Lewis ch 47 Renal Disorders NCLEX
NCLEX renal disorder questions from Lewis Chapter 47 focusing on acute kidney injury (AKI) causes, including prerenal, intrarenal, postrenal factors, and acute tubular necrosis (ATN) scenarios.
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Lewis ch 47 Renal Disorders NCLEX
What are intrarenal causes of acute kidney injury (AKI) (select all diac apply)?
a. Anaphylaxis
b. Renal stones
c. Bladder cancer
d. Nephrotoxic drugs
e. Acute glomemlor.ephritis
f. Tubular obstruction by myoglobin -
d, e, f. Intrarenal causes of acute kidney injury (AKI)
include conditions that cause direct damage to rhe
kidney tissue, including nephrotoxic drugs, acute
glomerulonephritis, and tubular obstruction by myoglobin, or prolonged ischemia.
Anaphylaxis and ocher prerenal problems are frequently rhe initial cause of AKI. Renal stones
and bladder cancer are among the posrrenal causes of AKI.
An 83-year-old female patient was found hung on the bathroom floor. She said she fell 2
days ago and has not been able to take her heart medicine or eat or drink anything since then.
What conditions could be causing prerenal AKI in this patient (select all that apply)?
a. Anaphylaxis
b. Renal calculi
c. Hypovolemia
d. Nephrotoxic drugs
e. Decreased cardiac output -
c, e.
Because the patient has had nothing to eat or drink
for 2 days, she is probably dehydrated and hypovolemic. Decreased cardiac output (CO) is
most likely because she is older and cakes heart medicine, which is probably for heart failure
or hypertension. Both hypovolemia and decreased CO cause prerenal AKI. Anaphylaxis is
also a cause of prerer.al AKI bur is not likely in this situation. Nephrotoxic drugs would
contribute to intrarenal causes of AKI and renal calculi would be a postrenal cause of AKI.
Acute tubular necrosis (ATN) is the most common cause of intrarenal AKI. Which patient is
most likely to
develop ATN?
a. Patient with diabetes mellitus
b. Patient with hypertensive crisis
c. Patient who tried co overdose on acetaminophen
d. Patient with major surgery who required a blood transfusion -
d. Acute tubular necrosis (ATN) is primarily the result
of ischemia, nephrotoxins, or sepsis. Major surgery
is most likely to cause severe kidney ischemia in the
patient requiring a blood transfusion. A blood transfusion hemoh tic reaction produces
nephrotoxic injury if it occurs. Diabetes mellitus, hypertension, and acetaminophen overdose
will not contribute to ATN.
Priority Decision: A dehydrated patient is in the Injury stage of the RIFLE staging of AKI.
What would ±e nurse
What are intrarenal causes of acute kidney injury (AKI) (select all diac apply)?
a. Anaphylaxis
b. Renal stones
c. Bladder cancer
d. Nephrotoxic drugs
e. Acute glomemlor.ephritis
f. Tubular obstruction by myoglobin -
d, e, f. Intrarenal causes of acute kidney injury (AKI)
include conditions that cause direct damage to rhe
kidney tissue, including nephrotoxic drugs, acute
glomerulonephritis, and tubular obstruction by myoglobin, or prolonged ischemia.
Anaphylaxis and ocher prerenal problems are frequently rhe initial cause of AKI. Renal stones
and bladder cancer are among the posrrenal causes of AKI.
An 83-year-old female patient was found hung on the bathroom floor. She said she fell 2
days ago and has not been able to take her heart medicine or eat or drink anything since then.
What conditions could be causing prerenal AKI in this patient (select all that apply)?
a. Anaphylaxis
b. Renal calculi
c. Hypovolemia
d. Nephrotoxic drugs
e. Decreased cardiac output -
c, e.
