NUR 2063 Essentials of Pathophysiology Exam 1 2026/2027
Actual Exam | 150 Real Exam Questions & Correct Verified
Answers with Detailed Rationales | Rasmussen | Pass
Guaranteed - A+ Graded EXAM with Questions and
Answers/Plus a Rationale Updated 2026 A+/Instant Download
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EXAM COVERAGE
1. Cellular Biology, Adaptation, Injury, and Death Mechanisms
2. Genetic Alterations, Chromosomal Abnormalities, and Epigenetic Influences
3. Fluid, Electrolyte, and Acid-Base Homeostatic Imbalances
4. Inflammation, Innate Immunity, and Wound Healing Pathophysiology
5. Adaptive Immunity, Hypersensitivity Reactions, and Immunodeficiencies
1. A 46-year-old male with a 30-pack-year smoking history undergoes routine bronchoscopy.
Histological examination of his bronchial mucosa reveals replacement of normal ciliated
pseudostratified columnar epithelium with stratified squamous epithelium. What
pathophysiological process does this represent?
A. Cellular atrophy secondary to chronic ischemic deprivation.
B. Metaplasia as a reversible, adaptive substitution of one adult cell type for another.
C. Dysplasia characterized by irreversible genetic mutations and loss of tissue organization.
D. Hyperplasia driven by excessive hormonal stimulation and uncontrolled cell division.
CORRECT ANSWER : B
Rationale: Metaplasia is a reversible structural adaptation where one differentiated cell type is
replaced by another cell type better suited to withstand chronic environmental irritation, such as
cigarette smoke. It is reversible if the irritant is removed, unlike dysplasia, which involves
disordered growth and pre-malignant atypia.
,2. A 62-year-old female presents with acute left ventricular failure following a massive myocardial
infarction. Myocardial biopsy reveals cellular swelling, severe mitochondrial dysfunction, and
rupture of lysosomal membranes. What is the fundamental mechanism driving this initial cellular
change?
A. Upregulation of anti-apoptotic Bcl-2 proteins leading to unchecked cellular proliferation.
B. Depletion of intracellular ATP resulting in failure of the Na+/K+ ATPase pump and
cellular edema.
C. Increased intracellular potassium concentration driving excessive water retention and lysis.
D. Activation of extracellular matrix remodeling pathways by resident fibroblasts.
CORRECT ANSWER : B
Rationale: Ischemia rapidly halts oxidative phosphorylation, causing profound ATP depletion.
This cripples the Na+/K+ ATPase membrane pump, causing intracellular accumulation of
sodium and water, resulting in acute cellular swelling (oncosis), whereas potassium leaks out.
3. A 55-year-old chronic alcoholic develops severe hepatic steatosis (fatty liver). Which subcellular
organelle is primarily impaired in its ability to synthesize lipoproteins, leading to the intracellular
accumulation of triglycerides?
A. Mitochondria producing insufficient ATP for basic metabolic needs.
B. Rough and smooth endoplasmic reticulum and Golgi apparatus dysfunction.
C. Lysosomes failing to digest excess glycogen stores.
D. Peroxisomes lacking catalase enzymes required for fatty acid oxidation.
CORRECT ANSWER : B
Rationale: Hepatocytes convert free fatty acids into triglycerides, which must bind with
apolipoproteins synthesized in the endoplasmic reticulum to form lipoproteins for export.
Alcohol toxicity impairs endoplasmic reticulum function and apolipoprotein synthesis, trapping
triglycerides inside hepatocytes.
4. A 28-year-old male sustains a crush injury to his right lower extremity during a construction
accident, resulting in compartment syndrome and subsequent rhabdomyolysis. Upon reperfusion
of the ischemic tissue, cellular damage is paradoxically exacerbated. Which cytotoxic
mechanism is primarily responsible for reperfusion injury?
A. Rapid intracellular accumulation of exogenous bicarbonate ions.
, B. Generation of reactive oxygen species (free radicals) that damage cellular membranes
and DNA.
C. Massive upregulation of protein synthesis by ribosomes.
D. Depletion of intracellular calcium ions halting all enzymatic activity.
CORRECT ANSWER : B
Rationale: Reperfusion of ischemic tissue introduces a sudden influx of oxygen, which damaged
cellular enzyme systems convert into reactive oxygen species and free radicals. These molecules
attack membrane lipids via peroxidation, worsening tissue injury.
5. A pathologist examines a tissue sample from a patient who died of a mesenteric infarct
(coagulative necrosis of the bowel). What is the primary microscopic hallmark of coagulative
necrosis?
A. Complete liquefaction of tissue into a viscous fluid mass due to leukocyte enzymes.
B. Preservation of the general structural outline of the necrotic cells for days due to
denaturation of structural proteins and enzymes.
C. Caseous cottage-cheese-like architecture surrounded by a distinct inflammatory granuloma.
D. Enzymatic fat digestion combined with calcium soap precipitation.
CORRECT ANSWER : B
Rationale: Coagulative necrosis, typical of ischemic injury in organs like the heart and kidneys,
occurs when protein denaturation outlasts enzymatic lysis, preserving tissue architecture
temporarily. Liquefactive necrosis involves enzymatic dissolution, seen in the brain.
6. A 70-year-old female with chronic atherosclerosis of the lower extremities experiences dry
gangrene of the right great toe. What pathophysiological process distinguishes dry gangrene
from wet gangrene?
A. Massive bacterial invasion and liquefactive necrosis secondary to neutrophil infiltration.
B. Coagulative necrosis resulting from ischemic coagulopathy without secondary bacterial
infection.
