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MR, 21 yo SNG
cc: irregular menses
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between menses no consult was done or medications taken as she thought it was normal
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ovarian cyst
Patient was then given Lady pills which she took for 8 months
was negative
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lung disease
(-) allergies No previous operations
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thyroid disease
Family History
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Menstrual History
Menarche: 11 years old, regular; every 28-30 days,
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,
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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21/minute, regular; Temperature: 36.9 C; Weight: 71 kg; Height: 152 cm; BMI = 30 kg/m2
Moist skin, no active dermatosis
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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Physical Examination
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Abdominal Exam
Abdomen globular, soft, non-tender, no palpable
masses
Physical Examination
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SUBJECTIVE
21 SNG irregular menses since 13 y/o Menarche at 11 with regular menses for 2 years
OBJECTIVE
BMI = 30 kg/m2
Salient Features
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endocrinopathy typified by oligo-ovulation or anovulation, signs of androgen excess, and multiple small ovarian cysts approximately 4 to 12 percent
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
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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PCOS Page 20
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PCOS : Etiology
multifactorial
CYP11a gene
encodes the cholesterol side-chain cleavage enzyme, the enzyme that performs the ratelimiting step in steroid biosynthesis
PCOS Page 21
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PCOS : Pathophysiology
Inappropriate
gonadotropin secretion
LH > FSH Increased levels
PCOS Page 22
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PCOS : Pathophysiology
Inappropriate
gonadotropin secretion
LH > FSH Increased levels
PCOS Page 23
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PCOS : Pathophysiology
Insulin resistance
Hyperinsulinemia
appears to be due
1. 2. 3.
PCOS Page 24
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PCOS : Pathophysiology
Increased
androgen levels
insulin and LH
PCOS Page 25
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PCOS : Pathophysiology
Decreased
SHBG
Produced in the
testosterone levels
PCOS Page 26
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PCOS : Pathophysiology
Anovulation
Mechanism is
unclear
Hypersecretion of LH Insulin-resistence
PCOS Page 27
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Menstrual Dysfunction
Oligo- and amenorrhea
Chronic estrogen exposure
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Hyperandrogenism
typically manifested
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Insulin-Resistance
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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Obesity
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
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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
anovulation, and neoplastic changes in the endometrium are felt to arise from chronic unopposed estrogen (Coulam, 1983).
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cycles
Women with PCOS who
become pregnant are known to experience an increased rate (30 to 50 percent) of early miscarriage
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a two- to threefold higher risk of gestational diabetes, pregnancyinduced hypertension, preterm birth, and perinatal mortality, unrelated to multifetal gestations
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DIAGNOSIS
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Sonography
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
Here comes your footer Page 41
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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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TREATMENT
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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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Observation
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
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menstrual cycles.
Decrease androgen
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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
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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
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PROGNOSIS
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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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Monitoring
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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