NSG 430 exam II
NSG 430 exam II – UPDATED Questions with 100% Verified
Answers
Grand Canyon University
NSG 430
NSG 430 exam II
Q1 What it acute decompensated heart failure
A Exacerbation of chronic heart failure
Q2 What are the clinical manifestations of acute decompensated heart failure
A Fluid overload, SOB, fatigue
Q3 Symptoms of acute decompensated heart failure
A Jugular Vein Distension (JVD) edema dyspnea orthopnea paroxysmal nocturnal dyspnea N/V
weight gain or loss hepamegaly pulmonary rales cardiac gallops S3 or S4 pleural effusion
Q4 What can acute decompensated heart failure lead to
A pulmonary edema
Q5 What is acute kidney injury (AKI)?
A - Abrupt reduction in renal function with elevated BUN and creatinine and Cystatin C levels
(biomarker of kidney function). - Usually associated with oliguria (<30 mL/hr or <400
mL/day) - GFR decreases - Can be reversed if diagnosed and treated early
Q6 Types of AKI
A Prerenal Intrarenal Postrenal
Q7 Labs to diagnose AKI
A GFR creatinine electrolytes (particularly potassium)
Q8 Symptoms of AKI
Page 1
, NSG 430 exam II
A Fatigue, dizziness, swelling, decreased urine output oliguria (<500 ml urine), azotemia
(increased urea in blood)
Q9 Interventions for AKI
A treat underlying cause of AKI fluid restrictions nutrition -enteral nutrition (low sodium, low
potassium, high calcium) -total parental nutrition (TPN) medications -diuretics * -calcium
channel blockers * drug of choice to treat AKI nephrotoxins -dose adjustment based on
kidney function
Q10 What is acute tubular necrosis
A destruction of tubular epithelial cells with acute suppression of renal function poor blood
flow to kidneys / poor oxygenation
Q11 Cause of acute tubular necrosis
A Patients at risk for developing this: trauma, massive transfusion Nephrotoxic agents cause
necrosis of tubular epithelial cells, which slough off and plug the tubules. Other risks
associated with developing ATN while in the hospital include major surgery, shock, blood
transfusion reaction, muscle injury from trauma, and prolonged hypotension Atenolol
Q12 Bradycardia
A slow heart rate (less than 60 bpm)
Q13 Symptoms of bradycardia
A fatigue, low perfusion, shortness of breath, hypotension
Q14 Medication of bradycardia
A atropine increases heart rate
Q15 Other treatment of bradycardia
Page 2
NSG 430 exam II – UPDATED Questions with 100% Verified
Answers
Grand Canyon University
NSG 430
NSG 430 exam II
Q1 What it acute decompensated heart failure
A Exacerbation of chronic heart failure
Q2 What are the clinical manifestations of acute decompensated heart failure
A Fluid overload, SOB, fatigue
Q3 Symptoms of acute decompensated heart failure
A Jugular Vein Distension (JVD) edema dyspnea orthopnea paroxysmal nocturnal dyspnea N/V
weight gain or loss hepamegaly pulmonary rales cardiac gallops S3 or S4 pleural effusion
Q4 What can acute decompensated heart failure lead to
A pulmonary edema
Q5 What is acute kidney injury (AKI)?
A - Abrupt reduction in renal function with elevated BUN and creatinine and Cystatin C levels
(biomarker of kidney function). - Usually associated with oliguria (<30 mL/hr or <400
mL/day) - GFR decreases - Can be reversed if diagnosed and treated early
Q6 Types of AKI
A Prerenal Intrarenal Postrenal
Q7 Labs to diagnose AKI
A GFR creatinine electrolytes (particularly potassium)
Q8 Symptoms of AKI
Page 1
, NSG 430 exam II
A Fatigue, dizziness, swelling, decreased urine output oliguria (<500 ml urine), azotemia
(increased urea in blood)
Q9 Interventions for AKI
A treat underlying cause of AKI fluid restrictions nutrition -enteral nutrition (low sodium, low
potassium, high calcium) -total parental nutrition (TPN) medications -diuretics * -calcium
channel blockers * drug of choice to treat AKI nephrotoxins -dose adjustment based on
kidney function
Q10 What is acute tubular necrosis
A destruction of tubular epithelial cells with acute suppression of renal function poor blood
flow to kidneys / poor oxygenation
Q11 Cause of acute tubular necrosis
A Patients at risk for developing this: trauma, massive transfusion Nephrotoxic agents cause
necrosis of tubular epithelial cells, which slough off and plug the tubules. Other risks
associated with developing ATN while in the hospital include major surgery, shock, blood
transfusion reaction, muscle injury from trauma, and prolonged hypotension Atenolol
Q12 Bradycardia
A slow heart rate (less than 60 bpm)
Q13 Symptoms of bradycardia
A fatigue, low perfusion, shortness of breath, hypotension
Q14 Medication of bradycardia
A atropine increases heart rate
Q15 Other treatment of bradycardia
Page 2
