UR 210/ NUR210 Exam 2 – Principles
N
of Pharmacology Guide ACTUAL EXAM
2026/2027 | Principles of
Pharmacology Guide | Verified Q&A |
Pass Guaranteed - A+ Graded
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========
PART A – MULTIPLE CHOICE (Q1–60)
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* *Q1 (Anticoagulants – warfarin monitoring):**
A 68-year-old patient with atrial fibrillation is prescribed warfarin. Which INR range indicates
therapeutic anticoagulation for this indication?
A) 1.5–2.0
B) 2.0–3.0
C) 2.5–3.5
D) 3.0–4.0
* *[CORRECT]** B
*Rationale: The American College of Cardiology/American Heart Association guidelines
recommend an INR of 2.0–3.0 for atrial fibrillation and most venous thromboembolism
indications. Option A (1.5–2.0) is subtherapeutic and increases stroke risk. Option C (2.5–3.5) is
reserved for mechanical heart valves. Option D (3.0–4.0) carries excessive bleeding risk without
additional benefit for this indication. Clinical pearl: Always verify the specific indication when
interpreting INR goals; mechanical mitral valves require higher targets than aortic valves.*
* *Q2 (Anticoagulants – heparin monitoring):**
A patient receiving unfractionated heparin for a pulmonary embolism has an aPTT of 48
seconds (control 30 seconds). Which action is most appropriate?
A) Increase the heparin infusion rate by 2 units/kg/hour
B) Continue the current heparin dose; the aPTT is therapeutic
C) Decrease the heparin infusion rate and recheck in 2 hours
D) Discontinue heparin and initiate a direct oral anticoagulant
,* *[CORRECT]** B
*Rationale: Therapeutic aPTT for unfractionated heparin is 1.5–2.5 times the control (45–75
seconds for a 30-second control). An aPTT of 48 seconds falls within this therapeutic range.
Option A would cause supratherapeutic anticoagulation and bleeding risk. Option C is
unnecessary as the value is therapeutic, not supratherapeutic. Option D is inappropriate during
acute treatment when heparin is preferred for rapid onset and reversibility. Clinical pearl: Always
use the institution-specific therapeutic range as reagent sensitivity varies; obtain aPTT 6 hours
after any rate change; transition to warfarin requires 5 days of overlap with therapeutic aPTT
and INR 2.0–3.0 for at least 24 hours.*
* *Q3 (Anticoagulants – DOAC reversal):**
A patient on apixaban presents with life-threatening gastrointestinal bleeding. Which reversal
agent is appropriate?
A) Vitamin K 10 mg IV
B) Protamine sulfate 50 mg IV
C) Andexanet alfa (Factor Xa decoy)
D) Fresh frozen plasma 2 units
* *[CORRECT]** C
*Rationale: Andexanet alfa is the FDA-approved specific reversal agent for Factor Xa inhibitors
(apixaban, rivaroxaban, edoxaban). It acts as a decoy that binds and sequesters the drug.
Option A (vitamin K) reverses warfarin only (requires synthesis of new clotting factors). Option B
(protamine) reverses heparin only by forming a stable complex. Option D (FFP) contains all
clotting factors but is less effective than 4-factor PCC for warfarin reversal and has no role in
DOAC reversal. Clinical pearl: Idarucizumab (Praxbind) is the specific reversal agent for
dabigatran (direct thrombin inhibitor); 4F-PCC can be used off-label for Factor Xa inhibitor
reversal if andexanet alfa is unavailable.*
* *Q4 (Beta-blockers – adverse effects):**
A patient on metoprolol for hypertension reports several symptoms. Which adverse effect is the
nurse most concerned about?
