• PCOS could be defined when two of the
three following criteria are present:
1)polycystic ovaries (either 12 or more
peripheral follicles 2-9mm in diameter or
increased ovarian volume > 10 cm3).
2)oligo- or anovulation.
3)clinical and/or biochemical signs of
• About 5- 10 % of reproductive age
females have clinical or biochemical signs
of anovulation and androgen excess .
• No one is quite sure what causes PCOS, and it
is likely to be the result of:
3)Metabolic disorder (IR)
• 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
• Dietary consumption
• Sedentary life style
• Lead to obesity
• BMI > 30
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.
PHENOTYPES OF IR
• PCOS + IR (70 % )
• PCOS without IR
PCOS WITH IR
Acanthosis Nigericans ( Marker of IR).
• Acanthosis nigricans is traditionally characterized by
hyperpigmented, velvety plaques of body folds.
• 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.
• Diagnosis of PCOS can only be made
when other etiologies have been excluded
(thyroid dysfunction, congenital adrenal
androgen-secreting tumours and Cushing
• In the past (before 2003) :
Necessary Lab Tests or USG
• Now ( after 2003):
Clinical grounds + USG
Lab,only for( IR & DD & Risks ).
• A raised luteinising hormone/follicle-stimulating
hormone ratio is no longer a diagnostic criteria
for PCOS owing to its inconsistency.
• Elevated free testosterone level (total
testosterone divided by sex hormone binding
globulin (SHBG) x 100 to give a calculated free
- Raised in total testosteronereduced
SHBG=doubling free testosterone
PCO VS MULTICYSTIC OVARIES
• Polycystic ovaries
– Multiple cysts
– Cyst dia <10 mm
– Stroma increased
• Multicystic ovaries
– Multiple cysts
– Cyst dia > 10 mm
– Stroma not
• Aimed at relieving symptoms and preventing
adverse long term effects.
• The target symptoms are:
• First line treatment- prevention of peripupertal
obesity (50% of PCOS In adolescents are50% of PCOS In adolescents are
• Life- style modifications:
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.
LONG TERM EFFECTS OF PCOS
• 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.
• It has been suggested that women with PCOS
may have a higher cardiovascular risk than
weight-matched controls with normal ovarian
• Increased cardiovascular risk factors such as
obesity, hyperandrogenism, hyperlipidaemia and
• Their abnormal lipid profiles mainly consist of
raised triglycerides, total and low-density
• 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.
• 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
• 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