UNIVERSITY OF CENTRAL FLORIDA
Course Code: NUR3145
Instructor:
Date: 2026
FINAL EXAM – PHARMACOLOGY FOR NURSING
PRACTICE
A 67-year-old male with heart failure (EF 35%), chronic kidney disease
stage 3 (eGFR 38 mL/min/1.73m²), and atrial fibrillation is prescribed
digoxin 0.125 mg daily. Three days after initiation, he presents with
nausea, visual disturbances described as yellow-green halos around
lights, and a heart rate of 44 bpm. His serum digoxin level is 2.6 ng/mL
and serum potassium is 3.1 mEq/L. Which factor most directly
potentiates digoxin toxicity in this patient, and what is the mechanism?
A) Atrial fibrillation increases digoxin's bioavailability by altering first-pass
metabolism in the liver B) Hypokalemia potentiates digoxin toxicity because
potassium and digoxin compete for the same binding site on the Na-K-
ATPase pump, and low extracellular potassium increases digoxin binding
affinity C) CKD increases digoxin toxicity by accelerating hepatic conversion
to active toxic metabolites D) Heart failure increases digoxin toxicity by
increasing volume of distribution and prolonging the drug's half-life in cardiac
tissue
Correct Answer: B
Rationale: Digoxin inhibits the Na-K-ATPase pump on cardiomyocytes.
Potassium and digoxin compete for the same binding site on this pump;
when extracellular potassium is low (hypokalemia), there is less competition,
and digoxin binds more readily, increasing its inhibitory effect and amplifying
toxicity. This is one of the most pharmacologically critical drug-electrolyte
interactions in clinical nursing. Compounding this, CKD reduces renal
excretion of digoxin (which is 60 to 80% renally eliminated unchanged),
leading to drug accumulation. Classic manifestations of toxicity include
1
,bradydysrhythmias, GI symptoms (nausea, vomiting, anorexia), and visual
disturbances (yellow-green chromatopsia, halos). Treatment involves holding
digoxin, correcting hypokalemia, cardiac monitoring, and potentially
administering digoxin immune Fab (Digibind) for severe toxicity.
A 58-year-old female with rheumatoid arthritis is being treated with
methotrexate 15 mg weekly. She presents to the clinic with oral ulcers,
macrocytic anemia, and fatigue. Her CBC shows: WBC 2,800/mcL, Hgb
9.2 g/dL, MCV 108 fL, platelets 88,000/mcL. Which mechanism explains
these adverse effects, and which supplement should be routinely co-
administered with methotrexate to reduce their incidence?
A) Methotrexate causes direct bone marrow suppression through alkylation
of DNA; leucovorin (folinic acid) 5 mg weekly is co-administered B)
Methotrexate competitively inhibits dihydrofolate reductase, depleting
tetrahydrofolate needed for purine and pyrimidine synthesis, causing folate
deficiency; folic acid 1 mg daily is co-administered on non-methotrexate days
C) Methotrexate causes hemolytic anemia through oxidative damage to red
blood cells; vitamin B12 supplementation corrects the anemia D)
Methotrexate activates the complement cascade causing autoimmune
cytopenias; corticosteroids are co-administered to suppress this response
Correct Answer: B
Rationale: Methotrexate is a folate antimetabolite that competitively and
irreversibly inhibits dihydrofolate reductase (DHFR), the enzyme that reduces
dietary folate to tetrahydrofolate (THF). THF is the active coenzyme required
for de novo synthesis of purines and thymidylate, essential for DNA
replication and cell division. Deficiency produces a megaloblastic picture
(elevated MCV, macrocytic anemia) and impairs rapidly dividing cells
including GI mucosa (oral ulcers) and hematopoietic precursors
(pancytopenia). Folic acid 1 mg daily supplementation on non-methotrexate
days reduces mucosal and hematological toxicity without significantly
compromising the anti-inflammatory efficacy of methotrexate in rheumatoid
arthritis. Leucovorin (folinic acid) is used for high-dose methotrexate rescue
in oncology settings and is not routinely used in low-dose rheumatological
regimens.