A) Mild fatigue and decreased exercise tolerance
B) Heart rate of 52 bpm at rest
C) Blood glucose of 68 mg/dL without adrenergic warning symptoms
D) Mild peripheral edema in the ankles
* *[CORRECT]** C
*Rationale: Beta-blockers block glycogenolysis and mask the adrenergic warning symptoms
(tremors, tachycardia, sweating) of hypoglycemia while preserving sweating (cholinergic). This
places diabetic patients at risk for unrecognized severe hypoglycemia. Option A is expected and
usually tolerable. Option B (HR 52) is mild bradycardia and acceptable if asymptomatic. Option
D is not a beta-blocker adverse effect; it is associated with calcium channel blockers
(amlodipine). Clinical pearl: Non-selective beta-blockers (propranolol, nadolol) are absolutely
, ontraindicated in asthma; even cardioselective agents (metoprolol, atenolol) lose selectivity at
c
higher doses and can precipitate bronchospasm.*
* *Q5 (ACE inhibitors – cough and angioedema):**
A patient on lisinopril develops a persistent dry cough. Which mechanism explains this adverse
effect?
A) Histamine release from mast cells in the respiratory tract
B) Bradykinin and substance P accumulation due to ACE inhibition
C) Direct irritation of the cough reflex center in the medulla
D) Increased prostaglandin E2 production in the lungs
* *[CORRECT]** B
*Rationale: ACE inhibitors block the conversion of angiotensin I to II but also inhibit bradykinin
degradation; accumulated bradykinin and substance P stimulate cough receptors in the
respiratory tract. This occurs in 5–20% of patients and is more common in women and
nonsmokers. Option A describes histamine-mediated reactions (penicillin allergy). Option C
describes central cough suppression (dextromethorphan mechanism). Option D is incorrect;
ACE inhibitors actually reduce prostaglandin production. Clinical pearl: Switching to an ARB
(losartan, valsartan) resolves cough in 90% of patients as ARBs do not affect bradykinin
metabolism; angioedema (airway-threatening swelling) requires immediate discontinuation and
lifetime avoidance of all ACE inhibitors.*
* *Q6 (Calcium channel blockers – adverse effects):**
A patient on amlodipine for hypertension develops bilateral ankle edema. Which mechanism
explains this finding?
A) Sodium and water retention from mineralocorticoid receptor activation
B) Arteriolar vasodilation exceeds venous vasodilation, increasing capillary hydrostatic pressure
C) Right-sided heart failure from negative inotropic effects
D) Lymphatic obstruction from drug-induced inflammation
* *[CORRECT]** B
*Rationale: Dihydropyridine calcium channel blockers (amlodipine, nifedipine) preferentially
dilate arterioles over venules, increasing hydrostatic pressure in capillary beds and causing fluid
extravasation into interstitial tissues (peripheral edema). This is NOT responsive to diuretics.
Option A describes mineralocorticoid effects (spironolactone deficiency or primary
hyperaldosteronism). Option C describes right heart failure (cor pulmonale, tricuspid
regurgitation). Option D is not a CCB mechanism. Clinical pearl: Adding an ACE inhibitor or
ARB (which dilate both arterioles and venules) reduces CCB-induced edema by 50–70%;
switching to a non-dihydropyridine CCB (verapamil, diltiazem) may also help.*
* *Q7 (Diuretics – hypokalemia):**
A patient on furosemide 40 mg twice daily has a serum potassium of 3.0 mEq/L. Which ECG
finding is most concerning?
A) Peaked T waves
, ) Flattened T waves and prominent U waves
B
C) Shortened PR interval
D) Delta waves and short PR interval
* *[CORRECT]** B
*Rationale: Loop diuretics (furosemide, bumetanide) cause hypokalemia by increasing distal
tubular sodium delivery, which drives potassium secretion via aldosterone-sensitive
mechanisms. Hypokalemia causes flattened T waves, ST depression, and prominent U waves
(best seen in V2–V3); severe hypokalemia (<2.5 mEq/L) can cause ventricular arrhythmias.
