CH 51: Acute Kidney Injury Flashcards

Question

Which of the following are known causes of intrarenal AKI? (SATA) A. Severe hypotension B. Systemic lupus erythematosus C. Contrast media D. Enlarged prostate E. Hemoglobin release from hemolysis

Answer 1

A. Severe hypotension B. Systemic lupus erythematosus C. Contrast media E. Hemoglobin release from hemolysis Rationale: All options except the enlarged prostate are intrarenal causes. BPH is a postrenal cause. Intrarenal injury stems from ischemia, autoimmune disease, nephrotoxins, and obstruction by heme pigments.

Answer 2

C. Ensure adequate hydration before and after the procedure Rationale: Hydration helps dilute and flush contrast media, reducing nephrotoxic effects on renal tubules.

Answer 3

D. Aggressive IV fluid resuscitation Rationale: Rhabdomyolysis releases myoglobin, which can damage kidneys. Fluid resuscitation dilutes toxins and prevents tubular obstruction.

Answer 4

B. Necrosis of tubular epithelial cells causing obstruction Rationale: Nephrotoxins cause necrosis of epithelial cells, which slough off and plug the tubules, disrupting kidney function and leading to ATN.

Answer 5

A. Intrarenal AKI Rationale: Lupus can cause glomerulonephritis and immune complex-mediated injury, leading to intrarenal damage and impaired nephron function.

Answer 6

A. Prolonged hypoperfusion Rationale: Sepsis often leads to systemic hypotension, reducing renal perfusion. Prolonged ischemia contributes to acute tubular necrosis, a common cause of intrarenal AKI.

Answer 7

A. Sepsis B. Contrast-induced nephropathy D. Blood transfusion reaction E. Muscle injury from trauma Rationale: ATN is caused by ischemia or nephrotoxins, including sepsis, contrast agents, transfusion reactions (hemolysis), and muscle trauma (rhabdomyolysis). Ureteral obstruction is a postrenal issue.

Answer 8

C. A patient receiving IV vancomycin and has elevated creatinine Rationale: Vancomycin is nephrotoxic, and rising creatinine suggests intrarenal injury. This is a classic case of nephrotoxic ATN due to direct damage to tubular epithelium.

Answer 9

D. Bilateral flank pain and decreased urine output Rationale: Postrenal AKI results from mechanical obstruction of urine flow, often presenting with bilateral flank pain due to hydronephrosis and reduced urine output. These are hallmark signs of bilateral ureteral obstruction.

Answer 10

C. Insert an indwelling urinary catheter Rationale: A distended bladder in a patient with known prostate cancer suggests bladder outlet obstruction. Inserting a catheter relieves the obstruction and can reverse postrenal AKI if done early.

Answer 11

A. Prostate cancer B. Bilateral ureteral obstruction D. Ureteral trauma E. Kidney stones Rationale: Postrenal AKI is caused by any obstruction in the urinary outflow tract, including tumors (like prostate cancer), trauma, bilateral obstruction, and calculi. Severe burns are typically a prerenal cause.

Answer 12

C. Reflux of urine into the renal pelvis causing increased pressure Rationale: In postrenal AKI, obstruction causes urine to back up into the kidneys, increasing hydrostatic pressure, leading to impaired filtration and possible tubular atrophy.

Answer 13

B. Obstruction of urinary outflow from the prostate Rationale: BPH causes mechanical blockage at the bladder neck, which is a classic postrenal cause of AKI. This leads to backflow of urine and kidney dysfunction.

Answer 14

B. Increased urine output and stabilized creatinine levels Rationale: Relief of a postrenal obstruction should restore urine flow and improve kidney function. Rising output and stable creatinine reflect a positive response.

Answer 15

D. It is caused by mechanical blockage of urine and is potentially reversible if treated early. Rationale: Postrenal AKI results from mechanical obstruction and accounts for less than 10% of cases. If addressed within 48 hours, recovery is often complete.

Answer 16

B. A patient with sepsis and prolonged hypotension Rationale: Septic shock leads to decreased peripheral vascular resistance and renal hypoperfusion, making it a prerenal cause of AKI.

Answer 17

B. Decreased renal perfusion Rationale: Cardiogenic shock leads to decreased cardiac output, a hallmark prerenal cause of AKI due to hypoperfusion of the kidneys.

Answer 18

A. Prolonged prerenal ischemia B. Acute glomerulonephritis D. Exposure to ethylene glycol E. Acute pyelonephritis Rationale: Intrarenal AKI is due to direct kidney tissue damage. BPH is a postrenal cause.

Answer 19

C. Prerenal Rationale: Dehydration leads to reduced circulating volume, making this a classic example of prerenal AKI.

Answer 20

A. Postrenal from obstructed urine outflow Rationale: Trauma to the pelvis can result in urinary tract obstruction, a postrenal cause of AKI.

Answer 21

A. Use of NSAIDs and sulfonamides Rationale: These drugs are associated with allergic interstitial nephritis, a type of intrarenal AKI.

Answer 22

A. MI B. Hypoalbuminemia C. Anaphylaxis E. GI losses Rationale: All options except BPH (a postrenal cause) lead to decreased renal perfusion and are classified as prerenal.

Answer 23

C. Nephrotoxic injury Rationale: IV contrast is a known nephrotoxin and contributes to intrarenal AKI.

Answer 24

C. Elevated serum creatinine Rationale: Ethylene glycol is a nephrotoxic chemical; rising creatinine indicates impaired renal function.

Answer 25

D. BPH Rationale: Benign prostatic hyperplasia causes obstruction of urine flow and is a leading postrenal cause of AKI in older males.

Answer 26

A. Gentamicin B. Amphotericin B C. Lead E. Carbon tetrachloride Rationale: These are nephrotoxic substances. ACE inhibitors are associated with interstitial nephritis.

Answer 27

C. Decreased urine output Rationale: Prerenal AKI leads to oliguria due to decreased renal perfusion. BUN often rises out of proportion to creatinine.

Answer 28

A. Atrial fibrillation Rationale: Atrial fibrillation increases embolic risk, which may lead to renal artery thrombosis, a prerenal cause of AKI.

Answer 29

C. Impaired bladder emptying Rationale: Neuromuscular disorders can cause bladder atony or dysfunction, resulting in urinary retention and postrenal obstruction.

Answer 30

D. Intrarenal from prolonged ischemia Rationale: In septic shock, prolonged hypotension can cause ischemic injury to nephrons, progressing to intrarenal AKI.

Answer 31

B. Intrarenal due to glomerular inflammation Rationale: SLE can lead to glomerulonephritis, which damages the glomeruli and causes intrarenal AKI.

Answer 32

A. Embolism B. Renal artery thrombosis D. Hepatorenal syndrome Rationale: These conditions specifically affect blood flow to the kidneys. Burns and cardiogenic shock reduce overall perfusion, but not specifically renovascular flow.

Answer 33

D. Amikacin Rationale: Amikacin is an aminoglycoside and is nephrotoxic, making it a high-risk drug for intrarenal AKI.

Answer 34

C. Postrenal Rationale: Bladder cancer can obstruct urinary outflow, especially if bilateral, leading to postrenal AKI.

Answer 35

B. A patient with recent Epstein-Barr virus infection and NSAID use Rationale: Viral infections and NSAIDs are known triggers for interstitial nephritis, an intrarenal cause of AKI.

