NRMS 5190 ADVANCED PATHOPHYSIOLOGY EXAM 3
COMPREHENSIVE REVIEW | QUESTIONS AND ANSWERS WITH
RATIONALES | 2026/27 UPDATE | 100% CORRECT -SUNY
DOWNSTATE MEDICAL CENTER
144 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
NRMS 5190 ADVANCED PATHOPHYSIOLOGY EXAM 3 COMPREHENSIVE REVIEW | QUESTIONS AND
ANSWERS WITH RATIONALES | 2026/27 UPDATE | 100% CORRECT -SUNY DOWNSTATE MEDICAL
CENTER. It contains 144 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 144 Questions
Foundations - Application - NRMS 5190 Advanced Pathophysiology 3 Comprehensive Review AND WITH
Rationales 2026/27 Update 100 Correct -suny Downstate Medical Center Advanced Pathophysiology 3
Cardiovascular Renal Respiratory Endocrine Neuro Hematologic GI Immune Musculoskeletal Integumentary
Graduate Msn/dnp-level Advanced Pathophysiology
All answers with rationales
,Table of Contents
Content Area Questions Key Topics
Cellular Injury Adaptation 1-24 Mechanism, Explains, Syndrome, Chronic, Acute
AND Death
Inflammation Immunity AND 25-48 Mechanism, Explains, Pathophysiologic, Diabetes, Elevated
Infection
Genetics AND Genetic 49-72 Mechanism, Pathophysiologic, Explains, Acute, Diabetes
Disorders
Neoplasia AND Cancer 73-96 Pathophysiologic, Mechanism, Explains, Syndrome, Directly
Pathophysiology
Cardiovascular System 97-120 Pathophysiologic, Explains, Mechanism, Fruity Breath,
Disorders Pathophysiology
Respiratory System 121-144 Explains, Mechanism, Pathophysiologic, Acute, Chronic
Disorders
TOTAL 144 All questions include answers and detailed rationales
,Section A - Cellular Injury Adaptation AND Death
Q1.
A patient with chronic kidney disease has an arterial blood gas showing pH 7.28, PaCO2
30 mm Hg, and HCO3- 14 mEq/L. Which acid-base disturbance is present?
A. Acute respiratory acidosis with metabolic B. Metabolic acidosis with respiratory
compensation compensation
C. Mixed metabolic acidosis and respiratory D. Metabolic alkalosis with respiratory
alkalosis acidosis
Correct: B - Metabolic acidosis with respiratory compensation
Rationale:Low pH with low HCO3- indicates metabolic acidosis; the low PaCO2 reflects
compensatory hyperventilation (respiratory compensation). The pH is not normalized, so it is
not a mixed disorder with a coexisting primary respiratory alkalosis. Renal failure impairs
HCO3- regeneration, producing the primary metabolic acidosis.
Why the other answers are wrong:
A. pH is acidemic but PaCO2 is low, not high, ruling out respiratory acidosis.
C. A mixed disorder would typically show a pH closer to normal or a PaCO2 inconsistent with
full compensation; here the changes are directionally appropriate for compensation.
D. Low HCO3- rules out metabolic alkalosis as the primary disturbance.
Reference: McCance, K.L. & Huether, S.E. (2024). Pathophysiology: The Biologic Basis for Disease, 9th
Ed., Ch. 3
Q2.
Which mechanism best explains the hypoxemia seen in a patient with acute respiratory
distress syndrome (ARDS)?
A. Alveolar hypoventilation due to B. Intrapulmonary shunt from alveolar
neuromuscular weakness flooding and atelectasis
C. Diffusion limitation from thickened D. Reduced inspired oxygen tension at
alveolar-capillary membrane alone altitude
Correct: B - Intrapulmonary shunt from alveolar flooding and atelectasis
Rationale:ARDS causes increased permeability pulmonary edema, surfactant inactivation,
and atelectasis, producing intrapulmonary shunting (perfusion of non-ventilated alveoli) that is
refractory to supplemental oxygen. Hypoventilation and low inspired O2 are not the primary
mechanisms, and diffusion limitation plays a minor role compared with shunt.
