NURSING PATHOPHYSIOLOGY EXAM 2 COMPLETE
STUDY GUIDE |300 QUESTIONS WITH VERIFIED ANSWERS &
DETAILED RATIONALES 2026/2027 UPDATED
TABLE OF CONTENTS
SECTION 1: CELLULAR ADAPTATION, INJURY & DEATH ................ Q 1–60
SECTION 2: INFLAMMATION & IMMUNE RESPONSE ..................... Q 61–120
SECTION 3: FLUID, ELECTROLYTE & ACID-BASE BALANCE ............. Q 121–170
SECTION 4: HEMATOLOGIC DISORDERS .............................. Q 171–220
SECTION 5: CARDIOVASCULAR DISORDERS ........................... Q 221–260
SECTION 6: RESPIRATORY DISORDERS & NGN CASE SCENARIOS ........ Q 261–300
SECTION 1: CELLULAR ADAPTATION, INJURY & DEATH (Q 1–60)
Q1. Which of the following best describes the mechanism by which hypoxia leads
to cellular swelling?
A) Increased ATP production and activation of the sodium-potassium pump
B) Decreased ATP production causing failure of the sodium-potassium pump and
intracellular accumulation of sodium and water
C) Enhanced oxidative phosphorylation with increased free radical scavenging
D) Stimulation of apoptosis through mitochondrial cytochrome c release
Answer: B
Rationale: Hypoxia impairs oxidative phosphorylation, reducing ATP production.
Without sufficient ATP, the sodium-potassium pump fails, allowing sodium and
water to accumulate intracellularly, causing cellular swelling. Increased ATP
production and enhanced oxidative phosphorylation are not consequences of
hypoxia. Apoptosis is a separate process from hypoxic cellular swelling.
Q2. A 58-year-old male with long-standing hypertension develops thickening of
the left ventricular wall. Which cellular adaptation does this represent?
A) Atrophy
B) Hyperplasia
C) Hypertrophy
D) Metaplasia
Answer: C
Rationale: Hypertrophy is an increase in cell size in response to increased
workload. Cardiac myocytes enlarge to compensate for the increased pressure
load caused by hypertension. Atrophy is a decrease in cell size. Hyperplasia
1
,involves an increase in cell number. Metaplasia is the replacement of one adult
cell type with another.
Q3. What is the primary difference between necrosis and apoptosis?
A) Necrosis is programmed cell death, while apoptosis is passive cell death
B) Necrosis causes inflammation, while apoptosis does not
C) Apoptosis affects groups of cells, while necrosis affects single cells
D) Apoptosis is always pathological, while necrosis is always physiological
Answer: B
Rationale: Necrosis is passive cell death resulting from irreversible injury and
triggers an inflammatory response due to the release of cellular contents.
Apoptosis is programmed cell death that does not cause inflammation and
typically affects individual cells.
Q4. A pathologist examines a tissue section showing cells with enlarged nuclei,
prominent nucleoli, and a high nuclear-to-cytoplasmic ratio. Some cells exhibit
basophilic cytoplasmic granules and mitotic figures with abnormal spindles.
Which pattern of cellular adaptation or injury is predominantly present?
A) Metaplasia with compensatory hyperplasia
B) Dysplasia with potential for malignant transformation
C) Reversible cell injury with hydropic change
D) Apoptosis with autophagic vacuole formation
Answer: B
Rationale: Dysplasia is characterized by disordered cell growth, nuclear
pleomorphism, increased mitoses (including abnormal), and loss of uniformity.
These features are distinct from metaplasia, reversible injury, and apoptosis.
Q5. A researcher treats cultured endothelial cells with a high dose of bacterial
lipopolysaccharide (LPS) for 6 hours. Compared to controls, the treated cells show
upregulated surface expression of E-selectin, ICAM-1, and increased production of
IL-6. Which phase of the inflammatory response is predominantly activated?
A) Chronic granulomatous inflammation
B) Acute vascular permeability phase
C) Leukocyte recruitment mediated by adhesion molecules
D) Resolution phase with angiogenesis
Answer: C
2
,Rationale: LPS stimulates endothelial cells to express selectins and adhesion
molecules, which mediate leukocyte rolling and firm adhesion. This is a key step in
acute inflammation.
Q6. A patient presents with acute hemolytic anemia, thrombocytopenia, and
acute kidney injury after receiving a blood transfusion. Laboratory findings show
low haptoglobin, elevated LDH, and schistocytes on peripheral smear. Which type
of hypersensitivity mechanism is most likely responsible?
