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NR 567 Exam 2 V1 | NR 567 Advanced Pharmacology for the AGACNP | Actual Q&A with Rationale (NR567 Exam 2) | Chamberlain College of Nursing

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NR 567 Exam 2 V1 | NR 567 Advanced Pharmacology for the AGACNP | Actual Q&A with Rationale (NR567 Exam 2) | Chamberlain College of Nursing

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NR 567 Exam 2 V1 | NR 567 Advanced
Pharmacology for the AGACNP | Actual
Q&A with Rationale (NR567 Exam 2) |
Chamberlain College of Nursing
1. A 64-year-old male with chronic heart failure (HFrEF) presents for a follow-up. He is

currently taking Lisinopril and Carvedilol. Which of the following findings would most likely

necessitate a dosage adjustment or temporary discontinuation of the ACE inhibitor?

A. Heart rate of 58 beats per minute


B. Serum potassium level of 4.2 mEq/L


C. Trace peripheral edema


D. Serum creatinine increase from 1.1 to 1.8 mg/dL


Answer: D


Rationale: ACE inhibitors can cause a reduction in glomerular filtration rate by

dilating the efferent arteriole. A significant rise in serum creatinine, typically defined

as greater than 30% from baseline, requires careful re-evaluation of the medication.

The AGACNP must monitor renal function and electrolytes closely when initiating or

titrating these agents.


2. A patient is being started on Warfarin for atrial fibrillation. Which of the following

statements regarding the mechanism of action is correct?

A. It directly inhibits Thrombin (Factor IIa)

,B. It inhibits the enzyme vitamin K epoxide reductase


C. It activates Antithrombin III


D. It inhibits Factor Xa in the final common pathway


Answer: B


Rationale: Warfarin works by interfering with the cyclic interconversion of vitamin K

and its epoxide. This action inhibits the synthesis of vitamin K-dependent clotting

factors II, VII, IX, and X. Because it affects synthesis rather than existing factors, it

takes several days to achieve full therapeutic effect.


3. Which of the following is considered a primary side effect of loop diuretics that the

AGACNP must monitor in a patient with acute decompensated heart failure?

A. Hyperkalemia


B. Hypertension


C. Hypercalcemia


D. Hypomagnesemia


Answer: D


Rationale: Loop diuretics like furosemide promote the excretion of sodium, potassium,

and magnesium in the thick ascending limb of the loop of Henle. Chronic or high-dose

therapy often leads to electrolyte depletion, specifically hypokalemia and

,hypomagnesemia. These imbalances increase the risk of cardiac arrhythmias and

require regular laboratory surveillance.


4. A patient with a history of severe asthma is being managed in the ICU. Which of the

following medications should be utilized with caution or avoided due to the risk of

bronchospasm? Select all that apply.

A. Propranolol


B. Aspirin


C. Timolol ophthalmic drops


D. Amlodipine


E. Ibuprofen


F. Ipratropium


Answer: A, B, C, E


Rationale: Non-selective beta-blockers like propranolol and even topical agents like

timolol can cause significant bronchoconstriction in susceptible asthma patients.

Additionally, NSAIDs and aspirin can trigger aspirin-exacerbated respiratory disease

(AERD) in up to 10-20% of adult asthmatics. Calcium channel blockers and

anticholinergics do not typically carry this specific risk for bronchospasm.

, 5. The AGACNP is reviewing the lipid profile of a patient on high-intensity statin therapy. The

patient complains of significant muscle pain. Which laboratory test is the priority to assess for

statin-induced rhabdomyolysis?

A. Alanine aminotransferase (ALT)


B. Aspartate aminotransferase (AST)


C. Alkaline phosphatase


D. Creatine kinase (CK)


Answer: D


Rationale: Creatine kinase is the specific marker used to evaluate muscle injury

associated with statin use. While statins can cause elevations in liver transaminases,

muscle-related adverse effects are more common and can range from simple myalgia

to life-threatening rhabdomyolysis. If CK levels are significantly elevated, the statin

must be discontinued immediately to prevent renal failure.


6. Which of the following describes the mechanism of action of Digoxin in the treatment of

heart failure?

A. Inhibition of the Na+/K+-ATPase pump


B. Antagonism of beta-1 adrenergic receptors


C. Direct stimulation of adenylyl cyclase


D. Blockade of calcium channels in the sarcoplasmic reticulum

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