Answer 36

A. Prerenal AKI Rationale: Prerenal AKI, when treated early and before any nephron damage occurs, typically resolves quickly with volume restoration. This reversible nature distinguishes it from intrarenal or prolonged postrenal causes.

Answer 37

A. Progression through oliguric, diuretic, and recovery phases Rationale: Once kidney tissue damage occurs, as with intrarenal AKI, the clinical course typically progresses through three distinct phases: oliguric (low urine output), diuretic (gradual increase in urine output), and recovery (stabilization and return of kidney function).

Answer 38

B. The AKI was postrenal and resolved before intrarenal damage occurred. Rationale: Postrenal AKI from obstruction (such as BPH) that is treated early—before nephron damage—can resolve rapidly. A quick return of urine output and lab normalization supports this.

Answer 39

C. Failure Rationale: The RIFLE criteria progress from Risk (mildest) to Injury (moderate) to Failure (most severe of the three stages). “Loss” and “ESRD” are outcome classifications, not stages.

Answer 40

A. “Loss and End-stage renal disease refer to the potential outcomes of AKI.” Rationale: RIFLE includes three graded stages of AKI severity—Risk, Injury, Failure—and two outcome categories: Loss (complete loss of kidney function for >4 weeks) and End-stage renal disease (ESRD), which is complete loss for >3 months.

Answer 41

C. Oliguria occurring within 1 week Rationale: Nephrotoxic injury can delay the onset of oliguria for up to a week after the initial insult, whereas ischemic causes typically result in oliguria within 24 hours.

Answer 42

A. Urine output of 200 mL/day B. Fixed urine specific gravity of 1.010 D. Urinalysis with WBCs and RBCs Rationale: Oliguria is defined as urine output <400 mL/day. Fixed specific gravity around 1.010 and the presence of RBCs/WBCs on urinalysis are signs of tubular damage. Creatinine would typically be elevated in AKI, and urine osmolality would not be high due to loss of concentrating ability.

Answer 43

B. Urinary tract obstruction Rationale: Anuria (no urine output) is most commonly associated with urinary tract obstruction (postrenal AKI).

Answer 44

C. Prerenal AKI Rationale: Hypovolemia and hypotension point toward decreased renal perfusion, which is a prerenal cause. Oliguria is common in prerenal AKI.

Answer 45

D. Fixed specific gravity of 1.010 Rationale: A fixed specific gravity around 1.010 reflects an inability of the tubules to concentrate urine, indicating damage to the tubular epithelium.

Answer 46

B. Intrarenal tubular damage Rationale: Casts are formed when necrotic tubular epithelial cells slough off and take the shape of the tubules, indicating tubular injury typical in ATN.

Answer 47

A. Urine output of 100 mL/day B. Occurrence of the phase within 1 day in ischemic injury D. Potential duration of 2 weeks or more Rationale: Oliguria is <400 mL/day, and ischemia causes it to occur rapidly, usually within 24 hours. This phase may last 10–14 days or even months. Specific gravity is usually fixed, not increased, and recovery is not rapid.

Answer 48

C. Loss of kidney concentrating ability Rationale: A urine osmolality equal to plasma osmolality (~300 mOsm/kg) indicates that the kidney has lost its ability to concentrate urine, commonly due to tubular damage in intrarenal AKI.

Answer 49

B. Intrarenal AKI Rationale: The presence of proteinuria and epithelial cell casts in the setting of nephrotoxin exposure is consistent with tubular injury, an intrarenal cause.

Answer 50

D. Prolonged oliguric phase beyond 3 weeks Rationale: The longer the oliguric phase lasts, the worse the prognosis for full recovery of renal function. Recovery is less likely if it extends beyond 2–3 weeks.

Answer 51

B. Glomerular membrane dysfunction Rationale: Proteinuria is typically a sign of glomerular membrane damage, commonly seen in conditions like glomerulonephritis.

Answer 52

D. Intrarenal AKI due to myoglobin-induced nephropathy Rationale: Myoglobin from necrotic muscle causes tubular obstruction and vasoconstriction, resulting in intrarenal AKI (acute tubular necrosis).

Answer 53

A. Fluid replacement to correct hypovolemia Rationale: Fluid replacement is crucial in prerenal AKI, especially when hypovolemia is the cause. Rehydration helps restore kidney perfusion and prevent further damage.

Answer 54

B. Bounding pulse and distended neck veins Rationale: Fluid retention causes vascular congestion, leading to distended neck veins and a bounding pulse due to the increased fluid volume.

Answer 55

B. Congestive heart failure Rationale: Fluid overload in AKI can lead to heart failure as the excess fluid burden causes the heart to work harder, potentially leading to CHF and pulmonary edema.

Answer 56

C. Administer fluids cautiously to avoid further overload Rationale: Fluid management must be cautious, as the patient may already be experiencing fluid overload. Overzealous fluid administration can worsen the situation and lead to complications like pulmonary edema or heart failure.

Answer 57

A. Hypertension B. Pulmonary edema D. Hyperkalemia E. Pericardial effusion Rationale: Severe fluid overload can lead to hypertension, pulmonary edema, and pericardial effusion due to increased fluid retention. Hyperkalemia may also occur as a result of kidney dysfunction and inability to excrete potassium. Decreased urine output is a hallmark of AKI, but it is a primary manifestation, not a consequence of fluid overload.

Answer 58

D. Decreased pH Rationale: In metabolic acidosis, the body’s inability to excrete hydrogen ions and the depletion of bicarbonate lead to a decrease in pH, resulting in acidosis. The increased respiratory rate and deep respirations are compensatory mechanisms to expel CO2 and try to normalize pH.

Answer 59

B. Rapid, deep respirations to expel CO2 Rationale: The body compensates for metabolic acidosis by increasing respiratory rate and depth (Kussmaul respirations) to expel CO2, which helps raise the pH by decreasing carbonic acid levels.

Answer 60

A. Monitor the patient’s respiratory rate and depth closely to assess for compensation Rationale: In metabolic acidosis, the body compensates by increasing respiratory rate and depth to expel CO2. Monitoring the patient’s breathing pattern will help assess the effectiveness of this compensatory mechanism.

Answer 61

D. Increased CO2 exhalation Rationale: Kussmaul respirations are deep, rapid breaths that occur as a compensatory mechanism to expel CO2, which helps to reduce carbonic acid levels and increase pH, counteracting the effects of metabolic acidosis.

Answer 62

A. Decreased pH and impaired buffering of acids Rationale: Impaired kidney function in metabolic acidosis results in an inability to excrete hydrogen ions or regenerate bicarbonate, leading to a decreased pH and impaired acid buffering capacity, which worsens acidosis.

Answer 63

B. Normal or below-normal serum sodium Rationale: Damaged tubules in AKI cannot effectively conserve sodium, leading to increased urinary sodium excretion. This typically results in normal or below-normal serum sodium levels, as the kidneys are unable to retain sodium properly.

Answer 64

C. Heart failure Rationale: Excessive sodium intake in AKI can lead to volume expansion, increasing blood volume and contributing to hypertension and heart failure due to the increased fluid burden on the heart.

Answer 65

B. Cerebral edema Rationale: Uncontrolled hyponatremia or water excess can cause cerebral edema, a dangerous complication that can lead to altered mental status and increased intracranial pressure.

