Graded A+ Premium Exam Tested And Verified
Subject Area NUR 2349 - PN1 Exam 3
Description Comprehensive examination on NUR 2349 - PN1 Exam 3.
Expected Grade A+
Total Questions 90
Duration 3 hours
Learning Outcomes 1. Demonstrate mastery of core concepts
Accreditation Aligned with US university standards.
Page 1
,1. Which of the following best describes the mechanism by which loop diuretics
cause ototoxicity?
A. Direct damage to the hair cells of the organ of Corti due to inhibition of the Na-K-2Cl
cotransporter in the stria vascularis
B. Vasoconstriction of the labyrinthine artery leading to ischemic injury of the cochlea
C. Accumulation of drug in the endolymph causing osmotic disruption of hair cell function
D. Competitive antagonism of GABA receptors in the auditory nerve
Answer: A. Direct damage to the hair cells of the organ of Corti due to inhibition of
the Na-K-2Cl cotransporter in the stria vascularis
Loop diuretics inhibit the Na-K-2Cl cotransporter in the stria vascularis, which alters
the ionic composition of endolymph and can damage hair cells. Option B is incorrect
because vasoconstriction is not the primary mechanism. Option C misrepresents the
mechanism; accumulation is not the cause. Option D is unrelated to loop diuretic
pharmacology.
2. A patient with chronic kidney disease (GFR 25 mL/min) is prescribed a
medication that is primarily eliminated by the kidneys. Which pharmacokinetic
parameter is most likely to be significantly altered?
A. Bioavailability due to decreased first-pass metabolism
B. Volume of distribution due to increased plasma protein binding
C. Half-life due to reduced renal clearance
D. Peak concentration due to faster absorption
Answer: C. Half-life due to reduced renal clearance
Reduced renal function prolongs the elimination half-life of renally cleared drugs.
Bioavailability (A) is not directly affected by renal impairment. Volume of distribution
(B) may increase due to fluid overload, not protein binding changes. Peak concentration
(D) is influenced by absorption rate, not renal elimination.
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,3. A patient receiving intravenous heparin develops a platelet count drop from
250,000 to 90,000/mm³ over 5 days. Which antibody is most likely responsible for
this condition?
A. IgG antibodies against platelet factor 4-heparin complexes
B. IgM antibodies against von Willebrand factor
C. IgA antibodies against glycoprotein IIb/IIIa
D. IgE antibodies against heparin itself
Answer: A. IgG antibodies against platelet factor 4-heparin complexes
Heparin-induced thrombocytopenia (HIT) is caused by IgG antibodies that bind to
platelet factor 4-heparin complexes, activating platelets. IgM (B) is not typical. IgA (C)
is associated with other autoimmune thrombocytopenias. IgE (D) mediates allergic
reactions, not thrombocytopenia.
4. A patient with type 2 diabetes is started on metformin. Which laboratory value
should be monitored to detect the most serious adverse effect?
A. Serum creatinine
B. Serum lactate
C. Hemoglobin A1c
D. Liver transaminases
Answer: B. Serum lactate
Metformin can cause lactic acidosis, a rare but potentially fatal adverse effect, so serum
lactate should be monitored. Serum creatinine (A) is monitored to assess renal function
before starting metformin but does not directly detect lactic acidosis. Hemoglobin A1c
(C) monitors glycemic control. Liver transaminases (D) are not affected by metformin.
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, 5. A nurse is caring for a patient with heart failure receiving digoxin. The patient's
serum potassium level is 3.2 mEq/L. Which electrocardiographic change is most
likely to occur?
A. Prolonged PR interval
B. Peaked T waves
C. Widened QRS complex
D. Shortened QT interval
Answer: A. Prolonged PR interval
Hypokalemia potentiates digoxin toxicity, which commonly manifests as PR interval
prolongation (first-degree AV block). Peaked T waves (B) are seen in hyperkalemia.
Widened QRS (C) is associated with quinidine or hyperkalemia. Shortened QT (D) is
not typical of digoxin toxicity.
6. A patient with a history of asthma is prescribed propranolol for migraine
prophylaxis. Which adverse effect is most anticipated?
A. Bronchospasm due to beta-2 receptor blockade
B. Hypoglycemia due to increased insulin secretion
C. Tachycardia due to reflex sympathetic activation
D. Hypertension due to alpha receptor stimulation
Answer: A. Bronchospasm due to beta-2 receptor blockade
Propranolol is a non-selective beta-blocker that blocks beta-2 receptors in the lungs,
causing bronchospasm in asthmatics. Hypoglycemia (B) is not increased; beta-blockers
may mask hypoglycemia. Tachycardia (C) is paradoxical; beta-blockers cause
bradycardia. Hypertension (D) is not a direct effect; beta-blockers lower blood
pressure.
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