Because the patient has had nothing to eat or drink
for 2 days, she is probably dehydrated and hypovolemic. Decreased cardiac output (CO) is
most likely because she is older and cakes heart medicine, which is probably for heart failure
or hypertension. Both hypovolemia and decreased CO cause prerenal AKI. Anaphylaxis is
also a cause of prerer.al AKI bur is not likely in this situation. Nephrotoxic drugs would
contribute to intrarenal causes of AKI and renal calculi would be a postrenal cause of AKI.
Acute tubular necrosis (ATN) is the most common cause of intrarenal AKI. Which patient is
most likely to
develop ATN?
a. Patient with diabetes mellitus
b. Patient with hypertensive crisis
c. Patient who tried co overdose on acetaminophen
d. Patient with major surgery who required a blood transfusion -
d. Acute tubular necrosis (ATN) is primarily the result
of ischemia, nephrotoxins, or sepsis. Major surgery
is most likely to cause severe kidney ischemia in the
patient requiring a blood transfusion. A blood transfusion hemoh tic reaction produces
nephrotoxic injury if it occurs. Diabetes mellitus, hypertension, and acetaminophen overdose
will not contribute to ATN.
Priority Decision: A dehydrated patient is in the Injury stage of the RIFLE staging of AKI.
What would ±e nurse
first anticipate in the treatment of this patient?
a. Assess daily weight
b. IV administration of fluid and furosemide (Lasix)
c. IV administration of insulin and sodium bicarbonate
d. Urinalysis to check for sediment, osmolality, sodium, and specific gravity -
b. IV administration of fluid and furosemide (Lasix)
Injur,' is the stage of RIFLE classification when urine
output is less than 0.5 mL kg hr for 12 hours, the serum
creatinine is increased times two or the glomerular
filtration rate (GFR) is decreased by 50%. This stage may
be reversible by treating the cause or, in this patient, the dehydration by administering IV
fluid and a low dose of a loop diuretic, furosemide (Lasix). Assessing the daily weight will be
done to monitor fluid changes but it is not the first treatment the nurse should anticipate. IV
administration of insulin and sodium bicarbonate would be used for hyperkalemia. Checking
the urinalysis will help to determine if the AKI has a prerenal, intrarenal, or postrenal cause
by what is seen in the urine but with this patient's dehydration, it is thought to be prerenal to
begin treatment.
What indicates to the nurse that a patient with oliguria has prerenal oliguria?
a. Urine testing reveals a low specific gravity.
b. Causative factor is malignant hypertension.
c. Urine testing reveals a high sodium concentration.
d. Reversal of oliguria occurs with fluid replacement. -
d. In prerenal oliguria, the oliguria is caused by a decrease
in circulating blood volume and there is no damage
yet to the renal tissue. It can be reversed by correcting
the precipitating factor, such as fluid replacement for
hypovolemia. Prerenal oliguria is characterized by urine
with a high specific gravity and a low sodium concentration,
whereas oliguria of intrarenal failure is characterized
by urine with a low specific gravity and a high sodium
concentration. Malignant hypertension causes damage to
renal tissue and intrarenal oliguria.
Metabolic acidosis occurs in the oliguric phase of AKI as a result of impairment of
a. ammonia synthesis.
b. excretion of sodium.
c. excretion of bicarbonate.
d. conservation of potassium. -
a. Metabolic acidosis occurs in AKI because the kidney’s
cannot synthesize ammonia or excrete acid products of
metabolism, resulting in ar. increased acid load. Sodium
is lost in urine because the kidney's cannot conserve
sodium. Impaired excretion of potassium results in
hyperkalemia. Bicarbonate is normally generated and
reabsorbed by the functioning kidney to maintain acidbase balance.
