NURS 6501 Knowledge Check Women’s and Men’s Health, Infections, and Hematologic Disorders

Question 1

4 out of 4 points

Scenario 1: Polycystic Ovarian Syndrome (PCOS)

A 29-year-old female presents to the clinic with a complaint of hirsutism and irregular menses. She describes irregular and infrequent menses (five or six per year) since menarche at 11 years of age. She began to develop dark, coarse facial hair when she was 13 years of age, but her parents did not seek treatment or medical opinion at that time. The symptoms worsened after she gained weight in college. She got married 3 years ago and has been trying to get pregnant for the last 2 years without success. Height 66 inches and weight 198. BMI 32 kg.m². Moderate hirsutism without virilization noted. Laboratory data reveal CMP within normal limits (WNL), CBC with manual differential (WNL), TSH 0.9 IU/L SI units (normal 0.4-4.0 IU/L SI units), a total testosterone of 65 ng/dl (normal 2.4-47 ng/dl), and glycated hemoglobin level of 6.1% (normal value ≤5.6%). Based on this information, the APRN diagnoses the patient with polycystic ovarian syndrome (PCOS) and refers her to the Women’s Health APRN for further workup and management.

Question

1. What is the pathogenesis of PCOS?

Selected Answer:

Polycystic Ovary Syndrome (PCOS) has an underlying genetic component that causes irregular ovulation, increased androgens, and ovaries with polycystic characteristics (McCance & Huether, 2019). Glucose intolerance and insulin resistance increase androgen secretion via the ovaries’ supportive structures and reduce sex-hormone-binding globulin (McCance & Huether, 2019). Elevated leptin levels act on the hypothalamus interfering with hormone production. Follicular growth and apoptosis alterations influence the absence of ovulation, creating inappropriate functioning of FSH and LH. Cortical thickening increases subcortical stroma, and hyperplasia occurs (McCance & Huether, 2019)

Polycystic ovary syndrome (PCOS) is a hormonal disorder common among women of reproductive age. Women with PCOS may have infrequent or prolonged menstrual periods or excess male hormone (androgen) levels. The ovaries m

ay develop numerous small collections of fluid (follicles) and fail to release eggs regularly.

other factors that may contribute to the development of PCOS include:

· Excess insulin. Insulin is the hormone produced in the pancreas that allows cells to use sugar, your body’s primary energy supply. If your cells become resistant to the action of insulin, then your blood sugar levels can rise, and your body might produce more insulin. Excess insulin might increase androgen production, causing difficulty with ovulation.

· Low-grade inflammation. This term describes white blood cells’ production of substances to fight infection. Research has shown that women with PCOS have a type of low-grade inflammation that stimulates polycystic ovaries to produce androgens, leading to heart and blood vessel problems.

· Excess androgen. The ovaries produce abnormally high androgen levels, resulting in hirsutism and acne. Early diagnosis of PCOS and treatment and weight loss may reduce the risk of long-term complications such as type 2 diabetes and heart disease.

Complications of PCOS can include: Infertility, Gestational diabetes or pregnancy-induced high blood pressure, miscarriage or premature birth, Nonalcoholic steatohepatitis, Metabolic syndrome including high blood pressure, high blood sugar, and abnormal cholesterol or triglyceride levels that significantly increase your risk of cardiovascular disease, Type 2 diabetes or prediabetes, Sleep apnea, Depression, anxiety and eating disorders, Abnormal uterine bleeding, and cancer of the uterine lining (endometrial cancer). It is important to note that these complications are more severe in overweight women.

Correct Answer:

The pathogenesis of PCOS has been linked to altered luteinizing hormone (LH) action, insulin resistance, and a possible predisposition to hyperandrogenism. One theory maintains that underlying insulin resistance exacerbates hyperandrogenism by suppressing synthesis of sex hormone–binding globulin and increasing adrenal and ovarian synthesis of androgens, thereby increasing androgen levels. These androgens then lead to irregular menses and physical manifestations of hyperandrogenism. The hyperandrogenic state is a cardinal feature of PCOS but glucose intolerance/insulin resistance and hyperinsulinemia often run parallel to and markedly aggravate the hyperandrogenic state, thus contributing to the severity of signs and symptoms of PCOS.

