NR507 Advanced Pathophysiology
Final Exam Review Guide 2026-2027
Questions & Answers
100 Multiple Choice Questions with Answers & Rationales
Select the BEST answer. Each question = 1 point. Total: 100 points. Time: 180 minutes.
Name: Class/Section: Student ID:
____________________________ ____________________________ ____________________________
__ __ __
I. Cellular Adaptation, Injury & Necrosis (Q1–Q8)
1. A 68-year-old patient with a 20-year history of smoking presents with chronic cough. A bronchial biopsy
reveals replacement of the normal ciliated columnar epithelium with stratified squamous epithelium. This
cellular adaptation is best described as:
A. Atrophy
B. Hypertrophy
C. Metaplasia
D. Dysplasia
Answer: C. Metaplasia
Rationale: Metaplasia is the reversible replacement of one differentiated cell type with another. Chronic exposure to
cigarette smoke injures the respiratory epithelium, and the body replaces the vulnerable ciliated columnar cells with
more resilient stratified squamous epithelium. This is an adaptive mechanism, though the new tissue is more susceptible
to malignancy. Atrophy refers to decreased cell size; hypertrophy to increased cell size; and dysplasia to disordered,
potentially precancerous cellular changes.
2. A 55-year-old male with essential hypertension develops left ventricular hypertrophy. Which of the following
best describes the mechanism of this adaptation?
A. Increased workload leads to increased cell number through mitotic division
B. Increased workload leads to increased cell size by adding sarcomeres
C. Decreased blood supply leads to cellular shrinkage and organelle loss
D. Hormonal stimulation leads to glandular epithelial cell proliferation
Answer: B. Increased workload leads to increased cell size by adding sarcomeres
Rationale: Pathologic hypertrophy occurs when increased workload (such as from chronic hypertension causing
increased afterload) stimulates myocardial cells to increase in size by synthesizing more contractile proteins and
sarcomeres. This allows the heart to generate greater force. Unlike hyperplasia, which involves increased cell number,
hypertrophy involves increased cell size. Myocardial cells are terminally differentiated and cannot divide, so they adapt
by enlarging.
1
,3. A patient presents with a painful, swollen right lower extremity after prolonged immobilization following
femoral fracture. The tissue has a foul odor and is dark-colored. Which type of necrosis is most likely present?
A. Coagulative necrosis
B. Liquefactive necrosis
C. Caseous necrosis
D. Wet (liquefactive) gangrene
Answer: D. Wet (liquefactive) gangrene
Rationale: Wet gangrene develops when there is superimposed bacterial infection on necrotic tissue in a setting of
compromised arterial blood supply. The liquefactive component of bacterial enzymatic digestion combines with
coagulative necrosis from ischemia. This produces a foul-smelling, dark, swollen lesion. Dry gangrene is slow, dry, and
without infection. Coagulative necrosis preserves tissue architecture; liquefactive necrosis is typical of brain infarcts;
and caseous necrosis is characteristic of tuberculosis.
4. A researcher is studying programmed cell death and notes that the process involves cytochrome c release from
mitochondria, activation of caspases, cell shrinkage, and formation of apoptotic bodies without inflammation.
Which of the following distinguishes this process from necrosis?
A. Necrosis is ATP-dependent, while this process is ATP-independent
B. This process does not elicit an inflammatory response, while necrosis always triggers inflammation
C. Necrosis involves DNA fragmentation, while this process does not affect nuclear material
D. This process causes cellular swelling, while necrosis causes cellular shrinkage
Answer: B. This process does not elicit an inflammatory response, while necrosis always triggers inflammation
Rationale: Apoptosis (programmed cell death) is an energy-dependent, tightly regulated process that does NOT elicit an
inflammatory response. Apoptotic cells shrink, form membrane-bound apoptotic bodies that are rapidly phagocytosed
by macrophages, and undergo internucleosomal DNA cleavage. In contrast, necrosis involves loss of membrane
integrity, cellular swelling, release of intracellular contents that trigger an intense inflammatory reaction, and is
generally a pathologic process.
