Final Exam: NUR 2063
Essentials of Pathophysiology
Review Guide Questions and Verified Answers
100% Correct | Grade A
Rasmussen University
Latest Update
100 Comprehensive Questions | 7 Sections
Section 1: Cellular Adaptation, Injury, Neoplasia, Fluid/Electrolyte/Acid-Base, and
Inflammation/Immunity
Q1: A 68-year-old patient with a history of chronic smoking presents with persistent cough and weight
loss. A biopsy reveals squamous cell carcinoma. Which cellular adaptation most likely preceded the
malignant transformation in this patient's bronchial epithelium?
A. Atrophy
B. Hypertrophy
C. Metaplasia [CORRECT]
D. Hyperplasia
Correct Answer: C
Rationale: C. Metaplasia is the most likely preceding adaptation. Chronic smoking irritates the bronchial epithelium,
causing the normal ciliated columnar epithelium to transform into stratified squamous epithelium (squamous metaplasia).
This adaptive change is reversible initially but can progress to dysplasia and eventually malignancy if the irritant persists.
Atrophy is a decrease in cell size, not a change in cell type. Hypertrophy is an increase in cell size without cell division.
,NUR 2063 Essentials of Pathophysiology | Final Exam | Rasmussen University 2026/2027
Hyperplasia is an increase in the number of cells, which may occur but does not involve the change in cell differentiation
seen in metaplasia.
Q2: A nurse is caring for a patient who has been bedridden for 6 weeks following a stroke. Assessment
reveals decreased muscle mass and weakness in the lower extremities. Which type of cellular adaptation is
occurring?
A. Physiologic hypertrophy
B. Pathologic atrophy [CORRECT]
C. Pathologic hyperplasia
D. Metaplasia
Correct Answer: B
Rationale: B. Pathologic atrophy is the correct answer. Disuse atrophy occurs when there is a lack of normal mechanical or
neural stimulation, as seen with prolonged bed rest or immobilization. The muscle cells decrease in size and organelle
content, leading to reduced muscle mass and weakness. This is pathologic because it results from disease or injury (the stroke
and subsequent immobility). Physiologic hypertrophy involves an increase in cell size due to normal hormonal or functional
demands (e.g., enlarged uterus during pregnancy). Pathologic hyperplasia is an abnormal increase in cell number.
Metaplasia is a reversible change from one differentiated cell type to another.
Q3: A 45-year-old patient with long-standing hypertension presents with left ventricular hypertrophy on
echocardiogram. Which cellular adaptation mechanism best explains the thickening of the left ventricular
wall?
A. Hyperplasia of cardiomyocytes
B. Hypertrophy of cardiomyocytes [CORRECT]
C. Metaplasia of cardiac tissue
D. Dysplasia of the myocardium
Correct Answer: B
Rationale: B. Hypertrophy of cardiomyocytes is the correct mechanism. Cardiac muscle cells (cardiomyocytes) are
terminally differentiated and cannot undergo hyperplasia (cell division) in response to increased workload. Instead, they
increase in size (hypertrophy) by synthesizing more sarcomeres and organelles to compensate for the increased afterload
from chronic hypertension. Hyperplasia is incorrect because adult cardiac cells lose the ability to divide. Metaplasia involves
a change in cell type, which does not occur here. Dysplasia refers to abnormal cell maturation and is a preneoplastic change,
not an adaptive response to mechanical stress.
Q4: A 50-year-old woman undergoes an endometrial biopsy that reveals endometrial hyperplasia. The
pathologist notes atypical cells. Which statement best describes the clinical significance of atypical
hyperplasia?
A. It is a fully reversible change with no cancer risk
B. It is considered a premalignant condition with increased risk of endometrial cancer [CORRECT]
C. It represents metastatic spread from another primary site
D. It is a normal physiologic response to estrogen stimulation
Correct Answer: B
Rationale: B. Atypical hyperplasia is considered a premalignant condition. Unlike simple or typical hyperplasia, atypical
hyperplasia involves architectural and cytologic abnormalities that significantly increase the risk of progression to
Page 1
,NUR 2063 Essentials of Pathophysiology | Final Exam | Rasmussen University 2026/2027
endometrial carcinoma. The atypical cells demonstrate disorganized growth patterns and nuclear abnormalities. It is not
fully reversible without intervention and carries a substantially elevated cancer risk compared to typical hyperplasia.