What indicates to the nurse that a patient with AKI is in the recovery phase?
a. A return to normal weight
a. Assess daily weight
b. IV administration of fluid and furosemide (Lasix)
c. IV administration of insulin and sodium bicarbonate
d. Urinalysis to check for sediment, osmolality, sodium, and specific gravity -
b. IV administration of fluid and furosemide (Lasix)
Injur,' is the stage of RIFLE classification when urine
output is less than 0.5 mL kg hr for 12 hours, the serum
creatinine is increased times two or the glomerular
filtration rate (GFR) is decreased by 50%. This stage may
be reversible by treating the cause or, in this patient, the dehydration by administering IV
fluid and a low dose of a loop diuretic, furosemide (Lasix). Assessing the daily weight will be
done to monitor fluid changes but it is not the first treatment the nurse should anticipate. IV
administration of insulin and sodium bicarbonate would be used for hyperkalemia. Checking
the urinalysis will help to determine if the AKI has a prerenal, intrarenal, or postrenal cause
by what is seen in the urine but with this patient's dehydration, it is thought to be prerenal to
begin treatment.
What indicates to the nurse that a patient with oliguria has prerenal oliguria?
a. Urine testing reveals a low specific gravity.
b. Causative factor is malignant hypertension.
c. Urine testing reveals a high sodium concentration.
d. Reversal of oliguria occurs with fluid replacement. -
d. In prerenal oliguria, the oliguria is caused by a decrease
in circulating blood volume and there is no damage
yet to the renal tissue. It can be reversed by correcting
the precipitating factor, such as fluid replacement for
hypovolemia. Prerenal oliguria is characterized by urine
with a high specific gravity and a low sodium concentration,
whereas oliguria of intrarenal failure is characterized
by urine with a low specific gravity and a high sodium
concentration. Malignant hypertension causes damage to
renal tissue and intrarenal oliguria.
Metabolic acidosis occurs in the oliguric phase of AKI as a result of impairment of
a. ammonia synthesis.
b. excretion of sodium.
c. excretion of bicarbonate.
d. conservation of potassium. -
a. Metabolic acidosis occurs in AKI because the kidney’s
cannot synthesize ammonia or excrete acid products of
metabolism, resulting in ar. increased acid load. Sodium
is lost in urine because the kidney's cannot conserve
sodium. Impaired excretion of potassium results in
hyperkalemia. Bicarbonate is normally generated and
reabsorbed by the functioning kidney to maintain acidbase balance.
What indicates to the nurse that a patient with AKI is in the recovery phase?
a. A return to normal weight
b. A urine output of 3700 mL/day
c. Decreasing sodium and potassium levels
d. Decreasing blood urea nitrogen (BUN) and creatinine levels -
d. The blood urea nitrogen (BUN) and creatinine levels
remain high during the oliguric and diuretic phases of
AKI . The recovery phase begins when the glomerular
filtration returns to a rate at which BUN and creatinine
stabilize and then decrease. Urinary output of 3 to 5 U
day, decreasing sodium and potassium levels, and
fluid weight loss are characteristic of the diuretic
phase of AKI.
While caring for the patient in the oliguric phase of AKI, the nurse monitors the patient for
associated collaborative problems. When should the nurse notify die health care prorider?
a. Urine output is 300 mL day.
b. Edema occurs in the feet, legs, and sacral area.
c. Cardiac monitor reveals a depressed T wave and elevated ST segment.
d. The patient experiences increasing muscle weakness and abdominal cramping. -
d. Hyperkalemia is a potentially life-threatening
complication of AKI in the oliguric phase. Muscle
weakness and abdominal cramping are signs of the
neuromuscular impairment that occurs with hyperkalemia. Jr. addition, h}'perkalemia car.
cause the cardiac conduction abnormalities of peaked T wave, prolonged PR interval,
prolonged QRS interval, and depressed ST segment. Urine output of 300 mL day is expected
during the oliguric phase, as is rhe development of peripheral edema.
In caring for rhe patient with AKI, what should the nurse be aware of?
a. The most common cause of death in xAKI is irreversible metabolic acidosis.
b. During the oliguric phase of AKI, daily fluid intake is limited co 1000 mL plus the prior
day's measured fluid loss.
c. Dietar}7 sodium and potassium during the oliguric phase of AKI are managed according to
the patient's urinary output.
d. One of the most important nursing measures in managing fluid balance in the patient with
AKI is taking accurate daily weights. -
d. Measuring, daily weights with the same scale at the
same time each day allows for the evaluation and detection of excessive body fluid gains or
losses. Infection is the leading cause of death in AKI, so meticulous aseptic technique is
critical. The fluid limitation in the oliguric phase is 600 mL plus the prior day's measured
fluid loss. Dietar}7 sodium and potassium intake are managed according to the plasma levels.
