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Understanding Polycystic Ovary Syndrome

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0% found this document useful (0 votes)
15 views26 pages

Understanding Polycystic Ovary Syndrome

Uploaded by

Zainab Sayyed
Copyright
© All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd

POLYCYSTIC OVARY SYNDROME

LALI PKHALADZE, MD, Ph.D.

TSU
Zhordania and Khomasuridze Institute of
Reproductology
Prevalence
 Polycystic Ovary Syndrome (PCOS) - a common disorder in
reproductological, gynecological, and endocrinological
practice.
 The prevalence varies by ethnicity: 6 - 29 %.
 PCOS - national disease of georgian women!
Etiology
Multifactorial disease:
 Genetic predisposition;
 Intrauterine factors;
 Environmental factors.
Stein IF, Leventhal ML.
Amenorrhea associated with bilateral polycystic ovaries.
Am J Obstet Gynecol 1935; 29: 181-910

7 women with variety of clinical symptoms (obesity, hirsutism,acne,


amenorrhea) were associated with enlarged bilateral polycystic ovaries)
PCOS

STEIN- LEVENTHAL SYNDROME


POLYCYSTIC OVARIAN DESEASE
SCLEROCYSTOSIS OF OVARIES
POLYCYSTIC OVARIES
(ICD10 – E28.1)
Clinical Manifestations
 Hirsutism, acne, seborhea;
 Menstrual disturbances - oligomenorrhea, amenorrhea,

abnormal uterine bleeding;


 Excessive weight, obesity;

 Depression, anxiety;

 Infertility;

 Pregnancy complications: miscarriage, gestational diabetes,

pregnancy hypertension, premature birth;


 Long term health consequences: metabolic syndrome, type 2

diabetes, CVD, dyslipidemia, endometrial


hyperplasia/carcinoma.
Share of PCOS in women with
different conditions

During oligomenorrhea/amenorrhea – 85%


Among women with hirsutism-70-95% A
Cases of anovulatory infertility– 80%
Rotterdam diagnostic
criteria (ESHRE/ASRAM) 2003

 Oligo-anovulation(OD)
 Hyperandrogenism(HA)
 Polycystic Ovarian Morphology
(PCOM)

(requres the presence of 2 out of 3 varibles)


Exclusion criteria

 Hyperprolactinemia;
 Thyroid dysfunction;
 Congenital Adrenal Hyperplasia;
 Acromegaly, Cushing’s syndrome.
Pathogenesis
The increase of ovarian androgen production is a
fundamental characteristic of PCOS
 Genetically determined dysregulation of enzyme
cytochrome P450C17;
 local ovarian factors- Increase in Inhibin, Activin,
IGF1;
 Imbalances between proliferation and apoptosis of
cells;
 Insulin resistance with compensatory
hyperinsulinemia(defect on insulin receptor).
PATHOPHYSIOLOGY
Ovarian folliculogenesis
dysfunction

[Link] follicular growth,

[Link] within the excessive cohort


of the emergence of dominant
follicle-“ follicular arrest “,

3. Multiple follicules in ovaries.


CARBOHYDRATE METABOLISM

 Insulin resistance – 50-75% Arched and Thiers, 1821


“Bearded Diabetic Women”

 Glucose intolerance – 35%


 Type 2 diabetes – 7-10%
 Metabolic syndrome– 40-45%O
 Obesity – 35-60%
Production of ovarian androgens due to
hyperinsulinemia

Hyperinsulinemia

LH IGF-IBP

+ IGF-I
INS
rec
SHBG
IGF-I rec

LH rec P450
inositolo +
Free testosterone

androgeni

ANDROGENS
CLINICAL MANIFESTATIONS OF PCOS

REPRODUCTIVE PPREMENOPAUSE/
ADOLESCENCE
PERIOD POSTMENOPAUSE

• Irregular • Infertility METABOLIC


menses(oligo/amen • Pregnancy loss SYNDROME
orrhoea, • Type 2 diabetes
anovulation, + • Gestational
diabetes mellitus
+ • Ischaemic heart
disfunctional disease, arterial
• Hypertension of hypertension
uterine bleeding
• Cosmetic pregnant women • Dyslipidaemia
problems- • Endometrial
hirsutism, alopecia, hyperplasia,
acne carcinoma

Excess of weight /obesity


visceral distribution of fat, acanthosis nigricans,’’ climacteris hump’’
PCOS
Diagnostical and laboratory test

