Question 1:
A 28-year-old woman presents to the clinic with a chief complaint of hirsutism and irregular
menses. She describes irregular and infrequent menses (five or six per year) since menarche
at 12 years of age. She began to develop dark, coarse facial hair when she was
14 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 of 2:
What is the pathogenesis of PCOS?
Answer:
Polycystic ovary syndrome (PCOS) is a heterogeneous disorder characterized by
hyperandrogenism and chronic anovulation. Depending on diagnostic criteria, 6% to
20% of reproductive aged women are affected. PCOS presents as a phenotype
reflecting a self-perpetuating vicious cycle involving neuroendocrine, metabolic, and
ovarian dysfunction. PCOS reflects the interactions among multiple proteins and genes
influenced by epigenetic and environmental factors. Functional ovarian
hyperandrogenism due to ovarian steroidal dysregulation is at the center of the
pathogenesis of polycystic ovary syndrome. Functional ovarian hyperandrogenism due
to ovarian steroidal dysregulation is at the center of the pathogenesis of polycystic ovary
syndrome. This has both genetic and environmental factors. The genetic factors are
polycystic ovary morphology, insulin resistance, hyperandrogenemia, defects in insulin
secretion. The steroidal dysregulation may lead to anovulation, irregular menses,
virilization, hirsutism and infertility. Insulin resistance may also occur.
How does PCOS affect a woman’s fertility or infertility?
Answer:
Women with PCOS have hormonal imbalances showing increased levels of
testosterone. This hormonal imbalance prevents development and release of mature
eggs. This prevents ovulation thus preventing pregnancy to occur.
Question 2:

A 20-year-old female college student presents to the Student Health Clinic with a chief
complaint of abdominal pain, foul smelling vaginal discharge, and fever and chills for the
past 4 days. She denies nausea, vomiting, or difficulties with defecation. 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:
What is the pathophysiology of PID?
Answer:
Pelvic Inflammatory Disease is mainly caused due to Neisseria gonorrhea (gonococci) or
Chlamydia trachomatis. Neisseria gonorrhea use host Sialic acid to evade the complement
attack and releases surface fragments that destroy the epithelial cells in cervix,
endometrium, or fallopian tubes. Chlamydia has auto-transported polymorphic membrane
proteins which helps the organism to penetrate the host cells and trigger a immune
response.
An Infection of the upper genital tract occurs (mainly by Gonococci and/ or Chlamydia or
other bacteria such as Bacteroides, Gardnerella vaginalis, Hemophilus influenza,
Mycoplasma, Escherichia coli) leading to pathological changes in the columnar epithelium
of the genital tract and produces inflammation in cervix, endometrium of uterus or fallopian
tubes. Microbial invasion, disruption of normal flora, alteration of cervical mucus barrier host
immune defense mechanisms against infectious agent leads to inflammatory response,
edema, and local tissue damage. If Gonococci, it enters the fallopian tubes, it will cause
inflammation and damage whereas Chlamydial infection leads to permanent scarring of the
fallopian tubes. The infectious agents then gain access to the abdominal cavity via fallopian
or uterine tubes leading to Pelvic inflammatory Disease (PID).
QUESTION 4
1. A 27-year-old male comes to the clinic with a chief complaint of a “sore on my penis”
that has been there for 3 days. He says it burns and leaked a little fluid. He denies