A 72-year-old male with type 2 diabetes is started on linagliptin (a DPP-
4 inhibitor) for glycemic control. His provider considers him a good
candidate because he has CKD stage 4 (eGFR 22 mL/min/1.73m²).
Which pharmacokinetic property of linagliptin makes it uniquely
appropriate for this patient compared to other agents in the same drug
class?
A) Linagliptin undergoes extensive renal glucuronidation, making it safer in
renal impairment B) Linagliptin is primarily eliminated via the bile and feces
2
,through enterohepatic recirculation and does not require dose adjustment in
any degree of renal impairment C) Linagliptin is dialyzable and removed
efficiently during hemodialysis sessions D) Linagliptin is converted to an
inactive metabolite by the kidney, making renal impairment clinically
irrelevant
Correct Answer: B
Rationale: Among the DPP-4 inhibitors (sitagliptin, saxagliptin, alogliptin,
linagliptin), linagliptin is unique in that it is predominantly eliminated via the
enterohepatic system (bile and feces), with less than 5% excreted renally.
This means no dose adjustment is required across all stages of CKD,
including end-stage renal disease on dialysis. In contrast, sitagliptin,
saxagliptin, and alogliptin are renally eliminated and require dose reductions
in moderate to severe CKD. DPP-4 inhibitors enhance incretin effect by
preventing degradation of GLP-1 and GIP, increasing glucose-dependent
insulin secretion and suppressing glucagon. They carry low hypoglycemia
risk as monotherapy because their effect is glucose-dependent. UCF nursing
students must understand pharmacokinetics as a basis for individualized
drug selection in patients with organ impairment.
A 34-year-old female with a history of bipolar disorder type I is
stabilized on lithium carbonate 900 mg twice daily (serum level 0.9
mEq/L). She is seen in the clinic complaining of three days of profuse
diarrhea and vomiting following a viral gastroenteritis. Today she
presents with coarse tremor, slurred speech, ataxia, confusion, and
muscle twitching. Her serum lithium level is 2.4 mEq/L. Which
pharmacokinetic mechanism explains the rapid rise in her lithium level
in the context of her illness?
A) Dehydration from fluid losses reduced renal blood flow and glomerular
filtration rate, decreasing lithium clearance, since lithium is entirely renally
eliminated without protein binding or hepatic metabolism B) Viral
gastroenteritis increased lithium absorption from the GI tract by altering
intestinal motility and pH C) The fever associated with illness increased
lithium's volume of distribution, paradoxically concentrating it in the CNS D)
Vomiting caused metabolic alkalosis, which increased tubular reabsorption of
lithium in exchange for hydrogen ions
Correct Answer: A
Rationale: Lithium has an extremely narrow therapeutic index (therapeutic
range 0.6 to 1.2 mEq/L; toxic above 1.5 mEq/L). It is not protein-bound, not
metabolized hepatically, and is entirely eliminated by the kidneys through
glomerular filtration and tubular reabsorption. Critically, lithium is reabsorbed
in the proximal tubule by the same mechanism as sodium. In states of
sodium and volume depletion (vomiting, diarrhea, fever, diuretic use, low-
sodium diet), the kidney compensates by avidly reabsorbing sodium, and
3
, lithium is co-reabsorbed proportionally, causing serum accumulation and
toxicity. This explains why NSAIDs (reduce GFR), thiazide diuretics (sodium
depletion), and low-sodium diets are major lithium drug and dietary
interactions. Signs of toxicity progress from tremor and GI distress (1.5 to 2.0
mEq/L) to ataxia, confusion, and dysarthria (2.0 to 2.5 mEq/L) to seizures,
coma, and cardiovascular collapse (above 2.5 mEq/L).
A nurse is preparing to administer IV vancomycin 1500 mg over 90
minutes to a patient with MRSA endocarditis. Fifteen minutes into the
infusion, the patient develops flushing, erythema, and pruritus
spreading from the face down the neck and upper chest, accompanied
by hypotension and tachycardia. There is no urticaria or angioedema.
