Lewis ch 47 Renal Disorders NCLEX
What are intrarenal causes of acute kidney injury (AKI) (select all that apply)?
a. Anaphylaxis
b. Renal stones
c. Bladder cancer
d. Nephrotoxic drugs
e. Acute glomerulonephritis
f. Tubular obstruction by myoglobin - d, e, f. Intrarenal causes of acute kidney injury
(AKI)
include conditions that cause direct damage to the kidney tissue, including
nephrotoxic drugs, acute glomerulonephritis, and tubular obstruction by
myoglobin, or prolonged ischemia.
Anaphylaxis and other prerenal problems are frequently the initial cause of AKI. Renal stones
and bladder cancer are among the postrenal causes of AKI.
An 83-year-old female patient was found lying 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
takes heart medicine, which is probably for heart failure or hypertension. Both hypovolemia
and decreased CO cause prerenal AKI. Anaphylaxis is also a cause of prerenal AKI but 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 to 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 hemolytic
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 the nurse
1|Page
,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)
Injury 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 kidneys cannot synthesize ammonia
or excrete acid products of metabolism, resulting in an increased acid load.
Sodium is lost in urine because the kidneys 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
2|Page
, 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 L/ 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 the health care
provider? 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. In addition, hyperkalemia can 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 the development of peripheral edema.
In caring for the patient with AKI, what should the nurse be aware of?
a. The most common cause of death in AKI is irreversible metabolic acidosis.
b. During the oliguric phase of AKI, daily fluid intake is limited to 1000 mL plus the prior
day's measured fluid loss.
c. Dietary 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. Dietary 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 mEq/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
3|Page
What are intrarenal causes of acute kidney injury (AKI) (select all that apply)?
a. Anaphylaxis
b. Renal stones
c. Bladder cancer
d. Nephrotoxic drugs
e. Acute glomerulonephritis
f. Tubular obstruction by myoglobin - d, e, f. Intrarenal causes of acute kidney injury
(AKI)
include conditions that cause direct damage to the kidney tissue, including
nephrotoxic drugs, acute glomerulonephritis, and tubular obstruction by
myoglobin, or prolonged ischemia.
Anaphylaxis and other prerenal problems are frequently the initial cause of AKI. Renal stones
and bladder cancer are among the postrenal causes of AKI.
An 83-year-old female patient was found lying 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
takes heart medicine, which is probably for heart failure or hypertension. Both hypovolemia
and decreased CO cause prerenal AKI. Anaphylaxis is also a cause of prerenal AKI but 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 to 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 hemolytic
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 the nurse
1|Page
,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)
Injury 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 kidneys cannot synthesize ammonia
or excrete acid products of metabolism, resulting in an increased acid load.
Sodium is lost in urine because the kidneys 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
2|Page
, 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 L/ 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 the health care
provider? 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. In addition, hyperkalemia can 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 the development of peripheral edema.
In caring for the patient with AKI, what should the nurse be aware of?
a. The most common cause of death in AKI is irreversible metabolic acidosis.
b. During the oliguric phase of AKI, daily fluid intake is limited to 1000 mL plus the prior
day's measured fluid loss.
c. Dietary 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. Dietary 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 mEq/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
3|Page
