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Case Discussion

Genevie Ramos Ombao February 28, 2012

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MR, 21 yo SNG
cc: irregular menses

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History of Present Illness

Menarche at 11 years old (10 years PTC)
Regular menstrual cycles every 28-30 days, 3 days duration,

consuming 4 pads per day, fully-soaked

13 years old (8 years PTC)

Started having irregular menses, going as long as 6 months in

between menses no consult was done or medications taken as she thought it was normal

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History of Present Illness

Patient continued to have irregular menstrual cycles , still no

consult done until

2010 (2 years PTC)

Consulted a local OBGYN for her complaint Pelvic ultrasound was done which allegedly showed an ovarian

cyst in the left

Patient was advised observation

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History of Present Illness

Sought a 2nd opinion where TRS done allegedly still showed left

ovarian cyst
Patient was then given Lady pills which she took for 8 months

affording relief of irregular menses

Aug 2011: stopped taking the pills
Patient since has had no menses; pregnancy test done at home

was negative

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No hypertension, heart disease, thyroid disease, or

lung disease
(-) allergies No previous operations

Past Medical History

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Non-smoker Alcoholic beverage non-drinker

Personal and Social History

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No hypertension, diabetes, bronchial asthma,

thyroid disease

Family History

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Menstrual History
Menarche: 11 years old, regular; every 28-30 days,

lasts for 3 days, 4 pads per day, (-) pain

Subsequent Menses: irregular, lasts for 3 days, 4

pads per day, (-) pain

LMP: September 2011
PMP: August 2011

Menstrual History

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Single, nulligravid

OB History

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Contraception History
OCP use x 8 months

NO Pap smear

Gynecologic History

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General: no weight loss or gain, anorexia, fever Skin: no skin changes Eyes: no blurring of vision, redness, itchiness, discharge, pain Nose: No discharge, epistaxis, anosmia Mouth & Throat: No bleeding, circumoral cyanosis, hoarseness,

soreness, difficulty of swallowing

Pulmonary: no cough (-) hemoptysis, chest wall abnormalities

Review of Systems

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Heart: No palpitations, chest pain, chest heaviness Gastrointestinal: no changes in bowel habits Genitourinary: no hematuria, frequency, urgency, flank pain Vascular: no excessive bleeding, easy bruisability Neurologic: no headaches, no seizure episodes, weakness or numbness Endocrinologic : no tremors, no polyuira, no polydipsia , no polyphagia , no excessive growth of facial hair or baldness

Review of Systems

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BP: 120/80; Pulse rate: 81/minute, regular; Respiratory rate:

21/minute, regular; Temperature: 36.9 C; Weight: 71 kg; Height: 152 cm; BMI = 30 kg/m2
Moist skin, no active dermatosis

No facial involuntary movement, edema, masses

Pink palpebral conjunctivae, anicteric sclerae, patent external

auditory canal, non-congested turbinates, no nasal discharge, supple neck, no lymphadenopathies, no palpable anterior neck mass
Symmetrical chest expansions, clear breath sounds in all lung fields,

no retractions

Physical Examination

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Adynamic precordium, normal rate, regular rhythm,

S1>S2 apex, S2>S1 base, PMI at 5th LICS, no murmurs

Pulses full and equal Conscious, coherent, oriented to 3 spheres No sensorimotor deficits Deep tendon reflexes of upper and lower extremities: ++

Physical Examination

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Abdominal Exam
Abdomen globular, soft, non-tender, no palpable


Physical Examination

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21 SNG irregular menses since 13 y/o Menarche at 11 with regular menses for 2 years

BMI = 30 kg/m2

Salient Features

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Polycystic Ovarian Syndrome (PCOS)

endocrinopathy typified by oligo-ovulation or anovulation, signs of androgen excess, and multiple small ovarian cysts approximately 4 to 12 percent

most common endocrine disorder of reproductive-aged women and affects

PCOS Page 18

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Ovarian Hyperthecosis

condition characterized by nests of luteinized theca cells distributed throughout the ovarian stroma deepening of the voice

frank virilization signs such as clitoromegaly, temporal balding, and

HAIRAN Syndrome
hyperandrogenic-insulin resistant-acanthosis nigricans
may represent either a variant of PCOS or a distinct genetic syndrome

PCOS Page 19

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The underlying cause of PCOS is unknown

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PCOS : Etiology


increased prevalence has been noted between affected individuals and

their sisters (32 to 66 percent) and mothers (24 to 52 percent)

studies of human ovarian theca cells have suggested dysregulation of the

CYP11a gene

encodes the cholesterol side-chain cleavage enzyme, the enzyme that performs the ratelimiting step in steroid biosynthesis

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PCOS : Pathophysiology

gonadotropin secretion
LH > FSH Increased levels

of LH in more than 50% of patients

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PCOS : Pathophysiology

gonadotropin secretion
LH > FSH Increased levels

of LH in more than 50% of patients

PCOS Page 23

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PCOS : Pathophysiology
Insulin resistance
appears to be due

to a postbinding abnormality in insulin receptor-mediated signal transduction Long-term effects:

1. 2. 3.

