PCOS Flashcards
Clinical presentation
Hyperandrogenism: Hirsutism, Acne, Alopecia
Menstrual disturbances: amenorrhea, oligomenorrhea, anovulation
Overweight or obese
Pathophysiology
Primary defect is unknown
- inappropriate gonadotropin secretion
- insulin resistance with hyperinsulinemia
- Excessive androgen production
Inappropriate gonadotropin secretion
- increase in GnRH
- Cause increase in LH surge too soon
- No rise in FSH
- No dominant follicle
- No ovulation
- Unopposed estrogen
- Luteal phase never happens
- Elevated levels of androgen
Regular Menstrual cycle vs. PCOS Cycle
Normal: normal GnRH level
LH and FSH levels spike during the cycle
One dominant follicle form
PCOS: Increase in GnRH
High LH level in baseline
FSH levels stay normal
No dominant follicle form
Insulin resistance
occurs in obese and non-obese women
potential defects in insulin receptor
In ovary: Insulin +/- LH increase androgens
Excess Androgen production
normally produced in ovary to facilitate follicular growth
Hypersecretion of LH and insulin leads to increase androgen production
-abnormal sex steroid synthesis
-hyperandrogenism
-hyperandrogenemia
increase in free testosterone concentrations
PCOS Diagnosis criteria
- Hyperandrogenism
- Chronic anovulation
- Polycystic ovaries
2 of the 3 must be present
Complications from PCOS
Infertility
CV
VTE
Type 2 diabetes
Dyslipidemia
Hypertension
Non-alcoholic fatty liver disease
Endometrial hyperplasia and cancer
Depression and anxiety
Obstructive sleep apnea
Pregnancy complications
Treatment decision considerations
- patient priorities
- efficacy vs. risks of treatment
- desire to become pregnant
NON PHARM TREATMENT
WEIGHT LOSS–> 5-15% (or more)
-improved pregnancy rates/reduce miscarriages
-improve ovarian function
-reduce free testosterone
-reduce hyperinsulinemia
EXERCISE
-30 minutes of moderate-vigorous physical activity daily
-reduce blood pressure and insulin levels
PHARMACOLOGIC TREATMENT
1ST LINE: COC
Estrogen component: lowest effective dose (20 mcg-30 mcg EE)
20 mcg EE for high risk VTE (obese or >39
< 35 mcg EE
LH suppression decrease androgen production
Progestin component: prefer low androgenic effects: norgestimate, norethindrone LOWER VTE RISK
NO COC HAS PROVEN SUPERIORITY FOR CLINICAL HYPERANDROGENISM
MONOPHASIC COC COMMON
Pharmacologic Treatment anti-androgen therapy
Spironolactone
50-100 mg BID
Blocks androgenic effects at follicle
Adverse effects: vaginal bleeding, beast tenderness, headache, dizziness
Takes 6-9 months to work
Used as an add on therapy
5 alpha reductase inhibitor
prevent conversion of testosterone to DHT
when COC and spironolactone are relatively ineffective for severe hirsutism
Finasteride 2.5-5 mg daily
headache, orthostasis
MUST use reliable forms of contraception
Insulin sensitizer
Metformin is 1st line of treatment in PCOS with type 2 diabetes and failed lifestyle modifications
2nd line: reduces insulin concentration and androgen production in ovary
500 mg PO DAILY or 100 mg BID
Up to 6 months to see results
GI side effects decrease after 2-3 weeks, taken with meal
Consider d/c if pregnant
No endometrial protection until regular menses and ovulation is reached
Treatment: insulin resistance
- Lifestyle modifications
- Metformin