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NR 341/ NR341 COMPLEX ADULT HEALTH EXAM 200 LATEST
VERSION2025/2026 REAL EXAM QUESTIONS AND CORRECT
ANSWERS|A+GRADE|
S/SX of the diuretic phase of acute kidney injury (AKI): - ......ANSWER........Urine output 1-
3L/day
Decreased K & Na
S/SX of the risk stage of acute kidney injury (AKI): - ......ANSWER........Cr >1.5xbaseline
Urine output <0.5ml/kg/hr. for 6+ hours
S/SX of the injury stage of acute kidney injury (AKI): - ......ANSWER........Cr >2xbaseline
Urine output <0.5ml/kg/hr. for 12+ hours
S/SX of the risk failure of acute kidney injury (AKI): - ......ANSWER........Cr >3xbaseline
Urine output <0.3ml/kg/hr for 12+ hours
Priority assessment findings of acute kidney injury (AKI): - ......ANSWER........Respiratory:
Crackles
Pleural Effusion
Kussmaul respirations
Cardiovascular:
CHF, hypo/hypertension
Cardiac dysrhythmias
Pericarditis, pericardial effusion
Neurologic:
Altered mentation, confusion, lethargy
,2 of 38
Decreased seizure threshold
S/SX of hypovolemic shock: - ......ANSWER........Elevated HR, decreased BP, tachypnea,
oliguria, cool pale skin, decreased mental status, flat neck veins, decreased CO CI RAP
PAP PAOP, elevated SVR, decreased SvO2.
Dehydration causes elevated HCT
Blood loss causes decreased HCT
Possible causes of hypovolemic shock: - ......ANSWER........External loss of blood
External loss of fluid
Internal sequestration of blood fluid (3rd spacing)
Management of hypovolemic shock: - ......ANSWER........Eliminate and treat the cause
Replace lost volume with appropriate fluid (NS or LR)
Initial shock - ......ANSWER........Inadequate intravascular volume
Initial shock clinical presentation: - ......ANSWER........There are no obvious clinical
indications of hypoperfusion seen in this stage of shock
May see a drop in cardiac output
Compensatory shock - ......ANSWER........Inadequate myocardial contractility
Compensatory shock neural compensation S/SX: - ......ANSWER........HR & contractility
increase
Systemic vasoconstriction and redistribution of blood occur
Venous vasoconstriction augments venous return to the heart
,3 of 38
Blood is shunted from the kidneys, GI tract, and skin
Respiratory rate and depth are increased
Increased blood glucose levels
Dilated pupils, peripheral vasoconstriction, sweat gland activity causing cool moist skin
Compensatory shock endocrine compensation S/SX: - ......ANSWER........Increased blood
glucose
Reabsorption of salt and water increasing intravascular volume and BP
RAAS >Renin > Angiotensinogen > Angiotensinogen 1 > Angiotensinogen 2 > increases BP
and venous return to the heart
Angiotensinogen 2 activates the adrenal cortex for the release of aldosterone
Compensatory shock chemical compensation S/SX: - ......ANSWER........Perfusion begins
to decline
Rate and depth of respiration increase
Hyperventilation >CO2 is released > Respiratory alkalosis occurs
Vasoconstriction of cerebral blood vessels occurs > Cerebral hypoxia & ischemia may
result
Compensatory shock clinical presentation: - ......ANSWER........Elevated HR
Narrowed pulse pressure
Rapid, deep respirations causing respiratory alkalosis
Thirst
Cool, moist skin
Oliguria
Diminished bowel sounds
Restlessness > confusion
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Hyperglycemia
Increased urine specific gravity
Decreased creatinine clearance
Progressive shock S/SX: - ......ANSWER........Ischemia in extremities
Weak or absent peripheral pulses
Altered body defense
Decreased capillary refill
Cellular hypoxia
Metabolic acidosis
Failure of the sodium-potassium pump
Edema
Progressive shock - ......ANSWER........Respiratory system is the first to fail
Decrease cardiac output
Decreased capillary permeability
AKI & liver injury
Progressive shock clinical presentation: - ......ANSWER........Dysrhythmias
Decreased BP
Narrow pulse pressure
Tachypnea
Cool, clammy skin
