PCOS

It is a medical educational Presentation.

1. POLYCYSTIC OVARIAN
SYNDROME
DR POLY BEGUM
Assistant Professor
DAMC, Faridpur

2. INTRODUCTION
Polycystic Ovarian Syndrome was originally
described in 1935 by Stein and Leventhal as a
syndrome .
PCOS could be defined when two of the three
following criteria(Rotterdam criteria) are present:
1)Oligomenorrhoea and / or anovulation.
2)clinical and/or biochemical signs of
hyperandrogenism.
3)polycystic ovaries with exclusion of other
aetiologies.

5. PREVALENCE
About 5- 10 % of reproductive
age females have clinical or
biochemical signs of
anovulation and androgen
excess .

6. ETIOLOGIES
No one is quite sure what causes
PCOS, and it is likely to be the
result of:
1)genetic (inherited)
2)environmental factors.
3)Metabolic disorder (IR)

7. GENETIC FACTOR
Women with PCOS often have a
mother or sister with the
condition, and researchers are
examining the role that
genetics or gene mutations
might play in its development.

8. ENVIRONMENTAL FACTOR
Dietary consumption
Sedentary life style
Lead to obesity
BMI > 30

9. INSULIN RESISTANCE (IR)
A malfunction of the body's blood
sugar control system (insulin
system) is frequent in women with
PCOS, who often have insulin
resistance and elevated blood
insulin levels, and researchers
believe that these abnormalities
may be related to the development
of PCOS.

10. PHENOTYPES OF IR
PCOS + IR (70 % )
PCOS without IR

11. PCOS WITH IR
Abdominal obesity
Acanthosis Nigericans
( Marker of IR).

12. Acanthosis nigricans is traditionally characterized
by hyperpigmented, velvety plaques of body folds.

13. PCOS WITHOUT IR
Majority are lean

14. Pathophysiology
•The hyperandrogenism and
anovulation that accompany PCOS may
be caused by abnormalities in four
endocrinologically active compartments:
–(i) the ovaries
– (ii) the adrenal glands
– (iii) the periphery (fat)
–(iv) the hypothalamus–pituitary
compartment

15. It is also known that the
ovaries of women with PCOS
produce excess amounts of
male hormones known as
androgens. This excessive
production of male hormones
may be a result of or related to
the abnormalities in insulin
production.

16. CLINICAL FEATURES OF PCOS
Ovulatory dysfunction
Amenorrhea
Oligomenorrhea
Irregular uterine bleeding
Infertility
Androgen excess
Hirsutism
Seborrhea
Acne
Alopecia
Virilization
Insulin resistance
Acanthosis nigricans
Obesity

21. DIAGNOSIS
Diagnosis of PCOS can only be
made when other etiologies
have been excluded (thyroid
dysfunction, congenital adrenal
hyperplasia,
hyperprolactinaemia,
androgen-secreting tumours
and Cushing syndrome).

22. INVESTIGATION
USG – Ovaries are enlarge in volume (
≥10cm
3
). Increased number of cyst (>12).Diameter of
cyst (2-9mm), peripherally arranged.
Serum values –
LH level is elevated and/or the ratio LH:FSH is >2:1.
Raised level of oestradiol and oestrone
SHBG level is reduced.
Raised serum testosterone (>150ngm/dl)
Insulin resistance: Raised fasting insulin levels >25µ
iu/ml and fasting glucose/insulin ratio <4.5 suggests
IR.
Laparoscopy – Bilateral polycystic ovary.

26. PCO VS MULTICYSTIC
OVARIES
Polycystic
ovaries
Bilateral
Multiple cysts
Cyst dia <10
mm
Stroma
increased
Multicystic
ovaries
Bilateral
Multiple
cysts
Cyst dia > 10
mm
Stroma not
increased

27. DIFFERENTIAL DIAGNOSIS
Late onset congenital adrenal hyperplasia
DHEAS > 18mmol/l
17 OH Prog > 6 mmol/l
Ovarian + adrenal androgen secreting tumours
V. high testosterone > 6mmol/l
Cushings Syndrome
- Dexamethsone suppression test
- 24 hours urinary cortisol
- DHEAS > 13 mmol/l
Iatrogenic and illegal androgen ingestion
Hypothyroidisms
Hyperprolactinemia.

