NR-507 ADVANCED
PATHOPHYSIOLOGY
– MIDTERM EXAM
Section 1: Cellular Adaptation, Injury & Death
1. A 52-year-old male with chronic alcoholism presents with hepatocytes showing
enlarged, pale-staining cytoplasm containing lipid vacuoles. This cellular change is
best described as:
A. Hyperplasia
B. Hypertrophy
C. Steatosis (fatty change)
D. Metaplasia
Rationale: Steatosis is the abnormal accumulation of triglycerides within hepatocytes,
commonly caused by alcohol abuse, diabetes, or obesity. The cells appear enlarged with
vacuolated cytoplasm. This is a form of reversible cellular injury, not an adaptive change
like hyperplasia or metaplasia .
2. A 45-year-old woman with a history of smoking develops chronic hypoxia. Her
erythrocyte count is elevated. This cellular adaptation is best described as:
A. Physiologic hyperplasia
B. Compensatory hyperplasia of erythroid precursors
C. Pathologic hypertrophy
D. Metaplasia
Rationale: Chronic hypoxia stimulates erythropoietin production, causing compensatory
hyperplasia of erythroid cell lines in the bone marrow. This increases oxygen-carrying
capacity. Metaplasia occurs in airway epithelium due to smoking but does not explain
elevated erythrocytes .
,3. What is the earliest reversible morphologic sign of cell injury?
A. Nuclear fragmentation
B. Cellular swelling (hydropic change)
C. Karyolysis
D. Fatty change
Rationale: Cellular swelling is the earliest reversible sign of cell injury, caused by ATP
depletion leading to failure of the Na⁺/K⁺-ATPase pump and subsequent water influx.
This is followed by fatty change in some organs. Nuclear changes indicate irreversible
injury .
4. The irreversible marker of cell death on electron microscopy is:
A. Cellular swelling
B. Nuclear pyknosis
C. Mitochondrial amorphous (flocculent) densities
D. Membrane blebbing
Rationale: Flocculent densities in the mitochondrial matrix are an irreversible marker of
cell death, indicating severe membrane damage. This represents the "point of no return"
where cell death is inevitable even if the stressor is removed .
5. Which type of cell adaptation occurs when normal columnar ciliated epithelial
cells of the bronchial lining are replaced by stratified squamous epithelial cells?
A. Hyperplasia
B. Metaplasia
C. Dysplasia
D. Anaplasia
Rationale: Metaplasia is the reversible replacement of one mature cell type by another,
sometimes less differentiated cell type. The classic example is replacement of normal
columnar ciliated epithelial cells of the bronchial lining by stratified squamous epithelial
cells in smokers .
6. A 60-year-old female smoker has a lung biopsy revealing anaplastic cells with
high mitotic rate and areas of necrosis. The term "anaplasia" refers to:
A. Decreased nuclear-to-cytoplasmic ratio
B. Loss of cellular differentiation and pleomorphism
C. Slow growth with abundant stroma
D. Benign, non-invasive growth pattern
,Rationale: Anaplasia is the hallmark of malignancy and refers to a lack of differentiation,
pleomorphic cells, hyperchromatic nuclei, increased mitotic figures, and loss of normal
tissue architecture .
7. How do free radicals cause cell damage?
A. Stealing the cell's oxygen to stabilize the electron, thus causing hypoxia
B. Stimulating the release of lysosomal enzymes that digest the cell membranes
C. Transferring one of its charged, stabilized atoms to the cell membrane, which causes
lysis
D. Giving up an electron, which causes injury to the chemical bonds of the cell
membrane
Rationale: A free radical is an electrically uncharged atom or group of atoms having an
unpaired electron. To stabilize, the molecule gives up an electron to another molecule or
steals one, forming injurious chemical bonds with proteins, lipids, or carbohydrates—key
molecules in membranes and nucleic acids .
8. What is a consequence of plasma membrane damage to the mitochondria?
A. Enzymatic digestion halts DNA synthesis
B. Influx of calcium ions halts ATP production
C. Edema from an influx in sodium causes a reduction in ATP production
D. Potassium shifts out of the mitochondria, which destroys the infrastructure
Rationale: Cell membrane injury leads to calcium influx into the cell. An influx of
calcium ions from the extracellular compartment activates multiple enzyme systems,
resulting in cytoskeleton disruption, membrane damage, activation of inflammation, and
eventually DNA degradation. Calcium overload impairs mitochondrial function and ATP
production .