5. A patient with severe ischemic heart disease undergoes coronary artery bypass grafting. Upon reperfusion of
the previously ischemic myocardium, there is paradoxically increased tissue damage. Which of the following is
the primary mechanism of ischemia-reperfusion injury?
A. Accumulation of lactic acid during ischemia
B. Generation of reactive oxygen species (ROS) upon restoration of blood flow
C. Calcium depletion in the cytoplasm of myocardial cells
D. Activation of anaerobic metabolism pathways
Answer: B. Generation of reactive oxygen species (ROS) upon restoration of blood flow
Rationale: Ischemia-reperfusion injury occurs because the return of oxygenated blood to ischemic tissue paradoxically
causes additional damage. The primary mechanism is the burst of reactive oxygen species (ROS) generated by
mitochondrial dysfunction, xanthine oxidase activation, and NADPH oxidase in activated neutrophils. During ischemia,
ATP is depleted, leading to accumulation of hypoxanthine. Upon reperfusion, xanthine oxidase uses oxygen to convert
hypoxanthine to uric acid, generating superoxide radicals that cause lipid peroxidation, membrane damage, and cell
death.
6. A 42-year-old female with Cushing syndrome presents with muscle weakness in her proximal limbs. Muscle
biopsy reveals decreased myofibril size and reduced cytoplasmic volume. This finding is an example of:
A. Physiologic hypertrophy
B. Pathologic atrophy
2
, C. Hyperplasia
D. Metaplasia
Answer: B. Pathologic atrophy
Rationale: Pathologic atrophy is a decrease in cell size due to adverse stimuli. Cushing syndrome (excess
glucocorticoids) causes protein catabolism and decreased protein synthesis, leading to muscle atrophy — particularly in
proximal muscles (proximal myopathy). Glucocorticoids stimulate ubiquitin-proteasome pathways and inhibit protein
synthesis. This is pathologic because it results from hormonal excess rather than normal physiologic disuse or aging.
7. A 45-year-old woman undergoes a Pap smear that reveals abnormal epithelial cells with nuclear
hyperchromasia, pleomorphism, and disorganized maturation. Biopsy confirms dysplasia of the cervix. Which
statement best characterizes dysplasia?
A. Dysplasia is always irreversible and definitively progresses to carcinoma
B. Dysplasia represents a fully malignant transformation with invasive potential
C. Dysplasia involves disordered cellular growth and maturation that is potentially reversible if the
inciting stimulus is removed
D. Dysplasia is characterized by replacement of one mature cell type with another mature cell type
Answer: C. Dysplasia involves disordered cellular growth and maturation that is potentially reversible if the
inciting stimulus is removed
Rationale: Dysplasia is characterized by abnormal cell growth involving changes in cell size, shape, and organization
(pleomorphism, hyperchromasia, loss of normal polarity). It is a potentially reversible change if the causative stimulus
is removed (e.g., cessation of smoking, elimination of HPV infection). However, dysplasia is considered a premalignant
lesion because it can progress to carcinoma if the stimulus persists. Metaplasia involves replacement of one cell type
with another (not dysplasia).
8. A 60-year-old alcoholic presents with upper abdominal pain. Liver biopsy reveals hepatocytes with large
cytoplasmic vacuoles that stain positively with Oil Red O. This pathologic finding is best described as:
A. Coagulative necrosis of hepatocytes
B. Fatty change (steatosis) resulting from reversible cellular injury
C. Irreversible cellular injury with mitochondrial calcification
D. Metaplastic transformation of hepatic parenchyma
Answer: B. Fatty change (steatosis) resulting from reversible cellular injury
Rationale: Fatty change (steatosis) is a form of reversible cellular injury in which triglycerides accumulate within
hepatocytes. Alcohol metabolism generates excess NADH, which shifts hepatocyte metabolism toward fatty acid
synthesis and inhibits fatty acid oxidation. The resulting lipid vacuoles are initially reversible if the insult is removed,
but persistent fatty change can progress to steatohepatitis, fibrosis, and cirrhosis. Oil Red O stains neutral lipids,
confirming the fatty nature of the vacuoles.
