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NUR 210/ NUR210 Exam 2 – Principles of Pharmacology Review ACTUAL EXAM 2026/2027 | Principles of Pharmacology Review | Verified Q&A | Pass Guaranteed - A+ Graded

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Excel on your NUR 210 Exam 2 with this 2026/2027 complete actual exam for Principles of Pharmacology Review at Galen. This 100% verified question set covers critical pharmacology topics: autonomic nervous system agents, cardiovascular and renal drugs, analgesic and anti-inflammatory medications, antimicrobial and antibiotic therapy, and endocrine pharmacology including insulin and thyroid agents. Each answer includes a detailed rationale to reinforce safe medication administration and clinical decision-making. Backed by our Pass Guarantee. Download now.

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Institution
NUR 210/ NUR210
Course
NUR 210/ NUR210

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​ UR 210/ NUR210 Exam 2 –​
N
​Principles of Pharmacology Review​
​ACTUAL EXAM 2026/2027 |​
​Principles of Pharmacology Review​
​| Verified Q&A | Pass Guaranteed -​
​A+ Graded​
​ =======================================================================​
=
​========​
​PART A – MULTIPLE CHOICE (Q1–60)​
​========================================================================​
​========​

*​ *Q1 (Anticoagulants – warfarin reversal):**​
​A patient on warfarin (Coumadin) presents with an INR of 6.5 and active bleeding. Which​
​intervention is most appropriate?​
​A. Administer protamine sulfate​
​B. Administer vitamin K (phytonadione) 5–10 mg IV​
​C. Administer andexanet alfa​
​D. Administer fresh frozen plasma (FFP) only​

*​ *[CORRECT]** B​
​*Rationale: The American College of Chest Physicians (CHEST) guidelines recommend vitamin​
​K (phytonadione) 5–10 mg IV for warfarin-associated major bleeding with INR >4.5. Protamine​
​sulfate (A) reverses heparin, not warfarin. Andexanet alfa (C) is indicated for​
​apixaban/rivaroxaban reversal, not warfarin. FFP alone (D) is insufficient because it does not​
​correct the underlying vitamin K-dependent factor deficiency.*​

*​ *Q2 (ACE inhibitors – adverse effects):**​
​A 62-year-old patient prescribed lisinopril (Prinivil) for hypertension returns complaining of a​
​persistent dry cough. Which mechanism explains this adverse effect?​
​A. Increased bradykinin levels​
​B. Decreased angiotensin II production​
​C. Increased prostaglandin synthesis​

,​D. Decreased aldosterone secretion​

*​ *[CORRECT]** A​
​*Rationale: ACE inhibitors block the conversion of angiotensin I to angiotensin II and also inhibit​
​the degradation of bradykinin, leading to accumulation and a dry, nonproductive cough in​
​5–20% of patients. Decreased angiotensin II (B) is the desired therapeutic effect. Prostaglandin​
​synthesis (C) is not the primary mechanism. Decreased aldosterone (D) causes hyperkalemia,​
​not cough.*​

*​ *Q3 (Beta-blockers – contraindications):**​
​Which condition is an absolute contraindication to the administration of metoprolol (Lopressor)?​
​A. Type 2 diabetes mellitus​
​B. Heart rate of 58 beats/minute​
​C. Severe bradycardia (HR <45 bpm)​
​D. Mild asthma​

*​ *[CORRECT]** C​
​*Rationale: Severe bradycardia (HR <45 bpm) is an absolute contraindication to beta-blocker​
​therapy because beta-blockers further decrease heart rate via beta-1 receptor blockade. Type 2​
​diabetes (A) is a relative contraindication due to masking of hypoglycemia symptoms, not​
​absolute. HR 58 bpm (B) warrants monitoring but is not an absolute contraindication. Mild​
​asthma (D) is a relative contraindication due to nonselective beta-blocker risk.*​

