesterone.
• Endometrial biopsy: Patients with greater than 3-month menstrual interval or an endometrial thickness of >=7mm on
ultrasound to assess the risk of hyperplasia.
28. • Diagnosing PCOS in children and adolescence is challenging because the normal pubertal
physiological events tend to mimic the signs and symptoms of PCOS.
• Diagnostic criteria for PCOS among adolescent has been problematic because irregular
menses, cystic acne, mild hyperandrogenism, and multi-follicular ovarian morphology occur
during normal pubertal maturation. These similarities between normal pubertal
development and the clinical features associated with PCOS confound the diagnosis
in adolescent girls.
• This overlap between normal puberty and the diagnostic pathological criteria of PCOS may
cause an over-diagnosis of PCOS among adolescent which can lead to unnecessary
treatment and psychological impairment.
29. Miscarriage: this
risk is confounded
by the high rate of
obesity in this
population.
Malignances: A
combination of
hyperinsulinemia,
hyperandrogenism,
and
oligoanovulation
increases the risk
of endometrial
cancer.
Psychiatric
disorder:
Increased risk of
anxiety,
depression,
binge-eating
disorder and
bipolar disorder.
32. SURGICAL OPTIONS
Ovarian drilling: tiny holes in ovaries can
reduce the level of androgens.
Oophorectomy: Removal of both the ovaries
Hysterectomy: Involves removal of all/ parts of
uterus.
Cyst aspiration: Fluid is removed from the cyst.
Approximately 84% ovulation induction rate and 56% pregnancy rate with maintenance of ovulation demonstrated for up to 20
years.
33. HOME
REMEDIES
Eating a healthy, well-
balanced diet including
plenty of fruits and
vegetables
Participating in
regular physical
activity
Maintaining a healthy
weight, to reduce
androgen levels and
reduce the risk of
diseases such as diabetes
and heart disease
Not smoking, as this
increases levels of
androgens and the
risk of heart disease
34. CONCLUSION
• PCOS is a chronic condition that can be successfully managed with close
surveillance.
• Maintaining good health is essential to prevent as well as treat hormonal
disturbances and conditions. The best treatment for PCOD/PCOS will include
timely diagnosis and the appropriate steps that can help overcome the
syndrome.
• Management of both those at risk for PCOS and those with a confirmed PCOS
diagnosis includes education, healthy lifestyle interventions, and therapeutic
interventions targeting their symptoms.
35. REFEREN
CES
• Marx, T.L. and Mehta, A.E., 2003. Polycystic ovary syndrome: pathogenesis and
treatment over the short and long term. Cleveland Clinic journal of
medicine, 70(1), pp.31-45.
• Ndefo, U.A., Eaton, A. and Green, M.R., 2013. Polycystic ovary syndrome: a
review of treatment options with a focus on pharmacological
approaches. Pharmacy and Therapeutics, 38(6), p.336.
• El Hayek, S., Bitar, L., Hamdar, L.H., Mirza, F.G. and Daoud, G., 2016. Poly
cystic ovarian syndrome: an updated overview. Frontiers in physiology, 7, p.124.
• Rosenfield, R.L. and Ehrmann, D.A., 2016. The pathogenesis of polycystic
ovary syndrome (PCOS): the hypothesis of PCOS as functional ovarian
hyperandrogenism revisited. Endocrine reviews, 37(5), pp.467-520.
