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NUR 6011 Final Exam Actual Exam V2 | NUR 6011 Advance Pharmacology (NUR6011 Final Exam) | William Paterson University

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NUR 6011 Final Exam Actual Exam V2 | NUR 6011 Advance Pharmacology (NUR6011 Final Exam) | William Paterson University

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NUR 6011 Final Exam Actual Exam V2 | NUR 6011 Advance
Pharmacology (NUR6011 Final Exam) | William Paterson University
1. A patient with chronic kidney disease (CKD) Stage 4 is prescribed a new medication that is
primarily excreted renally. Which pharmacokinetic principle is most critical for the nurse
practitioner to consider?
A. The drug’s half-life will likely be prolonged, requiring a dose reduction or interval
extension.

B. Loading doses must be increased to compensate for decreased clearance.

C. The drug’s volume of distribution will remain unchanged.

D. Renal excretion does not affect the steady-state concentration of a drug.

Answer: A
Rationale: In patients with renal impairment, the clearance of renally excreted drugs is
decreased, which directly leads to a prolonged half-life. The Advanced Practice Nurse must
adjust the dosage or the dosing interval to prevent drug accumulation and potential
toxicity. This decision is based on the patient’s estimated glomerular filtration rate (eGFR)
and the specific pharmacokinetic profile of the medication.

2. A 65-year-old male with a history of heart failure and a reduced ejection fraction (HFrEF) is
currently taking an ACE inhibitor, a beta-blocker, and a loop diuretic. He presents with a
serum potassium level of 3.2 mEq/L. Which medication addition or adjustment is most
appropriate?
A. Increase the dose of the ACE inhibitor.

B. Discontinue the beta-blocker immediately.

C. Switch the ACE inhibitor to an Angiotensin II Receptor Blocker (ARB).

D. Add Spironolactone (an aldosterone antagonist).

Answer: D
Rationale: Aldosterone antagonists like Spironolactone are indicated for patients with
HFrEF to improve survival and reduce hospitalizations. Additionally, because it is a
potassium-sparing diuretic, it can help mitigate the hypokalemia often caused by loop
diuretics. Monitoring serum potassium and renal function is essential when initiating this
therapy to avoid the risk of hyperkalemia.

3. Which of the following best describes the mechanism of action of Metformin in the
management of Type 2 Diabetes Mellitus?
A. Decreases hepatic glucose production and improves insulin sensitivity.

,B. Stimulates insulin secretion from the pancreatic beta cells.

C. Increases glucose excretion through the kidneys by inhibiting SGLT2.

D. Delays the absorption of carbohydrates in the small intestine.

Answer: A
Rationale: Metformin is a biguanide that primarily works by decreasing hepatic
gluconeogenesis and increasing peripheral glucose uptake and utilization. It does not
stimulate insulin secretion, which is why it has a lower risk of hypoglycemia compared to
sulfonylureas. This medication is considered first-line therapy for Type 2 Diabetes due to
its efficacy, safety profile, and cardiovascular benefits.

4. A patient is being started on Warfarin for atrial fibrillation. The nurse practitioner knows
that the initial effect of Warfarin may actually increase the risk of thrombosis because:
A. It stimulates the release of Vitamin K from the liver.

B. It has a very short half-life and wears off quickly.

C. It depletes Protein C and Protein S faster than it depletes clotting factors II, VII, IX, and X.

D. It causes immediate platelet aggregation.

Answer: C
Rationale: Warfarin inhibits the synthesis of Vitamin K-dependent clotting factors, but it
also inhibits the natural anticoagulants Protein C and Protein S. Because Protein C has a
shorter half-life than the procoagulant factors (like Factor II or X), a transient
prothrombotic state can occur during the initial days of therapy. This is why ‘bridging’ with
a rapid-acting anticoagulant like Heparin is often necessary for high-risk patients.

5. When prescribing an HMG-CoA reductase inhibitor (statin), which laboratory value must be
monitored if the patient reports new-onset muscle pain or weakness?
A. Serum creatinine

B. Hemoglobin A1c

C. Alkaline phosphatase

D. Creatine kinase (CK)

Answer: D
Rationale: Statin-associated muscle symptoms (SAMS) range from mild myalgia to life-
threatening rhabdomyolysis. If a patient reports significant muscle pain, the nurse
practitioner should order a creatine kinase (CK) level to assess for muscle damage. While
routine CK monitoring is not recommended for asymptomatic patients, it is a critical
diagnostic step for those presenting with clinical symptoms.

, 6. A patient with a history of asthma is diagnosed with hypertension. Which class of
antihypertensive medications should be used with extreme caution or avoided?
A. Calcium channel blockers

B. ACE inhibitors

C. Non-selective beta-blockers

D. Thiazide diuretics
Answer: C
Rationale: Non-selective beta-blockers, such as Propranolol, block both beta-1 and beta-2
receptors. Blocking beta-2 receptors in the lungs can lead to bronchoconstriction, which
can precipitate a life-threatening asthma exacerbation. If a beta-blocker is absolutely
necessary, a cardio-selective beta-1 blocker (like Metoprolol) is preferred, though caution
is still advised.

7. A patient is prescribed Amiodarone for the management of ventricular arrhythmias. Which
of the following organs is NOT typically associated with Amiodarone-induced toxicity?
A. Thyroid gland

B. Pancreas

C. Lungs

D. Liver

Answer: B
Rationale: Amiodarone has a very long half-life and a high iodine content, leading to
several potential toxicities. Common monitoring includes thyroid function tests (due to risk
of hypo/hyperthyroidism), pulmonary function tests (risk of fibrosis), and liver enzymes
(risk of hepatotoxicity). The pancreas is not a primary site for Amiodarone toxicity, unlike
the eyes (corneal microdeposits) and skin (blue-gray discoloration).

8. A patient taking Monoamine Oxidase Inhibitors (MAOIs) for depression must be educated
to avoid foods high in tyramine, such as aged cheeses and red wine, to prevent:
A. Serotonin syndrome

B. Anticholinergic toxicity

C. Extrapyramidal symptoms

D. Hypertensive crisis

Answer: D
Rationale: MAOIs inhibit the breakdown of tyramine in the gastrointestinal tract and liver.
Increased levels of tyramine cause a massive release of norepinephrine from storage

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