Polycystic Ovarian Syndrome Flashcards
PCOS information
Most common endocrinopathy in reproductive-aged women (12-45)
- most common cause of sub fertility, secondary amenorrhea and hirtuism
Affects 5-10% of women in the US and affects all races
Clinical features of PCOS
For younger than 20 = need all three in Rotterdam criteria
For adults = need only two for Rotterdam criteria
1) polycystic ovarian morphology on imaging
- usually > 12 follicles in ovary measuring 2-9mm in diameter. Looks like a “string of pearls”
- stems from arrestment of primary follicles
2) Ovulatory dysfunction
- amenorrhea (absence of menses >3 months)
- oligomenorrhea (cycle length >35 days or less than <10 a year)
- infertility
3) hyperandrogenism
- hirtuism
- inflammatory acne
- androgenic alopecia
- *while not 100% linked, most patients do show metabolic defects**
- insulin resistance
- overweight/obesity
- hyperinsulinemia
Pathophysiology of PCOS
90% of patients have intrinsic genetic defect in thecal cell androgen production
The excess androgens causes granulosa cell dysfunctions which impedes follicle maturity (negative feedback FSH in pituitary)
- leads to anovulation and multiple immature follicles in the ovary which turn into cysts
Ovulatory dysfunction
Anovulation results in amenorrhea due to lack of progesterone production from corpus luteum
This usually begins with menarche and persists throughout
Also estrogen over function induces endometrial hyperplasia which causes a instability of the thickening endometrium and leads to spotting/ unpredictable bleeding
- also high risk of endometrial cancer due to unopposed estrogen
PCOS is the most common cause of ovulatory dysfunction in reproductive aged women
Pregnancy complications
30-50% risk of early miscarriage
2-3x higher risk of
- gestational diabetes
- pregnancy-induced HTN
- preterm birth
- perinatal mortality
Increased risk of multiple pregnancies and morbidities due to fertility drugs
Hyperandrogenism
Excess androgen levels in females
Most common clinical manifestations are:
- hirtuism (60-75%) (PCOS is most common cause of this in women)
- Acne (15-25%)
- androgenic alopecia (5%)
Biochemical findings
- elevated total and free testosterone, androstenedione or DHEAS
Hirsutism DDX
PCOS (70-82%)
Idiopathic hyperandrogenemia (6-15%) - normal menstral cycle and fertility, just excess androgens
Adrenal hyperplasia (2-4%)
Androgen secreting tumor (0.2%)
Medications (iatrogenic hirtuism)
Hypertrichosis
Increased production of lanugo (soft, lightly pigmented hair)
- NOT associated with elevated androgens and no male pattern associated
need to rule this out from hirtuism although usually the hair differences clue you in
Causes
- congenital
- medications
- thyroid dysfunction
- anorexia nervosa
- malignancy
- porphyria
Acne
Frequent finding in adolescents and is common in PCOS
- is associated with androgen levels if severe and/or unresponsive to treatment
inflammatory refractive, persistent with age, late onset or being present in conjunction with other hyperandrogenism signs = PCOS work up
Androgenic alopecia
First a sign can be thinning or hair in temporal region typically in a “crown-like” shape
- usually rare for receding hair line but can show this still
Is caused by excess 5a-reductase converting testosterone -> DHT
Must exclude
- thyroid diseases
- anemia
- other chronic illnesses
Insulin resistance in PCOS
Manifestation is relative to severity of BMI
- PCOS patients with normal BMI can still have IR though
Causes compensatory hyperinsulinemia which causes
- increased GnRH pulse frequency
- decreases synthesis of SHBG and IGFBP-1 proteins = more circulating free androgens and estrogens and IGF-1
- the IGF free causes both IR over time and increased production of androgens from theca cells
Acanthosis nigricans
Cutaneous marker of insulin resistance
- is seen in 50% of obese women with PCOS (10% of non-obese women also show this)
Other metabolic defects of PCOS
metabolic syndrome is most likely
4x increased risk with T2DM
NFLAD
Sleep apnea
Dyslipidemia
CVD
Mood disorders
HTN
General work up for PCOS
PE and history
- calculate BMI
- use Gallwey score to determine hair growth and distribution
- check for signs of virilization
- abdomen exam = palpate for masses in lower areas
- breast exam and pelvic exam/i manual exam = galactorrhea, clitoromegaly and adnexal enlargement
- skin = acne and acanthosis nigricans
Laboratories
- perform pregnancy test (this is always first)
- free testosterone (more sensitive since this is the level to care about ) or total testosterone (less sensitive since it includes bound androgens)
- DHEAS testosterone level and androstenedione levels (determines if androgens are producing more from adrenal glands or ovaries respectively)
- measure SHBG levels (should be low)
- measure LH/FSH (LH:FSH should be >2)
- measure TSH, prolactin and 17-hydroxyprogesterone to rule out pregnancy
- thyroid antibodies (hashimotos)
Secondary screening for metabolic symptoms
- check BP and perform lipid panel (at every visit)
- do a 2-hr OGTT (screen regardless of BMI!!)
- check for OSA in overweight patients
- depression screening
Look for “ruling out symptoms” of PCOS (these symptoms DONT appear with PCOS usually)
- low body weight, eating disorder, excessive exercise
- hot flashes and urogential symptoms
- severe virilization
- cushings syndrome symptoms
- acromegaly signs
Clinical management of PCOS
Treat for:
- infertility
- regulating menses
- controlling hyperandrogenism features
Metabolic symptoms should be addressed in every patient
Treatments
- if pregnancy is NOT desired = OCPs are #1
- if pregnancy IS desired = clomphene + metformin
- if insulin resistance is present = metformin
- with acne: wants to conceive = topical creams; DOESNT want to conceive = OCPs
