PCOS

Page 1: Title and Authors

Polycystic Ovary Syndrome (PCOS)

  • Author: Ina S. Irabon, MD, FPOGS, FPSRM, FPSGE

  • Fields: Obstetrics and Gynecology, Reproductive Endocrinology and Infertility

Page 2: Additional Resources

  • Gynecology schedule for 2018-2019

  • Lecture decks available for download: Doc Ina's lectures for Obstetrics and Gynecology topics.

Page 3: References

Main Reference

  • Comprehensive Gynecology, 8th Edition, 2021Lobo RA, Gershenson DM, Lentz GM, Valea FA, editorsChapter 39, Polycystic Ovary Syndrome (pp. 824-836)

  • Yau TT, Ng NY, Cheung LP, Ma RC."Polycystic ovary syndrome: a common reproductive syndrome with long-term metabolic consequences."Hong Kong Med J. 2017 Dec; 23(6):622-634.doi: 10.12809/hkmj176308. Epub 2017 Nov 24.

Page 4: Outline of PCOS Presentation

Main Topics

  1. Diagnosis

  2. Insulin Resistance

  3. Hypertension

  4. Pathophysiology

  5. Consequences

  6. Treatment

Page 5: Overview of PCOS

  • Definition: Polycystic Ovary Syndrome (PCOS) is the most common endocrine disorder in reproductive-age women.

  • First described in 1935 by Stein and Leventhal as a syndrome involving amenorrhea, hirsutism, and obesity associated with enlarged polycystic ovaries.

  • Prevalence: Affects 15% to 20% of reproductive-age women, varying by ethnicity.

Page 6: Diagnosis Criteria for PCOS

Diagnosis Criteria

  • National Institute of Child Health and Human Development (1990):

    • Menstrual irregularity

    • Hyperandrogenism (clinical or biochemical)

  • ESHRE-ASRM (2003):

    • Menstrual irregularity

    • Hyperandrogenism

    • Polycystic ovaries on ultrasound (at least 2 of 3 criteria required)

  • AEPCOS Society (2006):

    • Hyperandrogenism (clinical or biochemical)

    • Menstrual irregularity

    • Polycystic ovaries on ultrasound (either or both)

  • NIH Workshop (2012): Endorsement of the Rotterdam criteria with recommendations for exclusion of other hormonal disorders.

Exclusions

  • Exclude conditions like non-classic adrenal hyperplasia, Cushing's syndrome, androgenic tumors, hyperprolactinemia, and thyroid disease.

Page 7: Ultrasound Criteria for Diagnosis

  • Classic definition requires 12 or more peripherally oriented cystic structures (2 to 9 mm) in at least one ovary.

  • Evolving criteria now recommend follicle number per ovary (FNPO) being most diagnostic: FNPO should be 19 to 20.

  • Ovarian volume of 10 mL or more is also a diagnostic parameter.

Page 8: Ovarian Morphology in PCOS

  • Antimüllerian hormone (AMH):

    • Value > 4.7 ng/mL can be a marker for polycystic ovaries but is not diagnostic on its own.

  • Polycystic appearing ovaries (PAO) are common in 10% to 25% of the normal reproductive-age population without PCOS symptoms.

  • Isolated findings of polycystic ovaries should not be mistaken for PCOS diagnosis but might indicate risk factors.

Page 9: PAO Insights

  • Not all women with isolated polycystic ovaries are diagnosed with PCOS.

  • Up to 20% of girls may have polycystic ovaries during adolescence.

  • The transition from normal to polycystic morphology may be influenced by genetics or environmental factors.

Page 10: Development of PCOS

  • Women with polycystic appearing ovaries (PAO) may have normal menstrual cycles and androgen levels but can later develop PCOS under susceptibility factors.

Page 11: Susceptibility Factors in PCOS Development

  • Heightened susceptibility due to genetic, environmental, or endocrine factors can lead to developing PCOS later in life.

Page 12: Menstrual Irregularity

  • Menstrual irregularity encompasses oligomenorrhea and amenorrhea with abnormal cycles indicating ovulatory issues. This is a strong correlate with insulin resistance in PCOS.

