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POLYCYSTIC OVARIAN
SYNDROME
DR LIM IRENE
INTRODUCTION
• 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
hyperandrogenism.
Polycystic Ovarian syndrome
Polycystic Ovarian syndrome
PREVALENCE
• About 5- 10 % of reproductive age
females have clinical or biochemical signs
of anovulation and androgen excess .
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)
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.
ENVIRONMENTAL FACTOR
• 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
Abdominal obesity
Acanthosis Nigericans ( Marker of IR).
• Acanthosis nigricans is traditionally characterized by
hyperpigmented, velvety plaques of body folds.
Polycystic Ovarian syndrome
Polycystic Ovarian syndrome
PCOS WITHOUT IR
• Majority are lean
• 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.
CLINICAL FEATURES OF PCOS
• Ovulatory dysfunction
– Amenorrhea
– Oligomenorrhea
– Irregular uterine bleeding
– Infertility
• Androgen excess
– Hirsutism
– Seborrhea
– Acne
– Alopecia
– Virilization
• Insulin resistance
– Acanthosis nigricans
– Obesity
Polycystic Ovarian syndrome
Polycystic Ovarian syndrome
Polycystic Ovarian syndrome
Polycystic Ovarian syndrome
Polycystic Ovarian syndrome
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).
• In the past (before 2003) :
Necessary Lab Tests or USG
• Now ( after 2003):
Clinical grounds + USG
Lab,only for( IR & DD & Risks ).
Polycystic Ovarian syndrome
• 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
testosterone level)
- Raised in total testosteronereduced
SHBG=doubling free testosterone
Polycystic Ovarian syndrome
Polycystic Ovarian syndrome
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
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.
TREATMENT
• Aimed at relieving symptoms and preventing
adverse long term effects.
• The target symptoms are:
-Infertility
-Hirsutism
-Amenorrhea
• First line treatment- prevention of peripupertal
obesity (50% of PCOS In adolescents are50% of PCOS In adolescents are
obese).obese).
• Life- style modifications:
Diet modification
Weight loss
Exercise
Psychosocial support.
Cessation smoking.
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.
Polycystic Ovarian syndrome
LONG TERM EFFECTS OF
PCOS
LONG TERM EFFECTS OF PCOS
PCOS
CVD
Gout
Obesity
Hirsutism
Infertility
Endometrial
Cancer
Gallbladder
Disease
NIDDM
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.
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.
• 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.
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.
• 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.
THANK YOU
FOR
YOUR ATTENTION

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Polycystic Ovarian syndrome

  • 2. INTRODUCTION • 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 hyperandrogenism.
  • 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.
  • 15. PCOS WITHOUT IR • Majority are lean
  • 16. • 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.
  • 17. CLINICAL FEATURES OF PCOS • Ovulatory dysfunction – Amenorrhea – Oligomenorrhea – Irregular uterine bleeding – Infertility • Androgen excess – Hirsutism – Seborrhea – Acne – Alopecia – Virilization • Insulin resistance – Acanthosis nigricans – Obesity
  • 23. 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).
  • 24. • In the past (before 2003) : Necessary Lab Tests or USG • Now ( after 2003): Clinical grounds + USG Lab,only for( IR & DD & Risks ).
  • 26. • 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 testosterone level) - Raised in total testosteronereduced SHBG=doubling free testosterone
  • 29. 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
  • 30. 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.
  • 31. TREATMENT • Aimed at relieving symptoms and preventing adverse long term effects. • The target symptoms are: -Infertility -Hirsutism -Amenorrhea
  • 32. • First line treatment- prevention of peripupertal obesity (50% of PCOS In adolescents are50% of PCOS In adolescents are obese).obese). • Life- style modifications: Diet modification Weight loss Exercise Psychosocial support. Cessation smoking.
  • 33. 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.
  • 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.