II. Inflammation & Immunity (Q9–Q16)
9. A 28-year-old male sustains a deep laceration to his forearm. Within minutes, the area becomes red, warm,
swollen, and tender. Which of the following vascular events occurs FIRST in the acute inflammatory response?
A. Margination and pavementing of neutrophils along the vascular endothelium
B. Vasodilation of arterioles causing increased blood flow (hyperemia)
C. Transmigration (diapedesis) of leukocytes between endothelial cells
D. Fibrin mesh formation and exudate coagulation
3
, Answer: B. Vasodilation of arterioles causing increased blood flow (hyperemia)
Rationale: The acute inflammatory response begins with transient vasoconstriction lasting seconds, followed
immediately by vasodilation of arterioles, which causes increased blood flow (hyperemia) to the injured area. This
vasodilation is mediated by histamine, prostaglandins, and nitric oxide. The resulting increased blood flow causes
redness (erythema) and warmth. Vasodilation is followed by increased vascular permeability (causing edema/swelling),
then leukocyte margination, rolling, adhesion, and transmigration.
10. A patient with a severe allergic reaction to bee venom develops urticaria, bronchospasm, and hypotension
within minutes. Laboratory testing reveals elevated tryptase levels. Which hypersensitivity reaction best
describes this pathophysiology?
A. Type I: IgE-mediated immediate hypersensitivity
B. Type II: Antibody-dependent cytotoxic hypersensitivity
C. Type III: Immune complex-mediated hypersensitivity
D. Type IV: T-cell-mediated delayed hypersensitivity
Answer: A. Type I: IgE-mediated immediate hypersensitivity
Rationale: This is a Type I (immediate) hypersensitivity reaction mediated by IgE antibodies bound to Fc receptors on
mast cells and basophils. Upon re-exposure to the allergen (bee venom), cross-linking of IgE triggers mast cell
degranulation, releasing histamine, tryptase, leukotrienes, and prostaglandins. These mediators cause vasodilation,
increased vascular permeability (urticaria), bronchoconstriction (wheezing), and hypotension (anaphylactic shock).
Tryptase is a specific marker of mast cell activation.
11. A 35-year-old patient with rheumatic fever develops Aschoff bodies in the myocardium. These
granulomatous lesions are composed primarily of:
A. Neutrophils and fibrin
B. Macrophages (Anitschkow cells), lymphocytes, and occasional giant cells
C. Plasma cells and eosinophils
D. Fibroblasts and collagen deposition
Answer: B. Macrophages (Anitschkow cells), lymphocytes, and occasional giant cells
Rationale: Aschoff bodies are pathognomonic granulomatous lesions of rheumatic fever found in the myocardium. They
consist of a central area of fibrinoid necrosis surrounded by macrophages (called Anitschkow cells, which have
caterpillar-like nuclear chromatin), lymphocytes, plasma cells, and occasionally multinucleated giant cells (Aschoff
giant cells). This is a classic example of chronic inflammation with granuloma formation resulting from a Type II
hypersensitivity reaction (antibody against streptococcal M proteins cross-reacting with cardiac antigens).
12. A patient with nephrotic syndrome develops generalized edema. Analysis of the accumulated fluid reveals
low protein content and specific gravity < 1.012. This fluid is best characterized as:
A. An exudate due to increased vascular permeability
B. A transudate due to decreased oncotic pressure
C. A purulent exudate due to bacterial infection
D. A hemorrhagic exudate due to vascular rupture
Answer: B. A transudate due to decreased oncotic pressure
Rationale: Transudates occur when there is an imbalance in hydrostatic and oncotic pressures without significant
inflammation. In nephrotic syndrome, massive proteinuria leads to hypoalbuminemia and decreased plasma oncotic
pressure, causing fluid to move from the vascular compartment into the interstitial space. Transudates are characterized
by low protein content (< 3 g/dL), low specific gravity (< 1.012), and few cells. Exudates, in contrast, result from
increased vascular permeability due to inflammation and have high protein, high specific gravity, and many cells.