Answer 66

B. Impaired potassium excretion Rationale: The kidneys are responsible for excreting 80-90% of the body’s potassium. In AKI, this ability is impaired, leading to the accumulation of potassium in the bloodstream and increasing the risk of hyperkalemia.

Answer 67

A. Release of potassium from damaged cells Rationale: Massive tissue trauma causes cellular destruction, which releases potassium into the extracellular fluid, increasing the risk of hyperkalemia in patients with AKI.

Answer 68

C. Hydrogen ions entering the cells, pushing potassium into the extracellular fluid Rationale: In metabolic acidosis, hydrogen ions enter the cells, displacing potassium into the extracellular fluid, which exacerbates hyperkalemia.

Answer 69

A. Peaked T waves, widening of the QRS complex, and ST segment depression Rationale: In patients with severe hyperkalemia, the ECG typically shows peaked T waves, widening of the QRS complex, and ST segment depression. These changes indicate the acute effect of elevated potassium on cardiac conduction.

Answer 70

A. Monitor for ECG changes Rationale: While the patient may be asymptomatic, the nurse must monitor for ECG changes, such as peaked T waves or widened QRS complex, as these are signs of severe hyperkalemia that may lead to life-threatening arrhythmias.

Answer 71

D. Give intravenous calcium to stabilize the cardiac membrane Rationale: Intravenous calcium helps stabilize the cardiac membrane and protect against life-threatening arrhythmias caused by hyperkalemia, which is the most urgent intervention.

Answer 72

C. Insulin and glucose Rationale: Insulin and glucose are used to shift potassium into the cells, lowering serum potassium levels in hyperkalemic patients. This is an essential treatment in the acute management of hyperkalemia.

Answer 73

D. Release of potassium from damaged red blood cells Rationale: Hemolysis of red blood cells, such as from bleeding or blood transfusions, can release potassium into the extracellular fluid, exacerbating hyperkalemia in patients with AKI.

Answer 74

B. Urinary system Rationale: In patients with AKI, the most common sites of infection are the urinary and respiratory systems, with the urinary system being particularly prone to infection due to decreased renal function and possible urinary stasis.

Answer 75

B. Infection Rationale: Leukocytosis, an elevated white blood cell count, is commonly seen in patients with AKI, especially when they have infections. Infection is the most common cause of death in AKI patients, and it often presents with leukocytosis.

Answer 76

B. Risk for infection due to leukocytosis Rationale: In patients with AKI and multiorgan failure, infection is the most common cause of death. Leukocytosis often occurs as a response to infection, so monitoring and managing infection risk is a priority in these patients.

Answer 77

C) BUN levels can be influenced by dehydration, corticosteroids, and catabolism, but creatinine levels are more reliable for diagnosing AKI. Rationale: Serum creatinine is considered the best serum indicator of AKI because it is not influenced by factors such as dehydration, corticosteroid use, or catabolism, whereas BUN levels can be affected by these conditions.

Answer 78

A) Recent corticosteroid therapy Rationale: An increase in BUN levels can be caused by dehydration, corticosteroid therapy, or catabolic states such as infections or fever, all of which increase protein metabolism.

Answer 79

B) Acute kidney injury Rationale: The elevated serum creatinine level is a more reliable indicator of acute kidney injury (AKI) than BUN because creatinine is not influenced by factors such as dehydration, corticosteroid use, or infection, making it the best marker for kidney function.

Answer 80

D) Serum creatinine Rationale: Serum creatinine is considered the best serum indicator of AKI because it reflects kidney function more reliably than BUN, which can be influenced by factors like hydration status, corticosteroid use, and catabolic states.

Answer 81

B) Fatigue and difficulty concentrating Rationale: Accumulation of nitrogenous waste products, such as urea, in the brain can lead to neurologic symptoms ranging from mild fatigue and difficulty concentrating to more severe manifestations like seizures, stupor, and coma.

Answer 82

B) Accumulation of nitrogenous waste products in the brain Rationale: Neurologic symptoms, such as fatigue and difficulty concentrating, can occur due to the accumulation of nitrogenous waste products in the brain and other nervous tissues during acute kidney injury (AKI).

Answer 83

A) Hyponatremia Rationale: During the diuretic phase of AKI, large volumes of urine are excreted, which increases the risk of electrolyte imbalances like hyponatremia, hypokalemia, and dehydration due to the loss of sodium and potassium.

Answer 84

D) Osmotic diuresis from high urea concentrations Rationale: Osmotic diuresis from high urea concentrations in the glomerular filtrate causes increased urine output during the diuretic phase of AKI, leading to fluid and electrolyte imbalances, including hypotension.

Answer 85

D) Hyponatremia Rationale: Excessive fluid and electrolyte losses during the diuretic phase of AKI can result in hyponatremia, hypokalemia, and dehydration due to the inability of the kidneys to concentrate urine effectively.

Answer 86

B) 1 to 3 L/day Rationale: During the diuretic phase of AKI, urine output typically increases to 1 to 3 L/day, and it may reach up to 5 L or more, though the kidneys still have difficulty concentrating the urine.

Answer 87

C) Hyponatremia Rationale: During the diuretic phase of AKI, large fluid losses increase the risk for electrolyte imbalances, such as hyponatremia, hypokalemia, and dehydration, due to the increased urine output and inability of the kidneys to concentrate urine.

Answer 88

B) Measuring fluid intake and output Rationale: Monitoring fluid intake and output is essential during the diuretic phase of AKI to manage fluid balance, monitor for dehydration, and detect electrolyte imbalances such as hyponatremia and hypokalemia.

Answer 89

A) Stabilization of acid-base and electrolyte levels Rationale: Near the end of the diuretic phase of AKI, the patient’s acid-base, electrolyte, and waste product levels (BUN, creatinine) stabilize, indicating recovery and improvement in kidney function.

Answer 90

C) Increased GFR with decreased BUN and creatinine Rationale: During the recovery phase of AKI, the glomerular filtration rate (GFR) increases, leading to a decrease in BUN and serum creatinine levels, reflecting improved kidney function.

Answer 91

B) A steady decrease in BUN and creatinine levels Rationale: A steady decrease in BUN and creatinine levels, along with an increase in GFR, indicates that kidney function is stabilizing and improving during the recovery phase of AKI.

Answer 92

B) Presence of multiple complications and comorbidities Rationale: The presence of multiple complications and comorbidities, such as cardiovascular disease, diabetes, or infection, can hinder recovery and increase the likelihood of progressing to end-stage renal disease (ESRD).

Answer 93

A) Older age Rationale: Older adults are less likely to experience a complete recovery of kidney function due to age-related changes in renal function, comorbidities, and overall health, which can affect the recovery phase of AKI.

Answer 94

B) Stable kidney function with no further deterioration Rationale: Patients who recover from AKI may achieve clinically normal kidney function but still remain in the early stages of CKD, where kidney function is stable but potentially susceptible to further deterioration in the future.

Answer 95

A) Prerenal cause Rationale: Prerenal causes of AKI are often due to decreased blood flow to the kidneys, which can result from dehydration, hypotension, or blood loss. These factors cause the kidneys to be deprived of adequate perfusion.