9. Which process describes the decrease in cellular size caused by aging, disuse, or
reduced blood supply?
A. Hypertrophy
B. Hyperplasia
C. Atrophy
D. Metaplasia
Rationale: Atrophy is the decrease in cellular size due to aging, disuse, or reduced
blood supply. Hypertrophy is an increase in cell size; hyperplasia is an increase in cell
number; metaplasia is the replacement of one cell type with another .
, 10. A 60-year-old male undergoes cardiac catheterization and experiences
reperfusion injury after clot dissolution. Which cellular event is the primary driver
of reperfusion injury in this scenario?
A. Calcium overload leading to mitochondrial permeability transition
B. Immediate restoration of ATP without any cellular consequences
C. Suppression of inflammatory cytokine release from neutrophils
D. Decreased generation of reactive oxygen species in myocardium
Rationale: Reperfusion causes calcium overload and mitochondrial damage, the primary
mechanism of reperfusion injury. ATP restoration is beneficial, and ROS generation
increases rather than decreases during reperfusion .
Section 2: Inflammation & Immunity
11. Which immune mechanism is primarily responsible for the immediate
hypersensitivity reaction seen in anaphylaxis?
A. Type I hypersensitivity involving IgE-mediated mast cell degranulation
B. Type II hypersensitivity with antibody-mediated cytotoxicity
C. Type III hypersensitivity due to immune complex deposition
D. Type IV hypersensitivity involving T-cell activation
Rationale: Anaphylaxis is a classic Type I hypersensitivity reaction where allergens cross-
link IgE on mast cells and basophils, triggering rapid degranulation and release of
histamine, leukotrienes, and prostaglandins, leading to vasodilation,
bronchoconstriction, and hypotension .
12. During acute inflammation, which cell type is the first responder to the site of
injury?
A. Neutrophils migrating via chemotaxis
B. Macrophages for phagocytosis
C. Lymphocytes for adaptive immunity
D. Eosinophils for parasitic defense
Rationale: Neutrophils are the earliest responders in acute inflammation, attracted by
chemotactic factors like C5a and IL-8, where they phagocytose debris and release
enzymes. Macrophages dominate chronic inflammation .
PATHOPHYSIOLOGY
– MIDTERM EXAM
Section 1: Cellular Adaptation, Injury & Death
1. A 52-year-old male with chronic alcoholism presents with hepatocytes showing
enlarged, pale-staining cytoplasm containing lipid vacuoles. This cellular change is
best described as:
A. Hyperplasia
B. Hypertrophy
C. Steatosis (fatty change)
D. Metaplasia
Rationale: Steatosis is the abnormal accumulation of triglycerides within hepatocytes,
commonly caused by alcohol abuse, diabetes, or obesity. The cells appear enlarged with
vacuolated cytoplasm. This is a form of reversible cellular injury, not an adaptive change
like hyperplasia or metaplasia .
2. A 45-year-old woman with a history of smoking develops chronic hypoxia. Her
erythrocyte count is elevated. This cellular adaptation is best described as:
A. Physiologic hyperplasia
B. Compensatory hyperplasia of erythroid precursors
C. Pathologic hypertrophy
D. Metaplasia
Rationale: Chronic hypoxia stimulates erythropoietin production, causing compensatory
hyperplasia of erythroid cell lines in the bone marrow. This increases oxygen-carrying
capacity. Metaplasia occurs in airway epithelium due to smoking but does not explain
elevated erythrocytes .
,3. What is the earliest reversible morphologic sign of cell injury?
A. Nuclear fragmentation
B. Cellular swelling (hydropic change)
C. Karyolysis
D. Fatty change
Rationale: Cellular swelling is the earliest reversible sign of cell injury, caused by ATP
depletion leading to failure of the Na⁺/K⁺-ATPase pump and subsequent water influx.
This is followed by fatty change in some organs. Nuclear changes indicate irreversible
injury .
4. The irreversible marker of cell death on electron microscopy is:
A. Cellular swelling
B. Nuclear pyknosis
C. Mitochondrial amorphous (flocculent) densities
D. Membrane blebbing
Rationale: Flocculent densities in the mitochondrial matrix are an irreversible marker of
cell death, indicating severe membrane damage. This represents the "point of no return"
where cell death is inevitable even if the stressor is removed .
