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NSG 3253 Pharmacotherapeutics for Nursing Practice II Final Exam | Comprehensive Question Bank with Verified Answers

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NSG 3253 Pharmacotherapeutics for Nursing Practice II Final Exam | Comprehensive Question Bank with Verified Answers

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NSG 3253 Pharmacotherapeutics for Nursing
Practice II Final Exam | Comprehensive Question
Bank with Verified Answers

Question 1
Why are angiotensin-converting enzyme (ACE) inhibitors strictly
contraindicated during the second and third trimesters of pregnancy?
• A. They cause severe fetal renal damage, oligohydramnios, and
skull hypoplasia.
• B. They induce rapid maternal hypoglycemia and gestational
diabetes.
• C. They cause permanent closure of the ductus arteriosus
prematurely.
• D. They stimulate massive uterine hyperstimulation and abrupt
labor.
Correct Answer: A. They cause severe fetal renal damage,
oligohydramnios, and skull hypoplasia.
Detailed Rationale: ACE inhibitors and ARBs act on the renin-
angiotensin-aldosterone system, which is critical for normal fetal renal
development. Exposure during the second and third trimesters leads to
fetotoxicity, renal failure, oligohydramnios, and skeletal deformities.
Question 2

,Which clinical manifestations are classic early signs of digitalis toxicity in
a patient receiving digoxin therapy?
• A. Anorexia, nausea, vomiting, and visual disturbances such as
yellow-green halos around lights
• B. Uncontrolled hypertension, tachycardia, and excessive sweating
• C. Severe watery diarrhea, high fever, and sudden hair loss
• D. Rapid weight gain, pitting peripheral edema, and wheezing
Correct Answer: A. Anorexia, nausea, vomiting, and visual disturbances
such as yellow-green halos around lights
Detailed Rationale: Digitalis toxicity frequently presents with
gastrointestinal symptoms (anorexia, nausea, vomiting) and
characteristic neurological/visual changes, including xanthopsia (yellow-
green vision or halos), along with cardiac arrhythmias.
Question 3
What is the specific pharmacological reversal agent administered for a
severe hemorrhage induced by a heparin overdose?
• A. Protamine sulfate
• B. Vitamin K phytadione
• C. Fresh frozen plasma alone without additives
• D. Calcium gluconate
Correct Answer: A. Protamine sulfate
Detailed Rationale: Protamine sulfate is a positively charged basic
protein that binds chemically to negatively charged heparin molecules,

,forming an inactive stable complex and neutralizing its anticoagulant
effect rapidly.
Question 4
What crucial dietary teaching should the nurse provide to a patient
prescribed chronic warfarin therapy?
• A. Maintain a consistent, stable daily intake of green leafy
vegetables containing vitamin K rather than drastically increasing
or eliminating them.
• B. Eliminate all dietary sources of vitamin K entirely from daily
meals.
• C. Increase vitamin K intake threefold whenever bleeding gums
occur.
• D. Avoid all forms of dietary protein and dairy products.
Correct Answer: A. Maintain a consistent, stable daily intake of green
leafy vegetables containing vitamin K rather than drastically increasing
or eliminating them.
Detailed Rationale: Warfarin is a vitamin K antagonist. Fluctuations in
dietary vitamin K can destabilize INR levels. Consistency, rather than
total avoidance, allows the healthcare provider to maintain a stable
therapeutic warfarin dose.
Question 5
Which electrolyte imbalance must the nurse monitor closely when
administering spironolactone, a potassium-sparing diuretic, particularly
if the patient is concurrently taking an ACE inhibitor?

, • A. Hyperkalemia
• B. Hypokalemia
• C. Hyponatremia
• D. Hypercalcemia
Correct Answer: A. Hyperkalemia
Detailed Rationale: Spironolactone blocks aldosterone receptors,
reducing potassium excretion. When combined with ACE inhibitors
(which also decrease aldosterone and raise potassium), the risk of
severe, life-threatening hyperkalemia increases significantly.
Question 6
Why are non-selective beta-adrenergic blockers (such as propranolol)
contraindicated in patients with asthma or chronic obstructive
pulmonary disease (COPD)?
• A. They block beta-2 receptors in bronchial smooth muscle,
precipitating severe bronchoconstriction and airway resistance.
• B. They stimulate massive histamine release from pulmonary mast
cells.
• C. They destroy alveolar surfactant membranes permanently.
• D. They cause acute respiratory depression by paralyzing the
diaphragm.
Correct Answer: A. They block beta-2 receptors in bronchial smooth
muscle, precipitating severe bronchoconstriction and airway resistance.
Detailed Rationale: Non-selective beta-blockers inhibit both beta-1
(cardiac) and beta-2 (bronchial and vascular) receptors. Blocking beta-2

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