A postmenopausal client presenting to the clinic with describing abdominal pain and an episode of unexplained vaginal Nearing receives a Pap smear (Papanicolaou test). Which medical history information should the nurse expect places the client at most risk for developing cervical cancer,
Herpes simplex virus.
Vulvovaginitis.
Human papillomavirus (HPV).
Chronic yeast infections.
The Correct Answer is C
A. Herpes simplex virus:
While herpes simplex virus (HSV) infection is a sexually transmitted infection that can cause genital ulcers and lesions, it is not directly associated with an increased risk of cervical cancer. However, individuals with genital herpes may have an increased risk of acquiring human papillomavirus (HPV), which is a significant risk factor for cervical cancer.
B. Vulvovaginitis:
Vulvovaginitis refers to inflammation or infection of the vulva and vagina and can be caused by various factors, including bacterial, fungal, or viral infections. While chronic inflammation or infection may contribute to cellular changes in the cervix, it is not a direct risk factor for cervical cancer.
C. Human papillomavirus (HPV):
Human papillomavirus (HPV) infection is the most significant risk factor for developing cervical cancer. Certain high-risk strains of HPV, particularly HPV types 16 and 18, are strongly associated with the development of cervical dysplasia and cervical cancer. Persistent infection with high-risk HPV strains can lead to cellular changes in the cervix, eventually progressing to cervical cancer.
D. Chronic yeast infections:
Chronic yeast infections, also known as recurrent vulvovaginal candidiasis, are caused by the overgrowth of Candida species in the vaginal area. While chronic yeast infections can cause discomfort and recurrent symptoms, they are not directly linked to an increased risk of cervical cancer. However, chronic irritation or inflammation in the genital area may increase the susceptibility to other infections, including HPV.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is C
Explanation
A) An increase in afterload results in decreased systolic pressure, which creates a decreased cardiac output:
This statement is incorrect. According to the Frank-Starling law, afterload refers to the resistance against which the heart must pump blood during systole. An increase in afterload typically results in increased systolic pressure, not decreased, as the heart works harder to overcome the increased resistance. However, increased afterload can lead to decreased cardiac output due to the increased work of the heart.
B) A decrease in afterload causes the cardiac muscles to hypertrophy, resulting in increased diastolic volume:
This statement is incorrect. A decrease in afterload typically reduces the workload on the heart, which may lead to reverse remodeling and a reduction in cardiac hypertrophy. Increased diastolic volume may occur due to reduced afterload, but it's not the direct result of hypertrophy.
C) An increase in preload results in greater shortening of myocardial fibers, thereby increasing contractility:
Correct. The Frank-Starling law states that an increase in preload (end-diastolic volume or stretch of myocardial fibers) leads to greater overlap of actin and myosin filaments within myocardial fibers during systole. This increased overlap results in stronger myocardial contraction (increased contractility), leading to an increased stroke volume and cardiac output.
D) A decrease in preload results in increasing diastolic muscle fiber length, which impedes contractility:
This statement is incorrect. Preload refers to the degree of stretch of the myocardial fibers at the end of diastole. A decrease in preload would lead to decreased stretch of the myocardial fibers, not increasing diastolic muscle fiber length. Decreased preload typically results in decreased contractility rather than an impediment to contractility due to reduced myocardial stretch.
Correct Answer is A
Explanation
A) Histamine-mediated vascular permeability leading to fluid transudation:
Correct. Ankle edema following an ankle sprain is often due to inflammation and increased vascular permeability. Histamine, released from mast cells and basophils during the inflammatory response, causes vasodilation and increases vascular permeability. This leads to the leakage of fluid from the blood vessels into the surrounding tissues, resulting in edema.
B) Bradykinin cascade resulting in the accumulation of substance P:
While bradykinin is involved in the inflammatory response and can contribute to pain and vasodilation, it does not directly cause fluid transudation leading to edema in the context of an ankle sprain.
C) Thromboxane A activation of chemical mediators:
Thromboxane A is involved in platelet aggregation and vasoconstriction rather than increasing vascular permeability and edema formation.
D) Neutrophil migration secondary to chemotaxis:
Neutrophil migration is part of the inflammatory response and can contribute to tissue damage and inflammation, but it is not the primary mechanism responsible for the development of edema following an ankle sprain.
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