Page 13: Hyperandrogenism

  • Symptoms of excess include hirsutism, acne, and alopecia.

  • Blood tests may show normal levels of testosterone despite symptoms, complicating diagnoses.

Page 14: Androgens in PCOS

  • 11-oxygenated androgens from adrenal glands are significant, affecting lipid metabolism and insulin resistance in women with PCOS.

Page 15: Assessment of Hirsutism

  • Hirsutism is evaluated using the modified Ferriman-Gallwey score; ethnic variations affect expressions of hyperandrogenism.

Page 16: Ferriman-Gallwey Scoring

  • The scoring system rates hair growth in nine body areas on a scale from 0 to 4. A score ≥6 typically indicates hirsutism.

Page 17: Phenotypes of PCOS

Different Phenotypes

  1. Type A: Hyperandrogenism + Chronic anovulation + Polycystic ovaries.

  2. Type B: Hyperandrogenism + Chronic anovulation.

  3. Type C: Hyperandrogenism + Polycystic ovaries.

  4. Type D: Chronic anovulation + Polycystic ovaries.

Page 18: Hyperandrogenism + Oligo-ovulation

  • Emphasizes hormonal disturbances associated with various types of PCOS.

Page 19: Phenotypic Diversity

  • Redefining PCOS based on its diverse presentations such as hyperandrogenism and irregular menses.

Page 20: Characteristics of Non-Hyperandrogenic PCOS

  • Non-hyperandrogenic type with irregular menses and polycystic ovaries counts as Type D.

Page 21: Endocrine Findings in PCOS

Key Findings

  • Abnormal gonadotropin secretion.

  • Elevated LH levels linked to obesity in PCOS.

Page 22: Gonadotropin Characteristics

  • Increased sensitivity to GnRH leads to elevated LH levels and abnormal LH/FSH ratios.

Page 23: Diagnosing PCOS

  • Elevated LH/FSH ratio has limited specificity for PCOS diagnosis and should not be solely relied upon.

Page 24: Estradiol in PCOS

  • High levels of biologically active estradiol arise from low SHBG levels, contributing to the risk of endometrial hyperplasia.

Page 25: Androgens in PCOS Risk Assessment

  • Measuring total testosterone, DHEAS, and conversion rates to DHT provides insights into symptomatology and risk factors associated with hirsutism.

Page 26: Elevated Prolactin Levels

  • About 20-30% of women with PCOS may show elevated prolactin levels related to increased GnRH pulsatility.

Page 27: Pathophysiology Overview

Major Pathways in PCOS

  1. Ovulatory dysfunction

  2. Disordered gonadotropin release

  3. Insulin resistance

Page 28: Genetic and Environmental Factors

  • Genetic susceptibility and environmental factors contribute to the complexity of PCOS pathogenesis.

Page 29: Disordered Gonadotropin Release

  • Increased LH secretion impacts ovarian androgen production.

Page 30: Ovulatory Dysfunction

  • PCOS leads to disrupted follicle growth due to several hormonal disturbances.

Page 31: Insulin Resistance Impact

  • Insulin resistance exacerbates hormonal derangements, impacting normal biochemical processes and cycle regularity.

Page 32: Effects of Insulin Resistance

  • Insulin directly influences testosterone levels and follicle development.

Page 33: Overproduction of AMH

  • Excess AMH can interfere with FSH action in small follicles, promoting follicular arrest.

Page 34: Insulin Resistance Details

  • Both genetic predisposition and lifestyle factors contribute significantly to the development of insulin resistance in PCOS.

Page 35: Insulin Signaling Abnormalities

  • Lower levels of IGFBP enhance bioavailability of IGF-1, stimulating ovarian activity and androgen production.

Page 36: Role of Adipose Tissue

  • Adipostatic changes contribute to further insulin resistance and metabolic dysfunction.

Page 37: Assessing Insulin Resistance

  • Diagnostic focus on ruling out diabetes, evaluating glucose tolerance, and tracking fasting glucose and insulin levels.