5. Which type of cell adaptation occurs when normal columnar ciliated epithelial
cells of the bronchial lining are replaced by stratified squamous epithelial cells?
A. Hyperplasia
B. Metaplasia
C. Dysplasia
D. Anaplasia
Rationale: Metaplasia is the reversible replacement of one mature cell type by another,
sometimes less differentiated cell type. The classic example is replacement of normal
columnar ciliated epithelial cells of the bronchial lining by stratified squamous epithelial
cells in smokers .
6. A 60-year-old female smoker has a lung biopsy revealing anaplastic cells with
high mitotic rate and areas of necrosis. The term "anaplasia" refers to:
A. Decreased nuclear-to-cytoplasmic ratio
B. Loss of cellular differentiation and pleomorphism
C. Slow growth with abundant stroma
D. Benign, non-invasive growth pattern
,Rationale: Anaplasia is the hallmark of malignancy and refers to a lack of differentiation,
pleomorphic cells, hyperchromatic nuclei, increased mitotic figures, and loss of normal
tissue architecture .
7. How do free radicals cause cell damage?
A. Stealing the cell's oxygen to stabilize the electron, thus causing hypoxia
B. Stimulating the release of lysosomal enzymes that digest the cell membranes
C. Transferring one of its charged, stabilized atoms to the cell membrane, which causes
lysis
D. Giving up an electron, which causes injury to the chemical bonds of the cell
membrane
Rationale: A free radical is an electrically uncharged atom or group of atoms having an
unpaired electron. To stabilize, the molecule gives up an electron to another molecule or
steals one, forming injurious chemical bonds with proteins, lipids, or carbohydrates—key
molecules in membranes and nucleic acids .
8. What is a consequence of plasma membrane damage to the mitochondria?
A. Enzymatic digestion halts DNA synthesis
B. Influx of calcium ions halts ATP production
C. Edema from an influx in sodium causes a reduction in ATP production
D. Potassium shifts out of the mitochondria, which destroys the infrastructure
Rationale: Cell membrane injury leads to calcium influx into the cell. An influx of
calcium ions from the extracellular compartment activates multiple enzyme systems,
resulting in cytoskeleton disruption, membrane damage, activation of inflammation, and
eventually DNA degradation. Calcium overload impairs mitochondrial function and ATP
production .
9. Which process describes the decrease in cellular size caused by aging, disuse, or
reduced blood supply?
A. Hypertrophy
B. Hyperplasia
C. Atrophy
D. Metaplasia
Rationale: Atrophy is the decrease in cellular size due to aging, disuse, or reduced
blood supply. Hypertrophy is an increase in cell size; hyperplasia is an increase in cell
number; metaplasia is the replacement of one cell type with another .
, 10. A 60-year-old male undergoes cardiac catheterization and experiences
reperfusion injury after clot dissolution. Which cellular event is the primary driver
of reperfusion injury in this scenario?
A. Calcium overload leading to mitochondrial permeability transition
B. Immediate restoration of ATP without any cellular consequences
C. Suppression of inflammatory cytokine release from neutrophils
D. Decreased generation of reactive oxygen species in myocardium
Rationale: Reperfusion causes calcium overload and mitochondrial damage, the primary
mechanism of reperfusion injury. ATP restoration is beneficial, and ROS generation
increases rather than decreases during reperfusion .
Section 2: Inflammation & Immunity
11. Which immune mechanism is primarily responsible for the immediate
hypersensitivity reaction seen in anaphylaxis?
A. Type I hypersensitivity involving IgE-mediated mast cell degranulation
B. Type II hypersensitivity with antibody-mediated cytotoxicity
C. Type III hypersensitivity due to immune complex deposition
D. Type IV hypersensitivity involving T-cell activation
Rationale: Anaphylaxis is a classic Type I hypersensitivity reaction where allergens cross-
link IgE on mast cells and basophils, triggering rapid degranulation and release of
histamine, leukotrienes, and prostaglandins, leading to vasodilation,
bronchoconstriction, and hypotension .
12. During acute inflammation, which cell type is the first responder to the site of
injury?
A. Neutrophils migrating via chemotaxis
B. Macrophages for phagocytosis
C. Lymphocytes for adaptive immunity
D. Eosinophils for parasitic defense
Rationale: Neutrophils are the earliest responders in acute inflammation, attracted by
chemotactic factors like C5a and IL-8, where they phagocytose debris and release
enzymes. Macrophages dominate chronic inflammation .
