PCOS: Polycystic Ovarian Syndrome
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Transcript PCOS: Polycystic Ovarian Syndrome
PCOS: Polycystic Ovarian Syndrome
NURS 541: Women’s
Healthcare – Diagnosis
and Management
Objectives
Etiology
Clinical Presentation
Assessment
Diagnosing PCOS
Management
Patient Counseling
Introduction
Classified as a hyperandrogenic disorder
Affects 6-8% of women
Approximately 70% of women with clinical features of
PCOS have the disorder
Etiology
Imbalance of several reproductive hormones
Dehydroepiandrosterone sulfate (DHEA-S)
Dehydroepiandrosterone (DHEA)
Androstenedione
Testosterone
Most testosterone is bound to sex hormone-binding
globulin (SHBG)
The amount of free testosterone dictates the amount of
hyperandrogenic effects that are seen
Etiology
SHBG levels (and therefore the amount of testosterone
binding) are influenced by hormonal changes
Estrogen and thyroid hormone INCREASE levels
Androgens and insulin DECREASE levels
SHBG
free testosterone
effects
Testosterone converted into dihydrotestosterone (DHT) by
5α reductase (enzyme)
DHT responsible for androgenic symptoms
Etiology
Women with PCOS have more steady levels of
gonadotropins and sex hormones than women without
PCOS
Gonadotropin-releasing hormone (GnRH), and therefore
luteinizing hormone (LH) pulse frequently versus with the
menstrual cycle
Increased level of LH => decreased follicle-stimulating
hormone (FSH)
Decreased ovulation
Etiology
Typical cyclical LH surge
(below) compared to the
frequent LH surges seen in
PCOS (left)
Etiology
Determining the cause of the increased androgen production is
key to individualized treatment
Is it an issue of excess insulin?
Is it an issue of decreased thyroid hormone?
Is there too little estrogen?
Is there too much DHEA/DHEA-S/androstenedione?
Clinical Presentation
Clinical Presentation
Signs
Associated conditions
Hirsutism
Obesity
Alopecia
Infertility
Acne
Insulin resistance
Menstrual irregularities
Dyslipidemia
Polycystic ovaries
Metabolic syndrome
Virilization
Psychological effects
Cancer risks
Signs/Symptoms
Hirsutism
Excessive hair growth in most androgenic-sensitive areas
(face, chin, upper lip, areolae, lower abdomen, inner thighs,
perineum)
Alopecia
Androgen-related hair loss, usually frontal/crown region
Acne
Enlargement of sebaceous glands, sebum
Signs/Symptoms
Menstrual Irregularities
Irregular menses, anovulatory cycles
Possible heavy menses due to persistent endometrial
stimulation, endometrial hyperplasia
If normal cycles, may be still anovulatory – lack of
premenstrual symptoms indication
Polycystic ovaries
As a result of chronic anovulation
One or more ovaries with 12+ enlarged follicles and/or
enlarged ovarian volume over 10mL (2003 ESHRE/ASRM
consensus)
Signs/Symptoms
Virilization
Cluster of symptoms including clitoral hypertrophy, severe
hirsutism, deepening of the voice, increased muscle mass,
breast atrophy, and male pattern baldness
If rapidly progressing, may indicate less common cause of
hyperandrogenism
Ovarian or adrenal tumor
Congenital adrenal hyperplasia
Hyperthecosis
Associated conditions
Obesity
Approximately ½ of all women with PCOS are obese
Insulin resistance
Affects 50-70% of women with PCOS
Instrumental in hormonal changes associated with
hyperandrogenism
Increases risk for Type 2 Diabetes and glucose intolerance
Dyslipidemia
70% of women with PCOS have at least 1 elevated lipid level
Associated conditions
Metabolic syndrome
Cluster of conditions – obesity, insulin resistance,
dyslipidemia
Increases risk for CV disease and diabetes
Diagnostic criteria - 3 or more of the following:
Waist circumference ≥ 35 inches
Triglycerides ≥ 150mg/dL
HDL cholesterol ≤ 50 mg/dL
Systolic BP ≥ 130 mmHg and/or diastolic BP ≥ 85 mmHg
Fasting glucose ≥ 100 mg/dL
Associated conditions
Infertility
Related to anovulation
More than ½ of women with PCOS are fertile, although may
take longer to conceive
Psychological effects
Higher rates of depression, anxiety, binge eating higher for
women with PCOS
Cancer risks
3-fold increased risk of endometrial cancer
2-fold increased risk of ovarian cancer
