A client has decreased glomerular filtration due to vasoconstriction of the afferent arteriole. What outcome should the nurse anticipate?
Decreased urine output
Elevated glomerular pressure
Increased filtrate production
Increased blood urea nitrogen clearance
The Correct Answer is A
Rationale:
A. Vasoconstriction of the afferent arteriole reduces blood flow into the glomerulus, which lowers glomerular filtration rate (GFR). A reduced GFR results in less filtrate formation, leading to oliguria (decreased urine output). This is a common physiologic response in conditions such as hypovolemia or acute kidney injury, where the body attempts to conserve fluid.
B. Constriction of the afferent arteriole decreases hydrostatic pressure within the glomerular capillaries, lowering filtration pressure. Glomerular pressure would actually decrease, not increase, in this scenario.
C. Increased filtrate production is incorrect. Reduced blood flow into the glomerulus decreases the amount of plasma filtered across the glomerular membrane, so filtrate production declines rather than increases.
D. Increased blood urea nitrogen (BUN) clearance is incorrect. When GFR decreases, the kidneys filter less urea, leading to elevated BUN levels in the blood. Clearance of BUN is reduced, not increased, during afferent arteriole vasoconstriction.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is B
Explanation
Rationale:
A. Recurrent urinary frequency may occur as a symptom of urinary tract obstruction or irritation, but it is a relatively minor and common manifestation. While uncomfortable for the client, urinary frequency itself is not the most serious or life-threatening complication of hydronephrosis.
B. Renal failure is the primary concern in a client with hydronephrosis caused by an untreated kidney stone. Hydronephrosis occurs when urine flow is obstructed, leading to increased pressure within the renal pelvis and calyces. This pressure compresses renal tissue, impairs blood flow, and damages nephrons. If the obstruction persists, it can result in progressive kidney damage and potentially irreversible renal failure. The longer the obstruction remains untreated, the higher the risk of permanent loss of renal function, making renal failure the most serious and concerning complication.
C. Diabetic nephropathy is a form of chronic kidney disease caused by long-term diabetes mellitus. It is unrelated to hydronephrosis from urinary obstruction. While clients with diabetes may have an increased risk of kidney disease, diabetic nephropathy is not a direct complication of untreated kidney stones.
D. Orthostatic hypotension is a drop in blood pressure upon standing, often caused by dehydration, autonomic dysfunction, or certain medications. It is not a direct complication of hydronephrosis and is less clinically urgent than the risk of renal failure in this context.
Correct Answer is B
Explanation
Rationale:
A. Neprilysin is an enzyme that breaks down natriuretic peptides and other vasoactive substances but does not convert angiotensin I to angiotensin II. Its role in the RAAS is indirect and involves modulation of vasodilation rather than the direct formation of angiotensin II.
B. ACE is a key enzyme in the renin-angiotensin-aldosterone system (RAAS). It converts angiotensin I, an inactive decapeptide, into angiotensin II, a potent vasoconstrictor. Angiotensin II increases blood pressure by causing vasoconstriction, stimulating aldosterone release from the adrenal cortex, and promoting sodium and water reabsorption in the kidneys. This conversion is central to regulating blood pressure and fluid balance.
C. Aldosterone is a hormone released by the adrenal cortex in response to angiotensin II. It promotes sodium and water reabsorption in the distal tubules and collecting ducts, increasing blood volume and pressure, but it does not catalyze the conversion of angiotensin I to angiotensin II.
D. Renin is an enzyme secreted by the juxtaglomerular cells of the kidney in response to low blood pressure or sympathetic stimulation. It cleaves angiotensinogen into angiotensin I, the inactive precursor, but it does not convert angiotensin I to angiotensin II.
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