Option A (peaked T waves) indicates hyperkalemia. Option C is not associated with electrolyte
abnormalities. Option D describes Wolff-Parkinson-White syndrome. Clinical pearl: Potassium
replacement for loop diuretic-induced hypokalemia should include magnesium repletion
(hypomagnesemia causes refractory hypokalemia by impairing ROMK channel function);
consider a potassium-sparing diuretic (spironolactone, triamterene) for chronic management.*
* *Q8 (Antidysrhythmics – amiodarone toxicity):**
A patient on long-term amiodarone presents with dyspnea, nonproductive cough, and bilateral
interstitial infiltrates on chest X-ray. Which adverse effect is most likely?
A) Acute pulmonary embolism
B) Amiodarone-induced pulmonary toxicity (interstitial pneumonitis)
C) Congestive heart failure exacerbation
D) Community-acquired pneumonia
* *[CORRECT]** B
*Rationale: Amiodarone contains iodine (37% by weight) and accumulates in adipose tissue and
organs, causing dose-dependent pulmonary toxicity (interstitial pneumonitis, organizing
pneumonia, ARDS) in 1–5% of patients, especially with doses >400 mg/day, age >60, or
pre-existing lung disease. Baseline and periodic chest X-rays and pulmonary function tests are
recommended. Option A would show wedge-shaped infarcts and elevated D-dimer. Option C
would show cardiomegaly and pleural effusions. Option D would show lobar consolidation and
respond to antibiotics. Clinical pearl: Amiodarone also causes thyroid dysfunction (hypo- or
hyperthyroidism), hepatotoxicity (baseline and periodic LFTs), corneal microdeposits
(reversible), photosensitivity, and peripheral neuropathy; baseline ECG, thyroid function, LFTs,
and chest X-ray are required before initiation.*
* *Q9 (Antiplatelets – aspirin adverse effects):**
A 16-year-old patient with influenza is prescribed aspirin for fever. Which serious adverse effect
is the nurse most concerned about?
A) Gastrointestinal bleeding
B) Reye syndrome (acute encephalopathy and fatty liver)
C) Acute kidney injury
D) Thrombotic thrombocytopenic purpura
**[CORRECT]** B
N
of Pharmacology Guide ACTUAL EXAM
2026/2027 | Principles of
Pharmacology Guide | Verified Q&A |
Pass Guaranteed - A+ Graded
=======================================================================
=
========
PART A – MULTIPLE CHOICE (Q1–60)
========================================================================
========
* *Q1 (Anticoagulants – warfarin monitoring):**
A 68-year-old patient with atrial fibrillation is prescribed warfarin. Which INR range indicates
therapeutic anticoagulation for this indication?
A) 1.5–2.0
B) 2.0–3.0
C) 2.5–3.5
D) 3.0–4.0
* *[CORRECT]** B
*Rationale: The American College of Cardiology/American Heart Association guidelines
recommend an INR of 2.0–3.0 for atrial fibrillation and most venous thromboembolism
indications. Option A (1.5–2.0) is subtherapeutic and increases stroke risk. Option C (2.5–3.5) is
reserved for mechanical heart valves. Option D (3.0–4.0) carries excessive bleeding risk without
additional benefit for this indication. Clinical pearl: Always verify the specific indication when
interpreting INR goals; mechanical mitral valves require higher targets than aortic valves.*
* *Q2 (Anticoagulants – heparin monitoring):**
A patient receiving unfractionated heparin for a pulmonary embolism has an aPTT of 48
seconds (control 30 seconds). Which action is most appropriate?
A) Increase the heparin infusion rate by 2 units/kg/hour
B) Continue the current heparin dose; the aPTT is therapeutic
C) Decrease the heparin infusion rate and recheck in 2 hours
D) Discontinue heparin and initiate a direct oral anticoagulant
,* *[CORRECT]** B
*Rationale: Therapeutic aPTT for unfractionated heparin is 1.5–2.5 times the control (45–75
seconds for a 30-second control). An aPTT of 48 seconds falls within this therapeutic range.
