ATI PN Pediatric Nursing Proctored Exam
with NGN 2023–2026 | 70 Questions and
Answers
Exam
The ATI PN Pediatric Nursing Proctored Exam with NGN 2023–2026 contains 70
questions and answers covering child health, PN ATI Pediatric Nursing concepts, and
NGN-style exam questions.
Q: A patient with heart failure is receiving furosemide. They develop
muscle weakness, fatigue, and ECG changes showing flattened T-
waves. What electrolyte imbalance is most likely, and why?
A: Hypokalemia.
Rationale: Loop diuretics like furosemide cause potassium wasting.
Symptoms include muscle weakness, fatigue, and ECG changes
(flattened T-waves, U-waves). This is critical in heart failure patients
because hypokalemia increases sensitivity to digoxin toxicity and can
cause dangerous arrhythmias.
Q: A COPD patient presents with ABGs: pH 7.33, PaCO₂ 55 mmHg,
HCO₃⁻ 30 mEq/L. What is this imbalance, and is compensation
occurring?
A: Respiratory acidosis with metabolic compensation.
Rationale: The low pH indicates acidosis. The elevated PaCO₂ (>45)
points to respiratory cause. The elevated HCO₃⁻ (>26) indicates
,metabolic compensation (kidneys retaining bicarbonate). In chronic
COPD, renal compensation develops over time.
Q: Why does left-sided heart failure cause pulmonary edema, while
right-sided failure causes peripheral edema?
A: Different ventricular dysfunction locations.
Rationale: Left ventricular failure → blood backs up into left atrium →
pulmonary veins → pulmonary capillary pressure increases → fluid leaks
into alveoli (pulmonary edema). Right ventricular failure → blood backs
up into right atrium → systemic veins → increased venous pressure → fluid
leaks into tissues (peripheral edema, JVD, hepatomegaly).
Q: Compare the pathophysiology of diabetic ketoacidosis (DKA) and
hyperosmolar hyperglycemic state (HHS).
A: Both involve insulin deficiency but differ in severity and
presentation.
Rationale: DKA: Absolute insulin deficiency → cells can't use glucose →
fat breakdown for energy → ketone production → metabolic acidosis.
Occurs mainly in Type 1 DM. HHS: Relative insulin deficiency → severe
hyperglycemia → osmotic diuresis → profound dehydration →
hyperosmolarity. Minimal ketosis. Occurs mainly in Type 2 DM.
Q: Why does an emphysema patient have a barrel chest and pursed-lip
breathing?
A: Due to lung hyperinflation and air trapping.
Rationale: Destruction of alveolar walls reduces elastic recoil → airways
collapse during expiration → air trapping → increased AP diameter (barrel
chest). Pursed-lip breathing creates back pressure to keep airways open
longer during exhalation, reducing air trapping.
Q: A patient with chronic kidney disease has decreased erythropoietin
production. What is the resulting complication, and why?
,A: Anemia.
Rationale: Erythropoietin, produced by the kidneys, stimulates RBC
production in bone marrow. CKD → decreased erythropoietin →
decreased RBC production → normocytic, normochromic anemia. This
contributes to fatigue, pallor, and decreased tissue oxygenation.
Q: Describe the vascular phase of acute inflammation.
A: Vasodilation and increased permeability.
Rationale: 1) Vasodilation (histamine-mediated) increases blood flow →
redness/heat. 2) Increased capillary permeability allows plasma proteins
to leak into tissues → edema. 3) Endothelial cell contraction creates gaps
for fluid/exudate escape.
Q: Why is a patient with lupus (SLE) at risk for infections despite having
autoantibodies?
A: Due to immune system dysfunction and immunosuppressive
treatment.
Rationale: SLE involves B-cell hyperactivity producing autoantibodies,
but also has complement system deficiencies. Treatment with
corticosteroids and immunosuppressants further increases infection risk
by suppressing normal immune responses.
Q: Differentiate between the pathophysiology of ischemic vs.
hemorrhagic stroke.
A: Different mechanisms of brain injury.
Rationale: Ischemic: Occlusion of cerebral artery → decreased blood
flow → ischemia → infarction (80% of strokes). Hemorrhagic: Rupture of
, cerebral blood vessel → bleeding into brain tissue → compression,
increased ICP (more acutely fatal).
Q: How does portal hypertension lead to esophageal varices?
A: Increased pressure creates collateral circulation.
Rationale: Liver cirrhosis → increased resistance in portal vein → portal
hypertension → blood seeks alternative pathways → distends collateral
veins at lower esophagus/stomach → thin-walled varices prone to
rupture → life-threatening hemorrhage.
Q: According to Piaget, why would a 3-year-old think a tall glass holds
more than a short glass, even when shown equal amounts?
A: Preoperational stage limitations.
Rationale: Children ages 2-7 are in preoperational stage. They lack
conservation (understanding quantity remains same despite shape
change). They focus on one dimension (height) and cannot mentally
reverse the pouring action.
Q: Why are infants more susceptible to respiratory distress from RSV
than older children?
A: Anatomical and immunological factors.
