NURS6501 Pathophysiology Week 7 With Answers (21 Solved Questions)

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Question 1:A 28-year-old woman presents to the clinic with a chief complaint of hirsutism and irregularmenses. She describes irregular and infrequent menses (five or six per year) since menarcheat 12 years of age. She began to develop dark, coarse facial hair when she was14 years of age, but her parents did not seek treatment or medical opinion at that time. Thesymptoms worsened after she gained weight in college. She got married 3 years ago andhas been trying to get pregnant for the last 2 years without success. Height 66 inches andweight 198. BMI 32 kg.m2. Moderate hirsutism without virilization noted.Laboratory datareveal CMP within normal limits (WNL), CBC with manual differential (WNL), TSH 0.9 IU/L SIunits (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 thisinformation, the APRN diagnoses the patient with polycystic ovarian syndrome (PCOS) andrefers 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 byhyperandrogenism and chronic anovulation. Depending on diagnostic criteria, 6% to20% of reproductive aged women are affected. PCOS presents as a phenotypereflecting a self-perpetuating vicious cycle involving neuroendocrine, metabolic, andovarian dysfunction. PCOS reflects the interactions among multiple proteins and genesinfluenced by epigenetic and environmental factors. Functional ovarianhyperandrogenism due to ovarian steroidal dysregulation is at the center of thepathogenesis of polycystic ovary syndrome. Functional ovarian hyperandrogenism dueto ovarian steroidal dysregulation is at the center of the pathogenesis of polycystic ovarysyndrome. This has both genetic and environmental factors. The genetic factors arepolycystic ovary morphology, insulin resistance, hyperandrogenemia, defects in insulinsecretion. 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 oftestosterone. This hormonal imbalance prevents development and release of matureeggs. This prevents ovulation thus preventing pregnancy to occur.Question 2:

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A 20-year-old female college student presents to the Student Health Clinic with a chiefcomplaint of abdominal pain, foul smelling vaginal discharge, and fever and chills for thepast 4 days. She denies nausea, vomiting, or difficulties with defecation. Last bowelmovement this morning and was normal for her. Nothing has helped with the paindespite taking ibuprofen 200 mg orally several times a day. She describes the pain assharp and localizes the pain to her lower abdomen. Past medical historynoncontributory. GYN/Social history + for having had unprotected sex while at afraternity party. Physical exam: thin, Ill appearing anxious looking white female who ismoving around on the exam table and unable to find a comfortable position.Temperature 101.6F orally, pulse 120, respirations 22 and regular. Review of systemsnegative except for chief complaint. Focused assessment of abdomendemonstrated moderate pain to palpation left and right lower quadrants. Upperquadrants soft and non-tender. Bowel sounds diminished in bilateral lower quadrants.Pelvic exam demonstrated + adnexal tenderness, + cervical motion tenderness andcopious amounts of greenish thick secretions. The APRN diagnoses the patient ashaving pelvic inflammatory disease (PID).Question:What is the pathophysiology of PID?Answer:Pelvic Inflammatory Disease is mainly caused due to Neisseria gonorrhea (gonococci) orChlamydia trachomatis. Neisseria gonorrhea use host Sialic acid to evade the complementattack and releases surface fragments that destroy the epithelial cells in cervix,endometrium, or fallopian tubes. Chlamydia has auto-transported polymorphic membraneproteins which helps the organism to penetrate the host cells and trigger a immuneresponse.An Infection of the upper genital tract occurs (mainly by Gonococci and/ or Chlamydia orother bacteria such as Bacteroides, Gardnerella vaginalis, Hemophilus influenza,Mycoplasma, Escherichia coli) leading to pathological changes in the columnar epitheliumof the genital tract and produces inflammation in cervix, endometrium of uterus or fallopiantubes. Microbial invasion, disruption of normal flora, alteration of cervical mucus barrier hostimmune defense mechanisms against infectious agent leads to inflammatory response,edema, and local tissue damage. If Gonococci, it enters the fallopian tubes, it will causeinflammation and damage whereas Chlamydial infection leads to permanent scarring of thefallopian tubes. The infectious agents then gain access to the abdominal cavity via fallopianor uterine tubes leading to Pelvic inflammatory Disease (PID).QUESTION 41.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

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any other symptoms. Past medical history noncontributory. Social history: works as abartender and he states he often “hooks up” with some of the patrons, both maleand female after work. He does not always use condoms. Physical exam withinnormal 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 laboratorytests, 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 andthe epithelium and produces a granulomatosis tissue reaction called a chancre. somemicroorganism strain with lymph into adjacent lymph nodes. Within the nodes in at the siteof the canker, the cell mediated, and humoral immune responses are stimulated.Secondary syphilis is systemic. During this stage, blood borne bacteria spread to all majororgan systems. The secondary stage is followed by a period during which the immunesystem can suppress the infection. Even without treatment, spontaneous resolution of theskin lesions occurs, and the individual enters the latent stage of infection.Latent syphilis may be subdivided into early and late stages however, no specific criteriadelineates one from the other period medical history and serologic studies can show thatsyphilis is present, but the individual has no clinical manifestations. Transmission remainspossible during this phase.Tertiary syphilis is the most severe stage involving significant morbidity and mortality. Thepathogenesis 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 bya 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 51.A 19-year-old female presents to the clinic with a chief complaint of “fluid filledbumps” and intense pruritis of her vulva. She states these symptoms have beenpresent for about 10 days, but she thought she had a yeast infection. She self-medicated with over the counter (OTC) metronidazole (Flagyl™) intravaginally butthe symptoms got worse. No other complaints except for fatigue out of proportionto her activity level. Past medical history noncontributory. Social history: sexuallyactive 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 inguinalareas. The APRN diagnoses the patient with herpes simplex virus-type 2 known asgenital herpes.

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Question:What is the pathophysiology of HSV-2?Answer:Once initial exposure two HSV 2 takes place, the virus enters mucocutaneous sites orabraded skin, the virus undergoes replication locally in the dermis and epidermis. This leadsto cell destruction transportation and vesicle formation. The virus spreads to contiguouscells and eventually into sensory nerves this process often occurs and causes a systemic,inflammatory, immune response, especially with HSV 2 infection that includes fever andmalaise. In rare cases the herpes can cause CNS manifestations. Painful lesions can lastfrom days to weeks. Eventually the virus is transported intraxonally to the dorsal root whereit remains in the latent stage until it becomes reactivated. The viral envelope is secured byHSV glycoprotein C and assists in the viral entry. Recognition of HSV DNA by toll likereceptors results in the activation and the development of interferon gene products by theinnate an adaptive immune systems via a dynamic interplay between HSV virion proteinproducts and the immune system, viral suppression of whole sales responses andsubsequent 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 bycomplement 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 scrotalpain and swelling of the left testicle that started 2 days ago.The pain has gottenprogressively worse over the last 12 hours and he now complains of left flank pain. Hecomplains of dysuria, frequency, and urgency with urination. He states his urine smellsfunny. He denies nausea, vomiting, but admits to urethral discharge just prior to the start ofhis severe symptoms. He denies any recent heavy lifting or straining for bowelmovements. He says the only thing that makes the pain better is if he sits in his recliner andelevates 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 lefttesticle that is very tender to touch. There is positive left inguinal adenopathy. Clean catchurinalysis 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 causeepididymitis. The bacteria demonstrate retrograde ascent if there is bladder outflowsecondary to urethral stricture or prostate enlargement. Most cases of epididymitis arecaused by an infection, usually by the bacteria Mycoplasma or Chlamydia. Theseinfections often come by way of sexually transmitted diseases. The bacteriumE.

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