Answer 96

C) Renal biopsy Rationale: A renal biopsy is the best way to confirm intrarenal causes of AKI. It provides direct information about the kidney tissue, which is essential for diagnosing the underlying pathology.

Answer 97

D) Intrarenal cause Rationale: The presence of hematuria, pyuria, and casts in the urine suggests an intrarenal disorder, which is a common cause of AKI. These findings reflect damage to the renal tubules and glomeruli.

Answer 98

B) Kidney ultrasound Rationale: A kidney ultrasound is often the first test performed in suspected postrenal AKI, as it helps evaluate urinary tract obstruction, such as from bladder or prostate cancer, without exposing the patient to nephrotoxic contrast agents.

Answer 99

A) Decreased urine output and high specific gravity Rationale: In prerenal AKI, decreased urine output is often seen along with high specific gravity, reflecting the kidneys’ attempt to concentrate urine due to decreased perfusion. The urine sodium level is typically low in prerenal causes.

Answer 100

A) To assess kidney blood flow and tubular function Rationale: A renal scan is used to assess abnormalities in kidney blood flow, tubular function, and the collecting system, which can help determine the cause of AKI and evaluate kidney function.

Answer 101

C) MRI or MRA Rationale: MRI or MRA with gadolinium contrast should be avoided in patients with kidney failure because gadolinium contrast can be potentially fatal in these patients, particularly due to the risk of nephrogenic systemic fibrosis.

Answer 102

B) Urinalysis showing casts and proteins Rationale: In cases of intrarenal AKI caused by nephrotoxic drugs, a urinalysis showing casts, proteins, and possibly other cellular debris would help confirm the diagnosis of kidney damage from the toxic exposure.

Answer 103

A) Loss of more than 50% of kidney function Rationale: An increase in serum creatinine typically does not occur until more than 50% of kidney function has been lost. The BUN may rise earlier due to other factors such as dehydration, infection, or corticosteroid use.

Answer 104

C) Renal ultrasound Rationale: A renal ultrasound is typically the first diagnostic test performed to evaluate postrenal causes of AKI. It helps detect urinary tract obstructions without the use of nephrotoxic contrast agents.

Answer 105

A) Presence of casts and RBCs in the urine Rationale: The presence of casts and RBCs in the urine suggests an intrarenal cause of AKI, which is indicative of damage to the renal tubules or glomeruli, often caused by conditions like glomerulonephritis or acute tubular necrosis.

Answer 106

D) Kidney ultrasound Rationale: A kidney ultrasound is commonly used to evaluate kidney disease or urinary tract obstruction without exposing the patient to nephrotoxic contrast agents, making it a safer option for those with kidney issues.

Answer 107

A) Serum creatinine increased × 1.5 and urine output <0.5 mL/kg/hr for 6 hours Rationale: According to the RIFLE classification, the “Risk” stage is defined by a serum creatinine increase of 1.5 times the baseline, a GFR decrease of 25%, and urine output less than 0.5 mL/kg/hr for 6 hours. This patient’s serum creatinine is increased, and they are at risk for AKI.

Answer 108

B) Injury Rationale: The “Injury” stage of AKI is characterized by a serum creatinine increase of 2 times the baseline and a GFR decrease of 50%. The patient also has urine output of less than 0.5 mL/kg/hr for 12 hours, fitting the criteria for the “Injury” stage.

Answer 109

D) Failure Rationale: The “Failure” stage of AKI is defined by a serum creatinine increase of 3 times the baseline or a serum creatinine level greater than 4 mg/dL with an acute rise of at least 0.5 mg/dL. The patient’s serum creatinine and urine output meet the criteria for “Failure.”

Answer 110

D) Loss Rationale: The “Loss” stage in the RIFLE classification refers to persistent acute kidney failure, with complete loss of kidney function lasting more than 4 weeks. This patient’s condition indicates progression to this stage.

Answer 111

D) End-stage renal disease Rationale: “End-stage renal disease” in the RIFLE classification refers to complete loss of kidney function for more than 3 months. This patient’s condition aligns with this classification.

Answer 112

A) Serum creatinine increased × 1.5 Rationale: The “Risk” stage in the RIFLE classification is defined by a serum creatinine increase of 1.5 times the baseline and a decrease in GFR by 25%. The urine output must be less than 0.5 mL/kg/hr for 6 hours.

Answer 113

C) Failure Rationale: The “Failure” stage in the RIFLE classification is indicated by a serum creatinine increase of 3 times the baseline or a serum creatinine level greater than 4 mg/dL, with an acute rise of at least 0.5 mg/dL, and a urine output of less than 0.3 mL/kg/hr for 24 hours.

Answer 114

D) Loss Rationale: The “Loss” stage in the RIFLE classification is marked by persistent kidney failure and complete loss of kidney function lasting more than 4 weeks. This patient has been on dialysis for 3 weeks without improvement, indicating the “Loss” stage.

Answer 115

C) Failure Rationale: The “Failure” stage in the RIFLE classification requires a serum creatinine increase of 3 times the baseline or a serum creatinine level greater than 4 mg/dL with an acute rise of at least 0.5 mg/dL. The patient’s serum creatinine and urine output meet the criteria for “Failure.”

Answer 116

A) Risk Rationale: The “Risk” stage of AKI in the RIFLE classification is characterized by a serum creatinine increase of 1.5 times the baseline and a GFR decrease of 25%. A GFR of 35 mL/min/1.73 m2 is indicative of the “Risk” stage.

Answer 117

B) Failure Rationale: The patient meets the criteria for “Failure” in the RIFLE classification with a serum creatinine increase of 3 times the baseline and a urine output of less than 0.3 mL/kg/hr for 24 hours.

Answer 118

B) Serum creatinine >4 mg/dL with acute rise ≥0.5 mg/dL and urine output <0.3 mL/kg/hr for 24 hours Rationale: The “Failure” stage of AKI is defined by a serum creatinine increase of 3 times the baseline, a serum creatinine greater than 4 mg/dL with an acute rise of at least 0.5 mg/dL, and urine output of less than 0.3 mL/kg/hr for 24 hours.

Answer 119

D) Recovery Rationale: The “Recovery” phase is marked by stabilization of kidney function, including a stable or decreasing serum creatinine level. This phase may take several months for full recovery of kidney function.

Answer 120

D) Loss Rationale: The “Loss” stage of AKI in the RIFLE classification refers to persistent kidney failure with complete loss of kidney function lasting more than 4 weeks. This patient’s condition suggests they are in the “Loss” stage.

Answer 121

C) Failure Rationale: The patient’s serum creatinine has risen to 5.2 mg/dL, which is a 3-fold increase from baseline, and their urine output has decreased to less than 0.3 mL/kg/hr for 24 hours, indicating the “Failure” stage of AKI in the RIFLE classification.

Answer 122

C) “In the Risk stage, my serum creatinine will increase by 1.5 times my baseline, and my urine output will be reduced.” Rationale: The “Risk” stage in the RIFLE classification is defined by a 1.5-fold increase in serum creatinine, a 25% decrease in GFR, and a urine output of less than 0.5 mL/kg/hr for 6 hours. This patient’s statement reflects the criteria for the “Risk” stage.

Answer 123

D) Serum creatinine and BUN levels Rationale: Serum creatinine and BUN levels are the primary diagnostic indicators for evaluating kidney function and identifying the cause of AKI. These tests provide crucial information about kidney function.

