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
Acute leukemia, including acute myeloid leukemia (AML), involves the proliferation of abnormal myeloblasts (immature white blood cells) in the bone marrow, leading to decreased production of normal blood cells. Here's the breakdown of the pathophysiology contributing to bruising in acute leukemia:
A) Oxyhemoglobin provides less oxygen to tissues:
Oxyhemoglobin refers to hemoglobin bound to oxygen, and its role is in oxygen transport, not in the process of bruising. Therefore, this option is not directly related to the pathophysiology of bruising in acute leukemia.
B) Insufficient platelets delay the clotting process:
Correct. Thrombocytopenia, or low platelet count, is a common complication of acute leukemia due to the replacement of normal bone marrow cells with leukemia cells, leading to inadequate production of platelets. Platelets play a crucial role in hemostasis and clot formation. Insufficient platelets result in delayed clotting, leading to easy bruising and bleeding tendencies in patients with acute leukemia.
C) Phagocytic cells are inadequate in fighting infection:
Leukopenia, or low white blood cell count, can occur in acute leukemia due to suppression of normal hematopoiesis by leukemia cells in the bone marrow. While leukopenia predisposes patients to infections due to impaired immune function, it is not directly related to the pathophysiology of bruising.
D) Lack of iron causes hypochromic blood cells:
Iron deficiency anemia can result in hypochromic red blood cells, but this is not typically associated with the pathophysiology of bruising in acute leukemia. Anemia may contribute to other symptoms such as fatigue and pallor, but bruising primarily results from thrombocytopenia-induced clotting abnormalities.
Correct Answer is A
Explanation
A) Flank pain and profound hypotension:
Correct. Flank pain, often described as a deep, constant, gnawing, or throbbing sensation in the abdomen or back, can be a sign of impending rupture or dissection of an abdominal aortic aneurysm (AAA). Profound hypotension may occur if the AAA ruptures, leading to massive internal bleeding and shock. Prompt recognition of these signs is crucial for early intervention and surgical repair to prevent catastrophic consequences.
B) Acute shortness of breath and chest pain:
Acute shortness of breath and chest pain are more indicative of cardiovascular or pulmonary conditions such as myocardial infarction, pulmonary embolism, or acute coronary syndrome rather than an abdominal aortic aneurysm. While aortic dissection can present with chest pain, it is typically described as severe, tearing, or ripping pain that radiates to the back, not as acute shortness of breath.
C) Absent pedal pulses and darkened toes:
Absent pedal pulses and darkened toes may indicate peripheral vascular disease or critical limb ischemia but are not specific signs of an abdominal aortic aneurysm. While AAA can lead to peripheral ischemia in advanced cases, it is not typically associated with acute changes in pedal pulses or toe discoloration.
D) Tea-colored urine and decreased output:
Tea-colored urine and decreased urine output may indicate acute kidney injury or rhabdomyolysis but are not specific signs of an abdominal aortic aneurysm. While a ruptured AAA can lead to renal ischemia and acute kidney injury due to hypoperfusion, these symptoms are not the primary manifestations of AAA
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