Metastatic spread refers to cancer that has spread from another site, which is unrelated to hyperplasia. While estrogen
stimulation can cause typical hyperplasia, the presence of atypical cells elevates this beyond a normal physiologic response.
Q5: A patient presents with severe chest pain and is diagnosed with an acute myocardial infarction. The
cardiologist explains that the ischemic injury causes cellular damage. Which statement correctly describes
the sequence of events in ischemic cell injury?
A. Mitochondrial damage occurs first, followed by sodium-potassium pump failure
B. ATP depletion occurs first, leading to sodium-potassium pump failure and calcium influx [CORRECT]
C. Calcium influx occurs first, followed by ATP generation and cell recovery
D. Ribosomal detachment occurs first, leading to increased protein synthesis
Correct Answer: B
Rationale: B. ATP depletion is the initiating event in ischemic cell injury. When blood flow is interrupted, oxygen delivery
ceases and oxidative phosphorylation stops, causing ATP levels to drop rapidly. Without adequate ATP, the
sodium-potassium pump (Na+/K+-ATPase) fails, allowing sodium to accumulate intracellularly and potassium to leave the
cell. The resulting osmotic gradient causes water influx and cellular swelling. Concurrently, calcium pumps fail, leading to
intracellular calcium accumulation that activates destructive enzymes (phospholipases, proteases, endonucleases).
Mitochondrial damage is a consequence, not the cause, of the injury cascade. Ribosomal detachment reduces protein
synthesis; it does not increase it.
Q6: A 30-year-old patient suffers a crush injury to the lower extremity. Upon release of compression, the
affected tissue shows worsening damage despite restored blood flow. Which pathophysiologic mechanism
best explains this phenomenon?
A. Coagulative necrosis from direct trauma
B. Reperfusion injury from oxygen free radical generation [CORRECT]
C. Liquefactive necrosis from bacterial contamination
D. Fat necrosis from tissue disruption
Correct Answer: B
Rationale: B. Reperfusion injury is the correct mechanism. When blood flow is restored to previously ischemic tissue, the
returning oxygen is partially reduced to form reactive oxygen species (ROS) and free radicals. These highly reactive
molecules cause lipid peroxidation of cell membranes, protein denaturation, and DNA damage. The paradox is that the
restoration of blood flow, while necessary for tissue survival, causes additional damage beyond what the original ischemia
produced. Neutrophils also accumulate in reperfused tissue and release additional ROS and proteolytic enzymes.
Coagulative necrosis results from ischemia itself, not from reperfusion. Liquefactive necrosis is caused by enzymatic
degradation, typically from bacterial infection. Fat necrosis occurs specifically in adipose tissue due to lipase activity.
Q7: A forensic pathologist examines a tissue sample from a patient who died of a myocardial infarction.
Microscopic examination reveals preserved cell outlines with loss of nuclear detail and eosinophilic
cytoplasm. Which type of necrosis is present?
A. Liquefactive necrosis
B. Coagulative necrosis [CORRECT]
C. Caseous necrosis
D. Fat necrosis
Page 2
, NUR 2063 Essentials of Pathophysiology | Final Exam | Rasmussen University 2026/2027
Correct Answer: B
Rationale: B. Coagulative necrosis is the correct diagnosis. This pattern is characteristic of ischemic injury in most solid
organs, especially the heart, kidneys, and spleen. The underlying mechanism involves protein denaturation and enzymatic
digestion that is less complete than in liquefactive necrosis, so the basic cellular architecture is preserved as a "ghost"
outline of the dead cells. The nuclei disappear (karyolysis) or shrink (pyknosis), and the cytoplasm becomes eosinophilic.
Liquefactive necrosis, in contrast, results in complete dissolution of tissue, commonly seen in brain infarcts and bacterial
infections. Caseous necrosis has a cheese-like appearance and is characteristic of tuberculosis. Fat necrosis involves
saponification of fat and is seen in acute pancreatitis.
Q8: A patient with active tuberculosis has a lung biopsy that shows a granuloma with central area of
necrosis containing necrotic debris and epithelioid macrophages. Which type of necrosis is characteristic of
this finding?
