Polycystic ovary syndrome overview: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
There are several | There are several organs involved in the [[pathogenesis]] of polycystic ovary syndrome like [[ovary]], [[adrenal]], [[hypothalamus]], [[pituitary]], or [[insulin]]-sensitive tissues. The [[pathophysiology]] of Polycystic ovary syndrome is not well understood. [[Insulin resistance]] leads to compensatory insulin hypersecretion by the [[pancreas]] in order to maintain [[Blood sugar regulation|normoglycemia]]. The resulting [[hyperinsulinemia]] promotes [[ovarian]] [[androgen]] output and may also promote [[adrenal]] [[androgen]] output. | ||
==Causes== | ==Causes== | ||
Revision as of 14:54, 18 October 2017
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Polycystic ovary syndrome Microchapters |
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Differentiating Polycystic ovary syndrome from other Diseases |
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Diagnosis |
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Treatment |
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Polycystic ovary syndrome overview On the Web |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]
Overview
Polycystic ovary syndrome is the most common form of chronic anovulation associated with androgen excess. Polycystic ovary syndrome occurs in approximately 5% to 10% of reproductive-age women. The diagnosis of polycystic ovary syndrome is made by excluding other hyper androgenic disorders like non-classic adrenal hyperplasia, androgen-secreting tumors, hyperprolactinemia in women with chronic anovulation and androgen excess. Polycystic ovary syndrome can be diagnosed whenever two of following three criteria are present oligomenorrhea, hirsutism and/or hyperandrogenemia and polycystic ovaries. Prompt investigation and treatment is necessary for patients with excessive vaginal bleeding. The endometrium of the patient with polycystic ovary syndrome must be evaluated by biopsy because of long-term exposure to unopposed estrogen leaves patients at increased risk for endometrial cancer. Polycystic ovary syndrome is also associated with increased metabolic and cardiovascular disorders. Polycystic ovary syndrome is considered to be a heterogeneous disorder with multifactorial causes. Polycystic ovary syndrome risk is significantly increased with a positive family history of chronic anovulation and androgen excess, and this complex disorder may be inherited in a polygenic fashion. Treatment begins with weight loss and metformin, if either or both are indicated, and depending on the patient's reproductive needs oral contraception supplemented with antiandrogen therapy for patients not wishing to conceive or fertility treatments for patients desiring pregnancy. The prognosis is excellent with treatment. Complications of polycystic ovary syndrome include infertility, irregular uterine bleeding, and increased pregnancy loss
Historical Perspective
Polycystic ovary syndrome was first described in 1935 by American gynecologists Irving F. Stein, Sr. and Michael L. Leventhal, from whom its original name of Stein–Leventhal syndrome is taken. The earliest published description of polycystic ovary syndrome was in 1721 in Italy. Cyst-related changes to the ovaries were described in 1844.
Classification
Polycystic ovary syndrome (PCOS) may be classified into 4 types based on the severity of symptoms into asymptomatic form, mild form, classical form, and metabolic form.
Pathophysiology
There are several organs involved in the pathogenesis of polycystic ovary syndrome like ovary, adrenal, hypothalamus, pituitary, or insulin-sensitive tissues. The pathophysiology of Polycystic ovary syndrome is not well understood. Insulin resistance leads to compensatory insulin hypersecretion by the pancreas in order to maintain normoglycemia. The resulting hyperinsulinemia promotes ovarian androgen output and may also promote adrenal androgen output.
Causes
The underlying defect in patients with polycystic ovary syndrome remains unknown, but the harmonal imbalance between LH, FSH and estrogen are mainly responsible for the development of polycystic ovary syndrome. Most studies suggest that more than one factor could play a role in developing polycystic ovary syndrome.
Differentiating Polycystic ovary syndrome overview from Other Diseases
Polycystic ovary syndrome must be differentiated from other causes of irregular or absent menstruation and hirsutism, such as congenital adrenal hyperplasia, cushing's syndrome, hyperprolactinemia, and other pituitary or adrenal disorders.
Epidemiology and Demographics
Polycystic ovarian syndrome is one of the most common endocrine disorders of reproductive-age women, with a prevalence of 4-12% in the United States. Up to 10% of women are diagnosed with polycystic ovary syndrome.
Risk Factors
Common risk factors in the development of polycystic ovary syndrome are hyperinsulinemia secondary to insulin resistance, obesity, family history of polycystic ovary syndrome among first-degree relatives, premature adrenarche, fetal androgen exposure, and low birth weight.
Screening
According to Royal College of Obstetricians and Gynaecologists (RCOG) thyroid function tests, serum prolactin levels, and a free androgen index are baseline screening tests recommended for women with suspected polycystic ovarian syndrome.