4
Final Exam Review Guide 2026-2027
Questions & Answers
100 Multiple Choice Questions with Answers & Rationales
Select the BEST answer. Each question = 1 point. Total: 100 points. Time: 180 minutes.
Name: Class/Section: Student ID:
____________________________ ____________________________ ____________________________
__ __ __
I. Cellular Adaptation, Injury & Necrosis (Q1–Q8)
1. A 68-year-old patient with a 20-year history of smoking presents with chronic cough. A bronchial biopsy
reveals replacement of the normal ciliated columnar epithelium with stratified squamous epithelium. This
cellular adaptation is best described as:
A. Atrophy
B. Hypertrophy
C. Metaplasia
D. Dysplasia
Answer: C. Metaplasia
Rationale: Metaplasia is the reversible replacement of one differentiated cell type with another. Chronic exposure to
cigarette smoke injures the respiratory epithelium, and the body replaces the vulnerable ciliated columnar cells with
more resilient stratified squamous epithelium. This is an adaptive mechanism, though the new tissue is more susceptible
to malignancy. Atrophy refers to decreased cell size; hypertrophy to increased cell size; and dysplasia to disordered,
potentially precancerous cellular changes.
2. A 55-year-old male with essential hypertension develops left ventricular hypertrophy. Which of the following
best describes the mechanism of this adaptation?
A. Increased workload leads to increased cell number through mitotic division
B. Increased workload leads to increased cell size by adding sarcomeres
C. Decreased blood supply leads to cellular shrinkage and organelle loss
D. Hormonal stimulation leads to glandular epithelial cell proliferation
Answer: B. Increased workload leads to increased cell size by adding sarcomeres
Rationale: Pathologic hypertrophy occurs when increased workload (such as from chronic hypertension causing
increased afterload) stimulates myocardial cells to increase in size by synthesizing more contractile proteins and
sarcomeres. This allows the heart to generate greater force. Unlike hyperplasia, which involves increased cell number,
hypertrophy involves increased cell size. Myocardial cells are terminally differentiated and cannot divide, so they adapt
by enlarging.
1
,3. A patient presents with a painful, swollen right lower extremity after prolonged immobilization following
femoral fracture. The tissue has a foul odor and is dark-colored. Which type of necrosis is most likely present?
A. Coagulative necrosis
B. Liquefactive necrosis
C. Caseous necrosis
D. Wet (liquefactive) gangrene
Answer: D. Wet (liquefactive) gangrene
Rationale: Wet gangrene develops when there is superimposed bacterial infection on necrotic tissue in a setting of
compromised arterial blood supply. The liquefactive component of bacterial enzymatic digestion combines with
coagulative necrosis from ischemia. This produces a foul-smelling, dark, swollen lesion. Dry gangrene is slow, dry, and
without infection. Coagulative necrosis preserves tissue architecture; liquefactive necrosis is typical of brain infarcts;
and caseous necrosis is characteristic of tuberculosis.
4. A researcher is studying programmed cell death and notes that the process involves cytochrome c release from
mitochondria, activation of caspases, cell shrinkage, and formation of apoptotic bodies without inflammation.
Which of the following distinguishes this process from necrosis?
A. Necrosis is ATP-dependent, while this process is ATP-independent
B. This process does not elicit an inflammatory response, while necrosis always triggers inflammation
C. Necrosis involves DNA fragmentation, while this process does not affect nuclear material
D. This process causes cellular swelling, while necrosis causes cellular shrinkage
Answer: B. This process does not elicit an inflammatory response, while necrosis always triggers inflammation
Rationale: Apoptosis (programmed cell death) is an energy-dependent, tightly regulated process that does NOT elicit an
inflammatory response. Apoptotic cells shrink, form membrane-bound apoptotic bodies that are rapidly phagocytosed
by macrophages, and undergo internucleosomal DNA cleavage. In contrast, necrosis involves loss of membrane
integrity, cellular swelling, release of intracellular contents that trigger an intense inflammatory reaction, and is
generally a pathologic process.
