NRSG 2350 PATHOPHYSIOLOGY
& PHARMACOLOGY EXAM AND
CORRECT ANSWERS WITH
LATEST MOCK PRACTICE SET
180 Questions with Answers and Detailed Rationales
100 PERCENT GUARANTEED PASS
INSTANT DOWNLOAD ANSWERS INCLUDED
IMPORTANCE OF THIS DOCUMENT
This comprehensive examination preparation guide has been meticulously developed to help you succeed in the
NRSG 2350 PATHOPHYSIOLOGY & PHARMACOLOGY EXAM AND CORRECT ANSWERS WITH
RATIONALES.PDF. It contains 180 carefully selected questions that reflect the most current exam content and
testing strategies. Each question is accompanied by a correct answer and a detailed rationale that explains the
underlying pathophysiology, pharmacology, or clinical reasoning.
Self-Assessment – Test your knowledge and Exam Preparation – Familiarize yourself with the
identify areas requiring further question format and content
study areas
Concept Reinforcement – Deepen your Confidence Building – Develop test-taking
understanding through strategies and reduce
evidence-based exam anxiety
rationales
Time Management – Practice answering
questions under simulated
exam conditions
Review Summary 180 Questions
Foundations - Application - NRSG 2350 Pathophysiology & Pharmacology AND Correct WITH Rationales
PDF Pathophysiology & Pharmacology Undergraduate YEAR 3
All answers with rationales
,Table of Contents
Section A - Mechanism Section B - Prescribed
Questions 1 to 45 Questions 46 to 90
Section C - Chronic Section D - Heart
Questions 91 to 135 Questions 136 to 180
,Section A - Mechanism
Q1.
A patient with chronic heart failure is prescribed a beta-blocker. Which property of
beta-blockers is most critical for improving survival in this population?
A. Cardioselectivity (1 selectivity) B. Lipophilicity
C. Vasodilatory action D. Intrinsic sympathomimetic activity
Correct: C - Vasodilatory action
Rationale:Beta-blockers with vasodilatory action (e.g., carvedilol) have been shown to reduce
mortality in heart failure more than non-vasodilating agents. Cardioselectivity and lipophilicity
are less critical for survival benefit. Intrinsic sympathomimetic activity is actually detrimental in
heart failure.
Q2.
In a patient with type 2 diabetes and chronic kidney disease (eGFR 30 mL/min), which
medication class is preferred as first-line therapy to reduce cardiovascular risk and slow
CKD progression?
A. Sulfonylureas B. DPP-4 inhibitors
C. SGLT2 inhibitors D. Thiazolidinediones
Correct: C - SGLT2 inhibitors
Rationale:SGLT2 inhibitors (e.g., empagliflozin, dapagliflozin) have shown renoprotective and
cardioprotective effects in patients with diabetic kidney disease, irrespective of glycemic
control. Sulfonylureas and DPP-4 inhibitors lack these benefits. Thiazolidinediones may
cause fluid retention and are less preferred in CKD.
Q3.
A patient on warfarin develops a supratherapeutic INR of 6.5 without major bleeding. What
is the most appropriate next step?
A. Administer vitamin K 10 mg IV B. Administer fresh frozen plasma
C. Hold warfarin and administer vitamin K D. Administer prothrombin complex
1-2 mg orally concentrate
Correct: C - Hold warfarin and administer vitamin K 1-2 mg orally
Page 3
, Section A - Mechanism
Rationale: For a supratherapeutic INR without major bleeding, holding warfarin and giving
low-dose oral vitamin K is recommended per guidelines. IV vitamin K or FFP is reserved for
major bleeding. Prothrombin complex concentrate is for life-threatening bleeding.
Q4.
Which of the following mechanisms best explains the development of drug-induced lupus
erythematosus with procainamide?
A. Direct DNA damage leading to apoptosis B. Inhibition of central T-cell tolerance
C. Blockade of acetylcholine receptors D. Stimulation of anti-dsDNA antibody
production
Correct: B - Inhibition of central T-cell tolerance
Rationale:Drug-induced lupus is thought to result from inhibition of central T-cell tolerance,
allowing autoreactive T-cells to escape deletion. Procainamide and hydralazine are common
triggers. Anti-dsDNA antibodies are less common than in idiopathic SLE. Acetylcholine
receptor blockade is unrelated.
Q5.
A patient with severe sepsis and hypotension is started on norepinephrine. What is the
primary mechanism by which norepinephrine increases mean arterial pressure?
A. Activation of 2-adrenergic receptors B. Stimulation of 1-adrenergic receptors
causing bronchodilation causing vasoconstriction
C. Inhibition of phosphodiesterase D. Blockade of nitric oxide synthase
increasing cAMP in cardiac muscle reducing vasodilation
Correct: B - Stimulation of 1-adrenergic receptors causing vasoconstriction
Rationale:Norepinephrine primarily acts on ±1-adrenergic receptors on vascular smooth
muscle, causing vasoconstriction and increasing systemic vascular resistance and MAP. It
has minimal 2 effects. Phosphodiesterase inhibition is seen with milrinone, and nitric oxide
synthase blockade is not a major mechanism.
Q6.
Which of the following is the most likely cause of drug-induced QT prolongation leading
to torsades de pointes?