Natural History, Complications, and Prognosis
If left untreated patients with polycystic ovary syndrome can develop heart disease due to elevated cholesterol and increased levels of androgens. Increased lengths of time without a menstrual period leads to unopposed exposure of endometrium to estrogen can result in endometrial cancer. Complications that can develop as a result of polycystic ovary syndrome are insulin resistance/type II diabetes, high blood pressure, dyslipidemia, strokes, miscarriage, and infertility. The prognosis for fertility in patients with polycystic ovary syndrome is good with treatment, unless there are other unknown fertility problems.
Diagnosis
Diagnostic Criteria
Polycystic ovary syndrome was previously defined according to the proceedings of an expert conference sponsored by the National Institutes of Health (NIH) in 1990, which described the disorder as including hyperandrogenism or hyperandrogenemia (or both), oligo-ovulation, and exclusion of known disorders of androgen excess and anovulation. Another expert conference held in Rotterdam in 2003 defined Polycystic ovary syndrome, after the exclusion of related disorders, by the presence of two of the following three features oligo-ovulation or anovulation, clinical or biochemical signs of hyperandrogenism (or both), and polycystic ovaries. In essence, the Rotterdam 2003 criteria expanded the NIH 1990 definition by creating two new phenotypes ovulatory women with polycystic ovaries plus hyperandrogenism and oligo-anovulatory women with polycystic ovaries but without hyperandrogenism.
History and Symptoms
The significant information that needs to focused in the history of the patient includes menstrual abnormalities, infertility, signs of virilization on physical examination and family history of Polycystic ovary syndrome among first-degree relatives.The most common symptoms of Polycystic ovary syndrome include amenorrhea or oligomenorrhea, abnormal uterine bleeding and androgenization, including hirsutism, acne, oily skin.
Physical Examination
Patients with polycystic ovary syndrome usually appear obese. During the physical examination, it is essential to search for and document signs of androgen excess (hirsutism, virilization, or both), insulin resistance (acanthosis nigricans), and the presence of unopposed estrogen action (well-rugated vagina and stretchable, clear cervical mucus) to support the diagnosis of polycystic ovary syndrome
Laboratory Findings
Measurement of the plasma levels of several hormones is helpful in supporting the diagnosis of polycystic ovary syndrome and especially in excluding other disorders. Determining the LH/FSH ratio of 3:1 is virtually diagnostic of polycystic ovary syndrome. However, a normal ratio does not exclude the diagnosis, as LH levels fluctuate widely throughout the course of a day. Other androgens are measured to screen for other virilizing adrenal tumors. Fasting blood glucose is measured to look for diabetes, screening for lipid abnormalities is also employed. Testosterone is measured to exclude a virilizing tumor. Prolactin is measured to exclude a prolactinoma. Thyroid-stimulating hormone (TSH) is measured to rule out hypothyroidism.
Electrocardiogram Findings
There are electrocardiogram findings associated with polycystic ovary syndrome.
Abdominal X-ray Findings
There are no X-ray findings associated with polycystic ovary syndrome.
CT Findings
There are no CT findings associated with polycystic ovary syndrome.
MRI
There are no MRI findings associated with polycystic ovary syndrome.
Ultrasound Findings
The Rotterdam 2003 criteria include the use of ultrasound as a diagnostic tool in diagnosing polycystic ovary syndrome. The typical polycystic-appearing ovary may emerge in a nonspecific fashion on an ultrasound. Multiple (12+) subcapsular follicles ranging from 2 to 9 mm in diameter in a state of arrested development ('pearl necklace' appearance) in a single ovary is diagnostic for polycystic ovary syndrome on ultrasound.
Imaging Findings
There are no other imaging findings associated with polycystic ovary syndrome.
Other Diagnostic Studies
Endometrial biopsy is recommended in patients diagnosed with polycystic ovary syndrome because long-term unopposed estrogen stimulation leaves these patients at increased risk for endometrial cancer.
Treatment
Medical Therapy
The first step in the management of polycystic ovary syndrome is weight loss if the patient is obese, and treatment of type 2 diabetes with metformin. In significantly overweight patients, weight loss alone usually effects a cure and should always be vigorously attempted. Diet and exercise are recommended in all women with polycystic ovary syndrome. The next step is the initiation of treatment to break the self-perpetuating anovulatory cycling, either by stimulating ovulation or suppressing androgenic and ovarian activity. The drug regimen for polycystic ovary syndrome depends upon the desire for a pregnancy by the patient. All anti-androgen treatments will take at least 3 months to affect hirsutism. .
Surgery
Surgery is not considered first-line therapy for Polycystic ovary syndrome and it does not affect insulin resistance or obesity. Surgery is indicated in the treatment of Polycystic ovary syndrome only in patients desiring pregnancy in whom at least 1 year of conservative therapy has failed.
Prevention
There is no established method for prevention of Polycystic ovary syndrome.
Secondary Prevention
Secondary preventive measures for polycystic ovary syndrome include lifestyle modifications and use of metformin to prevent diabetes and atherosclerosis.