Anuria
Absent bowel sounds
Lethargy > coma
NR 341/ NR341 COMPLEX ADULT HEALTH EXAM 200 LATEST
VERSION2025/2026 REAL EXAM QUESTIONS AND CORRECT
ANSWERS|A+GRADE|
S/SX of the diuretic phase of acute kidney injury (AKI): - ......ANSWER........Urine output 1-
3L/day
Decreased K & Na
S/SX of the risk stage of acute kidney injury (AKI): - ......ANSWER........Cr >1.5xbaseline
Urine output <0.5ml/kg/hr. for 6+ hours
S/SX of the injury stage of acute kidney injury (AKI): - ......ANSWER........Cr >2xbaseline
Urine output <0.5ml/kg/hr. for 12+ hours
S/SX of the risk failure of acute kidney injury (AKI): - ......ANSWER........Cr >3xbaseline
Urine output <0.3ml/kg/hr for 12+ hours
Priority assessment findings of acute kidney injury (AKI): - ......ANSWER........Respiratory:
Crackles
Pleural Effusion
Kussmaul respirations
Cardiovascular:
CHF, hypo/hypertension
Cardiac dysrhythmias
Pericarditis, pericardial effusion
Neurologic:
Altered mentation, confusion, lethargy
,2 of 38
Decreased seizure threshold
S/SX of hypovolemic shock: - ......ANSWER........Elevated HR, decreased BP, tachypnea,
oliguria, cool pale skin, decreased mental status, flat neck veins, decreased CO CI RAP
PAP PAOP, elevated SVR, decreased SvO2.
Dehydration causes elevated HCT
Blood loss causes decreased HCT
Possible causes of hypovolemic shock: - ......ANSWER........External loss of blood
External loss of fluid
Internal sequestration of blood fluid (3rd spacing)
Management of hypovolemic shock: - ......ANSWER........Eliminate and treat the cause
Replace lost volume with appropriate fluid (NS or LR)
Initial shock - ......ANSWER........Inadequate intravascular volume
Initial shock clinical presentation: - ......ANSWER........There are no obvious clinical
indications of hypoperfusion seen in this stage of shock
May see a drop in cardiac output
Compensatory shock - ......ANSWER........Inadequate myocardial contractility
Compensatory shock neural compensation S/SX: - ......ANSWER........HR & contractility
increase
Systemic vasoconstriction and redistribution of blood occur
Venous vasoconstriction augments venous return to the heart
,3 of 38
Blood is shunted from the kidneys, GI tract, and skin
Respiratory rate and depth are increased
Increased blood glucose levels
Dilated pupils, peripheral vasoconstriction, sweat gland activity causing cool moist skin
Compensatory shock endocrine compensation S/SX: - ......ANSWER........Increased blood
glucose
Reabsorption of salt and water increasing intravascular volume and BP
RAAS >Renin > Angiotensinogen > Angiotensinogen 1 > Angiotensinogen 2 > increases BP
and venous return to the heart
Angiotensinogen 2 activates the adrenal cortex for the release of aldosterone
Compensatory shock chemical compensation S/SX: - ......ANSWER........Perfusion begins
to decline
Rate and depth of respiration increase
Hyperventilation >CO2 is released > Respiratory alkalosis occurs
Vasoconstriction of cerebral blood vessels occurs > Cerebral hypoxia & ischemia may
result
Compensatory shock clinical presentation: - ......ANSWER........Elevated HR
Narrowed pulse pressure
Rapid, deep respirations causing respiratory alkalosis
Thirst
Cool, moist skin
Oliguria
Diminished bowel sounds
Restlessness > confusion
, 4 of 38
Hyperglycemia
Increased urine specific gravity
Decreased creatinine clearance
Progressive shock S/SX: - ......ANSWER........Ischemia in extremities
Weak or absent peripheral pulses
Altered body defense
Decreased capillary refill
Cellular hypoxia
Metabolic acidosis
Failure of the sodium-potassium pump
Edema
Progressive shock - ......ANSWER........Respiratory system is the first to fail
Decrease cardiac output
Decreased capillary permeability
AKI & liver injury
Progressive shock clinical presentation: - ......ANSWER........Dysrhythmias
Decreased BP
Narrow pulse pressure
Tachypnea
Cool, clammy skin
Anuria
Absent bowel sounds
Lethargy > coma