Why the other answers are wrong:
A. Neuromuscular weakness causes hypoventilation with hypercapnia, not the classic shunt
Page 3
, Section A - Cellular Injury Adaptation AND Death
physiology of ARDS.
C. Membrane thickening contributes minimally; shunt is the dominant mechanism.
D. Altitude-related hypoxemia is due to low PiO2, not intrinsic lung pathology.
Reference: McCance, K.L. & Huether, S.E. (2024). Pathophysiology, 9th Ed., Ch. 26
Q3.
In heart failure with reduced ejection fraction, which compensatory mechanism initially
maintains cardiac output but ultimately worsens myocardial workload?
A. Increased parasympathetic vagal tone B. Activation of the
renin-angiotensin-aldosterone system and
sympathetic nervous system
C. Release of atrial natriuretic peptide D. Upregulation of beta-adrenergic
receptors on myocytes
Correct: B - Activation of the renin-angiotensin-aldosterone system and sympathetic
nervous system
Rationale:RAAS and sympathetic activation increase preload, afterload, and heart rate to
preserve cardiac output, but chronic activation promotes remodeling, fibrosis, and further
pump failure. Natriuretic peptides are counter-regulatory and promote vasodilation and
diuresis. Parasympathetic tone and beta-receptor upregulation are not the primary
maladaptive compensatory responses.
Why the other answers are wrong:
A. Increased vagal tone would slow heart rate and reduce cardiac output, not compensate for
it.
C. ANP is a compensatory vasodilator and natriuretic hormone that opposes RAAS, not a
mechanism that worsens workload.
D. Beta-receptors are typically downregulated in chronic heart failure due to sustained
catecholamine exposure.
Reference: Lehne, R.A. (2026). Pharmacology for Nursing Care, 12th Ed., Ch. 58
Q4.
Which finding is most characteristic of nephrotic syndrome compared with nephritic
syndrome?
A. Active urinary sediment with red blood B. Massive proteinuria (>3.5 g/day) with
cell casts hypoalbuminemia and edema
C. Oliguria with hypertension and azotemia D. Sterile pyuria with white blood cell casts
Correct: B - Massive proteinuria (>3.5 g/day) with hypoalbuminemia and edema
Page 4
COMPREHENSIVE REVIEW | QUESTIONS AND ANSWERS WITH
RATIONALES | 2026/27 UPDATE | 100% CORRECT -SUNY
DOWNSTATE MEDICAL CENTER
144 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
NRMS 5190 ADVANCED PATHOPHYSIOLOGY EXAM 3 COMPREHENSIVE REVIEW | QUESTIONS AND
ANSWERS WITH RATIONALES | 2026/27 UPDATE | 100% CORRECT -SUNY DOWNSTATE MEDICAL
CENTER. It contains 144 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 144 Questions
Foundations - Application - NRMS 5190 Advanced Pathophysiology 3 Comprehensive Review AND WITH
Rationales 2026/27 Update 100 Correct -suny Downstate Medical Center Advanced Pathophysiology 3
Cardiovascular Renal Respiratory Endocrine Neuro Hematologic GI Immune Musculoskeletal Integumentary
Graduate Msn/dnp-level Advanced Pathophysiology
All answers with rationales
,Table of Contents
Content Area Questions Key Topics
Cellular Injury Adaptation 1-24 Mechanism, Explains, Syndrome, Chronic, Acute
AND Death
Inflammation Immunity AND 25-48 Mechanism, Explains, Pathophysiologic, Diabetes, Elevated
Infection
Genetics AND Genetic 49-72 Mechanism, Pathophysiologic, Explains, Acute, Diabetes
Disorders
Neoplasia AND Cancer 73-96 Pathophysiologic, Mechanism, Explains, Syndrome, Directly
Pathophysiology
Cardiovascular System 97-120 Pathophysiologic, Explains, Mechanism, Fruity Breath,
Disorders Pathophysiology
Respiratory System 121-144 Explains, Mechanism, Pathophysiologic, Acute, Chronic
Disorders
TOTAL 144 All questions include answers and detailed rationales
,Section A - Cellular Injury Adaptation AND Death
Q1.
A patient with chronic kidney disease has an arterial blood gas showing pH 7.28, PaCO2
30 mm Hg, and HCO3- 14 mEq/L. Which acid-base disturbance is present?
