Summary NR 602 Week 6 Grand Rounds – PCOS. Complete Solution

NR 602 Week 6 Grand Rounds – PCOS

What is PCOS?

Women with Polycystic Ovarian Syndrome (PCOS) have
abnormalities with the metabolism of androgens and estrogen, which lead to
an increase in androgen production (Beena & Thomas, 2016). PCOS can
result from abnormal functioning within the hypothalamic-pituitary-ovarian
axis (Beena & Thomas, 2016; Williams, Mortada, & Porter, 2016). PCOS
can be diagnosed when a patient presents with two out of three of the
following findings: polycystic ovaries (which is when there are 12 or more
follicles in 1 ovary), hyperandrogenism, and ovulatory dysfunction
(Williams, Mortada, & Porter, 2016).

Pathophysiology

The pathophysiology of PCOS is complex and no single reason can be
confirmed one hundred percent, however, it is thought that insulin resistance
plays a key role (Williams, Mortada, & Porter, 2016). Patient’s with PCOS
are two times more likely to have metabolic syndrome when compared with
the general population and they are four times more likely to have type 2
diabetes (Williams, Mortada, & Porter, 2016). The pathophysiology is also
associated with altered luteinizing hormone (LH) action, a predisposition to
hyperandrogenism, and insulin resistance (Williams, Mortada, & Porter,
2016). It is believed that the underlying insulin resistance these patients have
exacerbate hyperandrogenism via suppression of the synthesis of the sex
hormone-binding globulin and increase ovarian and adrenal synthesis of
androgens, leading to an overall increase in androgen levels (Williams,
Mortada, & Porter, 2016). The increase in androgens is what causes the
menses to be irregular as well as the development of physical appearances of
hyperandrogenism (Williams, Mortada, & Porter, 2016). Patients with PCOS
have also been found to have an increased risk for developing nonalcoholic
fatty liver disease, hyperlipidemia, and sleep apnea (Williams, Mortada, &
Porter, 2016).

Epidemiology

PCOS is the most common cause of infertility due to anovulation
(Williams, Mortada, & Porter, 2016). It is believed that between 6 to 25
percent of reproductive age women have PCOS (Williams, Mortada, &

, Porter, 2016). The symptoms typically begin around the time the woman
begins her menses, therefore, the diagnosis is commonly made during
adolescence or young adulthood (Williams, Mortada, & Porter, 2016). It has
been found that these patients are at a higher risk for developing ovarian and
endometrial cancers (Williams, Mortada, & Porter, 2016).

Risk Factors for PCOS

It is not entirely clear what factors can predispose a person to PCOS,
however, it is believed that genetics may play a role in its development along
with obesity (Begum, Shariff, Ayman, Mohammed, & Housam, 2017).
Obesity contributes to hyperinsulinemia, which is thought to be a
predisposing factor for PCOS (Begum, Shariff, Ayman, Mohammed, &
Housam, 2017).

Clinical Physical Assessment Findings

Patients will present with variable symptoms, from asymptomatic to
metabolic, gynecologic, and dermatologic manifestations (Williams,
Mortada, & Porter, 2016). The physical assessment finding one might
discover include amenorrhea or oligomenorrhea, infertility, dysfunctional
uterine bleeding, hirsutism, insulin resistance, acne, alopecia, acanthosis
nigricans, and hypertension (Palomba et al, 2014; Williams, Mortada, &
Porter, 2016). It is important for the provider to remember that many
features of PCOS are actually normal in puberty-aged girls thanks to the
immaturity of the hypothalamic-pituitary-ovarian axis (Goodman et al,
2015). If oligomenorrhea persists 2 to 3 years past menarche, the likelihood
of an underlying adrenal or ovarian dysfunction should be considered
(Goodman et al, 2015; Legro et al, 2013). Young to adolescent girls with
severe acne or acnes resistant to topical and oral agents, especially Accutane,
have a 40 percent risk of developing PCOS (Goodman et al, 2015).


Differential Diagnosis (3)

Primary Ovarian Insufficiency, also known as premature ovarian failure, is
characterized by follicle dysfunction that leads to the impairment of ovary
functioning (Klein & Poth, 2013). Evidence suggests that there is a genetic
predisposition to primary ovarian syndrome (Klein & Poth, 2013). These