NRMS 5190 PATHOPHYSIOLOGY EXAM 1 STUDY GUIDE |
2026/27 UPDATE WITH COMPLETE SOLUTIONS | A+
GUIDE | SUNY DOWNSTATE MEDICAL CENTER.
145 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 PATHOPHYSIOLOGY EXAM 1 STUDY GUIDE | 2026/27 UPDATE WITH COMPLETE SOLUTIONS
| A+ GUIDE | SUNY DOWNSTATE MEDICAL CENTER.. It contains 145 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 145 Questions
Foundations - Application - NRMS 5190 Pathophysiology 1 Study Guide 2026/27 Update WITH Complete
Solutions A Guide SUNY Downstate Medical Center Pathophysiology Cellular Injury Inflammation Immunity
Genetics Neoplasia Fluids/electrolytes Hemodynamics Graduate Msn/dnp-level Basic Sciences SUNY
Downstate NRMS 5190
All answers with rationales
,Table of Contents
Content Area Questions Key Topics
Cellular Injury Adaptation 1-25 Responsible, Mechanism, Explains, Tumor, Response
AND Death
Inflammation AND Wound 26-50 Directly, Mechanism, Explains, Electrolyte, Consistent
Healing
Immunity AND Immune 51-75 Mechanism, Explains, Response, Chronic, Serum
Disorders
Genetics AND Genetic 76-100 Mechanism, Explains, Chronic, Describes, Cellular
Disorders
Fluid Electrolyte AND 101-125 Explains, Mechanism, Directly, Develops, Tumor Suppressor
Acid-base Imbalances
Neoplasia AND Cancer 126-145 Explains, Directly, Mechanism, Change, Chronic
Pathophysiology
TOTAL 145 All questions include answers and detailed rationales
,Section A - Cellular Injury Adaptation AND Death
Q1.
A tissue biopsy shows cell swelling, dispersed ribosomes, and blebs, but the plasma
membrane is intact and ATP is only modestly reduced. This pattern is best classified as
which of the following?
A. Coagulative necrosis B. Reversible cell injury (hydropic change)
C. Apoptosis D. Liquefactive necrosis
Correct: B - Reversible cell injury (hydropic change)
Rationale:Hydropic swelling with intact membrane, preserved ATP, and ribosomal dispersion
is the classic reversible injury pattern; these changes resolve if the stressor is removed.
Necrosis (coagulative or liquefactive) requires membrane loss and enzymatic/denaturing
changes, and apoptosis is an energy-dependent, non-inflammatory programmed death with
cell shrinkage and apoptotic bodies.
Why the other answers are wrong:
A. Coagulative necrosis requires irreversible injury with protein denaturation and loss of nuclei,
not preserved membrane and ATP.
C. Apoptosis shows cell shrinkage, chromatin condensation, and apoptotic bodies-not hydropic
swelling with blebs.
D. Liquefactive necrosis involves enzymatic digestion and membrane rupture, seen in brain
infarcts and abscesses.
Reference: Kumar, V., Abbas, A.K., Aster, J.C. (2025). Robbins & Cotran Pathologic Basis of Disease,
11th Ed., Ch. 2.
Q2.
Which cytokine profile best characterizes a Th2-predominant response in allergic asthma?
A. IFN- and IL-2 B. IL-4, IL-5, and IL-13
C. IL-12 and TNF- D. IL-17 and IL-22
Correct: B - IL-4, IL-5, and IL-13
Rationale:Th2 cells drive atopic asthma via IL-4 (IgE class switching), IL-5 (eosinophil
recruitment), and IL-13 (mucus production, airway hyperresponsiveness). IFN-/IL-2 denote
Th1, IL-17/IL-22 denote Th17, and IL-12/TNF- are not the defining Th2 signature.
Why the other answers are wrong:
A. IFN- and IL-2 are Th1 cytokines that antagonize Th2 responses.
C. IL-12 promotes Th1 differentiation and TNF- is a proinflammatory mediator, not
Th2-defining.
Page 3
, Section A - Cellular Injury Adaptation AND Death
D. IL-17 and IL-22 characterize Th17 responses involved in autoimmunity and mucosal
defense.
