NR 507 Advanced Pathophysiology Chamberlain College
Midterm Exam Practice Questions with Verified Answers | 2026/2027
EXACTLY 50 Questions | Pathophysiology Rationales Included
DOMAIN 1: CELLULAR BIOLOGY, ADAPTATION & INJURY (Questions 1-8)
Q1. A patient with chronic hypertension develops left ventricular wall thickening. This cellular
adaptation is best described as:
A. Atrophy
B. Hypertrophy [CORRECT]
C. Hyperplasia
D. Metaplasia
Correct Answer: B
Rationale: Hypertrophy is an increase in cell size (not number) resulting in organ enlargement,
occurring in cells with limited capacity to divide (e.g., cardiac myocytes). In chronic
hypertension, increased afterload causes ventricular myocytes to enlarge. Hyperplasia is
increased cell number. Atrophy is decreased cell size. Metaplasia is replacement of one
mature cell type with another.
Q2. [SATA]
Which of the following are characteristic features of apoptosis? Select all that apply.
A. Programmed cell death [CORRECT]
B. Inflammatory response present
C. Caspase activation [CORRECT]
D. Cell shrinkage and chromatin condensation [CORRECT]
E. Membrane rupture with cellular contents release
Correct Answers: A, C, D
Rationale: Apoptosis is programmed cell death characterized by caspase activation, cell
shrinkage, chromatin condensation, and formation of apoptotic bodies. Unlike necrosis,
apoptosis does NOT trigger inflammation, and the cell membrane remains intact without
releasing cellular contents.
,Q3. A 62-year-old male with a history of heavy smoking is found to have Barrett esophagus on
endoscopy. The pathologist notes the replacement of normal squamous epithelium with
columnar epithelium. This cellular adaptation represents:
A. Dysplasia
B. Metaplasia [CORRECT]
C. Hyperplasia
D. Anaplasia
Correct Answer: B
Rationale: Metaplasia is the reversible replacement of one mature differentiated cell type
with another mature cell type. In Barrett esophagus, chronic reflux causes squamous
epithelium to be replaced by columnar epithelium (intestinal metaplasia). While metaplasia is
adaptive, it increases cancer risk. Dysplasia involves disordered cell growth with nuclear
atypia. Anaplasia refers to loss of differentiation in malignant cells.
Q4. [Case Study]
A 58-year-old patient presents with crushing chest pain. Cardiac catheterization reveals 95%
occlusion of the left anterior descending artery. Laboratory studies show elevated troponin I.
Within 24 hours, the myocardial tissue shows preserved tissue architecture with increased
eosinophilia and loss of nuclei. What type of necrosis has occurred?
A. Liquefactive necrosis
B. Coagulative necrosis [CORRECT]
C. Caseous necrosis
D. Fat necrosis
Correct Answer: B
Rationale: Coagulative necrosis is the most common type of necrosis, characterized by protein
denaturation that preserves tissue architecture for several days. It occurs in ischemic injury to
all solid organs except the brain (which undergoes liquefactive necrosis). The elevated
troponin and clinical scenario confirm myocardial infarction. Liquefactive necrosis occurs in
brain infarcts and abscesses. Caseous necrosis is seen in tuberculosis. Fat necrosis occurs in
pancreatitis and breast trauma.
Q5. [SATA]
, A patient with carbon monoxide poisoning presents with cellular hypoxia. Which of the
following mechanisms contribute to cellular injury in hypoxic states? Select all that apply.
A. Decreased ATP production [CORRECT]
B. Failure of the sodium-potassium pump [CORRECT]
C. Decreased intracellular calcium
D. Generation of reactive oxygen species upon reperfusion [CORRECT]
E. Cellular alkalosis
Correct Answers: A, B, D
Rationale: Hypoxia causes decreased oxidative phosphorylation and ATP depletion. Without
ATP, the Na+/K+-ATPase pump fails, leading to cellular edema and calcium influx. When
oxygen is reintroduced (reperfusion), reactive oxygen species (free radicals) are generated,
causing additional membrane damage. Hypoxia causes intracellular acidosis (not alkalosis)
due to anaerobic glycolysis and lactic acid accumulation.
Q6. A patient presents with acute pancreatitis. CT imaging shows areas of chalky white
deposits within the pancreatic fat. Microscopically, these deposits show basophilic calcium
soaps. This represents:
A. Coagulative necrosis
B. Fat necrosis [CORRECT]
C. Caseous necrosis
D. Liquefactive necrosis
Correct Answer: B
Rationale: Fat necrosis occurs when lipases break down triglycerides into fatty acids, which
combine with calcium to form insoluble calcium soaps (saponification), appearing as chalky
white deposits. This occurs in acute pancreatitis (due to released pancreatic lipases) and
traumatic fat necrosis (commonly breast tissue). The basophilic staining on microscopy is
characteristic.
Q7. [SATA]
Regarding the sodium-potassium (Na+/K+) ATPase pump, which statements are correct?
Select all that apply.
