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Understanding Polycystic Ovarian Syndrome

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0% found this document useful (0 votes)
15 views24 pages

Understanding Polycystic Ovarian Syndrome

Uploaded by

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

Polycystic Ovarian Syndrome

(PCOS)
MBChB yr 6
Introduction
• Polycystic ovary syndrome (PCOS) is the most
common metabolic abnormality reproductive age
women
• One of most common cause of infertility in
women
• A number of genomic variants has been
associated with PCOS
• Non-genetic factors such as nutrition and physical
activity have strong influence on the
development of PCOS
Characteristics
• PCOS characterized by:
• Oligoamenorhoea / amenorrhoea
• Signs androgen excess e.g. acne, hirsutism
• Laboratory criteria of
– Hyperandrogenemia
– Hyperinsulinemia
• Polycystic ovaries on US
Criteria for diagnosis
ROTTERDAM CRITERIA (2003)
• 2 out of 3 of the following
– Polycystic ovaries (>12 peripheral follicles or increased
ovarian volume >10cm3)
– Oligo- or anovulation
– Clinical and/or biochemical signs of hyperandrogenism
– And exclusion of other etiologies such as
hypothyroidism, hyperprolactinemia, congenital
adrenal hyperplasia, cushing syndrome, androgen
secreting tumors
Pathogenesis
• Abnormal Pituitary Function— Altered Negative
Feedback Loop
– Increased GnRH from hypothalamus
– Excessive LH secretion relative to FSH by pituitary
gland
– Ineffective suppression of the LH pulse frequency by
estradiol and progesterone
• LH stimulates excessive androgen production
– Intraovarian androgen excess causes excessive growth
of small ovarian follicles
– Inhibition of follicular maturation
– Thecal and stromal hyperplasia in ovary
Pathogenesis
• Hyperandrogenism causes:
– Reduced sex-hormone-binding globulin (SHBG) resulting in
more free testosterone
– Insulin insensitivity
– Lipid abnormalities
– Abdominal obesity
– Symptoms of androgen excess
• 50-90% patients have elevated serum androgen levels
• Causes hirsutism, acne, male pattern balding, alopecia
• Deepening voice, clitoromegaly
Pathogenesis
• Insulin resistance
– Genetic link
– Mutation of the insulin receptor gene in the peripheral
target tissues, results in hyperinsulinemia
– Favors anovulation, reduced SHBG and androgen excess
– Insulin resistance in PCOS is independent of obesity
– Increased risk for impaired glucose tolerance and type 2
DM in PCOS women
– Obese women with PCOS tend to be more insulin resistant
than normal-weight counterparts
– Linked with metabolic syndrome and abdominal obesity
Presentation
• MENSTRUAL DYSFUNCTION
– Oligo or amenorrhea typically begins in the
peripubertal period
– Reduction in ovulatory events leads to deficient
progesterone secretion
– Chronic estrogen stimulation of the endometrium
with no progesterone results in intermittent
breakthrough bleeding or DUB
– Increased risk for endometrial hyperplasia and/or
endometrial CA
Presentation
• Hirsutism, male type hair growth
– Ferriman Gallaway score >8
• 9 areas(upper lip, chin, chest, back, abdomen, arms,thighs)
• Score 1-4
• 0-absence of terminal hair
• 4-extensive terminal hair growth
• Acne
• Baldness
• Central Obesity
• Acanthosis Nigricans
Investigations
• Hyperandrogenism
– Elevated total testosterone
• Most values in PCOS <150 ng/dl (if >200 ng/dl, consider
ovarian or adrenal tumor)
– LH/FSH ratio
– Levels vary over menstrual cycle, released in
pulsatile fashion, affected by OCPs
– LH/FSH ratio >2 has little diagnostic sensitivity
Lab investigations
• Hyperinsulinemia
– Fasting glucose level of 5.6 to 6.9 mmol/L
– Glucose level of 7.8 mmol/L to 11.0 mmol/L after
75 gm glucose challenge test
– Stimulated testing with OGTT may be more
sensitive than fasting measurements
– Levels above that suggests diabetes
Investigations
• Metabolic Syndrome
– Waist circumference:
• Women>88 cm (>35 in)
– Triglycerides >150 mg/dL
– HDL cholesterol:
• Women<50 mg/dL
– Blood pressure 130/ 85 mm Hg
– Fasting glucose > 5.6 mmol/L