* Anamnesis
* Objective data – preasence of hirsutism, acne ,
seborrhea, allopecia, acanthothis nigricans,BMI, fat
distribution
* Gynecological examination
* Body basal temperature
* Biochemical markers (TSH, PRL, 17OHP, FSH, LH,
T, F T, DHEA-S, A4, SHBG, IRI,Glucose,lipids)

*USS
PCOS
Biochemical markers of hyperandrogenism
l line investigations

• Total testosterone (TT)


• Sex hormone binding globulin (SHBG)
• Free androgen index ( FAI )
• Free testosterone (FT)

II line investigatioins

• Androsterone ( A4 )
• Dehydroepiandrosterone- sulfate (DHEA-S)
• LH, FSH, LH/FSH ratio
• Antimiulerian hormone (AMH)
PCOS
Investigation related to metabolic abnormalities

 Glucosa (fasting)
 Insuline(basal)
 Index of insulinresistancy

HOMA index = insuline(basal) X glucose (fasting)


22,5

> 2,5 (insulinresistance)


PCOS
ON ULTRASOUND SCAN

• Preasence of 12 or more antral follicles in each


ovaries on different stage of maturation sized 2-5 mm
• Ovarian volume >10 mL (bylateral or unilateral enlarged
(2-6 fold) ovaries)
• The thikness of capsule is increased more than 10 fold
PCOS
METABOLIC SCREEN

* Glucose intolerance: glucose- 7,8-11 mmol/l after gucose


tolerance test
* Type 2 diabete: fasting glucose- ≥ 7,0 mmol/l or after 2 h
75 g glucose challenge- 11,1 mmol/l
PCOS
INCREASED RISK FOR METABOLIC
SYNDROME

• DYSLIPIDEMIA– LDL HDL TRG 

• GLUCOSE  5,6 mmol/l

• TRG  1,7 mmol/l

• HDL < 1,29 mmol/l


Management
The options should be focus on the main
concern of women

 Nonpharmacological: healthy life style with


hypocaloric diet and phisical activity;
 Pharmacological: COC, insulin sensitizers,
antiandrogens, antiestrogens for ovulation
induction;

Gibson-Helm et al. 2018; Teede et al. 2018; Domecq et al. 2013Martin et al. 2008.
For women who do not seek conceive
 Lifestyle modification -dietition, exercise(Cornstone in an
overweight women. Weight loss in 5% can improve
symptoms);
 Combine Oral Contraceptives (Combined oral contraceptives)-
reduces serum androgen levels by increasing SHBG levels,
providing regular monthly withdrowal bleed and beneficial
anti- androgenic effects;
 Progestins (Medroxsyprogesterone acetate);
 Insulinsensitaizers (Metformin);
 Antiandrogenes – spironolactone, flutamid, finasteride(can be
used to help with acne and hirsutism- take 6-9 month to
improve hear growth, avoid pregnancy- feminize a male
fetus);
 Cosmetic (depilatory cream, eleqtroepilation, eleqtrolizis,
lazerovaporization, fotoepilation).
Subfertility
• Weight loss alone may achieve
spontaneous ovulation;
• Ovulation induction with antiesrogens
or gonadotropins;
• Laparascopic ovarian diathermy;
• IVF if ovulation cannot be achieved or
does not succseed in pregnancy;
• Women with PCOS who undergo IVF
are at increased risk of ovarian
hyprtstimulation syndrome.
Management of infertility in women with PCOS
I line
optionNE
Farmacologic
Nonfarmacological al
Lifestyle Letrozol or
Clomifen Metformine
modification-
citrate (BMI≥30)
healty diet,
( BMI≤25)
Dexametazone +Clomifen
exercise
citrate
(in cases of combined forms
of PCOS)
II line option
Clomifen
citrate+ laparasc Bariatric Inhibitor
Metformi Gonad opy- surgery(BMI≥ s of
Metform ne otropi ovarian 30, 6 Month aromataz
in (BMI≤30) of uneffective
(BMI≥30
ns drilling
treatment )
e
)
III line option

Alternative methods of treatment- IVF


PSYCHOLOGICAL ISSUE
• Difficult to manage PCOS
patients;
• Patients requre additional
motivation;
• Symptoms can be distressing
and result in low self- esteem;
• Patients should be manage
sensitively, adopt a holistoc
approach incorporating all
members of the

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