Diabetes mellitus Cardiovascular disease Endometrial cancer

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PCOS : Pathophysiology

androgen levels
insulin and LH

stimulate ovarian theca cell androgen production

Elevated free

testosterone 7080%; Elevated DHEAS 25-65%

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PCOS : Pathophysiology

Produced in the

liver and binds to sex steroids

Supressed by

insulin and androgens


testosterone levels
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PCOS : Pathophysiology
Mechanism is


Hypersecretion of LH Insulin-resistence

PCOS Page 27

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Menstrual Dysfunction
Oligo- and amenorrhea
Chronic estrogen exposure

unopposed by the effects of postovulatory progesterone

Unstable thickened

endometrium unpredictable bleeding pattern

Irregular menstrual cycles

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typically manifested

clinically by hirsutism, acne, and/or androgenic alopecia

Different from virilization (

increased muscle mass, deepening of voice, clitoromegaly) !!!

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both lean and obese women

with PCOS have increased rates of insulin resistance and type 2 diabetes mellitus (DM) compared with weightmatched controls without PCOS (Dunaif, 1989, 1992).

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Women with PCOS are more

likely to be obese, as reflected by an elevated body mass index (BMI) and waist:hip ratio (Talbott, 1995).
Apple shaped android or

central type of obesity

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Metabolic Syndrome and Cardiovascular Disease

characterized by insulin

resistance, obesity, atherogenic dyslipidemia, and hypertension

reported to be approximately

45 percent in women with PCOS compared with 4 percent in age-adjusted controls (Dokras, 2005).

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Endometrial Neoplasia
threefold increased risk of

endometrial cancer has been reported

long-term risks of chronic

anovulation, and neoplastic changes in the endometrium are felt to arise from chronic unopposed estrogen (Coulam, 1983).

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Infertility and Pregnancy Loss

results from anovulatory

Women with PCOS who

become pregnant are known to experience an increased rate (30 to 50 percent) of early miscarriage

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Other Pregnancy Complications

Women with PCOS have

a two- to threefold higher risk of gestational diabetes, pregnancyinduced hypertension, preterm birth, and perinatal mortality, unrelated to multifetal gestations

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Polycystic ovarian syndrome is often referred to as a diagnosis of exclusion

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PCOS-mimickers: Thyroid Disease

also can manifest with

menstrual dysfunction and obesity

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Histologically a polycystic ovary

(PCO) displays increases in volume, number of ripening and atretic follicles, cortical stromal thickness, and number of hilar cell nests
Sonographic criteria for

polycystic ovaries from the 2003 Rotterdam conference include 12 small cysts (2 to 9 mm in diameter) or an increased ovarian volume (>10 mL) or both
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Insulin Resistance
Although the consensus meeting

in Rotterdam suggested that tests of insulin resistance are not required to diagnose or treat PCOS, these tests are often used to evaluate glucose metabolism and impaired insulin secretion in these women

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The choice of treatment for each symptom of PCOS depends on a woman's goals and the severity of endocrine dysfunction.

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PCOS patients with fairly regular cycle intervals (8 to 12

menses per year) and mild hyperandrogenism may choose not to be treated

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Weight Loss
lifestyle changes focused on diet and exercise are

paramount to treatment at each stage of life

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Combination Oral Contraceptive Pills

first-line treatment

for menstrual irregularities

induce regular

menstrual cycles.
Decrease androgen

levels , increase SHBG levels

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Combination Oral Contraceptive Pills

How to?
if a woman's last menses was more

than 4 weeks prior, do a pregnancy test!

If negative, progesterone is given to produce a withdrawal bleed prior to COC initiation.

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Combination Oral Contraceptive Pills

How to?
Typical regimens include:

medroxyprogesterone acetate (MPA) (Provera, Pfizer, New York, NY), 10 mg orally daily for 10 days; MPA, 10 mg orally twice daily for 5 days; or micronized progesterone (Prometrium, Solvay Pharmaceuticals, Marietta, GA), 200 mg orally daily for 10 days.
Lady Pills : Levonorgestrel 150

mcg, ethinyl estradiol 30 mcg

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Insulin-Sensitizing Agents
improves peripheral insulin sensitivity

by reducing hepatic glucose production and increasing target tissue sensitivity to insulin
decreases androgens in both lean and

obese women, leading to increased rates of spontaneous ovulation

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PCOS is a chronic condition. There is no cure. Thus, management options are targeted at alleviating the signs and symptoms to reduce morbidity. Another goal of treatment is to prevent the development of complications
- BMJ, 2011

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PCOS Prognosis
therapy is generally continued throughout the

reproductive years. If treatments are stopped during that time, symptoms generally recur
Once a woman with PCOS reaches

menopause, hyperandrogenic manifestations may improve as ovarian function declines, allowing withdrawal of therapies directed against hyperandrogenism
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Patients should be evaluated every 3 months for

treatment response and development of any adverse effects. Once stable, monitoring is every 6 months.
Combination therapy may be required to achieve results

in ameliorating hyperandrogenism.

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Thank you

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