NSG 5140 Advanced Pathophysiology
Midterm Exam Review 2 2026 | South
College | Practice Questions, Verified
Answers & Rationales | Just Released This
Year PDF | Updated This Year
NSG 5140 ADVANCED PATHOPHYSIOLOGY MIDTERM EXAM REVIEW 2026
South College | Practice Questions with Verified Answers & Rationales
DOCUMENT OVERVIEW
• This comprehensive practice exam contains verified multiple-choice questions
designed to assess mastery of pathophysiology concepts across all major body
systems and disease processes covered in NSG 5140, with detailed rationales for
each correct answer to strengthen clinical understanding and retention.
• Study this material by working through questions systematically, reviewing
rationales carefully even for correct answers, identifying weak topic areas, and
using this guide as both a diagnostic tool and a reinforcement mechanism to build
confidence and clinical reasoning skills before your midterm examination.
EXAM QUESTIONS
1. A 45-year-old patient develops acute kidney injury following major surgery.
Which of the following best describes the primary pathophysiologic
mechanism in acute tubular necrosis (ATN)?
A) Glomerular filtration barrier damage with proteinuria
B) Tubular epithelial cell necrosis and loss of function
C) Interstitial inflammation without parenchymal damage
D) Afferent arteriole vasoconstriction with decreased blood flow
E) Immune complex deposition along the basement membrane
,CORRECT ANSWER: B) Tubular epithelial cell necrosis and loss of function is
the primary pathophysiologic mechanism in acute tubular necrosis.
Acute tubular necrosis represents direct damage to the tubular epithelial cells,
resulting in loss of their structural integrity and functional capacity. The tubular
epithelium provides critical functions including selective reabsorption, secretion,
and active transport. When these cells undergo necrosis, they cannot perform
these essential functions, leading to decreased glomerular filtration rate and
oliguria. ATN can result from ischemia (most common in post-surgical settings) or
nephrotoxic injury. Option A describes nephrotic syndrome patterns. Option C
describes interstitial nephritis. Option D describes hemodynamic acute kidney
injury. Option E describes membranous nephropathy. The key distinguishing
feature of ATN is the actual death of tubular cells themselves.
2. A 28-year-old woman with systemic lupus erythematosus presents with
hemolytic anemia. Which mechanism best explains the destruction of red
blood cells in this autoimmune condition?
A) Decreased erythropoietin production by kidneys
B) IgG antibody binding to RBC membranes followed by complement-mediated lysis
and phagocytosis
C) Increased osmotic fragility due to membrane lipid peroxidation
D) Bone marrow suppression from corticosteroid therapy
E) Hypersplenism from portal hypertension
CORRECT ANSWER: B) IgG antibody binding to RBC membranes followed by
complement-mediated lysis and phagocytosis is the primary mechanism in
SLE-related hemolysis.
In systemic lupus erythematosus, autoantibodies (primarily IgG) bind to antigens on
the red blood cell membrane. These antibody-coated RBCs are then recognized as
foreign by complement proteins and by macrophages in the spleen, which express
Fc receptors. Complement activation leads to formation of the membrane attack
complex (C5b-9), causing osmotic lysis of cells. Additionally, antibody-opsonized
,RBCs are phagocytosed by splenic macrophages, resulting in extravascular
hemolysis. This represents Type II hypersensitivity reactions. Option A would cause
normocytic anemia without hemolysis. Option C is not the primary mechanism in
SLE. Option D can contribute but is not the primary pathophysiology. Option E
contributes but is secondary to the autoimmune process.
3. A 62-year-old male with chronic obstructive pulmonary disease experiences
acute respiratory failure. Which of the following best explains Type II
respiratory failure in COPD?
A) Hypoxemia due to ventilation-perfusion mismatch without hypercapnia
B) Hypoxemia and hypercapnia due to inadequate alveolar ventilation
C) Pulmonary edema from left ventricular dysfunction
D) Shunting of blood through consolidated lung tissue
E) Acute increase in airway resistance without loss of elastic recoil
CORRECT ANSWER: B) Hypoxemia and hypercapnia due to inadequate alveolar
ventilation is the defining characteristic of Type II respiratory failure.