Which reaction is occurring, what is its mechanism, and what is the
appropriate nursing intervention?
A) IgE-mediated anaphylaxis; administer epinephrine 0.3 mg IM immediately
and discontinue vancomycin permanently B) Red man syndrome; a non-
immune-mediated direct mast cell degranulation reaction caused by rapid
vancomycin infusion; stop or slow the infusion and administer
diphenhydramine, then resume at a slower rate C) Vancomycin-induced
thrombocytopenia; discontinue the infusion, obtain a CBC, and notify the
provider regarding permanent discontinuation D) Type III immune complex
hypersensitivity reaction; administer corticosteroids IV and discontinue
vancomycin
Correct Answer: B
Rationale: Red man syndrome (RMS) is a predictable, rate-dependent, non-
immunological adverse reaction to vancomycin caused by direct stimulation
of mast cells and basophils to release histamine, independent of IgE
antibody production. It is characterized by flushing, erythema, pruritus, and
hypotension classically following the distribution of the neck, face, and upper
torso ("red man" distribution). Unlike true anaphylaxis, RMS does not involve
bronchospasm or angioedema as primary features and is not a
contraindication to future vancomycin use. Management: stop the infusion
immediately, administer diphenhydramine 25 to 50 mg IV, wait for symptoms
to resolve, and resume the infusion at a slower rate (typically over at least 90
to 120 minutes, with rates not exceeding 10 mg/min). Vancomycin should
always be infused at no faster than 500 mg per 30 minutes in adults. RMS
can be prevented with premedication with antihistamines and adequate
infusion time.
A 61-year-old male with type 2 diabetes, heart failure with reduced
ejection fraction (HFrEF, EF 30%), and CKD stage 2 is being evaluated
for optimization of his diabetes regimen. His current HbA1c is 9.1%. In
addition to metformin, which class of glucose-lowering agents has
4
Course Code: NUR3145
Instructor:
Date: 2026
FINAL EXAM – PHARMACOLOGY FOR NURSING
PRACTICE
A 67-year-old male with heart failure (EF 35%), chronic kidney disease
stage 3 (eGFR 38 mL/min/1.73m²), and atrial fibrillation is prescribed
digoxin 0.125 mg daily. Three days after initiation, he presents with
nausea, visual disturbances described as yellow-green halos around
lights, and a heart rate of 44 bpm. His serum digoxin level is 2.6 ng/mL
and serum potassium is 3.1 mEq/L. Which factor most directly
potentiates digoxin toxicity in this patient, and what is the mechanism?
A) Atrial fibrillation increases digoxin's bioavailability by altering first-pass
metabolism in the liver B) Hypokalemia potentiates digoxin toxicity because
potassium and digoxin compete for the same binding site on the Na-K-
ATPase pump, and low extracellular potassium increases digoxin binding
affinity C) CKD increases digoxin toxicity by accelerating hepatic conversion
to active toxic metabolites D) Heart failure increases digoxin toxicity by
increasing volume of distribution and prolonging the drug's half-life in cardiac
tissue
Correct Answer: B
Rationale: Digoxin inhibits the Na-K-ATPase pump on cardiomyocytes.
Potassium and digoxin compete for the same binding site on this pump;
when extracellular potassium is low (hypokalemia), there is less competition,
and digoxin binds more readily, increasing its inhibitory effect and amplifying
toxicity. This is one of the most pharmacologically critical drug-electrolyte
interactions in clinical nursing. Compounding this, CKD reduces renal
excretion of digoxin (which is 60 to 80% renally eliminated unchanged),
leading to drug accumulation. Classic manifestations of toxicity include
1
,bradydysrhythmias, GI symptoms (nausea, vomiting, anorexia), and visual
disturbances (yellow-green chromatopsia, halos). Treatment involves holding
digoxin, correcting hypokalemia, cardiac monitoring, and potentially
administering digoxin immune Fab (Digibind) for severe toxicity.