Answer 124

B) Calculate the patient’s daily fluid balance and adjust intake accordingly. Rationale: Fluid restriction should be based on the patient’s total fluid balance, including the 24-hour fluid loss. This ensures that the patient does not experience fluid overload or dehydration.

Answer 125

A) The degree of catabolism Rationale: The degree of catabolism (breakdown of body tissue) determines the patient’s protein needs. Higher protein intake may be necessary if there is significant catabolism, which is common in AKI.

Answer 126

B) Enteral nutrition Rationale: Enteral nutrition is appropriate for patients unable to consume food orally. It helps maintain adequate nutrition and supports the gut’s normal function.

Answer 127

D) Continuous renal replacement therapy (CRRT) may be used if dialysis is not effective. Rationale: Continuous renal replacement therapy (CRRT) is a form of dialysis that is often used in critically ill patients with AKI. It is typically used when traditional dialysis methods are not suitable.

Answer 128

A) Potassium Rationale: Potassium restrictions are critical in managing AKI because the kidneys may have difficulty excreting potassium, leading to the risk of hyperkalemia. Other electrolyte restrictions may also be necessary, but potassium is a priority.

Answer 129

A) Serum calcium levels Rationale: Calcium supplements should be administered cautiously, and serum calcium levels should be closely monitored to avoid hypercalcemia, which can occur if calcium is over-supplemented.

Answer 130

A) Administer sodium bicarbonate to shift potassium into cells. Rationale: Administering sodium bicarbonate helps to shift potassium from the extracellular space into cells, effectively lowering the potassium level. This intervention is necessary to prevent life-threatening arrhythmias associated with hyperkalemia.

Answer 131

C) Canned soups Rationale: Canned soups are typically high in sodium and should be avoided by patients on a low-sodium diet. Fresh fruits, vegetables, and grilled chicken are generally low in sodium.

Answer 132

C) Weight and urine output Rationale: Monitoring weight and urine output is critical for detecting fluid overload. A sudden increase in weight or a decrease in urine output can indicate that the patient is retaining fluid, which may lead to complications such as pulmonary edema.

Answer 133

A) Renal ultrasound Rationale: Renal ultrasound is commonly used to evaluate kidney disease and detect any urinary tract obstructions, making it a standard diagnostic test in the management of AKI.

Answer 134

B. Administer calcium gluconate Rationale: Calcium gluconate temporarily stabilizes the myocardium and raises the threshold for dysrhythmias in patients with hyperkalemia. This intervention is critical in reducing the risk of life-threatening cardiac arrhythmias before other measures like potassium removal are considered.

Answer 135

B. Manage the underlying cause and prevent complications Rationale: The main goals in treating AKI are to eliminate the cause, manage symptoms, and prevent complications while the kidneys recover. Immediate renal replacement therapy (RRT) is not always necessary unless the clinical condition requires it.

Answer 136

C. Monitor closely for complications while initiating conservative therapy Rationale: Conservative therapy is often sufficient for managing AKI unless it is refractory to treatment. Monitoring and supporting the patient with fluid management, electrolytes, and other therapies are appropriate in this phase. Immediate initiation of RRT is not indicated unless certain critical factors are met.

Answer 137

D. Pericarditis, pericardial effusion, or cardiac tamponade Rationale: Indications for initiating RRT in AKI include volume overload, high serum potassium, metabolic acidosis (serum HCO3 <15 mEq/L), BUN >120 mg/dL, changes in mental status, and pericarditis, pericardial effusion, or cardiac tamponade.

Answer 138

B. 600 mL plus the previous 24-hour fluid loss Rationale: The fluid restriction during the oliguric phase is calculated by adding all losses from the previous 24 hours (urine, diarrhea, emesis, blood) plus 600 mL for insensible losses, such as respiration and diaphoresis.

Answer 139

A. Hypotension Rationale: Rapid fluid shifts during HD can cause hypotension, which is a common complication. Hypotension during dialysis needs prompt attention to prevent further complications.

Answer 140

A. Furosemide Rationale: Furosemide (Lasix) is a loop diuretic commonly used to manage fluid overload in AKI when the patient has adequate intravascular volume and cardiac output. Mannitol is used for osmotic diuresis but is not typically used in all AKI cases.

Answer 141

C. Peritonitis Rationale: Peritonitis is a serious complication of peritoneal dialysis (PD) and can occur when the catheter or peritoneal cavity becomes infected. Proper aseptic technique is essential to prevent this complication.

Answer 142

D. Serum creatinine Rationale: Serum creatinine is the best indicator of kidney function in AKI because it is not affected by factors such as hydration status or protein intake, unlike BUN.

Answer 143

A. It is administered over 24 hours Rationale: CRRT is administered continuously over 24 hours and has slower blood flow rates compared to intermittent hemodialysis (HD). It does not involve rapid fluid shifts and is typically used for long-term management in critically ill patients.

Answer 144

B. Restrict fluids based on previous losses plus 600 mL Rationale: Fluid restriction during the oliguric phase is essential to prevent fluid overload, which can worsen the condition. The correct formula for fluid restriction is to add all losses from the previous 24 hours plus 600 mL for insensible losses.

Answer 145

C. Administer calcium gluconate Rationale: Calcium gluconate is used first to stabilize the myocardium in the presence of hyperkalemia, reducing the risk of life-threatening dysrhythmias. Other treatments such as sodium bicarbonate or Kayexalate may follow.

Answer 146

C. Clinical status of the patient Rationale: The decision to initiate RRT is based on the clinical status of the patient, including volume overload, high potassium, acidosis, or changes in mental status, rather than just lab values like serum creatinine or BUN.

Answer 147

B. Hypotension Rationale: Rapid fluid shifts during HD can lead to hypotension. It is important to monitor for signs of hypotension during and after treatment and manage it appropriately to prevent further complications.

Answer 148

A. CRRT can be used for patients who are hemodynamically unstable Rationale: CRRT is used in hemodynamically unstable patients because it provides slow, continuous fluid and solute removal, which is less likely to cause hypotension compared to HD. It requires specialized equipment and is performed continuously over 24 hours.

Answer 149

B. 0.8–1.0 g/kg/day Rationale: The appropriate protein intake for patients with AKI is 0.8–1.0 g/kg/day, depending on the degree of catabolism. Higher protein intake may be required for patients with increased metabolic needs.

Answer 150

C. Constipation Rationale: Sodium polystyrene sulfonate (Kayexalate) can cause constipation as a side effect, and the nurse should monitor the patient for bowel movement changes.

Answer 151

B. Hyponatremia Rationale: Loop diuretics, such as furosemide, can cause electrolyte imbalances, including hyponatremia. The nurse should monitor sodium levels closely when administering these medications.

Answer 152

A. Hemodialysis catheter and anticoagulation therapy Rationale: CRRT requires a hemodialysis catheter and anticoagulation therapy to prevent clotting of the dialysis circuit due to the slower blood flow rates compared to intermittent hemodialysis.

Answer 153

D. Decreased urine output Rationale: The oliguric phase of AKI is characterized by a significant decrease in urine output, typically less than 400 mL per day. This phase often occurs in the first 1-7 days following the insult.

Answer 154

D. Serum potassium Rationale: Diuretics can cause potassium depletion, which can lead to hypokalemia. The nurse should closely monitor potassium levels to prevent complications such as cardiac arrhythmias.