A. Coagulative necrosis
B. Liquefactive necrosis
C. Caseous necrosis [CORRECT]
D. Gangrenous necrosis
Correct Answer: C
Rationale: C. Caseous necrosis is the characteristic necrotic pattern in tuberculosis granulomas. It has a distinctive
cheese-like (caseous) appearance on gross examination, appearing soft and granular. Microscopically, the necrotic area
shows amorphous, granular debris with complete loss of cellular structure, surrounded by epithelioid macrophages,
Langhans giant cells, and lymphocytes. This pattern is a combination of coagulative and liquefactive necrosis features.
Coagulative necrosis preserves tissue architecture and is seen in infarcts. Liquefactive necrosis completely digests tissue and
is seen in brain infarcts and bacterial abscesses. Gangrenous necrosis refers to necrosis of a limb or organ, typically with
superimposed bacterial infection.
Q9: A nurse is reviewing a patient's laboratory results and notes a potassium level of 6.8 mEq/L. The
patient complains of muscle weakness and palpitations. The nurse recognizes that hyperkalemia is the
most life-threatening electrolyte imbalance primarily because of its effect on which organ system?
A. Central nervous system causing seizures
B. Hepatic system causing liver failure
C. Cardiovascular system causing cardiac arrest [CORRECT]
D. Pulmonary system causing respiratory failure
Correct Answer: C
Rationale: C. Hyperkalemia is the most life-threatening electrolyte imbalance because of its direct effect on the cardiac
conduction system. Elevated potassium alters the resting membrane potential of cardiac myocytes, leading to depolarization.
ECG changes progress from peaked T waves and widened QRS complexes to sine wave patterns, and ultimately ventricular
fibrillation or asystole (cardiac arrest). The muscle weakness reported is due to hyperpolarization of skeletal muscle cells,
making them less excitable. While severe electrolyte imbalances can affect multiple systems, hyperkalemia is uniquely
dangerous because it can cause sudden cardiac death. Seizures are more commonly associated with severe hyponatremia.
Liver failure is not a direct consequence of hyperkalemia. Respiratory failure is more associated with hypokalemia affecting
respiratory muscle function.
Q10: A patient with diabetic ketoacidosis (DKA) presents with deep, rapid respirations (Kussmaul
respirations). Which acid-base disorder is present, and what is the compensatory mechanism?
Page 3
Essentials of Pathophysiology
Review Guide Questions and Verified Answers
100% Correct | Grade A
Rasmussen University
Latest Update
100 Comprehensive Questions | 7 Sections
Section 1: Cellular Adaptation, Injury, Neoplasia, Fluid/Electrolyte/Acid-Base, and
Inflammation/Immunity
Q1: A 68-year-old patient with a history of chronic smoking presents with persistent cough and weight
loss. A biopsy reveals squamous cell carcinoma. Which cellular adaptation most likely preceded the
malignant transformation in this patient's bronchial epithelium?
A. Atrophy
B. Hypertrophy
C. Metaplasia [CORRECT]
D. Hyperplasia
Correct Answer: C
Rationale: C. Metaplasia is the most likely preceding adaptation. Chronic smoking irritates the bronchial epithelium,
causing the normal ciliated columnar epithelium to transform into stratified squamous epithelium (squamous metaplasia).
This adaptive change is reversible initially but can progress to dysplasia and eventually malignancy if the irritant persists.
Atrophy is a decrease in cell size, not a change in cell type. Hypertrophy is an increase in cell size without cell division.
,NUR 2063 Essentials of Pathophysiology | Final Exam | Rasmussen University 2026/2027
Hyperplasia is an increase in the number of cells, which may occur but does not involve the change in cell differentiation
seen in metaplasia.
Q2: A nurse is caring for a patient who has been bedridden for 6 weeks following a stroke. Assessment
reveals decreased muscle mass and weakness in the lower extremities. Which type of cellular adaptation is
occurring?
A. Physiologic hypertrophy
B. Pathologic atrophy [CORRECT]
C. Pathologic hyperplasia
D. Metaplasia
Correct Answer: B
Rationale: B. Pathologic atrophy is the correct answer. Disuse atrophy occurs when there is a lack of normal mechanical or
neural stimulation, as seen with prolonged bed rest or immobilization. The muscle cells decrease in size and organelle
content, leading to reduced muscle mass and weakness. This is pathologic because it results from disease or injury (the stroke
and subsequent immobility). Physiologic hypertrophy involves an increase in cell size due to normal hormonal or functional
demands (e.g., enlarged uterus during pregnancy). Pathologic hyperplasia is an abnormal increase in cell number.