A. Acute respiratory acidosis with metabolic B. Metabolic acidosis with respiratory
compensation compensation
C. Mixed metabolic acidosis and respiratory D. Metabolic alkalosis with respiratory
alkalosis acidosis
Correct: B - Metabolic acidosis with respiratory compensation
Rationale:Low pH with low HCO3- indicates metabolic acidosis; the low PaCO2 reflects
compensatory hyperventilation (respiratory compensation). The pH is not normalized, so it is
not a mixed disorder with a coexisting primary respiratory alkalosis. Renal failure impairs
HCO3- regeneration, producing the primary metabolic acidosis.
Why the other answers are wrong:
A. pH is acidemic but PaCO2 is low, not high, ruling out respiratory acidosis.
C. A mixed disorder would typically show a pH closer to normal or a PaCO2 inconsistent with
full compensation; here the changes are directionally appropriate for compensation.
D. Low HCO3- rules out metabolic alkalosis as the primary disturbance.
Reference: McCance, K.L. & Huether, S.E. (2024). Pathophysiology: The Biologic Basis for Disease, 9th
Ed., Ch. 3
Q2.
Which mechanism best explains the hypoxemia seen in a patient with acute respiratory
distress syndrome (ARDS)?
A. Alveolar hypoventilation due to B. Intrapulmonary shunt from alveolar
neuromuscular weakness flooding and atelectasis
C. Diffusion limitation from thickened D. Reduced inspired oxygen tension at
alveolar-capillary membrane alone altitude
Correct: B - Intrapulmonary shunt from alveolar flooding and atelectasis
Rationale:ARDS causes increased permeability pulmonary edema, surfactant inactivation,
and atelectasis, producing intrapulmonary shunting (perfusion of non-ventilated alveoli) that is
refractory to supplemental oxygen. Hypoventilation and low inspired O2 are not the primary
mechanisms, and diffusion limitation plays a minor role compared with shunt.
Why the other answers are wrong:
A. Neuromuscular weakness causes hypoventilation with hypercapnia, not the classic shunt
Page 3
, Section A - Cellular Injury Adaptation AND Death
physiology of ARDS.
C. Membrane thickening contributes minimally; shunt is the dominant mechanism.
D. Altitude-related hypoxemia is due to low PiO2, not intrinsic lung pathology.
Reference: McCance, K.L. & Huether, S.E. (2024). Pathophysiology, 9th Ed., Ch. 26
Q3.
In heart failure with reduced ejection fraction, which compensatory mechanism initially
maintains cardiac output but ultimately worsens myocardial workload?
A. Increased parasympathetic vagal tone B. Activation of the
renin-angiotensin-aldosterone system and
sympathetic nervous system
C. Release of atrial natriuretic peptide D. Upregulation of beta-adrenergic
receptors on myocytes
Correct: B - Activation of the renin-angiotensin-aldosterone system and sympathetic
nervous system
Rationale:RAAS and sympathetic activation increase preload, afterload, and heart rate to
preserve cardiac output, but chronic activation promotes remodeling, fibrosis, and further
pump failure. Natriuretic peptides are counter-regulatory and promote vasodilation and
diuresis. Parasympathetic tone and beta-receptor upregulation are not the primary
maladaptive compensatory responses.
Why the other answers are wrong:
A. Increased vagal tone would slow heart rate and reduce cardiac output, not compensate for
it.
C. ANP is a compensatory vasodilator and natriuretic hormone that opposes RAAS, not a
mechanism that worsens workload.
D. Beta-receptors are typically downregulated in chronic heart failure due to sustained
catecholamine exposure.
Reference: Lehne, R.A. (2026). Pharmacology for Nursing Care, 12th Ed., Ch. 58
Q4.
Which finding is most characteristic of nephrotic syndrome compared with nephritic
syndrome?
A. Active urinary sediment with red blood B. Massive proteinuria (>3.5 g/day) with
cell casts hypoalbuminemia and edema
C. Oliguria with hypertension and azotemia D. Sterile pyuria with white blood cell casts
Correct: B - Massive proteinuria (>3.5 g/day) with hypoalbuminemia and edema
Page 4
