The development of atherosclerosis is a process of sequential events. Arrange the pathophysiological events in order of occurrence. Place the first event on top, and the last on the bottom.
Arterial endothelium injury causes Inflammation.
Vessel narrowing results in ischemia.
Foam cells release growth factors for smooth muscle cells.
Macrophages consume low-density lipoprotein (LDL), creating foam cells.
Smooth muscle grows over fatty streaks creating fibrous plaques.
The Correct Answer is A,D,C,E,B
This sequence starts with an injury to the arterial endothelium, leading to inflammation. Macrophages then consume LDL, forming foam cells. These foam cells release growth factors that stimulate the growth of smooth muscle cells. The smooth muscle cells grow over the fatty streaks, creating fibrous plaques. Finally, as these plaques grow, they narrow the vessel, which can result in ischemia. This is a simplified explanation of a complex process that involves many other factors and steps. It’s also important to note that this process can take many years to develop.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is C
Explanation
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.
Correct Answer is B
Explanation
Polycystic kidney disease (PKD) is a genetic disorder characterized by the formation of multiple fluid-filled cysts in the kidneys. One of the complications associated with PKD is hypertension, which often occurs due to activation of the renin-angiotensin-aldosterone system (RAAS). Here's how the pathophysiological process of the RAAS contributes to the client's elevated blood pressure:
A) Intravascular fluid deficit:
In polycystic kidney disease, the development of multiple cysts in the kidneys can impair renal function and lead to decreased filtration and reabsorption capacity. However, this impairment typically leads to fluid retention rather than intravascular fluid deficit, contributing to hypertension rather than hypotension.
B) Renin angiotensin mechanism:
Correct. In PKD, the cysts disrupt normal kidney architecture and function, leading to activation of the renin-angiotensin-aldosterone system (RAAS). Reduced renal blood flow and glomerular filtration rate (GFR) stimulate the release of renin from the juxtaglomerular cells of the kidneys. Renin acts on angiotensinogen to convert it into angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme (ACE). Angiotensin II is a potent vasoconstrictor that increases peripheral vascular resistance, leading to elevated blood pressure. Additionally, angiotensin II stimulates the secretion of aldosterone, which promotes sodium and water retention, further contributing to hypertension.
C) Inflammatory process of bladder mucosa:
This option is not directly related to the pathophysiological process of hypertension in polycystic kidney disease. Flank pain and hematuria in PKD are often associated with cyst rupture or hemorrhage within the cysts rather than an inflammatory process of the bladder mucosa.
D) Mineral precipitation in urine:
Mineral precipitation in urine, such as the formation of kidney stones, can occur in polycystic kidney disease but is not directly associated with hypertension. Kidney stones may contribute to flank pain and hematuria but do not typically cause systemic hypertension.
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