any other symptoms. Past medical history noncontributory. Social history: works as a
bartender and he states he often “hooks up” with some of the patrons, both male
and female after work. He does not always use condoms. Physical exam within
normal limits except for a lesion on the lateral side of the penis adjacent to the glans.
The area is indurated with a small round raised lesion. The APRN orders laboratory
tests, but feels the patient has syphilis.
Question:
Describe the 4 stages of syphilis.
Answer:
Primary syphilis begins at the site of bacterial invasion. Where T. Palladium multiplies and
the epithelium and produces a granulomatosis tissue reaction called a chancre. some
microorganism strain with lymph into adjacent lymph nodes. Within the nodes in at the site
of the canker, the cell mediated, and humoral immune responses are stimulated.
Secondary syphilis is systemic. During this stage, blood borne bacteria spread to all major
organ systems. The secondary stage is followed by a period during which the immune
system can suppress the infection. Even without treatment, spontaneous resolution of the
skin lesions occurs, and the individual enters the latent stage of infection.
Latent syphilis may be subdivided into early and late stages however, no specific criteria
delineates one from the other period medical history and serologic studies can show that
syphilis is present, but the individual has no clinical manifestations. Transmission remains
possible during this phase.
Tertiary syphilis is the most severe stage involving significant morbidity and mortality. The
pathogenesis of syphilitic manifestations at the stage remains unclear. The destructive skin,
bone, and soft tissue lesions also called gummas of tertiary syphilis probably are caused by
a severe hypersensitivity reaction to the microorganism. Within the cardiovascular system,
infection with T. palladium may cause aneurysms, heart valve insufficiency's, in heart failure.
QUESTION 5
1. A 19-year-old female presents to the clinic with a chief complaint of “fluid filled
bumps” and intense pruritis of her vulva. She states these symptoms have been
present for about 10 days, but she thought she had a yeast infection. She self-
medicated with over the counter (OTC) metronidazole (Flagyl™) intravaginally but
the symptoms got worse. No other complaints except for fatigue out of proportion
to her activity level. Past medical history noncontributory. Social history: sexually
active with several men and did forget to use a condom during one sexual encounter.
Physical exam negative except for pelvic exam which revealed multiple fluid filled
(vesicular) lesions on the vulva and introitus. Positive lymph nodes in inguinal
areas. The APRN diagnoses the patient with herpes simplex virus-type 2 known as
genital herpes.

Question:
What is the pathophysiology of HSV-2?
Answer:
Once initial exposure two HSV 2 takes place, the virus enters mucocutaneous sites or
abraded skin, the virus undergoes replication locally in the dermis and epidermis. This leads
to cell destruction transportation and vesicle formation. The virus spreads to contiguous
cells and eventually into sensory nerves this process often occurs and causes a systemic,
inflammatory, immune response, especially with HSV 2 infection that includes fever and
malaise. In rare cases the herpes can cause CNS manifestations. Painful lesions can last
from days to weeks. Eventually the virus is transported intraxonally to the dorsal root where
it remains in the latent stage until it becomes reactivated. The viral envelope is secured by
HSV glycoprotein C and assists in the viral entry. Recognition of HSV DNA by toll like
receptors results in the activation and the development of interferon gene products by the
innate an adaptive immune systems via a dynamic interplay between HSV virion protein
products and the immune system, viral suppression of whole sales responses and
subsequent evasion of the immune system is achieved. In the early stages of the infection,
the HSV protein virion host shutoff or VHS is developed to suppressed host-cell responses.
In addition, glycoprotein C binds to complement C3B, inhibits immunity mediated by
complement and plays a role in inhibiting neutralization of antibodies.
Question 6:
A 27-year-old male presents to the clinic with a chief complaint of a gradual onset of scrotal
pain and swelling of the left testicle that started 2 days ago. The pain has gotten
progressively worse over the last 12 hours and he now complains of left flank pain. He
complains of dysuria, frequency, and urgency with urination. He states his urine smells
funny. He denies nausea, vomiting, but admits to urethral discharge just prior to the start of
his severe symptoms. He denies any recent heavy lifting or straining for bowel
movements. He says the only thing that makes the pain better is if he sits in his recliner and
elevates his scrotum on a small pillow. Past medical history negative. Social history +
for sexual activity only with his wife of 3 years. Physical exam reveals red, swollen left
testicle that is very tender to touch. There is positive left inguinal adenopathy. Clean catch
urinalysis in the clinic + for 3+ bacteria. The APRN diagnoses the patient with epididymitis.
Question:
Discuss how bacteria in the urine causes epididymitis.
Answer:
Bacteria in urine as evidenced by the urinalysis results bacteria 3+ can cause
epididymitis. The bacteria demonstrate retrograde ascent if there is bladder outflow
secondary to urethral stricture or prostate enlargement. Most cases of epididymitis are
caused by an infection, usually by the bacteria Mycoplasma or Chlamydia. These
infections often come by way of sexually transmitted diseases. The bacterium E.

NURS6501 Pathophysiology Week 7 With Answers (21 Solved Questions)

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