Presence of any 2 of 5 criteria


Investigations
• Ultrasound
– Increased ovarian area (>5.5 cm2) or volume (>11 ml)
with presence of:
– >12 follicles measuring 2-9 mm in diameter
– Thickened sclerotic cortex
– Multiple follicles in peripheral location
– Polycystic ovaries not specific for PCOS
– 80% of women with PCOS have classic cysts
– Approx 20% normal women have incidental polycystic
ovaries
Polycystic ovaries, US
Polycystic ovaries; lapscope
Differential Diagnosis
• 1. Hyperprolactinemia/ hypothyroidism
– Prominent menstrual dysfunction
– mild hyperandrogenism
• 2. Congenital Adrenal Hyperplasia
– morning serum 17-hydroxyprogesterone
concentration greater than 200 ng/dL in the early
follicular phase strongly suggests the diagnosis
Differential Diagnosis
• 3. Ovarian and adrenal tumors
– serum testosterone concentrations > than 150
ng/dL
– adrenal tumors: serum DHEA-S concentrations >
800 mcg/dL
– LOW serum LH concentrations
• 4. Cushing’s syndrome
• 5. Drugs: danazol; OCPs with high
androgenicity
Treatment
• Depends on the main symptom to be addressed
• Acne
• Obesity
• Menstrual abnormality
• Hisrutism
• Long-term issues
– Insulin resistance
– Cardiovascular risk
– Obstructive sleep apnea
– Malignancy risk
Treatment
• Life style modification
• Diet and exercise
– In patients with PCOS who are obese, endocrine
metabolic parameters markedly improve after 4-12
weeks of dietary restriction
– Their SHBG levels rise and free testosterone levels fall
by 2-fold
– Serum insulin and IGF-1 levels also decrease
– Weight loss in patients with PCOS who are obese is
associated with a reduction of hirsutism and a return
of ovulatory cycles in 30% of women
– Target weight loss is 5% or more
Treatment
• Metformin
– Useful particularly in those who are overweight or obese
– Improves many metabolic abnormalities in PCOS and may
improve menstrual cyclicity and the potential for
pregnancy
– Improves insulin resistance and decreases
hyperinsulinemia in patients with PCOS
– Pretreatment with metformin has been shown to enhance
the efficacy of clomiphene for inducing ovulation
– The usual starting dose is 500 mg BD
– Target—1500-1800 mg / day
Treatment
• Combination estrogen-progestin pill first line
when fertility is not desired. MOA:
– Decrease in LH secretion and decrease in androgen
production
– Increase in hepatic production of sex-hormone
binding globulin
– Decreased bioavailablity of testosterone
– Decreased adrenal androgen secretion
– Regular withdrawal bleeds
– Prevention of endometrial hyperplasia
Treatment
• Anti androgens
• Mechanical hair removal
Plucking/shaving/electrolysis/laser
• Long term effects
– Cardiovascular Risk
• Increased prevalence of HTN
• Dyslipidemia (↑ TG, ↓ HDL, ↑ LDL)
• Predisposition to macrovascular disease and
thrombosis
• Multidisciplinary management
Treatment
Long term effects
• Obstructive Sleep Apnea (OSA)
– 30-fold increased risk of OSA, not explained by obesity
alone
– Insulin resistance strongest predictor of OSA (not BMI,
age, testosterone)
• Risk for malignancy
– 3 fold increased risk endometrial carcinoma in PCOS
– Increased risk of ovarian and breast cancer
– Warrants regular screening

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