Pathophysiology and Clinical Presentation-Correct Diagnosis

Polycystic Ovarian Syndrome (PCOS)

  

The Menstrual Cycle

(McCance & Huether, 2014)

Polycystic Ovarian Syndrome (PCOS) accounts for the vast majority of anovulation and ovulatory dysfunction in women with no underlying cause for the increased androgens.  Ovaries are female gonads which are the primary female reproductive organs.  In healthy ovaries, the two main functions are secretion of female sex hormone and development and release of ova; the female gametes. According to McCance (2014),” the commonly accepted cycle average is 28 (27 to 30) days, with rhythmic intervals of 21 to 35 days” (p. 778).

In PCOS, it affects 8-10 percent of women in their reproductive age (Thornton, Wald, & Hensen, 2015). However is suspected to have genetic components while various traits may be inherited (McCance & Huether, 2019).  According to Berkowitz (2007), “Diagnosis is confirmed by increased serum androgens (e.g., testosterone, androstenedione) and increased LH with normal FSH” (p. 176).  Diagnosing times and frequency varies amongst females.  While 22 to 30% of women have polycystic ovaries on ultrasounds with one or more other signs and symptoms; many women may have normal ovaries with one or more signs and symptoms (McCance & Huether, 2019).  In diagnosing, it is important to rule out any differential diagnoses that may mimic PCOS.  Currently the Endocrine Society supports The Rotterdam criteria in which the person must have two of the three following criteria: androgen excess, ovulatory dysfunction, and polycystic ovaries on ultrasound, in addition to excluding any endocrinopathies that may mimic PCOS (Thornton, Wald, & Hensen, 2015).

No one factor fully accounts for PCOS abnormalities; although it is an abnormality of both the reproductive and endocrine (metabolic) systems.  The person with the disease may have insulins resistance/ hyperinsulinemis, disorders of luteinizing hormone/follicle stimulating hormone release, decrease in sex hormone-binding globulin (SHBG) production, increased ovarian androgen production which all components can lead to anovulation causing PCOS.

Characteristics of PCOS usually present during puberty and include obesity, menstrual disturbances, oligomenorrhea, amenorrhea, hyperandrongenism, infertility, and some women maybe asymptomatic.  Other manifestations of PCOS included cardiovascular disease hypertension, dyslipidemia, diabetes mellitus and hormones disturbances such as increases in LH, insulin, androgens and prolactin.  Also includes decreases in SHBG, estrogen receptors and insulin-like growth factor.  Additionally, women with PCOS are at higher risk of developing gestational diabetes mellitus (McCance & Huether, 2019).

 Normal Female Reproductive Anatomy

(McCance & Huether, 2014)

 

PCOS Ovaries

(McCance & Huether, 2019)