C. Uncontrolled cellular replication driven by viral oncogenes.
D. Caseous necrosis localized strictly to dermal sweat glands.
CORRECT ANSWER : B
Actual Exam | 150 Real Exam Questions & Correct Verified
Answers with Detailed Rationales | Rasmussen | Pass
Guaranteed - A+ Graded EXAM with Questions and
Answers/Plus a Rationale Updated 2026 A+/Instant Download
EXAM COVERAGE
1. Cellular Biology, Adaptation, Injury, and Death Mechanisms
2. Genetic Alterations, Chromosomal Abnormalities, and Epigenetic Influences
3. Fluid, Electrolyte, and Acid-Base Homeostatic Imbalances
4. Inflammation, Innate Immunity, and Wound Healing Pathophysiology
5. Adaptive Immunity, Hypersensitivity Reactions, and Immunodeficiencies
1. A 46-year-old male with a 30-pack-year smoking history undergoes routine bronchoscopy.
Histological examination of his bronchial mucosa reveals replacement of normal ciliated
pseudostratified columnar epithelium with stratified squamous epithelium. What
pathophysiological process does this represent?
A. Cellular atrophy secondary to chronic ischemic deprivation.
B. Metaplasia as a reversible, adaptive substitution of one adult cell type for another.
C. Dysplasia characterized by irreversible genetic mutations and loss of tissue organization.
D. Hyperplasia driven by excessive hormonal stimulation and uncontrolled cell division.
CORRECT ANSWER : B
Rationale: Metaplasia is a reversible structural adaptation where one differentiated cell type is
replaced by another cell type better suited to withstand chronic environmental irritation, such as
cigarette smoke. It is reversible if the irritant is removed, unlike dysplasia, which involves
disordered growth and pre-malignant atypia.
,2. A 62-year-old female presents with acute left ventricular failure following a massive myocardial
infarction. Myocardial biopsy reveals cellular swelling, severe mitochondrial dysfunction, and
rupture of lysosomal membranes. What is the fundamental mechanism driving this initial cellular
change?
A. Upregulation of anti-apoptotic Bcl-2 proteins leading to unchecked cellular proliferation.
B. Depletion of intracellular ATP resulting in failure of the Na+/K+ ATPase pump and
cellular edema.
C. Increased intracellular potassium concentration driving excessive water retention and lysis.
D. Activation of extracellular matrix remodeling pathways by resident fibroblasts.
CORRECT ANSWER : B
Rationale: Ischemia rapidly halts oxidative phosphorylation, causing profound ATP depletion.
This cripples the Na+/K+ ATPase membrane pump, causing intracellular accumulation of
sodium and water, resulting in acute cellular swelling (oncosis), whereas potassium leaks out.
3. A 55-year-old chronic alcoholic develops severe hepatic steatosis (fatty liver). Which subcellular
organelle is primarily impaired in its ability to synthesize lipoproteins, leading to the intracellular
accumulation of triglycerides?
A. Mitochondria producing insufficient ATP for basic metabolic needs.
B. Rough and smooth endoplasmic reticulum and Golgi apparatus dysfunction.
C. Lysosomes failing to digest excess glycogen stores.
D. Peroxisomes lacking catalase enzymes required for fatty acid oxidation.
CORRECT ANSWER : B
Rationale: Hepatocytes convert free fatty acids into triglycerides, which must bind with
apolipoproteins synthesized in the endoplasmic reticulum to form lipoproteins for export.
Alcohol toxicity impairs endoplasmic reticulum function and apolipoprotein synthesis, trapping
triglycerides inside hepatocytes.
4. A 28-year-old male sustains a crush injury to his right lower extremity during a construction
accident, resulting in compartment syndrome and subsequent rhabdomyolysis. Upon reperfusion
of the ischemic tissue, cellular damage is paradoxically exacerbated. Which cytotoxic
mechanism is primarily responsible for reperfusion injury?
A. Rapid intracellular accumulation of exogenous bicarbonate ions.
, B. Generation of reactive oxygen species (free radicals) that damage cellular membranes
and DNA.
C. Massive upregulation of protein synthesis by ribosomes.
D. Depletion of intracellular calcium ions halting all enzymatic activity.
CORRECT ANSWER : B
Rationale: Reperfusion of ischemic tissue introduces a sudden influx of oxygen, which damaged
cellular enzyme systems convert into reactive oxygen species and free radicals. These molecules
attack membrane lipids via peroxidation, worsening tissue injury.
5. A pathologist examines a tissue sample from a patient who died of a mesenteric infarct
(coagulative necrosis of the bowel). What is the primary microscopic hallmark of coagulative
necrosis?
A. Complete liquefaction of tissue into a viscous fluid mass due to leukocyte enzymes.
B. Preservation of the general structural outline of the necrotic cells for days due to
denaturation of structural proteins and enzymes.
C. Caseous cottage-cheese-like architecture surrounded by a distinct inflammatory granuloma.
D. Enzymatic fat digestion combined with calcium soap precipitation.
CORRECT ANSWER : B
Rationale: Coagulative necrosis, typical of ischemic injury in organs like the heart and kidneys,
occurs when protein denaturation outlasts enzymatic lysis, preserving tissue architecture
temporarily. Liquefactive necrosis involves enzymatic dissolution, seen in the brain.
6. A 70-year-old female with chronic atherosclerosis of the lower extremities experiences dry
gangrene of the right great toe. What pathophysiological process distinguishes dry gangrene
from wet gangrene?
A. Massive bacterial invasion and liquefactive necrosis secondary to neutrophil infiltration.
B. Coagulative necrosis resulting from ischemic coagulopathy without secondary bacterial
infection.
C. Uncontrolled cellular replication driven by viral oncogenes.
D. Caseous necrosis localized strictly to dermal sweat glands.
CORRECT ANSWER : B