Type II respiratory failure is defined by the inability of the respiratory system to
eliminate carbon dioxide, resulting in hypercapnia (PaCO2 > 45 mmHg) regardless
of the oxygen levels. In COPD, this occurs due to inadequate alveolar ventilation
caused by airway obstruction, loss of elastic recoil from emphysema, and
respiratory muscle weakness. The fundamental problem is insufficient minute
ventilation to meet the body's metabolic demands for CO2 elimination. Type I
respiratory failure (Option A) involves hypoxemia without CO2 retention and occurs
in conditions with V/Q mismatch or diffusion impairment. Options C and D describe
mechanisms that may accompany COPD but are not the defining feature of Type II
failure. Option E describes airway obstruction but misses the ventilatory
insufficiency component.
, 4. A 55-year-old patient with acute myocardial infarction develops cardiogenic
shock. Which cardiac compensatory mechanism becomes maladaptive in this
condition?
A) Increased contractility from sympathetic stimulation
B) Venoconstriction to maintain preload
C) Increased heart rate to maintain cardiac output
D) Ventricular remodeling with increased chamber dilatation
E) Arteriolar constriction to maintain blood pressure
CORRECT ANSWER: D) Ventricular remodeling with increased chamber
dilatation becomes maladaptive in cardiogenic shock.
Ventricular remodeling is initially a compensatory mechanism where the heart
dilates to maintain cardiac output via the Frank-Starling mechanism. However,
excessive dilatation becomes pathologic because: (1) it increases wall tension and
myocardial oxygen demand, worsening ischemia; (2) it causes mechanical
dysfunction as the ventricle becomes spherical rather than elliptical; (3) it activates
neurohumoral systems that increase afterload; and (4) it can progress to dilated
cardiomyopathy. Additionally, in the context of acute MI with ventricular rupture
risk, excessive dilatation increases wall stress and rupture risk. While options A, B,
C, and E are initially compensatory responses, option D represents the maladaptive
consequence of these compensations. The adverse remodeling contributes to the
progressive hemodynamic deterioration in cardiogenic shock.
5. A 34-year-old woman presents with fatigue and dyspnea. Lab findings show:
Hgb 7.2 g/dL, MCV 65 fL, ferritin 8 ng/mL, TIBC 425 μg/dL. Which
pathophysiologic stage of iron deficiency anemia is this patient in?
A) Iron depletion stage with normal hemoglobin
B) Iron-deficient erythropoiesis with early anemia
C) Iron deficiency anemia with microcytic, hypochromic RBCs
Midterm Exam Review 2 2026 | South
College | Practice Questions, Verified
Answers & Rationales | Just Released This
Year PDF | Updated This Year
NSG 5140 ADVANCED PATHOPHYSIOLOGY MIDTERM EXAM REVIEW 2026
South College | Practice Questions with Verified Answers & Rationales
DOCUMENT OVERVIEW
• This comprehensive practice exam contains verified multiple-choice questions
designed to assess mastery of pathophysiology concepts across all major body
systems and disease processes covered in NSG 5140, with detailed rationales for
each correct answer to strengthen clinical understanding and retention.
• Study this material by working through questions systematically, reviewing
rationales carefully even for correct answers, identifying weak topic areas, and
using this guide as both a diagnostic tool and a reinforcement mechanism to build
confidence and clinical reasoning skills before your midterm examination.
EXAM QUESTIONS
1. A 45-year-old patient develops acute kidney injury following major surgery.
Which of the following best describes the primary pathophysiologic
mechanism in acute tubular necrosis (ATN)?
A) Glomerular filtration barrier damage with proteinuria
B) Tubular epithelial cell necrosis and loss of function
C) Interstitial inflammation without parenchymal damage
D) Afferent arteriole vasoconstriction with decreased blood flow
E) Immune complex deposition along the basement membrane
,CORRECT ANSWER: B) Tubular epithelial cell necrosis and loss of function is
the primary pathophysiologic mechanism in acute tubular necrosis.
Acute tubular necrosis represents direct damage to the tubular epithelial cells,
resulting in loss of their structural integrity and functional capacity. The tubular
epithelium provides critical functions including selective reabsorption, secretion,
and active transport. When these cells undergo necrosis, they cannot perform
these essential functions, leading to decreased glomerular filtration rate and
oliguria. ATN can result from ischemia (most common in post-surgical settings) or
nephrotoxic injury. Option A describes nephrotic syndrome patterns. Option C
describes interstitial nephritis. Option D describes hemodynamic acute kidney
injury. Option E describes membranous nephropathy. The key distinguishing
feature of ATN is the actual death of tubular cells themselves.
