NGN Exam Prep Questions & Detailed
Rationales (Pain & Inflammation Focus)
Question 1
Clinical Scenario
A 48-year-old female client with a history of rheumatoid
arthritis presents to the outpatient clinic with complaints of
epigastric pain, dark tarry stools, and fatigue over the past
week. She reports taking high-dose naproxen (500 mg twice
daily) for the past 6 months to manage joint stiffness. Her vital
signs are: BP 108/64 mmHg, HR 102 beats/min, RR 18
breaths/min, and SpO2 98% on room air. Laboratory results
reveal a hemoglobin of 8.2 g/dL (82 g/L) and hematocrit of 25%.
Question Stem
,Which provider order should the nurse anticipate implementing
first?
A. Administer misoprostol 200 mcg orally
B. Obtain a 12-lead electrocardiogram (ECG)
C. Discontinue naproxen therapy
D. Initiate an intravenous infusion of a proton pump inhibitor
Correct Answer
C. Discontinue naproxen therapy
Detailed Rationale
The client is demonstrating classic signs of a nonsteroidal anti-
inflammatory drug (NSAID)-induced upper gastrointestinal (GI)
bleed, including epigastric distress, melena (dark tarry stools),
tachycardia, and significant anemia (hemoglobin 8.2 g/dL).
Nonselective NSAIDs such as naproxen inhibit cyclooxygenase-1
(COX-1) enzymes, which are responsible for producing
prostaglandins that maintain the protective gastric mucosal
barrier, decrease gastric acid secretion, and promote mucosal
blood flow. Systemic inhibition of COX-1 leads to mucosal
erosion, ulceration, and potential hemorrhage.
The priority step in managing NSAID-induced GI toxicity is
immediate discontinuation of the offending agent to prevent
further injury to the gastric mucosa. While initiating an
,intravenous proton pump inhibitor (such as pantoprazole) and
administering mucosa-protective agents like misoprostol are
essential components of treatment, continuing to administer
the causative NSAID will exacerbate bleeding and delay mucosal
healing. Obtaining an ECG may be ordered if hemodynamic
instability progresses or if cardiac ischemia is suspected due to
anemia, but it is not the primary intervention for halting the
drug-induced cause.
Learning Objective
After completing this question, the learner should be able to:
• Recognize clinical manifestations of NSAID-induced
gastrointestinal ulceration and hemorrhage.
• Explain the physiological mechanism of COX-1 inhibition on
gastric mucosal protection.
• Prioritize nursing actions when managing adverse drug
reactions related to chronic NSAID therapy.
Medication Safety Focus
Adverse effect / Priority intervention
Question 2
Clinical Scenario
A 24-year-old male client is brought to the emergency
department by friends after being found lethargic in his
, apartment. The friends state he has been taking "a lot of over-
the-counter pain pills" for a severe toothache over the past 3
days. Assessment findings include jaundice of the sclera, right
upper quadrant abdominal tenderness, nausea, and vomiting.
Serum acetaminophen level is 180 mcg/mL (drawn 6 hours after
reported last ingestion), and alanine aminotransferase (ALT) is
1,250 U/L.
Question Stem
Which medication should the nurse prepare to administer
immediately?
A. Naloxone
B. Acetylcysteine
C. Activated charcoal
D. Flumazenil
Correct Answer
B. Acetylcysteine
Detailed Rationale
Acetaminophen toxicity is the leading cause of acute liver
failure. When taken in toxic amounts, the normal metabolic
pathways (glucuronide and sulfate conjugation) become
saturated, diverting acetaminophen metabolism to the
cytochrome P450 enzyme system. This produces a toxic reactive