Metaplasia is a reversible change from one differentiated cell type to another.
Q3: A 45-year-old patient with long-standing hypertension presents with left ventricular hypertrophy on
echocardiogram. Which cellular adaptation mechanism best explains the thickening of the left ventricular
wall?
A. Hyperplasia of cardiomyocytes
B. Hypertrophy of cardiomyocytes [CORRECT]
C. Metaplasia of cardiac tissue
D. Dysplasia of the myocardium
Correct Answer: B
Rationale: B. Hypertrophy of cardiomyocytes is the correct mechanism. Cardiac muscle cells (cardiomyocytes) are
terminally differentiated and cannot undergo hyperplasia (cell division) in response to increased workload. Instead, they
increase in size (hypertrophy) by synthesizing more sarcomeres and organelles to compensate for the increased afterload
from chronic hypertension. Hyperplasia is incorrect because adult cardiac cells lose the ability to divide. Metaplasia involves
a change in cell type, which does not occur here. Dysplasia refers to abnormal cell maturation and is a preneoplastic change,
not an adaptive response to mechanical stress.
Q4: A 50-year-old woman undergoes an endometrial biopsy that reveals endometrial hyperplasia. The
pathologist notes atypical cells. Which statement best describes the clinical significance of atypical
hyperplasia?
A. It is a fully reversible change with no cancer risk
B. It is considered a premalignant condition with increased risk of endometrial cancer [CORRECT]
C. It represents metastatic spread from another primary site
D. It is a normal physiologic response to estrogen stimulation
Correct Answer: B
Rationale: B. Atypical hyperplasia is considered a premalignant condition. Unlike simple or typical hyperplasia, atypical
hyperplasia involves architectural and cytologic abnormalities that significantly increase the risk of progression to
Page 1
,NUR 2063 Essentials of Pathophysiology | Final Exam | Rasmussen University 2026/2027
endometrial carcinoma. The atypical cells demonstrate disorganized growth patterns and nuclear abnormalities. It is not
fully reversible without intervention and carries a substantially elevated cancer risk compared to typical hyperplasia.
Metastatic spread refers to cancer that has spread from another site, which is unrelated to hyperplasia. While estrogen
stimulation can cause typical hyperplasia, the presence of atypical cells elevates this beyond a normal physiologic response.
Q5: A patient presents with severe chest pain and is diagnosed with an acute myocardial infarction. The
cardiologist explains that the ischemic injury causes cellular damage. Which statement correctly describes
the sequence of events in ischemic cell injury?
A. Mitochondrial damage occurs first, followed by sodium-potassium pump failure
B. ATP depletion occurs first, leading to sodium-potassium pump failure and calcium influx [CORRECT]
C. Calcium influx occurs first, followed by ATP generation and cell recovery
D. Ribosomal detachment occurs first, leading to increased protein synthesis
Correct Answer: B
Rationale: B. ATP depletion is the initiating event in ischemic cell injury. When blood flow is interrupted, oxygen delivery
ceases and oxidative phosphorylation stops, causing ATP levels to drop rapidly. Without adequate ATP, the
sodium-potassium pump (Na+/K+-ATPase) fails, allowing sodium to accumulate intracellularly and potassium to leave the
cell. The resulting osmotic gradient causes water influx and cellular swelling. Concurrently, calcium pumps fail, leading to
intracellular calcium accumulation that activates destructive enzymes (phospholipases, proteases, endonucleases).
Mitochondrial damage is a consequence, not the cause, of the injury cascade. Ribosomal detachment reduces protein
synthesis; it does not increase it.
Q6: A 30-year-old patient suffers a crush injury to the lower extremity. Upon release of compression, the
affected tissue shows worsening damage despite restored blood flow. Which pathophysiologic mechanism
best explains this phenomenon?
A. Coagulative necrosis from direct trauma
B. Reperfusion injury from oxygen free radical generation [CORRECT]
C. Liquefactive necrosis from bacterial contamination
D. Fat necrosis from tissue disruption
Correct Answer: B
Rationale: B. Reperfusion injury is the correct mechanism. When blood flow is restored to previously ischemic tissue, the
returning oxygen is partially reduced to form reactive oxygen species (ROS) and free radicals. These highly reactive
molecules cause lipid peroxidation of cell membranes, protein denaturation, and DNA damage. The paradox is that the
restoration of blood flow, while necessary for tissue survival, causes additional damage beyond what the original ischemia
produced. Neutrophils also accumulate in reperfused tissue and release additional ROS and proteolytic enzymes.