Response Feedback:

[None Given]

Question 2

Click here to ORDER an A++ paper from our Verified MASTERS and DOCTORATE WRITERS: NURS 6501 Knowledge Check Women’s and Men’s Health, Infections, and Hematologic Disorders

Scenario 1: Polycystic Ovarian Syndrome (PCOS)

Question

How does PCOS affect a woman’s fertility or infertility?

Selected Answer:

PCOS is the leading cause of infertility in women (McCance & Huether, 2019). Infertility results from alterations in androgen production, follicular disturbances, and an absence of ovulation. In other words, PCOS negatively impacts fertility because women with the condition do not ovulate or release an egg each month due to an overproduction of estrogen by the ovaries.

Correct Answer:

Ovulation problems are usually the primary cause of infertility in women with PCOS. Ovulation may not occur due to an increase in testosterone production or © 2020 Walden University 2 because follicles on the ovaries do not mature. Due to unbalanced hormones, ovulation and menstruation can be irregular. A hyperandrogenic state is a cardinal feature in the pathogenesis of PCOS. Excessive androgens affect follicular growth, and insulin affects follicular decline by suppressing apoptosis and enabling follicle to persist. There is dysfunction in ovarian follicle development. Inappropriate gonadotropin secretion triggers the beginning of a vicious cycle that perpetuates anovulation

Response Feedback:

[None Given]

Question 3

4 out of 4 points

Scenario 2: Pelvic Inflammatory Disease (PID)

A 30-year-old female comes to the clinic with a complaint of abdominal pain, foul smelling vaginal discharge, and fever and chills for the past 5 days. She denies nausea, vomiting, or difficulties with bowels. Last bowel movement this morning and was normal for her. Nothing has helped with the pain despite taking ibuprofen 200 mg orally several times a day. She describes the pain as sharp and localizes the pain to her lower abdomen. Past medical history noncontributory. GYN/Social history + for having had unprotected sex while at a fraternity party. Physical exam: thin, Ill appearing anxious looking white female who is moving around on the exam table and unable to find a comfortable position. Temperature 101.6F orally, pulse 120, respirations 22 and regular. Review of systems negative except for chief complaint. Focused assessment of abdomen demonstrated moderate pain to palpation left and right lower quadrants. Upper quadrants soft and non-tender. Bowel sounds diminished in bilateral lower quadrants. Pelvic exam demonstrated + adnexal tenderness, + cervical motion tenderness and copious amounts of greenish thick secretions. The APRN diagnoses the patient as having pelvic inflammatory disease (PID).

Question:

1. What is the pathophysiology of PID?

Selected Answer:

Pelvic inflammatory disease (PID) is a condition of inflammation related to infections and involves the uterus, fallopian tubes, ovaries, and the peritoneal cavity in severe cases. Infections combined with the normal vaginal microbiome’s failure allow the infecting microorganism to spread into the upper genital tract causing PID (McCance & Huether, 2019). Although often caused by gonorrhea or chlamydia, PID’s etiology can be caused by multiple bacteria when the pH of the vagina changes and alter the integrity of the mucus of the cervix (McCance & Huether, 2019). Altering the cervix’s integrity allows an inflammatory process to begin in the uterus and fallopian tubes with edema, obstruction, or necrosis. Gonorrhea pathogens secrete toxins increasing the inflammation and damage, and chlamydia replicates in the cells rupturing the cell membrane, with both pathogens capable of spreading into the abdominal cavity (McCance & Huether, 2019).

Correct Answer:

Pelvic inflammatory disease (PID) is an infectious and inflammatory disorder of the upper female genital tract, including the uterus, fallopian tubes, and adjacent pelvic structures. Infection and inflammation may spread to the abdomen, including perihepatic structures. PID is initiated by infection that ascends from the vagina and cervix into the upper genital tract. Chlamydia trachomatis is the predominant sexually transmitted organism associated with PID. Of all acute PID cases, less than 50% test positive for the sexually transmitted organisms such as Chlamydia trachomatis and Neisseria gonorrhea. Other organisms implicated in the pathogenesis of PID include, Gardnerella vaginalis (which causes bacterial vaginosis (BV), Haemophilus influenzae, and anaerobes such as Peptococcus and Bacteroides species. Inflammatory responses in the fallopian tubes and uterus causes swelling and sometimes necrosis of the area. This inflammation leads to scarring of the fallopian tubes and causes infertility. N gonorrhoeae is no longer the primary organism associated with PID, but gonorrhea remains the second most frequently reported sexually transmitted disease, after chlamydial infection.

Response Feedback:

[None Given]