Hirsutism, clitoral hypertrophy and menstrual dysfunction
A new female patient, C.Y. 32-year-old patient consults your office because she presents hirsutism, clitoral hypertrophy and menstrual dysfunction. She also stated she has gain weight lately. You suspect of Polycystic Ovary Syndrome (PCOS).
Discuss and described the pathophysiology and symptomology/clinical manifestations of Hyperandrogenism.
Discuss three differential diagnoses for AUB with ICD 10 numbers for each.
Discuss patient education.
Develop the management plan (pharmacological and nonpharmacological).
continue to discuss the 3 topics listed below for your case:
An effective health assessment incorporates not only physiological parameters; please suggest other parameters that should be considered and included on health assessments to reach maximal health potential on individuals.
Name the different family developmental stages and give examples of each one.
Describe family structure and function and the relationship with health care.
Your initial post should be at least 500 words, formatted and cited in current APA initial post is worth 8 points. Sources within 2020-2025
Sample Answer
Case Presentation: C.Y., a 32-Year-Old Female with Suspected PCOS
C.Y., a 32-year-old female, presents with hirsutism, clitoral hypertrophy, menstrual dysfunction, and recent weight gain. These symptoms raise a strong suspicion for Polycystic Ovary Syndrome (PCOS). This discussion will delve into hyperandrogenism, differential diagnoses for abnormal uterine bleeding (AUB), patient education, management strategies, and broader considerations for health assessment, family development, structure, and function.
Hyperandrogenism: Pathophysiology and Symptomatology
Hyperandrogenism, a hallmark of PCOS, refers to excessive androgen levels in the female body. The pathophysiology is complex and not fully understood, but it involves several key mechanisms:
- Increased Ovarian Androgen Production: The ovaries of women with PCOS produce abnormally high amounts of androgens, such as testosterone and androstenedione. This is often due to dysregulation of the enzymes involved in steroidogenesis.