5. A patient with severe ischemic heart disease undergoes coronary artery bypass grafting. Upon reperfusion of
the previously ischemic myocardium, there is paradoxically increased tissue damage. Which of the following is
the primary mechanism of ischemia-reperfusion injury?
A. Accumulation of lactic acid during ischemia
B. Generation of reactive oxygen species (ROS) upon restoration of blood flow
C. Calcium depletion in the cytoplasm of myocardial cells
D. Activation of anaerobic metabolism pathways
Answer: B. Generation of reactive oxygen species (ROS) upon restoration of blood flow
Rationale: Ischemia-reperfusion injury occurs because the return of oxygenated blood to ischemic tissue paradoxically
causes additional damage. The primary mechanism is the burst of reactive oxygen species (ROS) generated by
mitochondrial dysfunction, xanthine oxidase activation, and NADPH oxidase in activated neutrophils. During ischemia,
ATP is depleted, leading to accumulation of hypoxanthine. Upon reperfusion, xanthine oxidase uses oxygen to convert
hypoxanthine to uric acid, generating superoxide radicals that cause lipid peroxidation, membrane damage, and cell
death.
6. A 42-year-old female with Cushing syndrome presents with muscle weakness in her proximal limbs. Muscle
biopsy reveals decreased myofibril size and reduced cytoplasmic volume. This finding is an example of:
A. Physiologic hypertrophy
B. Pathologic atrophy
2
, C. Hyperplasia
D. Metaplasia
Answer: B. Pathologic atrophy
Rationale: Pathologic atrophy is a decrease in cell size due to adverse stimuli. Cushing syndrome (excess
glucocorticoids) causes protein catabolism and decreased protein synthesis, leading to muscle atrophy — particularly in
proximal muscles (proximal myopathy). Glucocorticoids stimulate ubiquitin-proteasome pathways and inhibit protein
synthesis. This is pathologic because it results from hormonal excess rather than normal physiologic disuse or aging.
7. A 45-year-old woman undergoes a Pap smear that reveals abnormal epithelial cells with nuclear
hyperchromasia, pleomorphism, and disorganized maturation. Biopsy confirms dysplasia of the cervix. Which
statement best characterizes dysplasia?
A. Dysplasia is always irreversible and definitively progresses to carcinoma
B. Dysplasia represents a fully malignant transformation with invasive potential
C. Dysplasia involves disordered cellular growth and maturation that is potentially reversible if the
inciting stimulus is removed
D. Dysplasia is characterized by replacement of one mature cell type with another mature cell type
Answer: C. Dysplasia involves disordered cellular growth and maturation that is potentially reversible if the
inciting stimulus is removed
Rationale: Dysplasia is characterized by abnormal cell growth involving changes in cell size, shape, and organization
(pleomorphism, hyperchromasia, loss of normal polarity). It is a potentially reversible change if the causative stimulus
is removed (e.g., cessation of smoking, elimination of HPV infection). However, dysplasia is considered a premalignant
lesion because it can progress to carcinoma if the stimulus persists. Metaplasia involves replacement of one cell type
with another (not dysplasia).
8. A 60-year-old alcoholic presents with upper abdominal pain. Liver biopsy reveals hepatocytes with large
cytoplasmic vacuoles that stain positively with Oil Red O. This pathologic finding is best described as:
A. Coagulative necrosis of hepatocytes
B. Fatty change (steatosis) resulting from reversible cellular injury
C. Irreversible cellular injury with mitochondrial calcification
D. Metaplastic transformation of hepatic parenchyma
Answer: B. Fatty change (steatosis) resulting from reversible cellular injury
Rationale: Fatty change (steatosis) is a form of reversible cellular injury in which triglycerides accumulate within
hepatocytes. Alcohol metabolism generates excess NADH, which shifts hepatocyte metabolism toward fatty acid
synthesis and inhibits fatty acid oxidation. The resulting lipid vacuoles are initially reversible if the insult is removed,
but persistent fatty change can progress to steatohepatitis, fibrosis, and cirrhosis. Oil Red O stains neutral lipids,
confirming the fatty nature of the vacuoles.