A 58-year-old female with rheumatoid arthritis is being treated with
methotrexate 15 mg weekly. She presents to the clinic with oral ulcers,
macrocytic anemia, and fatigue. Her CBC shows: WBC 2,800/mcL, Hgb
9.2 g/dL, MCV 108 fL, platelets 88,000/mcL. Which mechanism explains
these adverse effects, and which supplement should be routinely co-
administered with methotrexate to reduce their incidence?
A) Methotrexate causes direct bone marrow suppression through alkylation
of DNA; leucovorin (folinic acid) 5 mg weekly is co-administered B)
Methotrexate competitively inhibits dihydrofolate reductase, depleting
tetrahydrofolate needed for purine and pyrimidine synthesis, causing folate
deficiency; folic acid 1 mg daily is co-administered on non-methotrexate days
C) Methotrexate causes hemolytic anemia through oxidative damage to red
blood cells; vitamin B12 supplementation corrects the anemia D)
Methotrexate activates the complement cascade causing autoimmune
cytopenias; corticosteroids are co-administered to suppress this response
Correct Answer: B
Rationale: Methotrexate is a folate antimetabolite that competitively and
irreversibly inhibits dihydrofolate reductase (DHFR), the enzyme that reduces
dietary folate to tetrahydrofolate (THF). THF is the active coenzyme required
for de novo synthesis of purines and thymidylate, essential for DNA
replication and cell division. Deficiency produces a megaloblastic picture
(elevated MCV, macrocytic anemia) and impairs rapidly dividing cells
including GI mucosa (oral ulcers) and hematopoietic precursors
(pancytopenia). Folic acid 1 mg daily supplementation on non-methotrexate
days reduces mucosal and hematological toxicity without significantly
compromising the anti-inflammatory efficacy of methotrexate in rheumatoid
arthritis. Leucovorin (folinic acid) is used for high-dose methotrexate rescue
in oncology settings and is not routinely used in low-dose rheumatological
regimens.
A 72-year-old male with type 2 diabetes is started on linagliptin (a DPP-
4 inhibitor) for glycemic control. His provider considers him a good
candidate because he has CKD stage 4 (eGFR 22 mL/min/1.73m²).
Which pharmacokinetic property of linagliptin makes it uniquely
appropriate for this patient compared to other agents in the same drug
class?
A) Linagliptin undergoes extensive renal glucuronidation, making it safer in
renal impairment B) Linagliptin is primarily eliminated via the bile and feces
2
,through enterohepatic recirculation and does not require dose adjustment in
any degree of renal impairment C) Linagliptin is dialyzable and removed
efficiently during hemodialysis sessions D) Linagliptin is converted to an
inactive metabolite by the kidney, making renal impairment clinically
irrelevant
Correct Answer: B
Rationale: Among the DPP-4 inhibitors (sitagliptin, saxagliptin, alogliptin,
linagliptin), linagliptin is unique in that it is predominantly eliminated via the
enterohepatic system (bile and feces), with less than 5% excreted renally.
This means no dose adjustment is required across all stages of CKD,
including end-stage renal disease on dialysis. In contrast, sitagliptin,
saxagliptin, and alogliptin are renally eliminated and require dose reductions
in moderate to severe CKD. DPP-4 inhibitors enhance incretin effect by
preventing degradation of GLP-1 and GIP, increasing glucose-dependent
insulin secretion and suppressing glucagon. They carry low hypoglycemia
risk as monotherapy because their effect is glucose-dependent. UCF nursing
students must understand pharmacokinetics as a basis for individualized
drug selection in patients with organ impairment.
A 34-year-old female with a history of bipolar disorder type I is
stabilized on lithium carbonate 900 mg twice daily (serum level 0.9
mEq/L). She is seen in the clinic complaining of three days of profuse
diarrhea and vomiting following a viral gastroenteritis. Today she
presents with coarse tremor, slurred speech, ataxia, confusion, and
muscle twitching. Her serum lithium level is 2.4 mEq/L. Which
pharmacokinetic mechanism explains the rapid rise in her lithium level
in the context of her illness?
