The nurse is caring for a client who is admitted with polycystic kidney disease (PKD), flank pain, and hematuria. The client's blood pressure is 180/100 mm Hg. Which pathophysiological process supports the client's blood pressure finding?
Intravascular fluid deficit.
Renin angiotensin mechanism.
Inflammatory process of bladder mucosa.
Mineral precipitation in urine.
The Correct Answer is B
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.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is B
Explanation
A) Elevation in blood pressure:
While elevation in blood pressure could potentially cause discomfort at the arterial line insertion site, it is not the most likely physiological effect to induce sudden pain in this scenario. Blood pressure elevation would typically cause generalized symptoms rather than localized pain at the insertion site.
B) Vasospasm at insertion site:
Correct. Vasospasm refers to the sudden constriction of blood vessels, leading to reduced blood flow. It can occur in response to arterial puncture or manipulation during arterial line insertion, resulting in sudden pain at the insertion site.
C) Clot in the arterial catheter:
A clot in the arterial catheter could potentially cause obstruction and affect blood flow, but it is less likely to induce sudden pain at the insertion site unless there is associated ischemia or tissue damage.
D) Air lock in the transducer:
An air lock in the transducer could disrupt pressure monitoring but is not typically associated with sudden pain at the insertion site. It may lead to inaccurate pressure readings rather than localized pain.
Correct Answer is A
Explanation
A) Blockage of retinal capillaries causing ischemic damage of the central macular area:
Correct. Blurry central vision that worsens over time can be indicative of macular ischemia, often caused by blockage of retinal capillaries leading to ischemic damage of the central macular area. This condition can occur in diseases such as diabetic retinopathy or retinal vein occlusion.
B) Opaque spoke-like lines developing in the periphery of the lens to the center:
This description is more characteristic of cataracts, which cause visual disturbances such as glare or halos around lights rather than blurry central vision.
C) Tears in the retina that detach from the lining of the posterior eyeball:
Retinal tears and subsequent detachment can cause visual disturbances, but they typically present as sudden onset of floaters, flashes of light, and a curtain-like shadow over the visual field rather than blurry central vision.
D) An increase in intraocular pressure with loss of peripheral vision:
This description is indicative of glaucoma, which can lead to loss of peripheral vision (visual field defects) rather than blurry central vision. Glaucoma-related visual field loss usually begins peripherally and progresses inward, affecting central vision in later stages.
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