Coagulative necrosis results from ischemia itself, not from reperfusion. Liquefactive necrosis is caused by enzymatic
degradation, typically from bacterial infection. Fat necrosis occurs specifically in adipose tissue due to lipase activity.
Q7: A forensic pathologist examines a tissue sample from a patient who died of a myocardial infarction.
Microscopic examination reveals preserved cell outlines with loss of nuclear detail and eosinophilic
cytoplasm. Which type of necrosis is present?
A. Liquefactive necrosis
B. Coagulative necrosis [CORRECT]
C. Caseous necrosis
D. Fat necrosis
Page 2
, NUR 2063 Essentials of Pathophysiology | Final Exam | Rasmussen University 2026/2027
Correct Answer: B
Rationale: B. Coagulative necrosis is the correct diagnosis. This pattern is characteristic of ischemic injury in most solid
organs, especially the heart, kidneys, and spleen. The underlying mechanism involves protein denaturation and enzymatic
digestion that is less complete than in liquefactive necrosis, so the basic cellular architecture is preserved as a "ghost"
outline of the dead cells. The nuclei disappear (karyolysis) or shrink (pyknosis), and the cytoplasm becomes eosinophilic.
Liquefactive necrosis, in contrast, results in complete dissolution of tissue, commonly seen in brain infarcts and bacterial
infections. Caseous necrosis has a cheese-like appearance and is characteristic of tuberculosis. Fat necrosis involves
saponification of fat and is seen in acute pancreatitis.
Q8: A patient with active tuberculosis has a lung biopsy that shows a granuloma with central area of
necrosis containing necrotic debris and epithelioid macrophages. Which type of necrosis is characteristic of
this finding?
A. Coagulative necrosis
B. Liquefactive necrosis
C. Caseous necrosis [CORRECT]
D. Gangrenous necrosis
Correct Answer: C
Rationale: C. Caseous necrosis is the characteristic necrotic pattern in tuberculosis granulomas. It has a distinctive
cheese-like (caseous) appearance on gross examination, appearing soft and granular. Microscopically, the necrotic area
shows amorphous, granular debris with complete loss of cellular structure, surrounded by epithelioid macrophages,
Langhans giant cells, and lymphocytes. This pattern is a combination of coagulative and liquefactive necrosis features.
Coagulative necrosis preserves tissue architecture and is seen in infarcts. Liquefactive necrosis completely digests tissue and
is seen in brain infarcts and bacterial abscesses. Gangrenous necrosis refers to necrosis of a limb or organ, typically with
superimposed bacterial infection.
Q9: A nurse is reviewing a patient's laboratory results and notes a potassium level of 6.8 mEq/L. The
patient complains of muscle weakness and palpitations. The nurse recognizes that hyperkalemia is the
most life-threatening electrolyte imbalance primarily because of its effect on which organ system?
A. Central nervous system causing seizures
B. Hepatic system causing liver failure
C. Cardiovascular system causing cardiac arrest [CORRECT]
D. Pulmonary system causing respiratory failure
Correct Answer: C
Rationale: C. Hyperkalemia is the most life-threatening electrolyte imbalance because of its direct effect on the cardiac
conduction system. Elevated potassium alters the resting membrane potential of cardiac myocytes, leading to depolarization.
ECG changes progress from peaked T waves and widened QRS complexes to sine wave patterns, and ultimately ventricular
fibrillation or asystole (cardiac arrest). The muscle weakness reported is due to hyperpolarization of skeletal muscle cells,
making them less excitable. While severe electrolyte imbalances can affect multiple systems, hyperkalemia is uniquely
dangerous because it can cause sudden cardiac death. Seizures are more commonly associated with severe hyponatremia.
Liver failure is not a direct consequence of hyperkalemia. Respiratory failure is more associated with hypokalemia affecting
respiratory muscle function.
Q10: A patient with diabetic ketoacidosis (DKA) presents with deep, rapid respirations (Kussmaul
respirations). Which acid-base disorder is present, and what is the compensatory mechanism?
Page 3
