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Lewis Chapter 46 Acute Kidney Injury and Chronic Kidney Disease Questions with 100% Actual correct answers | verified | latest update | Graded A+ | Already Passed | Complete Solution CA$11.16   Add to cart
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Lewis Chapter 46 Acute Kidney Injury and Chronic Kidney Disease Questions with 100% Actual correct answers | verified | latest update | Graded A+ | Already Passed | Complete Solution

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Lewis Chapter 46 Acute Kidney Injury and Chronic Kidney Disease Questions with 100% Actual correct answers | verified | latest update | Graded A+ | Already Passed | Complete Solution

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Lewis Chapter 46: Acute Kidney Injury
and Chronic Kidney Disease
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.


We have an expert-written solution to this problem!
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
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. 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.


We have an expert-written solution to this problem!
In a patient with AKI, which laboratory urinalysis result indicates tubular
damage?
a. Hematuria
b. Specific gravity fixed at 1.010
c. Urine sodium of 12 mEq/L (12 mmol/L)
d. Osmolality of 1000 mOsm/kg (1000 mmol/kg)
b. A urine specific gravity that is consistently 1.010 and a
urine osmolality of about 300 mOsm/kg is the same specific gravity and
osmolality as plasma. This indicates that tubules are damaged and unable to
concentrate urine. Hematuria is more common with postrenal damage.
Tubular damage is associated with a high sodium concentration (greater than
40 mEq/L).


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
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.


We have an expert-written solution to this problem!
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,

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