2. A 28-year-old woman with systemic lupus erythematosus presents with
hemolytic anemia. Which mechanism best explains the destruction of red
blood cells in this autoimmune condition?
A) Decreased erythropoietin production by kidneys
B) IgG antibody binding to RBC membranes followed by complement-mediated lysis
and phagocytosis
C) Increased osmotic fragility due to membrane lipid peroxidation
D) Bone marrow suppression from corticosteroid therapy
E) Hypersplenism from portal hypertension
CORRECT ANSWER: B) IgG antibody binding to RBC membranes followed by
complement-mediated lysis and phagocytosis is the primary mechanism in
SLE-related hemolysis.
In systemic lupus erythematosus, autoantibodies (primarily IgG) bind to antigens on
the red blood cell membrane. These antibody-coated RBCs are then recognized as
foreign by complement proteins and by macrophages in the spleen, which express
Fc receptors. Complement activation leads to formation of the membrane attack
complex (C5b-9), causing osmotic lysis of cells. Additionally, antibody-opsonized
,RBCs are phagocytosed by splenic macrophages, resulting in extravascular
hemolysis. This represents Type II hypersensitivity reactions. Option A would cause
normocytic anemia without hemolysis. Option C is not the primary mechanism in
SLE. Option D can contribute but is not the primary pathophysiology. Option E
contributes but is secondary to the autoimmune process.
3. A 62-year-old male with chronic obstructive pulmonary disease experiences
acute respiratory failure. Which of the following best explains Type II
respiratory failure in COPD?
A) Hypoxemia due to ventilation-perfusion mismatch without hypercapnia
B) Hypoxemia and hypercapnia due to inadequate alveolar ventilation
C) Pulmonary edema from left ventricular dysfunction
D) Shunting of blood through consolidated lung tissue
E) Acute increase in airway resistance without loss of elastic recoil
CORRECT ANSWER: B) Hypoxemia and hypercapnia due to inadequate alveolar
ventilation is the defining characteristic of Type II respiratory failure.
Type II respiratory failure is defined by the inability of the respiratory system to
eliminate carbon dioxide, resulting in hypercapnia (PaCO2 > 45 mmHg) regardless
of the oxygen levels. In COPD, this occurs due to inadequate alveolar ventilation
caused by airway obstruction, loss of elastic recoil from emphysema, and
respiratory muscle weakness. The fundamental problem is insufficient minute
ventilation to meet the body's metabolic demands for CO2 elimination. Type I
respiratory failure (Option A) involves hypoxemia without CO2 retention and occurs
in conditions with V/Q mismatch or diffusion impairment. Options C and D describe
mechanisms that may accompany COPD but are not the defining feature of Type II
failure. Option E describes airway obstruction but misses the ventilatory
insufficiency component.
, 4. A 55-year-old patient with acute myocardial infarction develops cardiogenic
shock. Which cardiac compensatory mechanism becomes maladaptive in this
condition?
A) Increased contractility from sympathetic stimulation
B) Venoconstriction to maintain preload
C) Increased heart rate to maintain cardiac output
D) Ventricular remodeling with increased chamber dilatation
E) Arteriolar constriction to maintain blood pressure
CORRECT ANSWER: D) Ventricular remodeling with increased chamber
dilatation becomes maladaptive in cardiogenic shock.
Ventricular remodeling is initially a compensatory mechanism where the heart
dilates to maintain cardiac output via the Frank-Starling mechanism. However,
excessive dilatation becomes pathologic because: (1) it increases wall tension and
myocardial oxygen demand, worsening ischemia; (2) it causes mechanical
dysfunction as the ventricle becomes spherical rather than elliptical; (3) it activates
neurohumoral systems that increase afterload; and (4) it can progress to dilated
cardiomyopathy. Additionally, in the context of acute MI with ventricular rupture
risk, excessive dilatation increases wall stress and rupture risk. While options A, B,
C, and E are initially compensatory responses, option D represents the maladaptive
consequence of these compensations. The adverse remodeling contributes to the
progressive hemodynamic deterioration in cardiogenic shock.
5. A 34-year-old woman presents with fatigue and dyspnea. Lab findings show:
Hgb 7.2 g/dL, MCV 65 fL, ferritin 8 ng/mL, TIBC 425 μg/dL. Which
pathophysiologic stage of iron deficiency anemia is this patient in?
A) Iron depletion stage with normal hemoglobin
B) Iron-deficient erythropoiesis with early anemia
C) Iron deficiency anemia with microcytic, hypochromic RBCs