Option A would cause supratherapeutic anticoagulation and bleeding risk. Option C is
unnecessary as the value is therapeutic, not supratherapeutic. Option D is inappropriate during
acute treatment when heparin is preferred for rapid onset and reversibility. Clinical pearl: Always
use the institution-specific therapeutic range as reagent sensitivity varies; obtain aPTT 6 hours
after any rate change; transition to warfarin requires 5 days of overlap with therapeutic aPTT
and INR 2.0–3.0 for at least 24 hours.*
* *Q3 (Anticoagulants – DOAC reversal):**
A patient on apixaban presents with life-threatening gastrointestinal bleeding. Which reversal
agent is appropriate?
A) Vitamin K 10 mg IV
B) Protamine sulfate 50 mg IV
C) Andexanet alfa (Factor Xa decoy)
D) Fresh frozen plasma 2 units
* *[CORRECT]** C
*Rationale: Andexanet alfa is the FDA-approved specific reversal agent for Factor Xa inhibitors
(apixaban, rivaroxaban, edoxaban). It acts as a decoy that binds and sequesters the drug.
Option A (vitamin K) reverses warfarin only (requires synthesis of new clotting factors). Option B
(protamine) reverses heparin only by forming a stable complex. Option D (FFP) contains all
clotting factors but is less effective than 4-factor PCC for warfarin reversal and has no role in
DOAC reversal. Clinical pearl: Idarucizumab (Praxbind) is the specific reversal agent for
dabigatran (direct thrombin inhibitor); 4F-PCC can be used off-label for Factor Xa inhibitor
reversal if andexanet alfa is unavailable.*
* *Q4 (Beta-blockers – adverse effects):**
A patient on metoprolol for hypertension reports several symptoms. Which adverse effect is the
nurse most concerned about?
A) Mild fatigue and decreased exercise tolerance
B) Heart rate of 52 bpm at rest
C) Blood glucose of 68 mg/dL without adrenergic warning symptoms
D) Mild peripheral edema in the ankles
* *[CORRECT]** C
*Rationale: Beta-blockers block glycogenolysis and mask the adrenergic warning symptoms
(tremors, tachycardia, sweating) of hypoglycemia while preserving sweating (cholinergic). This
places diabetic patients at risk for unrecognized severe hypoglycemia. Option A is expected and
usually tolerable. Option B (HR 52) is mild bradycardia and acceptable if asymptomatic. Option
D is not a beta-blocker adverse effect; it is associated with calcium channel blockers
(amlodipine). Clinical pearl: Non-selective beta-blockers (propranolol, nadolol) are absolutely
, ontraindicated in asthma; even cardioselective agents (metoprolol, atenolol) lose selectivity at
c
higher doses and can precipitate bronchospasm.*
* *Q5 (ACE inhibitors – cough and angioedema):**
A patient on lisinopril develops a persistent dry cough. Which mechanism explains this adverse
effect?
A) Histamine release from mast cells in the respiratory tract
B) Bradykinin and substance P accumulation due to ACE inhibition
C) Direct irritation of the cough reflex center in the medulla
D) Increased prostaglandin E2 production in the lungs
* *[CORRECT]** B
*Rationale: ACE inhibitors block the conversion of angiotensin I to II but also inhibit bradykinin
degradation; accumulated bradykinin and substance P stimulate cough receptors in the
respiratory tract. This occurs in 5–20% of patients and is more common in women and
nonsmokers. Option A describes histamine-mediated reactions (penicillin allergy). Option C
describes central cough suppression (dextromethorphan mechanism). Option D is incorrect;
ACE inhibitors actually reduce prostaglandin production. Clinical pearl: Switching to an ARB
(losartan, valsartan) resolves cough in 90% of patients as ARBs do not affect bradykinin
metabolism; angioedema (airway-threatening swelling) requires immediate discontinuation and
lifetime avoidance of all ACE inhibitors.*
* *Q6 (Calcium channel blockers – adverse effects):**
A patient on amlodipine for hypertension develops bilateral ankle edema. Which mechanism
explains this finding?
