DNP 649 Module 2 Reproductive Physiology Case Study: PCOS Example

When the Cycle Stalls: A Reproductive Physiology Case Study of Polycystic Ovary Syndrome

Student Name

Edson College of Nursing and Health Innovation, Arizona State University

DNP 649: Advanced Physiology

Instructor Name

Month Day, Year

When the Cycle Stalls: A Reproductive Physiology Case Study of Polycystic Ovary Syndrome

Case

A 19-year-old woman reports periods every 45 to 90 days since menarche at 12, acne and coarse hair on her chin and abdomen. Her BMI is 31. Labs show total testosterone above the reference range, an LH to FSH ratio of about 3:1, a low sex hormone-binding globulin (SHBG), normal prolactin and TSH and a negative pregnancy test. A fasting insulin is elevated.

1. The Normal Cycle in Brief

In a normal cycle, the hypothalamus releases GnRH in pulses. Slower pulses favor FSH and faster pulses favor LH. FSH recruits follicles and, with LH, drives a two-cell system: theca cells make androgens under LH stimulation, and granulosa cells convert them to estradiol using aromatase under FSH stimulation (Hall & Hall, 2026). One dominant follicle matures, rising estradiol triggers the LH surge, ovulation occurs and the corpus luteum produces progesterone that prepares and then stabilizes the endometrium.

2. Interpreting Her Data

Irregular cycles of 45 to 90 days indicate oligo-ovulation. Elevated testosterone and hirsutism indicate hyperandrogenism. A raised LH to FSH ratio reflects altered gonadotropin secretion, though it is not required for diagnosis. Low SHBG means more of her testosterone is free and active. Normal prolactin and TSH and a negative pregnancy test help exclude other causes of irregular cycles. The elevated fasting insulin suggests insulin resistance.

Diagnosis. Under the Rotterdam criteria, polycystic ovary syndrome is diagnosed when at least two are present among irregular or absent ovulation, hyperandrogenism shown in the clinic or in the laboratory, and polycystic-appearing ovaries on ultrasound, once other causes have been ruled out (Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group, 2004). She meets two without imaging. The 2023 international guideline keeps this framework and notes that, in adults, anti-Müllerian hormone can be used instead of ultrasound to define polycystic ovarian morphology (Teede et al., 2023).

3. Explaining the Mechanisms

Faster GnRH pulses. In PCOS, GnRH pulse frequency is persistently high, which favors LH over FSH (Azziz et al., 2016). Relatively low FSH leaves follicles without enough stimulus to mature.

Theca cell overproduction. High LH drives theca cells to make more androgens, and theca cells in PCOS are intrinsically more active. Granulosa cells, short of FSH-driven aromatase, convert less of this androgen to estradiol, so androgens accumulate in the ovary and circulation.

Insulin resistance. Insulin resistance leads to compensatory high insulin. Insulin acts with LH to boost theca androgen production and suppresses the liver's production of SHBG, raising free testosterone (Azziz et al., 2016). This explains why weight and insulin levels influence her symptoms.

Follicle arrest. Local androgen excess and low FSH stop follicles at an early stage. Many small follicles accumulate, producing the polycystic appearance, but none becomes dominant, so the LH surge and ovulation do not occur.

Skin findings. Free androgens stimulate hair follicles and sebaceous glands, causing hirsutism and acne.

4. Why Missing Ovulation Matters

Without ovulation, there is no corpus luteum and no progesterone. Estrogen keeps acting on the endometrium with no progesterone to oppose it, leading to proliferation, irregular heavy bleeding and, over years, a higher risk of endometrial hyperplasia. This is why regular withdrawal bleeding, often with combined hormonal contraception, is part of management.

5. Implications for Practice

Understanding the mechanism guides treatment: lifestyle change and weight reduction lower insulin and androgens, combined hormonal contraceptives suppress LH and raise SHBG, and metformin targets insulin resistance. The guideline also recommends screening for metabolic risk, including glucose and lipids, and attention to mood (Teede et al., 2023).

References

Azziz, R., Carmina, E., Chen, Z., Dunaif, A., Laven, J. S. E., Legro, R. S., Lizneva, D., Natterson-Horowtiz, B., Teede, H. J., & Yildiz, B. O. (2016). Polycystic ovary syndrome. Nature Reviews Disease Primers, 2, Article 16057. https://doi.org/10.1038/nrdp.2016.57

Hall, J. E., & Hall, M. E. (2026). Guyton and Hall textbook of medical physiology (15th ed.). Elsevier.

Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group. (2004). Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome. Fertility and Sterility, 81(1), 19-25. https://doi.org/10.1016/j.fertnstert.2003.10.004

Teede, H. J., Tay, C. T., Laven, J. J. E., Dokras, A., Moran, L. J., Piltonen, T. T., Costello, M. F., Boivin, J., Redman, L. M., Boyle, J. A., Norman, R. J., Mousa, A., & Joham, A. E. (2023). Recommendations from the 2023 international evidence-based guideline for the assessment and management of polycystic ovary syndrome. Journal of Clinical Endocrinology & Metabolism, 108(10), 2447-2469. https://doi.org/10.1210/clinem/dgad463