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NUR 6011 Exam 2 Actual Exam V2 | NUR 6011 Advance Pharmacology (NUR6011 Exam 2) | William Paterson University

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NUR 6011 Exam 2 Actual Exam V2 | NUR 6011 Advance Pharmacology (NUR6011 Exam 2) | William Paterson University

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NUR 6011 Exam 2 Actual Exam V2 | NUR 6011 Advance Pharmacology
(NUR6011 Exam 2) | William Paterson University
1. A 65-year-old patient with heart failure is prescribed an ACE inhibitor. What is the
physiological mechanism behind the characteristic dry cough associated with this medication
class?
A. Inhibition of prostaglandin synthesis in the lungs

B. Direct irritation of the bronchial mucosa by the drug metabolite

C. Accumulation of bradykinin and substance P

D. Increased production of angiotensin II in pulmonary tissues
Answer: C
Rationale: ACE inhibitors prevent the breakdown of bradykinin, leading to its
accumulation in the respiratory tract. This accumulation triggers the cough reflex in
approximately 10-20% of patients. Switching to an Angiotensin II Receptor Blocker (ARB)
is usually the next clinical step as ARBs do not affect bradykinin levels.

2. When prescribing a statin for a patient with hyperlipidemia, which laboratory parameter
must be monitored to detect the most serious potential adverse effect?
A. Serum Creatinine

B. Alkaline Phosphatase

C. Blood Urea Nitrogen (BUN)

D. Creatine Kinase (CK)
Answer: D
Rationale: Elevated Creatine Kinase (CK) levels are a marker for muscle damage, ranging
from myalgia to life-threatening rhabdomyolysis. While liver enzymes were previously
monitored routinely, current guidelines emphasize baseline testing and monitoring only if
symptoms occur. Patients should be educated to report any unexplained muscle pain or
weakness immediately.

3. A patient is being started on Warfarin for atrial fibrillation. Which of the following
statements regarding the ‘bridging’ with Heparin is correct?
A. Heparin is unnecessary if the patient has no history of stroke

B. Heparin provides immediate anticoagulation while Warfarin depletes clotting factors

C. Warfarin causes an immediate anticoagulant effect within 2 hours

D. Warfarin inhibits the activity of existing thrombin molecules

,Answer: B
Rationale: Warfarin works by inhibiting the synthesis of Vitamin K-dependent clotting
factors, which takes several days to reach therapeutic levels. During the initial phase,
Protein C and S are depleted faster than other factors, creating a temporary prothrombotic
state. Bridging with Heparin or LMWH ensures the patient is protected until the INR
reaches the target therapeutic range.

4. Metformin is the first-line treatment for Type 2 Diabetes. What is the primary reason it is
contraindicated in patients with a significant reduction in glomerular filtration rate (eGFR <
30 mL/min)?
A. Risk of severe hypoglycemia

B. Reduced efficacy in glucose lowering

C. Increased risk of lactic acidosis

D. Potential for permanent renal tubule damage
Answer: C
Rationale: Metformin is renally excreted, and its accumulation in the setting of renal
failure can lead to the dangerous buildup of lactate. Lactic acidosis is a rare but potentially
fatal metabolic complication characterized by low pH and elevated lactate levels.
Healthcare providers must monitor renal function at least annually and adjust or
discontinue the drug as kidney function declines.

5. A patient with asthma is not well-controlled on a Short-Acting Beta Agonist (SABA) alone.
What is the preferred next step in pharmacotherapy according to GINA guidelines?
A. Add a Long-Acting Beta Agonist (LABA) as monotherapy

B. Add a Low-dose Inhaled Corticosteroid (ICS)

C. Switch SABA to an Oral Corticosteroid

D. Add a Theophylline supplement
Answer: B
Rationale: The addition of a low-dose Inhaled Corticosteroid (ICS) addresses the
underlying inflammation that drives asthma symptoms. Monotherapy with LABAs is
contraindicated in asthma due to an increased risk of asthma-related death. Consistent use
of ICS significantly reduces the risk of exacerbations and the need for rescue inhalers.

6. A patient taking Digoxin for heart failure presents with nausea, halo vision, and an irregular
heart rate. Which electrolyte abnormality most increases the risk of this toxicity?
A. Hypernatremia

B. Hypermagnesemia

, C. Hypokalemia

D. Hypocalcemia
Answer: C
Rationale: Digoxin competes with potassium for binding sites on the Na+/K+ ATPase
pump. When potassium levels are low, Digoxin binds more effectively, significantly
increasing its pharmacological effect and the risk of toxicity. Clinicians must closely
monitor potassium levels, especially in patients also taking loop diuretics.

7. A patient is prescribed Amiodarone for refractory ventricular arrhythmias. Which organ
system requires baseline and periodic monitoring due to the drug’s high iodine content?
A. Renal system

B. Thyroid gland

C. Pancreas

D. Bone marrow
Answer: B
Rationale: Amiodarone contains significant amounts of iodine and is structurally similar to
thyroxine, which can lead to both hyperthyroidism and hypothyroidism. Monitoring TSH
and T4 is essential for early detection of thyroid dysfunction during therapy. Additionally,
the drug has a very long half-life, meaning side effects can persist for months after
discontinuation.

8. Which of the following is a common adverse effect of Calcium Channel Blockers
(specifically Dihydropyridines like Amlodipine)?
A. Hyperkalemia

B. Peripheral edema

C. Dry cough

D. Bronchospasm
Answer: B
Rationale: Peripheral edema occurs due to the preferential dilation of precapillary
arterioles, which increases hydrostatic pressure in the capillaries. This leads to fluid
extravasation into the interstitial space, typically manifesting in the ankles. It is a dose-
dependent side effect and is often managed by adding an ACE inhibitor or reducing the
dose.

9. A patient with a history of Myocardial Infarction is prescribed Clopidogrel. Genetic testing
reveals the patient is a CYP2C19 ‘poor metabolizer’. What is the clinical implication?
A. The patient is at high risk for toxicity and bleeding

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