*​ *Q4 (Calcium channel blockers – adverse effects):**​
​A patient taking amlodipine (Norvasc) reports bilateral ankle edema. The nurse understands this​
​is caused by:​
​A. Sodium and water retention​
​B. Arteriolar vasodilation without venous vasodilation​
​C. Direct cardiac suppression​
​D. Increased capillary permeability​

*​ *[CORRECT]** B​
​*Rationale: Dihydropyridine calcium channel blockers (amlodipine) cause preferential arteriolar​
​vasodilation without compensatory venous vasodilation, leading to increased hydrostatic​
​pressure in capillary beds and peripheral edema. Sodium retention (A) is more characteristic of​
​dihydropyridine use in combination with heart failure. Direct cardiac suppression (C) occurs with​
​nondihydropyridines (verapamil, diltiazem). Capillary permeability (D) is not the mechanism.*​

*​ *Q5 (Diuretics – loop diuretics adverse effects):**​
​A patient receiving furosemide (Lasix) IV develops tinnitus and hearing loss. The nurse​
​recognizes this as:​
​A. An expected adverse effect requiring dose reduction​
​B. A sign of ototoxicity requiring immediate discontinuation​
​C. A hypersensitivity reaction​

, ​D. An indication of therapeutic effectiveness​

*​ *[CORRECT]** B​
​*Rationale: Loop diuretics (furosemide, bumetanide, torsemide) cause ototoxicity via damage to​
​the stria vascularis and hair cells of the cochlea, particularly with rapid IV administration or in​
​renal impairment. This is an indication for immediate discontinuation and audiology evaluation.​
​Dose reduction (A) is insufficient. Hypersensitivity (C) presents with rash or anaphylaxis.​
​Tinnitus is never a therapeutic indicator (D). Clinical pearl: Administer furosemide IV over 1–2​
​minutes to minimize ototoxicity risk.*​

*​ *Q6 (Antidysrhythmics – amiodarone):**​
​A patient on long-term amiodarone (Cordarone) therapy requires monitoring for which​
​potentially life-threatening adverse effect?​
​A. Acute liver failure​
​B. Pulmonary fibrosis​
​C. Aplastic anemia​
​D. Hemorrhagic cystitis​

*​ *[CORRECT]** B​
​*Rationale: Amiodarone (Class III antidysrhythmic) accumulates in lung tissue and can cause​
​potentially fatal pulmonary fibrosis, pneumonitis, or organizing pneumonia. Baseline and​
​periodic chest X-rays and pulmonary function tests are required. While hepatotoxicity occurs,​
​acute liver failure (A) is rare. Aplastic anemia (C) is associated with carbamazepine and​
​chloramphenicol. Hemorrhagic cystitis (D) is associated with cyclophosphamide.*​

*​ *Q7 (Antidysrhythmics – adenosine):**​
​When administering adenosine (Adenocard) for supraventricular tachycardia (SVT), the nurse​
​should expect:​
​A. A gradual decrease in heart rate over 5 minutes​
​B. Brief asystole followed by normal sinus rhythm​
​C. Sustained hypotension for 30 minutes​
​D. Immediate ventricular fibrillation​

*​ *[CORRECT]** B​
​*Rationale: Adenosine causes transient AV nodal blockade via activation of A1 receptors,​
​producing brief asystole (6–12 seconds) followed by restoration of normal sinus rhythm in 90%​
​of SVT cases. Rapid IV push followed by a 20 mL saline flush is required. Gradual decrease (A)​
​describes beta-blockers. Sustained hypotension (C) is not characteristic. Ventricular fibrillation​
​(D) is a rare complication, not an expected outcome.*​

*​ *Q8 (Anticoagulants – heparin monitoring):**​
​A patient receiving unfractionated heparin has an aPTT of 98 seconds (therapeutic range 60–80​
​seconds). What is the nurse's priority action?​
​A. Continue the current infusion rate​

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