Differential Diagnosis
Differential Diagnosis
PCOS (80%)
Nonclassical congenital adrenal hyperplasia (2%)
Hyperandrogenism, insulin resistance, and acanthosis nigricans
(HAIR-AN) syndrome (4%)
Androgen-producing tumors (rare) – ovarian or adrenal
Idiopathic hirsutism (5%)
Thyroid disorders, androgenic medication, pregnancy,
hyperprolactinemia, Cushing syndrome
Assessment
Assessment
History
Thorough menstrual history (menarche, menstrual pattern,
flow, symptoms)
Pregnancy history (ability to conceive, time to conception)
Symptoms/associated conditions of PCOS, including onset
and severity – rapid vs slow onset
Medication history
Family history of associated conditions
Assessment
Physical Exam
Anthropometric measurements – height, weight, BMI, waist
circumference
Blood pressure
Skin examination – look for hirsutism, acne, alopecia
Acanthosis nigricans often seen with insulin resistance
Thyroid exam
Breast exam
Pelvic exam – assess for uterine/ovarian masses
Assessment
Laboratory testing
Mixed evidence re: appropriate testing
Testing should reflect findings in history/exam
Hyperandrogenism and ovulatory dysfunction
TSH, prolactin, fasting lipid profile, 2hr OGTT (ACOG, AEPCOS, 2009)
Hyperandrogenism and regular menstrual cycles
Above, PLUS serum progesterone on day 20-24 of cycle
Less than 3-4 ng/mL = oligo-ovulatory cycle
Assessment
Laboratory testing (continued)
Testosterone testing – mixed evidence as to usefulness
If tumor suspected, total testosterone recommended, and
refer if > 150 ng/dL (100 ng/dL if menopausal)
17-OHP (hydroxyprogesterone)
If congenital adrenal hyperplasia is suspected
Imaging/Procedures
Pelvic ultrasonography
To identify ovarian cysts and endometrial hyperplasia
Endometrial biopsy – chronic anovulation
Diagnosing PCOS
Differential Diagnosis
PCOS (80%)
Nonclassical congenital adrenal hyperplasia (2%)
Hyperandrogenism, insulin resistance, and acanthosis nigricans
(HAIR-AN) syndrome (4%)
Androgen-producing tumors (rare) – ovarian or adrenal
Idiopathic hirsutism (5%)
Thyroid disorders, androgenic medication, pregnancy,
hyperprolactinemia, Cushing syndrome
Diagnosing PCOS
Two established criteria:
Rotterdam PCOS Consensus Group (2004)
Two of three of the following:
Oligo- or anovulation
Clinical and/or biochemical signs of hyperandrogenism
Polycystic ovaries
Androgen Excess and Polycystic Ovary Syndrome Society
Hyperandrogenism: hirsutism and/or hyperandrogenemia
Ovarian dysfunction: oligo-anovulation and/or polycystic ovaries
Exclusion of other androgen excess or related disorders
Management
Management
Non-pharmacologic modalities
Lifestyle modification – diet, nutrition, exercise
Mechanical hair removal
Management
Pharmacologic modalities
Combined hormonal contraceptives
Progestin with a non- or low androgenic potential preferred
Desogestrel, norgestimate, drospirenone
Signs/symptoms may be reduced/resolve within 2-12 months
Help protect against endometrial hyperplasia with monthly
withdrawal bleeds
Management
Pharmacologic modalities
Progestogens
To prevent endometrial hyperplasia and cancer
LNG-IUS, progestin-only pills, DMPA, implant
Medroxyprogesterone acetate 5-10mg or 200mg micronized
progesterone first 14 days of each month
Anti-androgens
For refractory hirsutism or alopecia
May be teratogenic so need effective contraception
Management
Pharmacologic management (continued)
Insulin sensitizing agents
Metformin – if impaired glucose tolerance, inability to lose
weight with diet and exercise or with those at normal weight
Not recommended for treatment of PCOS symptoms
Also helpful for those with infertility
Topical agent
Eflornithine HCl 13.9% (Vaniqa) – to treat hirsutism
When to Refer
If diagnosis other than PCOS
If initial treatment not successful
Women with infertility issues (not successful with
metformin)
If metabolic syndrome present
Patient Counseling
Follow up is necessary due to long-term risks of PCOS
Weight management, nutrition, exercise
Screening and management of BP, lipids, diabetes
Management of menstrual cycle, withdrawal bleeds
Support, encouragement, woman-centered care
Questions?