A. Blockade of voltage-gated sodium B. Inhibition of the hERG potassium channel
channels
C. Activation of L-type calcium channels D. Stimulation of 1-adrenergic receptors
Correct: B - Inhibition of the hERG potassium channel
Page 4
& PHARMACOLOGY EXAM AND
CORRECT ANSWERS WITH
LATEST MOCK PRACTICE SET
180 Questions with Answers and Detailed Rationales
100 PERCENT GUARANTEED PASS
INSTANT DOWNLOAD ANSWERS INCLUDED
IMPORTANCE OF THIS DOCUMENT
This comprehensive examination preparation guide has been meticulously developed to help you succeed in the
NRSG 2350 PATHOPHYSIOLOGY & PHARMACOLOGY EXAM AND CORRECT ANSWERS WITH
RATIONALES.PDF. It contains 180 carefully selected questions that reflect the most current exam content and
testing strategies. Each question is accompanied by a correct answer and a detailed rationale that explains the
underlying pathophysiology, pharmacology, or clinical reasoning.
Self-Assessment – Test your knowledge and Exam Preparation – Familiarize yourself with the
identify areas requiring further question format and content
study areas
Concept Reinforcement – Deepen your Confidence Building – Develop test-taking
understanding through strategies and reduce
evidence-based exam anxiety
rationales
Time Management – Practice answering
questions under simulated
exam conditions
Review Summary 180 Questions
Foundations - Application - NRSG 2350 Pathophysiology & Pharmacology AND Correct WITH Rationales
PDF Pathophysiology & Pharmacology Undergraduate YEAR 3
All answers with rationales
,Table of Contents
Section A - Mechanism Section B - Prescribed
Questions 1 to 45 Questions 46 to 90
Section C - Chronic Section D - Heart
Questions 91 to 135 Questions 136 to 180
,Section A - Mechanism
Q1.
A patient with chronic heart failure is prescribed a beta-blocker. Which property of
beta-blockers is most critical for improving survival in this population?
A. Cardioselectivity (1 selectivity) B. Lipophilicity
C. Vasodilatory action D. Intrinsic sympathomimetic activity
Correct: C - Vasodilatory action
Rationale:Beta-blockers with vasodilatory action (e.g., carvedilol) have been shown to reduce
mortality in heart failure more than non-vasodilating agents. Cardioselectivity and lipophilicity
are less critical for survival benefit. Intrinsic sympathomimetic activity is actually detrimental in
heart failure.
Q2.
In a patient with type 2 diabetes and chronic kidney disease (eGFR 30 mL/min), which
medication class is preferred as first-line therapy to reduce cardiovascular risk and slow
CKD progression?
A. Sulfonylureas B. DPP-4 inhibitors
C. SGLT2 inhibitors D. Thiazolidinediones
Correct: C - SGLT2 inhibitors
Rationale:SGLT2 inhibitors (e.g., empagliflozin, dapagliflozin) have shown renoprotective and
cardioprotective effects in patients with diabetic kidney disease, irrespective of glycemic
control. Sulfonylureas and DPP-4 inhibitors lack these benefits. Thiazolidinediones may
cause fluid retention and are less preferred in CKD.
Q3.
A patient on warfarin develops a supratherapeutic INR of 6.5 without major bleeding. What
is the most appropriate next step?
A. Administer vitamin K 10 mg IV B. Administer fresh frozen plasma
C. Hold warfarin and administer vitamin K D. Administer prothrombin complex
1-2 mg orally concentrate
Correct: C - Hold warfarin and administer vitamin K 1-2 mg orally
Page 3
, Section A - Mechanism
Rationale: For a supratherapeutic INR without major bleeding, holding warfarin and giving
low-dose oral vitamin K is recommended per guidelines. IV vitamin K or FFP is reserved for
major bleeding. Prothrombin complex concentrate is for life-threatening bleeding.
Q4.
Which of the following mechanisms best explains the development of drug-induced lupus
erythematosus with procainamide?
A. Direct DNA damage leading to apoptosis B. Inhibition of central T-cell tolerance
C. Blockade of acetylcholine receptors D. Stimulation of anti-dsDNA antibody
production
Correct: B - Inhibition of central T-cell tolerance
Rationale:Drug-induced lupus is thought to result from inhibition of central T-cell tolerance,
allowing autoreactive T-cells to escape deletion. Procainamide and hydralazine are common
triggers. Anti-dsDNA antibodies are less common than in idiopathic SLE. Acetylcholine
receptor blockade is unrelated.
Q5.
A patient with severe sepsis and hypotension is started on norepinephrine. What is the
primary mechanism by which norepinephrine increases mean arterial pressure?
A. Activation of 2-adrenergic receptors B. Stimulation of 1-adrenergic receptors
causing bronchodilation causing vasoconstriction
C. Inhibition of phosphodiesterase D. Blockade of nitric oxide synthase
increasing cAMP in cardiac muscle reducing vasodilation
Correct: B - Stimulation of 1-adrenergic receptors causing vasoconstriction
Rationale:Norepinephrine primarily acts on ±1-adrenergic receptors on vascular smooth
muscle, causing vasoconstriction and increasing systemic vascular resistance and MAP. It
has minimal 2 effects. Phosphodiesterase inhibition is seen with milrinone, and nitric oxide
synthase blockade is not a major mechanism.
Q6.
Which of the following is the most likely cause of drug-induced QT prolongation leading
to torsades de pointes?
A. Blockade of voltage-gated sodium B. Inhibition of the hERG potassium channel
channels
C. Activation of L-type calcium channels D. Stimulation of 1-adrenergic receptors
Correct: B - Inhibition of the hERG potassium channel
Page 4