Answer 155

A. Hypotension Rationale: Hemodialysis can cause hypotension due to the rapid removal of fluid and solutes. This drop in blood pressure can lead to dizziness, fainting, or shock if not managed properly.

Answer 156

B. Ensure the patient is well hydrated before the procedure Rationale: Renal biopsy requires the patient to be well hydrated before the procedure to prevent complications such as hypotension or reduced perfusion. The nurse should also ensure that the patient has no active bleeding risk.

Answer 157

B. Refractory hyperkalemia Rationale: Renal replacement therapy is indicated in cases of severe and refractory hyperkalemia, when medications and other measures are insufficient to control the potassium levels.

Answer 158

A. Document the weight gain and notify the physician Rationale: A 2 kg weight gain could indicate fluid retention, which is common in AKI. The nurse should notify the physician to evaluate the patient’s condition and adjust treatment as needed.

Answer 159

C. Prepare to administer sodium polystyrene sulfonate Rationale: Sodium polystyrene sulfonate (Kayexalate) is a medication used to treat hyperkalemia by exchanging sodium for potassium in the gastrointestinal tract. The nurse should anticipate this intervention for a potassium level of 6.5 mEq/L.

Answer 160

B. Continue to monitor the patient’s vital signs and urine output Rationale: After the administration of fluids, the nurse should continue to monitor the patient’s urine output and vital signs closely. Increased urine output is a positive sign, and fluid overload should be prevented.

Answer 161

A. Low-potassium diet Rationale: A low-potassium diet is crucial for patients with AKI to prevent hyperkalemia, which can lead to life-threatening arrhythmias. Potassium-rich foods should be avoided.

Answer 162

C. The patient’s renal function returns to baseline Rationale: In the recovery phase of AKI, the patient’s renal function begins to return to baseline, with normalization of urine output and improvement in laboratory values such as BUN and creatinine.

Answer 163

C. Checking for signs of electrolyte imbalance Rationale: A priority assessment for a patient receiving renal replacement therapy (RRT) is monitoring for signs of electrolyte imbalance, as RRT can alter electrolyte levels, including potassium, sodium, and calcium.

Answer 164

C. Notify the healthcare provider about the decrease in urine output Rationale: The nurse should notify the healthcare provider about the decrease in urine output, as this could indicate a need for adjustment in the CRRT or further intervention. Increasing the flow rate or administering diuretics without guidance could worsen the situation.

Answer 165

C. Insulin and glucose Rationale: Insulin and glucose are used together to promote the transient shift of potassium into cells, which can temporarily lower serum potassium levels in cases of hyperkalemia.

Answer 166

B. Assess for signs of hypokalemia Rationale: The nurse should first assess for signs and symptoms of hypokalemia (e.g., weakness, muscle cramps, cardiac arrhythmias) before taking further action. Hypokalemia can be life-threatening and may require immediate intervention.

Answer 167

B. Shift potassium into cells temporarily Rationale: Sodium bicarbonate temporarily shifts potassium into cells, which helps lower serum potassium levels. This intervention is used in the management of hyperkalemia, especially when it is severe.

Answer 168

D. Creatinine Rationale: During the recovery phase of AKI, creatinine levels are expected to return to baseline as kidney function improves and the kidneys begin to excrete waste products more effectively.

Answer 169

C. Constipation Rationale: Sodium polystyrene sulfonate (Kayexalate) works by exchanging sodium for potassium in the gastrointestinal tract, which can cause constipation as a side effect. The nurse should monitor for this and intervene as necessary.

Answer 170

B. Initiate continuous renal replacement therapy Rationale: For a patient with severe AKI (serum creatinine >4 mg/dL and oliguria), continuous renal replacement therapy (CRRT) is often initiated to manage fluid overload, electrolyte imbalances, and metabolic acidosis.

Answer 171

A. Decrease the CRRT flow rate Rationale: The nurse should decrease the CRRT flow rate to prevent further hypotension. Rapid fluid and solute removal during CRRT can cause hypotension, which can lead to inadequate perfusion and other complications.

Answer 172

D. Carbohydrates and fats Rationale: Carbohydrates and fats are the primary sources of energy in AKI nutrition therapy to prevent ketosis from fat breakdown and gluconeogenesis from muscle protein breakdown. This helps avoid catabolism and ensures adequate energy for recovery.

Answer 173

B. Serum potassium levels Rationale: For patients with AKI, it is important to monitor serum potassium levels because dietary potassium intake needs to be carefully managed to prevent hyperkalemia.

Answer 174

C. Daily dialysis to remove excess fluid Rationale: Parenteral nutrition (PN) may result in fluid overload, and the patient may need daily dialysis (such as hemodialysis or CRRT) to remove the excess fluid and maintain fluid balance.

Answer 175

B. To provide adequate calories and prevent catabolism Rationale: The primary goal of nutrition therapy in AKI is to provide adequate calories (30 to 35 kcal/kg) and protein (0.8–1.0 g/kg) to prevent catabolism and support the body’s recovery while managing fluid and electrolyte imbalances.

Answer 176

A. Restrict the patient’s sodium intake Rationale: When sodium levels are elevated in patients receiving PN, restricting sodium intake is appropriate to prevent further complications such as edema, hypertension, and fluid retention.

Answer 177

B. Monitoring serum potassium and sodium levels regularly Rationale: Monitoring serum potassium and sodium levels is essential for preventing electrolyte imbalances in patients with AKI, as these patients are at risk for both hyperkalemia and hyponatremia.

Answer 178

A. Prevent the breakdown of muscle protein and promote recovery Rationale: The goal of providing adequate calories from fats and carbohydrates while restricting protein in AKI is to prevent muscle protein breakdown, thus minimizing catabolism and promoting recovery without overwhelming the kidneys.

Answer 179

A. Administer diuretics as ordered Rationale: The presence of edema, neck vein distention, and crackles in the lungs suggests fluid overload. The nurse should prioritize administering diuretics as ordered to help manage fluid retention before considering other interventions.

Answer 180

B. The patient is in the oliguric phase of AKI Rationale: Dark urine and a high specific gravity (greater than 1.020) are common findings in the oliguric phase of AKI, indicating concentrated urine due to decreased urine output.

Answer 181

C. Provide oral care and offer sips of water frequently Rationale: Dry and inflamed oral mucosa is a common finding in AKI due to fluid imbalances. The nurse should provide frequent oral care and offer sips of water to help alleviate dryness and prevent further irritation.

Answer 182

D. It suggests fluid overload and heart failure Rationale: An S3 gallop is often associated with fluid overload and heart failure, which can occur in AKI due to the kidneys’ inability to manage fluid balance effectively.

Answer 183

D. Assess for signs of coagulation abnormalities or bleeding Rationale: The development of bruises and poor circulation may suggest coagulation abnormalities, which are common in AKI. The nurse should assess the patient for signs of bleeding and notify the healthcare provider if necessary.

Answer 184

B. Monitor the patient’s potassium levels Rationale: PVCs can be caused by electrolyte imbalances, particularly low potassium levels. The nurse should first assess the patient’s potassium levels and correct any deficiencies before taking further action.