28. TREATMENT
Aimed at relieving symptoms and
preventing adverse long term
effects.
The target symptoms are:
-Infertility
-Hirsutism
-Amenorrhea

29. First line treatment- prevention of peripupertal
obesity (50% of PCOS In adolescents are obese).50% of PCOS In adolescents are obese).
Life- style modifications:
Diet modification
Weight loss
Exercise
Psychosocial support.
Cessation smoking.

30. A weight loss of only 5% of total
body weight is associated with:
Decreased insulin levels
improved menstrual function
reduced hirsutism and acne
lower testosterone levels.

32. Management….
–Anovulation
•CLOMIPHENE CITRATE
•GONADOTROPINS
•SURGICAL METHOD
–WEDGE RESECTION
–LAPAROSCOPIC OVARIAN
SURGERY(LOS)

33. Ovarian Wedge Resection
•Bilateral ovarian wedge resection is associated with only
a transient reduction in androstenedione levels and a
prolonged minimal decrease in plasma testosterone .
• In patients with hirsutism and PCOS who had wedge
resection, hair growth was reduced by approximately
16% .
• Although Stein and Leventhal’s original report cited a
pregnancy rate of 85% following wedge resection and
maintenance of ovulatory cycles.
•subsequent reports show lower pregnancy rates and a
concerning incidence of periovarian adhesions Instances
of premature ovarian failure and infertility were
reported.

34. Laparoscopic Electrocautery
•Laparoscopic ovarian electrocautery is
used as an alternative to wedge
resection in patients with severe PCOS
whose condition is resistant to
clomiphene citrate.
•In a recent series, ovarian drilling was
achieved laparoscopically with an
insulated electrocautery needle, using
100-W cutting current to assist entry
and 40-W coagulating current to treat
each microcyst over 2 seconds (8-mm
needle in ovary)

35. LONG TERM EFFECTS
OF PCOS

36. LONG TERM EFFECTS OF
PCOS,
PCOS
CVD
Gout
Obesity
Hirsutism
Infertility
Endometrial
Cancer
Gallbladder
Disease
NIDDM

37. NIDDM
Type II DM or Insulin Resistance (IR)
Women presenting with PCOS,
particularly if:
-they are obese (BMI > 30)
-strong family history of type 2 diabetes or
-they are over the age of 40 years,
are at increased risk of type 2 diabetes
and should be offered a glucose
tolerance test.

38. CVD
It has been suggested that women with PCOS
may have a higher cardiovascular risk than
weight-matched controls with normal ovarian
function.
Increased cardiovascular risk factors such as
obesity, hyperandrogenism, hyperlipidaemia
and hyperinsulinaemia.

39. Their abnormal lipid profiles mainly
consist of raised triglycerides, total
and low-density lipoprotein
cholesterol.
The elevation of risk factors in
young women with PCOS may
therefore put them at higher risk of
developing accelerated
atherosclerosis resulting in
myocardial infarction.

40. ENDOMETRIAL Ca
It has been known for many years
that severe oligo- and amenorrhoea
in the presence of premenopausal
levels of estrogen can lead to
endometrial hyperplasia and
carcinoma.
In women with PCOS intervals
between menstruation of more than
3 months may be associated with
endometrial hyperplasia.

41. Regular induction of a withdrawal
bleed with cyclical gestogens, such
as progestogens, oral contraceptive
pills or the Mirena® intrauterine
system would be advisable in
oligomenorrhoeic women with
PCOS.

42. THANK YOU
FOR
YOUR
ATTENTION