Reference: Abbas, A.K., Lichtman, A.H., Pillai, S. (2024). Cellular and Molecular Immunology, 10th Ed.,
Ch. 10.
Q3.
A patient with severe diarrhea has ABG: pH 7.28, PaCO2 30, HCO3 14. What is the primary
acid-base disturbance and the expected respiratory response?
A. Metabolic acidosis with appropriate B. Respiratory acidosis with renal
respiratory compensation (hyperventilation) compensation
C. Metabolic alkalosis with hypoventilation D. Mixed respiratory and metabolic acidosis
Correct: A - Metabolic acidosis with appropriate respiratory compensation
(hyperventilation)
Rationale:Low HCO3 with acidemia indicates metabolic acidosis; the low PaCO2 reflects
hyperventilation, the expected respiratory compensation (Winter's formula predicts PaCO2
1.5×14+8 = 29 ± 2). Respiratory acidosis would show elevated PaCO2, and metabolic
alkalosis would show elevated HCO3 and pH.
Why the other answers are wrong:
B. Respiratory acidosis requires elevated PaCO2 and would not explain the low HCO3.
C. Metabolic alkalosis shows high pH and high HCO3, opposite of this ABG.
D. A mixed disorder would show a PaCO2 inconsistent with compensation; here it fits Winter's
formula.
Reference: Lehne, R.A. (2026). Pharmacology for Nursing Care, 12th Ed., Ch. 18 (Fluids and
Electrolytes).
Q4.
Which molecular event is most directly responsible for the initiation of apoptosis via the
intrinsic pathway?
A. Caspase-8 activation by death receptors B. Mitochondrial outer membrane
permeabilization and cytochrome c release
C. Perforin and granzyme B delivery by D. Complement-mediated membrane attack
cytotoxic T cells complex formation
Correct: B - Mitochondrial outer membrane permeabilization and cytochrome c release
Rationale:The intrinsic (mitochondrial) pathway is triggered by MOMP, releasing cytochrome
c that assembles the apoptosome and activates caspase-9. Caspase-8 and granzyme B
initiate the extrinsic/cytotoxic pathways, and MAC causes osmotic lysis, not programmed
apoptosis.
Page 4
2026/27 UPDATE WITH COMPLETE SOLUTIONS | A+
GUIDE | SUNY DOWNSTATE MEDICAL CENTER.
145 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 PATHOPHYSIOLOGY EXAM 1 STUDY GUIDE | 2026/27 UPDATE WITH COMPLETE SOLUTIONS
| A+ GUIDE | SUNY DOWNSTATE MEDICAL CENTER.. It contains 145 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 145 Questions
Foundations - Application - NRMS 5190 Pathophysiology 1 Study Guide 2026/27 Update WITH Complete
Solutions A Guide SUNY Downstate Medical Center Pathophysiology Cellular Injury Inflammation Immunity
Genetics Neoplasia Fluids/electrolytes Hemodynamics Graduate Msn/dnp-level Basic Sciences SUNY
Downstate NRMS 5190
All answers with rationales
,Table of Contents
Content Area Questions Key Topics
Cellular Injury Adaptation 1-25 Responsible, Mechanism, Explains, Tumor, Response
AND Death
Inflammation AND Wound 26-50 Directly, Mechanism, Explains, Electrolyte, Consistent
Healing
Immunity AND Immune 51-75 Mechanism, Explains, Response, Chronic, Serum
Disorders
Genetics AND Genetic 76-100 Mechanism, Explains, Chronic, Describes, Cellular
Disorders
Fluid Electrolyte AND 101-125 Explains, Mechanism, Directly, Develops, Tumor Suppressor
Acid-base Imbalances
Neoplasia AND Cancer 126-145 Explains, Directly, Mechanism, Change, Chronic
Pathophysiology
TOTAL 145 All questions include answers and detailed rationales
,Section A - Cellular Injury Adaptation AND Death
Q1.
A tissue biopsy shows cell swelling, dispersed ribosomes, and blebs, but the plasma
membrane is intact and ATP is only modestly reduced. This pattern is best classified as
which of the following?