A) Dehydration from fluid losses reduced renal blood flow and glomerular
filtration rate, decreasing lithium clearance, since lithium is entirely renally
eliminated without protein binding or hepatic metabolism B) Viral
gastroenteritis increased lithium absorption from the GI tract by altering
intestinal motility and pH C) The fever associated with illness increased
lithium's volume of distribution, paradoxically concentrating it in the CNS D)
Vomiting caused metabolic alkalosis, which increased tubular reabsorption of
lithium in exchange for hydrogen ions
Correct Answer: A
Rationale: Lithium has an extremely narrow therapeutic index (therapeutic
range 0.6 to 1.2 mEq/L; toxic above 1.5 mEq/L). It is not protein-bound, not
metabolized hepatically, and is entirely eliminated by the kidneys through
glomerular filtration and tubular reabsorption. Critically, lithium is reabsorbed
in the proximal tubule by the same mechanism as sodium. In states of
sodium and volume depletion (vomiting, diarrhea, fever, diuretic use, low-
sodium diet), the kidney compensates by avidly reabsorbing sodium, and
3
, lithium is co-reabsorbed proportionally, causing serum accumulation and
toxicity. This explains why NSAIDs (reduce GFR), thiazide diuretics (sodium
depletion), and low-sodium diets are major lithium drug and dietary
interactions. Signs of toxicity progress from tremor and GI distress (1.5 to 2.0
mEq/L) to ataxia, confusion, and dysarthria (2.0 to 2.5 mEq/L) to seizures,
coma, and cardiovascular collapse (above 2.5 mEq/L).
A nurse is preparing to administer IV vancomycin 1500 mg over 90
minutes to a patient with MRSA endocarditis. Fifteen minutes into the
infusion, the patient develops flushing, erythema, and pruritus
spreading from the face down the neck and upper chest, accompanied
by hypotension and tachycardia. There is no urticaria or angioedema.
Which reaction is occurring, what is its mechanism, and what is the
appropriate nursing intervention?
A) IgE-mediated anaphylaxis; administer epinephrine 0.3 mg IM immediately
and discontinue vancomycin permanently B) Red man syndrome; a non-
immune-mediated direct mast cell degranulation reaction caused by rapid
vancomycin infusion; stop or slow the infusion and administer
diphenhydramine, then resume at a slower rate C) Vancomycin-induced
thrombocytopenia; discontinue the infusion, obtain a CBC, and notify the
provider regarding permanent discontinuation D) Type III immune complex
hypersensitivity reaction; administer corticosteroids IV and discontinue
vancomycin
Correct Answer: B
Rationale: Red man syndrome (RMS) is a predictable, rate-dependent, non-
immunological adverse reaction to vancomycin caused by direct stimulation
of mast cells and basophils to release histamine, independent of IgE
antibody production. It is characterized by flushing, erythema, pruritus, and
hypotension classically following the distribution of the neck, face, and upper
torso ("red man" distribution). Unlike true anaphylaxis, RMS does not involve
bronchospasm or angioedema as primary features and is not a
contraindication to future vancomycin use. Management: stop the infusion
immediately, administer diphenhydramine 25 to 50 mg IV, wait for symptoms
to resolve, and resume the infusion at a slower rate (typically over at least 90
to 120 minutes, with rates not exceeding 10 mg/min). Vancomycin should
always be infused at no faster than 500 mg per 30 minutes in adults. RMS
can be prevented with premedication with antihistamines and adequate
infusion time.
A 61-year-old male with type 2 diabetes, heart failure with reduced
ejection fraction (HFrEF, EF 30%), and CKD stage 2 is being evaluated
for optimization of his diabetes regimen. His current HbA1c is 9.1%. In
addition to metformin, which class of glucose-lowering agents has
4