A) Sodium and water retention from mineralocorticoid receptor activation
B) Arteriolar vasodilation exceeds venous vasodilation, increasing capillary hydrostatic pressure
C) Right-sided heart failure from negative inotropic effects
D) Lymphatic obstruction from drug-induced inflammation
* *[CORRECT]** B
*Rationale: Dihydropyridine calcium channel blockers (amlodipine, nifedipine) preferentially
dilate arterioles over venules, increasing hydrostatic pressure in capillary beds and causing fluid
extravasation into interstitial tissues (peripheral edema). This is NOT responsive to diuretics.
Option A describes mineralocorticoid effects (spironolactone deficiency or primary
hyperaldosteronism). Option C describes right heart failure (cor pulmonale, tricuspid
regurgitation). Option D is not a CCB mechanism. Clinical pearl: Adding an ACE inhibitor or
ARB (which dilate both arterioles and venules) reduces CCB-induced edema by 50–70%;
switching to a non-dihydropyridine CCB (verapamil, diltiazem) may also help.*
* *Q7 (Diuretics – hypokalemia):**
A patient on furosemide 40 mg twice daily has a serum potassium of 3.0 mEq/L. Which ECG
finding is most concerning?
A) Peaked T waves
, ) Flattened T waves and prominent U waves
B
C) Shortened PR interval
D) Delta waves and short PR interval
* *[CORRECT]** B
*Rationale: Loop diuretics (furosemide, bumetanide) cause hypokalemia by increasing distal
tubular sodium delivery, which drives potassium secretion via aldosterone-sensitive
mechanisms. Hypokalemia causes flattened T waves, ST depression, and prominent U waves
(best seen in V2–V3); severe hypokalemia (<2.5 mEq/L) can cause ventricular arrhythmias.
Option A (peaked T waves) indicates hyperkalemia. Option C is not associated with electrolyte
abnormalities. Option D describes Wolff-Parkinson-White syndrome. Clinical pearl: Potassium
replacement for loop diuretic-induced hypokalemia should include magnesium repletion
(hypomagnesemia causes refractory hypokalemia by impairing ROMK channel function);
consider a potassium-sparing diuretic (spironolactone, triamterene) for chronic management.*
* *Q8 (Antidysrhythmics – amiodarone toxicity):**
A patient on long-term amiodarone presents with dyspnea, nonproductive cough, and bilateral
interstitial infiltrates on chest X-ray. Which adverse effect is most likely?
A) Acute pulmonary embolism
B) Amiodarone-induced pulmonary toxicity (interstitial pneumonitis)
C) Congestive heart failure exacerbation
D) Community-acquired pneumonia
* *[CORRECT]** B
*Rationale: Amiodarone contains iodine (37% by weight) and accumulates in adipose tissue and
organs, causing dose-dependent pulmonary toxicity (interstitial pneumonitis, organizing
pneumonia, ARDS) in 1–5% of patients, especially with doses >400 mg/day, age >60, or
pre-existing lung disease. Baseline and periodic chest X-rays and pulmonary function tests are
recommended. Option A would show wedge-shaped infarcts and elevated D-dimer. Option C
would show cardiomegaly and pleural effusions. Option D would show lobar consolidation and
respond to antibiotics. Clinical pearl: Amiodarone also causes thyroid dysfunction (hypo- or
hyperthyroidism), hepatotoxicity (baseline and periodic LFTs), corneal microdeposits
(reversible), photosensitivity, and peripheral neuropathy; baseline ECG, thyroid function, LFTs,
and chest X-ray are required before initiation.*
* *Q9 (Antiplatelets – aspirin adverse effects):**
A 16-year-old patient with influenza is prescribed aspirin for fever. Which serious adverse effect
is the nurse most concerned about?
A) Gastrointestinal bleeding
B) Reye syndrome (acute encephalopathy and fatty liver)
C) Acute kidney injury
D) Thrombotic thrombocytopenic purpura
**[CORRECT]** B