Answer 185

C. Remove the catheter and notify the healthcare provider Rationale: Inflammation and exudate at the dialysis access site could indicate an infection or complication. The nurse should notify the healthcare provider immediately for further evaluation and possible intervention.

Answer 186

D. The BUN level may indicate kidney dysfunction or azotemia Rationale: Elevated BUN levels are a common sign of kidney dysfunction and azotemia, which are key concerns in AKI. The nurse should monitor BUN levels as part of assessing the patient’s kidney function and overall condition.

Answer 187

B. Monitor serum electrolyte levels frequently Rationale: Monitoring serum electrolyte levels frequently is essential for managing electrolyte imbalances in AKI. Frequent monitoring allows the nurse to detect changes in electrolyte levels early and intervene to prevent complications such as arrhythmias or other life-threatening issues.

Answer 188

C. Offer relaxation techniques and provide information about the condition Rationale: Offering relaxation techniques and providing information about the patient’s condition can help alleviate anxiety. Education and reassurance are key components in managing anxiety, especially when the patient understands what is happening and what to expect in terms of treatment and recovery.

Answer 189

B. The patient will completely recover without any loss of kidney function. Rationale: The priority goal for a patient with AKI is to completely recover without any loss of kidney function. This goal ensures the restoration of kidney health and the prevention of long-term complications.

Answer 190

B. The patient will maintain normal fluid and electrolyte balance during hospitalization. Rationale: The goal of maintaining normal fluid and electrolyte balance is essential to preventing complications in AKI. This goal is realistic and focuses on the patient’s immediate needs during hospitalization.

Answer 191

A. The patient will demonstrate effective coping strategies. Rationale: The goal of demonstrating effective coping strategies is appropriate for addressing anxiety in a patient with AKI. This outcome focuses on equipping the patient with tools to manage their emotions and stress during hospitalization.

Answer 192

A. Prevention and early recognition of AKI Rationale: Prevention and early recognition are the most important aspects of care in preventing AKI. Identifying high-risk populations and monitoring them closely helps in preventing the onset of AKI.

Answer 193

C. A 65-year-old with chronic kidney disease (CKD) and heart failure Rationale: A patient with preexisting CKD, older age, heart failure, and other risk factors is at a significantly higher risk for developing AKI, particularly when they undergo stressors like surgery or trauma.

Answer 194

C. Hold metformin for 48 hours before and after the contrast procedure Rationale: Holding metformin for 48 hours before and after the use of contrast media is recommended to decrease the risk for lactic acidosis, a common complication in diabetic patients receiving contrast.

Answer 195

A. Preexisting chronic kidney disease Rationale: Preexisting chronic kidney disease (CKD) is a significant risk factor for AKI in hospitalized patients, especially if they are exposed to nephrotoxic drugs or undergo major surgery or trauma.

Answer 196

B. Weight, intake and output, and fluid balance Rationale: Monitoring weight, intake and output, and fluid balance helps assess kidney function and fluid volume status, which are critical in preventing and managing AKI.

Answer 197

D. Nonsteroidal anti-inflammatory drugs Rationale: NSAIDs can worsen kidney function, particularly in patients with CKD, by decreasing renal blood flow and increasing the risk of AKI.

Answer 198

B. Discontinue the ACE inhibitor if hyperkalemia is not controlled by other means Rationale: If hyperkalemia is not controlled by diet changes or diuretics, ACE inhibitors may need to be reduced or stopped because they can exacerbate hyperkalemia.

Answer 199

A. Ensure hydration and monitor renal function closely Rationale: Ensuring adequate hydration and closely monitoring renal function is crucial when administering nephrotoxic drugs to prevent or minimize kidney damage.

Answer 200

B. Ensure adequate hydration before, during, and after the procedure Rationale: Ensuring adequate hydration before, during, and after the procedure helps reduce the risk of CIN in high-risk patients by promoting renal perfusion and minimizing nephrotoxic effects.

Answer 201

D. Monitor for signs of hypotension and fluid imbalance Rationale: Aggressive diuretic therapy can lead to hypotension and fluid imbalance, so it is essential to monitor for these complications to prevent further kidney damage.

Answer 202

B. Promptly replace the fluid losses to prevent ischemic damage Rationale: Prompt replacement of significant fluid losses helps prevent ischemic tubular damage, especially in cases of trauma, burns, or extensive surgery, all of which increase the risk of AKI.

Answer 203

D. Closely monitor fluid and electrolyte balance Rationale: Patients with extensive burns are at high risk for AKI due to fluid and electrolyte imbalances. Close monitoring of fluid and electrolyte balance is essential to prevent kidney damage.

Answer 204

A. Monitoring for signs of hypotension and electrolyte imbalances Rationale: Monitoring for hypotension and electrolyte imbalances is crucial when a patient is receiving diuretic therapy, as these can lead to further complications such as dehydration and renal damage.

Answer 205

A. Monitor kidney function and fluid status regularly Rationale: Regular monitoring of kidney function and fluid status is crucial to detecting any signs of kidney damage early and preventing further injury when nephrotoxic medications are used.

Answer 206

B. Administer a low osmolality contrast agent Rationale: Using a low osmolality contrast agent reduces the nephrotoxic effect of contrast media and helps minimize the risk of CIN in high-risk patients.

Answer 207

A. Monitoring daily weight and intake and output Rationale: Monitoring daily weight and intake and output is critical during the oliguric phase to detect fluid retention or imbalance, which can lead to complications such as hypervolemia.

Answer 208

A. Monitoring blood glucose levels closely Rationale: In patients with AKI and comorbid conditions like diabetes, closely monitoring blood glucose is crucial to prevent further kidney damage, as poorly controlled glucose can exacerbate kidney injury.

Answer 209

B. Monitoring for signs of hypovolemia Rationale: In the diuretic phase of AKI, the patient may lose significant amounts of fluid, making it crucial to monitor for signs of hypovolemia, such as hypotension and dehydration.

Answer 210

A. Fever Rationale: Patients with AKI may have a blunted febrile response to infection, which means they may not exhibit the typical fever associated with infections such as pneumonia.

Answer 211

B. Implement strict aseptic techniques during invasive procedures Rationale: Strict aseptic techniques are essential in preventing infection in patients with AKI, as infection is a leading cause of death, and these patients may be at a higher risk of infection due to compromised immunity.

Answer 212

C. Antibiotic dosages should be decreased based on the patient’s level of kidney function Rationale: Antibiotics are often eliminated by the kidneys, so in patients with AKI, dosages may need to be adjusted based on the patient’s renal function to prevent toxicity and adverse effects.

Answer 213

A. Encourage frequent repositioning of the patient Rationale: Repositioning the patient frequently helps prevent pressure injuries, especially in patients with limited mobility. This reduces the risk of pressure ulcers, which are common in critically ill patients.

Answer 214

D. Maintaining good oral hygiene and mouth care Rationale: Maintaining good oral hygiene and mouth care is essential in preventing stomatitis in patients with AKI, as ammonia in saliva can irritate the mucous membranes.

Answer 215

B. Report the weight gain as it indicates potential fluid retention Rationale: A weight gain of 1 kg in one day is equivalent to 1000 mL of fluid and may indicate fluid retention, which should be reported to the healthcare provider to adjust the patient’s treatment plan accordingly.

Answer 216

A. Hyperkalemia Rationale: Hyperkalemia is most likely to occur during the oliguric phase of AKI due to decreased renal excretion of potassium, which can lead to dangerous cardiac arrhythmias.

