Pharmacology and the Nursing
Process
10th Edition
• Author(s)Linda Lane Lilley;
Shelly Rainforth Collins; Julie
S. Snyder
TEST BANK
,Question 1: Multiple-Choice Question (MCQ)
1. Clinical Scenario
A 74-year-old female patient with a history of chronic kidney
disease (CKD) Stage 3b and chronic heart failure is prescribed
digoxin 0.125 mg orally daily for ventricular rate control due to
atrial fibrillation. The patient’s baseline serum creatinine is 1.8
mg/dL (estimated glomerular filtration rate [eGFR] 32
mL/min/1.73 m²). She presents to the clinic complaining of mild
nausea, generalized weakness, and "blurry, slightly yellow
vision" over the past 3 days. Her current serum potassium level
is 3.3 mEq/L.
2. Question Stem
Which pharmacokinetic and pharmacodynamic principle
explains this patient’s presentation, and what is the priority
nursing action?
3. Answer Options
A. Digoxin has a wide therapeutic index; the symptoms are
likely due to age-related cataracts, so the nurse should reassure
the patient and check her blood pressure.
B. Digoxin is primarily metabolized by the liver; renal
impairment will not affect its clearance, so the nurse should
request an increase in dietary potassium.
,C. Digoxin clearance is reduced due to decreased renal
excretion, and hypokalemia potentiates digoxin toxicity; the
nurse must hold the dose and request a serum digoxin level.
D. Digoxin undergoes extensive first-pass metabolism; her visual
changes indicate acute optic nerve ischemia, so the nurse
should immediately administer digoxin immune Fab (Digibind).
4. Correct Answer
C
5. Comprehensive Rationale
Digoxin has a narrow therapeutic index ($0.5-2.0\text{ ng/mL}$
for arrhythmias; often lower, $0.5-0.9\text{ ng/mL}$, in heart
failure). It is primarily excreted unchanged by the kidneys via
glomerular filtration and active tubular secretion. This patient's
Stage 3b CKD causes a significant reduction in the renal
clearance of digoxin, leading to drug accumulation and an
increased risk of toxicity.
Furthermore, pharmacodynamically, digoxin inhibits the
$\text{Na}^+/\text{K}^+$-ATPase pump by binding
competitively to the same site as potassium. Hypokalemia
(serum potassium less than 3.5 mEq/L) means there are fewer
potassium ions to compete with digoxin for pump-binding sites,
significantly enhancing digoxin's binding and magnifying its
therapeutic and toxic effects even at lower or normal serum
, drug concentrations. Classic clinical manifestations of digoxin
toxicity include gastrointestinal disturbances (anorexia, nausea,
vomiting) and neurological/visual disturbances (generalized
weakness, blurred vision, xanthopsia/yellow-green halos
around objects). The immediate, priority nursing action is to
hold the scheduled dose to prevent further drug accumulation
and collaborate with the provider to obtain a serum digoxin
level and correct the hypokalemia.
6. Distractor Analysis
• A is incorrect: Digoxin has a narrow, not wide, therapeutic
index. Attributing classic visual halos to cataracts in a
patient on digoxin is a critical failure to recognize a toxic
drug effect.
• B is incorrect: Digoxin is primarily eliminated unchanged
by the kidneys, not metabolized by the liver. While
increasing dietary potassium is helpful, it is completely
inadequate as an isolated action without addressing the
potential toxicity and withholding the drug.
• D is incorrect: Digoxin has low first-pass metabolism when
given orally (bioavailability is 60–80%). While visual
changes are toxic manifestations, they do not signify optic
nerve ischemia. Digoxin immune Fab is reserved for life-
threatening toxicity (e.g., severe arrhythmias, severe
Process
10th Edition
• Author(s)Linda Lane Lilley;
Shelly Rainforth Collins; Julie
S. Snyder
TEST BANK
,Question 1: Multiple-Choice Question (MCQ)
1. Clinical Scenario
A 74-year-old female patient with a history of chronic kidney
disease (CKD) Stage 3b and chronic heart failure is prescribed
digoxin 0.125 mg orally daily for ventricular rate control due to
atrial fibrillation. The patient’s baseline serum creatinine is 1.8
mg/dL (estimated glomerular filtration rate [eGFR] 32
mL/min/1.73 m²). She presents to the clinic complaining of mild
nausea, generalized weakness, and "blurry, slightly yellow
vision" over the past 3 days. Her current serum potassium level
is 3.3 mEq/L.
2. Question Stem
Which pharmacokinetic and pharmacodynamic principle
explains this patient’s presentation, and what is the priority
nursing action?
3. Answer Options
A. Digoxin has a wide therapeutic index; the symptoms are
likely due to age-related cataracts, so the nurse should reassure
the patient and check her blood pressure.
B. Digoxin is primarily metabolized by the liver; renal
impairment will not affect its clearance, so the nurse should
request an increase in dietary potassium.
,C. Digoxin clearance is reduced due to decreased renal
excretion, and hypokalemia potentiates digoxin toxicity; the
nurse must hold the dose and request a serum digoxin level.
D. Digoxin undergoes extensive first-pass metabolism; her visual
changes indicate acute optic nerve ischemia, so the nurse
should immediately administer digoxin immune Fab (Digibind).
4. Correct Answer
C
5. Comprehensive Rationale
Digoxin has a narrow therapeutic index ($0.5-2.0\text{ ng/mL}$
for arrhythmias; often lower, $0.5-0.9\text{ ng/mL}$, in heart
failure). It is primarily excreted unchanged by the kidneys via
glomerular filtration and active tubular secretion. This patient's
Stage 3b CKD causes a significant reduction in the renal
clearance of digoxin, leading to drug accumulation and an
increased risk of toxicity.
Furthermore, pharmacodynamically, digoxin inhibits the
$\text{Na}^+/\text{K}^+$-ATPase pump by binding
competitively to the same site as potassium. Hypokalemia
(serum potassium less than 3.5 mEq/L) means there are fewer
potassium ions to compete with digoxin for pump-binding sites,
significantly enhancing digoxin's binding and magnifying its
therapeutic and toxic effects even at lower or normal serum
, drug concentrations. Classic clinical manifestations of digoxin
toxicity include gastrointestinal disturbances (anorexia, nausea,
vomiting) and neurological/visual disturbances (generalized
weakness, blurred vision, xanthopsia/yellow-green halos
around objects). The immediate, priority nursing action is to
hold the scheduled dose to prevent further drug accumulation
and collaborate with the provider to obtain a serum digoxin
level and correct the hypokalemia.
6. Distractor Analysis
• A is incorrect: Digoxin has a narrow, not wide, therapeutic
index. Attributing classic visual halos to cataracts in a
patient on digoxin is a critical failure to recognize a toxic
drug effect.
• B is incorrect: Digoxin is primarily eliminated unchanged
by the kidneys, not metabolized by the liver. While
increasing dietary potassium is helpful, it is completely
inadequate as an isolated action without addressing the
potential toxicity and withholding the drug.
• D is incorrect: Digoxin has low first-pass metabolism when
given orally (bioavailability is 60–80%). While visual
changes are toxic manifestations, they do not signify optic
nerve ischemia. Digoxin immune Fab is reserved for life-
threatening toxicity (e.g., severe arrhythmias, severe