A 68-year-old man with a history of heart failure resulting from hypertension has AKI as a
result of the effects of nephrotoxic diuretics. Currently his serum potassium is 6.2 iriEq.'L (6.2
mmol L) with cardiac changes, his BUN is 108 mg-’dL (38.6 mmoL'L), his serum creatinine is
4.1 mg dL (362 mmol L), and his serum HCO3- is 14 mEq.'L (14 mmol L). He is somnolent
and disoriented. Which treatment should the nurse expect to be used for him?
a. Loop diuretics
b. Renal replacement therapy
c. Insulin and sodium bicarbonate
d. Sodium polystyrene sulfonate (Kayexalate) -
b. This patient has at least three of the six common
c. Decreasing sodium and potassium levels
d. Decreasing blood urea nitrogen (BUN) and creatinine levels -
d. The blood urea nitrogen (BUN) and creatinine levels
remain high during the oliguric and diuretic phases of
AKI . The recovery phase begins when the glomerular
filtration returns to a rate at which BUN and creatinine
stabilize and then decrease. Urinary output of 3 to 5 U
day, decreasing sodium and potassium levels, and
fluid weight loss are characteristic of the diuretic
phase of AKI.
While caring for the patient in the oliguric phase of AKI, the nurse monitors the patient for
associated collaborative problems. When should the nurse notify die health care prorider?
a. Urine output is 300 mL day.
b. Edema occurs in the feet, legs, and sacral area.
c. Cardiac monitor reveals a depressed T wave and elevated ST segment.
d. The patient experiences increasing muscle weakness and abdominal cramping. -
d. Hyperkalemia is a potentially life-threatening
complication of AKI in the oliguric phase. Muscle
weakness and abdominal cramping are signs of the
neuromuscular impairment that occurs with hyperkalemia. Jr. addition, h}'perkalemia car.
cause the cardiac conduction abnormalities of peaked T wave, prolonged PR interval,
prolonged QRS interval, and depressed ST segment. Urine output of 300 mL day is expected
during the oliguric phase, as is rhe development of peripheral edema.
In caring for rhe patient with AKI, what should the nurse be aware of?
a. The most common cause of death in xAKI is irreversible metabolic acidosis.
b. During the oliguric phase of AKI, daily fluid intake is limited co 1000 mL plus the prior
day's measured fluid loss.
c. Dietar}7 sodium and potassium during the oliguric phase of AKI are managed according to
the patient's urinary output.
d. One of the most important nursing measures in managing fluid balance in the patient with
AKI is taking accurate daily weights. -
d. Measuring, daily weights with the same scale at the
same time each day allows for the evaluation and detection of excessive body fluid gains or
losses. Infection is the leading cause of death in AKI, so meticulous aseptic technique is
critical. The fluid limitation in the oliguric phase is 600 mL plus the prior day's measured
fluid loss. Dietar}7 sodium and potassium intake are managed according to the plasma levels.
A 68-year-old man with a history of heart failure resulting from hypertension has AKI as a
result of the effects of nephrotoxic diuretics. Currently his serum potassium is 6.2 iriEq.'L (6.2
mmol L) with cardiac changes, his BUN is 108 mg-’dL (38.6 mmoL'L), his serum creatinine is
4.1 mg dL (362 mmol L), and his serum HCO3- is 14 mEq.'L (14 mmol L). He is somnolent
and disoriented. Which treatment should the nurse expect to be used for him?
a. Loop diuretics
b. Renal replacement therapy
c. Insulin and sodium bicarbonate
d. Sodium polystyrene sulfonate (Kayexalate) -
b. This patient has at least three of the six common
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