Answer 217

B. Strictly limiting all fluid intake to avoid fluid overload Rationale: Monitoring blood pressure frequently is critical in preventing further kidney injury, especially in patients with comorbid conditions such as CVD, as hypertension can exacerbate AKI.

Answer 218

B. Assessing the patient’s renal output and urinary output trends Rationale: During the diuretic phase, it is important to assess the patient’s renal and urinary output trends, as this can help in determining whether the kidneys are recovering or if further interventions are needed.

Answer 219

A. Use standard precautions for all procedures Rationale: Standard precautions should be used for all patients to reduce the risk of infection. Patients with AKI may have a blunted immune response, increasing their susceptibility to infections.

Answer 220

B. Monitor the patient’s serum electrolytes regularly Rationale: Monitoring the patient’s serum electrolytes regularly is essential to identify and manage any imbalances that may occur during the course of AKI, such as hyperkalemia or hyponatremia.

Answer 221

A. “Monitor your urine output and report any decrease in the amount.” Rationale: Monitoring urine output and reporting any decrease is crucial in identifying recurrent kidney issues. Decreased urine output could indicate a recurrence of kidney damage or worsening of renal function.

Answer 222

A. Provide referrals for financial assistance and counseling Rationale: Referrals for financial assistance and counseling are crucial for patients dealing with the psychosocial and financial challenges of recovery. Addressing emotional well-being can aid in the overall recovery process.

Answer 223

B. “The recovery period may last anywhere from 3 to 12 months.” Rationale: Recovery from AKI can take 3 to 12 months, depending on the severity of the kidney injury and the patient’s overall health, including any comorbid conditions. It is important to set realistic expectations for recovery.

Answer 224

C. Monitor kidney function and adjust dietary recommendations accordingly Rationale: Kidney function directly affects protein and potassium requirements. The nurse should monitor kidney function and adjust the patient’s dietary recommendations to ensure they are not consuming excess protein or potassium that could worsen kidney function.

Answer 225

B. “The possibility of kidney transplant may be an option if dialysis becomes necessary.” Rationale: If kidneys do not recover, chronic dialysis or a kidney transplant may be necessary. Discussing the potential for a transplant is part of preparing the patient for ongoing renal management.

Answer 226

D. The patient’s electrolyte levels are within normal range Rationale: Maintaining normal electrolyte levels is a critical component of achieving normal fluid and electrolyte balance in patients with AKI. Monitoring electrolyte levels helps to evaluate the success of therapy and management of AKI.

Answer 227

A. The patient has no signs of complications and adheres to the treatment regimen Rationale: A complete recovery from AKI is most likely when the patient adheres to the treatment plan, experiences no complications, and regains normal kidney function. The absence of complications indicates that the patient’s condition is improving without further deterioration.

Answer 228

B. Dehydration due to polypharmacy and immobility Rationale: Older adults are at increased risk for AKI due to factors such as polypharmacy (e.g., diuretics and laxatives) and immobility, which can lead to dehydration. This combination of factors is a significant risk for kidney injury.

Answer 229

B. Reduced renal reserve and less ability to compensate for changes in fluid volume Rationale: Aging kidneys have reduced renal reserve and are less able to compensate for changes in fluid volume, solute load, and cardiac output, which makes older adults more susceptible to AKI.

Answer 230

C. Impaired function of other organ systems, such as CVD and diabetes Rationale: Impaired function of other organ systems, such as CVD and diabetes, increases the risk of AKI in older adults. These conditions contribute to decreased renal perfusion and kidney function.

Answer 231

A. Monitor for and prevent dehydration due to polypharmacy Rationale: Preventing dehydration due to polypharmacy (e.g., diuretics and laxatives) is crucial in older adults to reduce the risk of AKI. Dehydration is a significant predisposing factor in the development of kidney injury.

Answer 232

C. Patients over 65 years of age are less likely to recover from AKI. Rationale: Older adults are less likely to recover from AKI compared to younger adults. While mortality rates are similar, age and other comorbidities increase the likelihood of poor recovery.

Answer 233

D. All of the above Rationale: All of these factors contribute to the increased risk of AKI in older adults. Reduced renal reserve due to aging, nephrotoxic effects of aminoglycosides, and reduced mobility after surgery all increase the likelihood of kidney injury.

Answer 234

d. serum creatinine or urine output from baseline.

Answer 235

b. ECG changes. d. pulmonary edema.

Answer 236

c. Hypokalemia and hyponatremia

Answer 237

b. Rapid, deep respirations Rationale: Patients with metabolic acidosis caused by AKI may have Kussmaul respirations to eliminate carbon dioxide. Bounding pulses and vasodilation are not associated with metabolic acidosis. Because the patient is likely to have fluid retention, poor skin turgor would not be a finding in AKI.

Answer 238

c. Diluting nephrotoxic substances Rationale: The primary goal of treatment for acute kidney injury (AKI) is to eliminate the cause and provide supportive care while the kidneys recover. Because this patient‘s heart failure is causing AKI, the care will be directed toward treatment of the heart failure. Renal failure caused by hypertension, hypovolemia, or nephrotoxins would be managed by interventions specific to those problems.

Answer 239

c. Glomerular filtration rate (GFR) Rationale: Calculated GFR is a more accurate indicator of kidney function than BUN or creatinine. BUN levels can fluctuate based on factors such as fluid volume status and protein intake. Urine output can be normal or high in patients with AKI and does not accurately reflect kidney function. Creatinine alone is not an accurate reflection of renal function.

Answer 240

a. Limit movement of the left leg. Rationale: Temporary vascular catheters have high rates of infection, dislodgment, and malfunction; the patient with a left femoral vein catheter must avoid flexion of the left leg. Protein intake is likely to be increased when the patient is receiving dialysis. The retention catheter is likely to remain in place because accurate measurement of output will be needed. There is no indication that the patient needs continuous pulse oximetry.

Answer 241

a. Insert urethral catheter. Rationale: The patient‘s elevation in BUN is most likely associated with hydronephrosis caused by the acute urinary retention, so the insertion of an indwelling catheter is the first action to prevent ongoing postrenal failure for this patient. The other actions are appropriate but would be implemented after the catheter.

Answer 242

b. Urine output over an 8-hour period is 2500 mL. Rationale: The high urine output indicates a need to increase fluid intake to prevent hypovolemia. The other information is typical of AKI and will not require a change in therapy.

Answer 243

c. Check the patient‘s most recent potassium level. Rationale: The increasing QRS interval is suggestive of hyperkalemia, so the nurse would check the most recent potassium and then notify the patient‘s health care provider. The BUN and creatinine will be increased in a patient with AKI, but they would not directly affect the electrocardiogram (ECG). Documentation of the QRS interval is also appropriate, but interventions to decrease the potassium level are needed to prevent life-threatening dysrhythmias.

Answer 244

c. Place the patient on a cardiac monitor. Rationale: Because hyperkalemia can cause fatal dysrhythmias, the initial action would be to monitor the cardiac rhythm. Kayexalate and Epogen will take time to correct the hyperkalemia and anemia. The catheter allows monitoring of the urine output but does not correct the cause of the renal failure.

CH 51: Acute Kidney Injury Flashcards

(268 cards)