Page 38: Measurement Techniques

  • Various indices (e.g., HOMA-IR, QUICKI) help evaluate insulin sensitivity effectively.

Page 39: Acanthosis Nigricans

  • Present in obese, hyperandrogenic PCOS patients, denoting severe insulin resistance and heightened metabolic concerns.

Page 40: PCOS Pathophysiology Summary

  • PCOS is characterized by androgens, insulin resistance, and hormonal imbalances leading to various symptoms.

Page 41: Consequences of PCOS

  • Changes in health focus from reproductive to long-term metabolic outcomes.

Page 42: Multi-disciplinary Approach

  • Treatment necessitates collaboration among specialists in various fields addressing comprehensive health aspects.

Page 43: Weight and Metabolic Issues

  • Overweight exacerbates risks associated with PCOS. Standardized diagnostic criteria for metabolic syndrome applicable to evaluate associated risks.

Page 44: Diabetes Correlation

  • Rates of Type 2 diabetes are notably elevated in PCOS populations; screening is critical.

Page 45: Quality of Life Concerns

  • PCOS affects emotional well-being and can exacerbate mental health issues due to physical and reproductive challenges.

Page 46: Cardiovascular Risk in PCOS

  • Identification of increased cardiovascular risk factors in patients with traditional PCOS presentations.

Page 47: Cardiovascular Findings

  • Evaluation of lipid profiles and traditional risk factors for cardiovascular diseases in PCOS patients.

Page 48: Cardiovascular Risk Pattern

  • Milder phenotypes generally demonstrate reduced cardiovascular risks compared to classical presentations of PCOS.

Page 49: Cancer Risks

  • Increased risk of endometrial and ovarian cancers associated with long-term hormonal imbalances in PCOS.

Page 50: Cancer Management in PCOS

  • Management strategies involving oral contraceptives can normalize cancer risks enhanced by PCOS.

Page 51: Ovarian Aging and PCOS

  • Consequential risks heighten with aging; constant monitoring and management procedures are crucial.

Page 52: Treatment Overview

  • Tailored treatments based on individual complaints related to symptoms and concerns posed by PCOS.

Page 53: Treatment Goals

  • Management should include lifestyle changes and symptom-specific treatments to effectively mitigate PCOS symptoms.

Page 54: Lifestyle Modification

  • Emphasizing lifestyle interventions significantly impacts managing all aspects of PCOS.

Page 55: Androgen Excess Management

  • Treatments primarily include oral contraceptives or anti-androgen medications to counteract excessive androgen effects.

Page 56: Management of Irregular Bleeding

  • Progestogen therapy is crucial for preventing endometrial complications in anovulatory women.

Page 57: Progestogen Therapy Scheduling

  • Regimen includes cyclical dosing to manage endometrial health in PCOS patients.

Page 58: Ovulation Induction for Infertility

  • Medications and lifestyle changes should be aligned for effective fertility restoration in PCOS.

Page 59: Fertility Treatments

  • Options for ovulation induction include several pharmacological agents and procedures tailored to individual patient needs.

Page 60: Treatment for Fertility Challenges

  • Adjunct therapies may be required if first-line treatments do not yield success.

Page 61: IVF Considerations

  • While effective, managing potential risks like OHSS is essential during IVF treatment for PCOS patients.

Page 62: Metabolic Management Strategies

  • Comprehensive lifestyle and dietary changes complement pharmacological approaches for managing metabolic risks.

Page 63: Surgery for Obesity Management

  • For individuals who are morbidly obese, bariatric surgery may be indicated as part of treatment.

Page 64: Summary of Treatment Modalities

  • Table outlining specific treatments for infertility, skin manifestations, abnormal bleeding, and metabolic concerns in PCOS.

Page 65: Final Summary

  • Overview of critical key points on diagnosis, resistance, hypertension, pathophysiology, consequences, and treatment of PCOS.

Page 66: Thank You

  • Acknowledgment to the audience for their attention.

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