Rationale: 1) Smaller airways that obstruct easily with
inflammation/mucus. 2) Less developed immune system. 3) Less
respiratory reserve. 4) Inability to clear secretions effectively. 5)
Immature ciliary function.
with NGN 2023–2026 | 70 Questions and
Answers
Exam
The ATI PN Pediatric Nursing Proctored Exam with NGN 2023–2026 contains 70
questions and answers covering child health, PN ATI Pediatric Nursing concepts, and
NGN-style exam questions.
Q: A patient with heart failure is receiving furosemide. They develop
muscle weakness, fatigue, and ECG changes showing flattened T-
waves. What electrolyte imbalance is most likely, and why?
A: Hypokalemia.
Rationale: Loop diuretics like furosemide cause potassium wasting.
Symptoms include muscle weakness, fatigue, and ECG changes
(flattened T-waves, U-waves). This is critical in heart failure patients
because hypokalemia increases sensitivity to digoxin toxicity and can
cause dangerous arrhythmias.
Q: A COPD patient presents with ABGs: pH 7.33, PaCO₂ 55 mmHg,
HCO₃⁻ 30 mEq/L. What is this imbalance, and is compensation
occurring?
A: Respiratory acidosis with metabolic compensation.
Rationale: The low pH indicates acidosis. The elevated PaCO₂ (>45)
points to respiratory cause. The elevated HCO₃⁻ (>26) indicates
,metabolic compensation (kidneys retaining bicarbonate). In chronic
COPD, renal compensation develops over time.
Q: Why does left-sided heart failure cause pulmonary edema, while
right-sided failure causes peripheral edema?
A: Different ventricular dysfunction locations.
Rationale: Left ventricular failure → blood backs up into left atrium →
pulmonary veins → pulmonary capillary pressure increases → fluid leaks
into alveoli (pulmonary edema). Right ventricular failure → blood backs
up into right atrium → systemic veins → increased venous pressure → fluid
leaks into tissues (peripheral edema, JVD, hepatomegaly).
Q: Compare the pathophysiology of diabetic ketoacidosis (DKA) and
hyperosmolar hyperglycemic state (HHS).
A: Both involve insulin deficiency but differ in severity and
presentation.
Rationale: DKA: Absolute insulin deficiency → cells can't use glucose →
fat breakdown for energy → ketone production → metabolic acidosis.
Occurs mainly in Type 1 DM. HHS: Relative insulin deficiency → severe
hyperglycemia → osmotic diuresis → profound dehydration →
hyperosmolarity. Minimal ketosis. Occurs mainly in Type 2 DM.
Q: Why does an emphysema patient have a barrel chest and pursed-lip
breathing?
A: Due to lung hyperinflation and air trapping.
Rationale: Destruction of alveolar walls reduces elastic recoil → airways
collapse during expiration → air trapping → increased AP diameter (barrel
chest). Pursed-lip breathing creates back pressure to keep airways open
longer during exhalation, reducing air trapping.
Q: A patient with chronic kidney disease has decreased erythropoietin
production. What is the resulting complication, and why?
,A: Anemia.
Rationale: Erythropoietin, produced by the kidneys, stimulates RBC
production in bone marrow. CKD → decreased erythropoietin →
decreased RBC production → normocytic, normochromic anemia. This
contributes to fatigue, pallor, and decreased tissue oxygenation.
Q: Describe the vascular phase of acute inflammation.
A: Vasodilation and increased permeability.
Rationale: 1) Vasodilation (histamine-mediated) increases blood flow →
redness/heat. 2) Increased capillary permeability allows plasma proteins
to leak into tissues → edema. 3) Endothelial cell contraction creates gaps
for fluid/exudate escape.
Q: Why is a patient with lupus (SLE) at risk for infections despite having
autoantibodies?
A: Due to immune system dysfunction and immunosuppressive
treatment.
Rationale: SLE involves B-cell hyperactivity producing autoantibodies,
but also has complement system deficiencies. Treatment with
corticosteroids and immunosuppressants further increases infection risk
by suppressing normal immune responses.
Q: Differentiate between the pathophysiology of ischemic vs.
hemorrhagic stroke.
A: Different mechanisms of brain injury.
Rationale: Ischemic: Occlusion of cerebral artery → decreased blood
flow → ischemia → infarction (80% of strokes). Hemorrhagic: Rupture of
, cerebral blood vessel → bleeding into brain tissue → compression,
increased ICP (more acutely fatal).
Q: How does portal hypertension lead to esophageal varices?
A: Increased pressure creates collateral circulation.
Rationale: Liver cirrhosis → increased resistance in portal vein → portal
hypertension → blood seeks alternative pathways → distends collateral
veins at lower esophagus/stomach → thin-walled varices prone to
rupture → life-threatening hemorrhage.
Q: According to Piaget, why would a 3-year-old think a tall glass holds
more than a short glass, even when shown equal amounts?
A: Preoperational stage limitations.
Rationale: Children ages 2-7 are in preoperational stage. They lack
conservation (understanding quantity remains same despite shape
change). They focus on one dimension (height) and cannot mentally
reverse the pouring action.
Q: Why are infants more susceptible to respiratory distress from RSV
than older children?
A: Anatomical and immunological factors.
Rationale: 1) Smaller airways that obstruct easily with
inflammation/mucus. 2) Less developed immune system. 3) Less
respiratory reserve. 4) Inability to clear secretions effectively. 5)
Immature ciliary function.