A. Coagulative necrosis B. Reversible cell injury (hydropic change)
C. Apoptosis D. Liquefactive necrosis
Correct: B - Reversible cell injury (hydropic change)
Rationale:Hydropic swelling with intact membrane, preserved ATP, and ribosomal dispersion
is the classic reversible injury pattern; these changes resolve if the stressor is removed.
Necrosis (coagulative or liquefactive) requires membrane loss and enzymatic/denaturing
changes, and apoptosis is an energy-dependent, non-inflammatory programmed death with
cell shrinkage and apoptotic bodies.
Why the other answers are wrong:
A. Coagulative necrosis requires irreversible injury with protein denaturation and loss of nuclei,
not preserved membrane and ATP.
C. Apoptosis shows cell shrinkage, chromatin condensation, and apoptotic bodies-not hydropic
swelling with blebs.
D. Liquefactive necrosis involves enzymatic digestion and membrane rupture, seen in brain
infarcts and abscesses.
Reference: Kumar, V., Abbas, A.K., Aster, J.C. (2025). Robbins & Cotran Pathologic Basis of Disease,
11th Ed., Ch. 2.
Q2.
Which cytokine profile best characterizes a Th2-predominant response in allergic asthma?
A. IFN- and IL-2 B. IL-4, IL-5, and IL-13
C. IL-12 and TNF- D. IL-17 and IL-22
Correct: B - IL-4, IL-5, and IL-13
Rationale:Th2 cells drive atopic asthma via IL-4 (IgE class switching), IL-5 (eosinophil
recruitment), and IL-13 (mucus production, airway hyperresponsiveness). IFN-/IL-2 denote
Th1, IL-17/IL-22 denote Th17, and IL-12/TNF- are not the defining Th2 signature.
Why the other answers are wrong:
A. IFN- and IL-2 are Th1 cytokines that antagonize Th2 responses.
C. IL-12 promotes Th1 differentiation and TNF- is a proinflammatory mediator, not
Th2-defining.
Page 3
, Section A - Cellular Injury Adaptation AND Death
D. IL-17 and IL-22 characterize Th17 responses involved in autoimmunity and mucosal
defense.
Reference: Abbas, A.K., Lichtman, A.H., Pillai, S. (2024). Cellular and Molecular Immunology, 10th Ed.,
Ch. 10.
Q3.
A patient with severe diarrhea has ABG: pH 7.28, PaCO2 30, HCO3 14. What is the primary
acid-base disturbance and the expected respiratory response?
A. Metabolic acidosis with appropriate B. Respiratory acidosis with renal
respiratory compensation (hyperventilation) compensation
C. Metabolic alkalosis with hypoventilation D. Mixed respiratory and metabolic acidosis
Correct: A - Metabolic acidosis with appropriate respiratory compensation
(hyperventilation)
Rationale:Low HCO3 with acidemia indicates metabolic acidosis; the low PaCO2 reflects
hyperventilation, the expected respiratory compensation (Winter's formula predicts PaCO2
1.5×14+8 = 29 ± 2). Respiratory acidosis would show elevated PaCO2, and metabolic
alkalosis would show elevated HCO3 and pH.
Why the other answers are wrong:
B. Respiratory acidosis requires elevated PaCO2 and would not explain the low HCO3.
C. Metabolic alkalosis shows high pH and high HCO3, opposite of this ABG.
D. A mixed disorder would show a PaCO2 inconsistent with compensation; here it fits Winter's
formula.
Reference: Lehne, R.A. (2026). Pharmacology for Nursing Care, 12th Ed., Ch. 18 (Fluids and
Electrolytes).
Q4.
Which molecular event is most directly responsible for the initiation of apoptosis via the
intrinsic pathway?
A. Caspase-8 activation by death receptors B. Mitochondrial outer membrane
permeabilization and cytochrome c release
C. Perforin and granzyme B delivery by D. Complement-mediated membrane attack
cytotoxic T cells complex formation
Correct: B - Mitochondrial outer membrane permeabilization and cytochrome c release
Rationale:The intrinsic (mitochondrial) pathway is triggered by MOMP, releasing cytochrome
c that assembles the apoptosome and activates caspase-9. Caspase-8 and granzyme B
initiate the extrinsic/cytotoxic pathways, and MAC causes osmotic lysis, not programmed
apoptosis.
Page 4