A. It maintains the resting membrane potential [CORRECT]
Midterm Exam Practice Questions with Verified Answers | 2026/2027
EXACTLY 50 Questions | Pathophysiology Rationales Included
DOMAIN 1: CELLULAR BIOLOGY, ADAPTATION & INJURY (Questions 1-8)
Q1. A patient with chronic hypertension develops left ventricular wall thickening. This cellular
adaptation is best described as:
A. Atrophy
B. Hypertrophy [CORRECT]
C. Hyperplasia
D. Metaplasia
Correct Answer: B
Rationale: Hypertrophy is an increase in cell size (not number) resulting in organ enlargement,
occurring in cells with limited capacity to divide (e.g., cardiac myocytes). In chronic
hypertension, increased afterload causes ventricular myocytes to enlarge. Hyperplasia is
increased cell number. Atrophy is decreased cell size. Metaplasia is replacement of one
mature cell type with another.
Q2. [SATA]
Which of the following are characteristic features of apoptosis? Select all that apply.
A. Programmed cell death [CORRECT]
B. Inflammatory response present
C. Caspase activation [CORRECT]
D. Cell shrinkage and chromatin condensation [CORRECT]
E. Membrane rupture with cellular contents release
Correct Answers: A, C, D
Rationale: Apoptosis is programmed cell death characterized by caspase activation, cell
shrinkage, chromatin condensation, and formation of apoptotic bodies. Unlike necrosis,
apoptosis does NOT trigger inflammation, and the cell membrane remains intact without
releasing cellular contents.
,Q3. A 62-year-old male with a history of heavy smoking is found to have Barrett esophagus on
endoscopy. The pathologist notes the replacement of normal squamous epithelium with
columnar epithelium. This cellular adaptation represents:
A. Dysplasia
B. Metaplasia [CORRECT]
C. Hyperplasia
D. Anaplasia
Correct Answer: B
Rationale: Metaplasia is the reversible replacement of one mature differentiated cell type
with another mature cell type. In Barrett esophagus, chronic reflux causes squamous
epithelium to be replaced by columnar epithelium (intestinal metaplasia). While metaplasia is
adaptive, it increases cancer risk. Dysplasia involves disordered cell growth with nuclear
atypia. Anaplasia refers to loss of differentiation in malignant cells.
Q4. [Case Study]
A 58-year-old patient presents with crushing chest pain. Cardiac catheterization reveals 95%
occlusion of the left anterior descending artery. Laboratory studies show elevated troponin I.
Within 24 hours, the myocardial tissue shows preserved tissue architecture with increased
eosinophilia and loss of nuclei. What type of necrosis has occurred?
A. Liquefactive necrosis
B. Coagulative necrosis [CORRECT]
C. Caseous necrosis
D. Fat necrosis
Correct Answer: B
Rationale: Coagulative necrosis is the most common type of necrosis, characterized by protein
denaturation that preserves tissue architecture for several days. It occurs in ischemic injury to
all solid organs except the brain (which undergoes liquefactive necrosis). The elevated
troponin and clinical scenario confirm myocardial infarction. Liquefactive necrosis occurs in
brain infarcts and abscesses. Caseous necrosis is seen in tuberculosis. Fat necrosis occurs in
pancreatitis and breast trauma.
Q5. [SATA]
, A patient with carbon monoxide poisoning presents with cellular hypoxia. Which of the
following mechanisms contribute to cellular injury in hypoxic states? Select all that apply.
A. Decreased ATP production [CORRECT]
B. Failure of the sodium-potassium pump [CORRECT]
C. Decreased intracellular calcium
D. Generation of reactive oxygen species upon reperfusion [CORRECT]
E. Cellular alkalosis
Correct Answers: A, B, D
Rationale: Hypoxia causes decreased oxidative phosphorylation and ATP depletion. Without
ATP, the Na+/K+-ATPase pump fails, leading to cellular edema and calcium influx. When
oxygen is reintroduced (reperfusion), reactive oxygen species (free radicals) are generated,
causing additional membrane damage. Hypoxia causes intracellular acidosis (not alkalosis)
due to anaerobic glycolysis and lactic acid accumulation.
Q6. A patient presents with acute pancreatitis. CT imaging shows areas of chalky white
deposits within the pancreatic fat. Microscopically, these deposits show basophilic calcium
soaps. This represents:
A. Coagulative necrosis
B. Fat necrosis [CORRECT]
C. Caseous necrosis
D. Liquefactive necrosis
Correct Answer: B
Rationale: Fat necrosis occurs when lipases break down triglycerides into fatty acids, which
combine with calcium to form insoluble calcium soaps (saponification), appearing as chalky
white deposits. This occurs in acute pancreatitis (due to released pancreatic lipases) and
traumatic fat necrosis (commonly breast tissue). The basophilic staining on microscopy is
characteristic.
Q7. [SATA]
Regarding the sodium-potassium (Na+/K+) ATPase pump, which statements are correct?
Select all that apply.
A. It maintains the resting membrane potential [CORRECT]