II. Inflammation & Immunity (Q9–Q16)
9. A 28-year-old male sustains a deep laceration to his forearm. Within minutes, the area becomes red, warm,
swollen, and tender. Which of the following vascular events occurs FIRST in the acute inflammatory response?
A. Margination and pavementing of neutrophils along the vascular endothelium
B. Vasodilation of arterioles causing increased blood flow (hyperemia)
C. Transmigration (diapedesis) of leukocytes between endothelial cells
D. Fibrin mesh formation and exudate coagulation
3
, Answer: B. Vasodilation of arterioles causing increased blood flow (hyperemia)
Rationale: The acute inflammatory response begins with transient vasoconstriction lasting seconds, followed
immediately by vasodilation of arterioles, which causes increased blood flow (hyperemia) to the injured area. This
vasodilation is mediated by histamine, prostaglandins, and nitric oxide. The resulting increased blood flow causes
redness (erythema) and warmth. Vasodilation is followed by increased vascular permeability (causing edema/swelling),
then leukocyte margination, rolling, adhesion, and transmigration.
10. A patient with a severe allergic reaction to bee venom develops urticaria, bronchospasm, and hypotension
within minutes. Laboratory testing reveals elevated tryptase levels. Which hypersensitivity reaction best
describes this pathophysiology?
A. Type I: IgE-mediated immediate hypersensitivity
B. Type II: Antibody-dependent cytotoxic hypersensitivity
C. Type III: Immune complex-mediated hypersensitivity
D. Type IV: T-cell-mediated delayed hypersensitivity
Answer: A. Type I: IgE-mediated immediate hypersensitivity
Rationale: This is a Type I (immediate) hypersensitivity reaction mediated by IgE antibodies bound to Fc receptors on
mast cells and basophils. Upon re-exposure to the allergen (bee venom), cross-linking of IgE triggers mast cell
degranulation, releasing histamine, tryptase, leukotrienes, and prostaglandins. These mediators cause vasodilation,
increased vascular permeability (urticaria), bronchoconstriction (wheezing), and hypotension (anaphylactic shock).
Tryptase is a specific marker of mast cell activation.
11. A 35-year-old patient with rheumatic fever develops Aschoff bodies in the myocardium. These
granulomatous lesions are composed primarily of:
A. Neutrophils and fibrin
B. Macrophages (Anitschkow cells), lymphocytes, and occasional giant cells
C. Plasma cells and eosinophils
D. Fibroblasts and collagen deposition
Answer: B. Macrophages (Anitschkow cells), lymphocytes, and occasional giant cells
Rationale: Aschoff bodies are pathognomonic granulomatous lesions of rheumatic fever found in the myocardium. They
consist of a central area of fibrinoid necrosis surrounded by macrophages (called Anitschkow cells, which have
caterpillar-like nuclear chromatin), lymphocytes, plasma cells, and occasionally multinucleated giant cells (Aschoff
giant cells). This is a classic example of chronic inflammation with granuloma formation resulting from a Type II
hypersensitivity reaction (antibody against streptococcal M proteins cross-reacting with cardiac antigens).
12. A patient with nephrotic syndrome develops generalized edema. Analysis of the accumulated fluid reveals
low protein content and specific gravity < 1.012. This fluid is best characterized as:
A. An exudate due to increased vascular permeability
B. A transudate due to decreased oncotic pressure
C. A purulent exudate due to bacterial infection
D. A hemorrhagic exudate due to vascular rupture
Answer: B. A transudate due to decreased oncotic pressure
Rationale: Transudates occur when there is an imbalance in hydrostatic and oncotic pressures without significant
inflammation. In nephrotic syndrome, massive proteinuria leads to hypoalbuminemia and decreased plasma oncotic
pressure, causing fluid to move from the vascular compartment into the interstitial space. Transudates are characterized
by low protein content (< 3 g/dL), low specific gravity (< 1.012), and few cells. Exudates, in contrast, result from
increased vascular permeability due to inflammation and have high protein, high specific gravity, and many cells.
4