A) Type I IgE-mediated mast cell degranulation
B) Type II antibody-dependent cytotoxicity against mismatched RBC antigens
C) Type III immune complex deposition in renal glomeruli
D) Type IV delayed-type hypersensitivity mediated by cytotoxic T cells
Answer: B
Rationale: Transfusion reaction involves pre-existing antibodies binding to
incompatible RBC antigens, leading to complement activation, intravascular
hemolysis, and sequelae. This is a classic Type II hypersensitivity.
Q7. In a family with hereditary nonpolyposis colorectal cancer (Lynch syndrome),
a mutation in an MLH1 gene leads to defective mismatch repair. Which of the
following best describes the consequence for tumor suppressor gene function in
affected cells?
A) Loss of heterozygosity and accelerated accumulation of mutations
B) Enhanced apoptosis and cell cycle arrest
C) Increased DNA repair capacity and genomic stability
D) Activation of oncogenes and uncontrolled cell proliferation
Answer: A
Rationale: Defective mismatch repair leads to microsatellite instability and
accelerated accumulation of mutations in tumor suppressor genes and
oncogenes, contributing to cancer development.
Q8. In a patient with untreated type 1 diabetes mellitus, the excessive breakdown
of fatty acids leads to the production of which of the following metabolites,
resulting in a life-threatening acid-base imbalance?
A) Lactic acid
B) Pyruvic acid
C) Acetoacetic acid
D) Glucuronic acid
3
, Answer: C
Rationale: In the absence of insulin, the body shifts to fatty acid metabolism,
producing ketone bodies including acetoacetic acid, which leads to metabolic
acidosis.
Q9. Which of the following cellular adaptations is characterized by a decrease in
the size of individual cells, leading to a reduction in the overall size of an organ,
and is most commonly reversible upon removal of the stimulus?
A) Hyperplasia
B) Hypertrophy
C) Atrophy
D) Metaplasia
Answer: C
Rationale: Atrophy is a decrease in cellular size and function, which can be
physiological or pathological. It is generally reversible if the causative stimulus is
removed.
Q10. A patient presents with jaundice, dark urine, and pale stools. Laboratory
tests reveal elevated unconjugated bilirubin and normal urine urobilinogen.
Which of the following is the most likely underlying mechanism for this
presentation?
A) Intrahepatic cholestasis
B) Hemolytic anemia
C) Biliary duct obstruction
D) Hepatocellular failure
Answer: B
Rationale: In hemolytic anemia, excessive destruction of red blood cells leads to
overproduction of unconjugated bilirubin, which is water-insoluble and cannot be
excreted in urine. This results in elevated serum unconjugated bilirubin, causing
jaundice.
Q11. In the context of cellular injury, which of the following mechanisms is
primarily responsible for the irreversible stage of injury, characterized by severe
mitochondrial dysfunction and depletion of adenosine triphosphate (ATP)?
A) Loss of cell membrane integrity
B) Reversible swelling of the endoplasmic reticulum
C) ATP depletion
4
STUDY GUIDE |300 QUESTIONS WITH VERIFIED ANSWERS &
DETAILED RATIONALES 2026/2027 UPDATED
TABLE OF CONTENTS
SECTION 1: CELLULAR ADAPTATION, INJURY & DEATH ................ Q 1–60
SECTION 2: INFLAMMATION & IMMUNE RESPONSE ..................... Q 61–120
SECTION 3: FLUID, ELECTROLYTE & ACID-BASE BALANCE ............. Q 121–170
SECTION 4: HEMATOLOGIC DISORDERS .............................. Q 171–220
SECTION 5: CARDIOVASCULAR DISORDERS ........................... Q 221–260
SECTION 6: RESPIRATORY DISORDERS & NGN CASE SCENARIOS ........ Q 261–300
SECTION 1: CELLULAR ADAPTATION, INJURY & DEATH (Q 1–60)
Q1. Which of the following best describes the mechanism by which hypoxia leads
to cellular swelling?
A) Increased ATP production and activation of the sodium-potassium pump
B) Decreased ATP production causing failure of the sodium-potassium pump and
intracellular accumulation of sodium and water
C) Enhanced oxidative phosphorylation with increased free radical scavenging
D) Stimulation of apoptosis through mitochondrial cytochrome c release
Answer: B
Rationale: Hypoxia impairs oxidative phosphorylation, reducing ATP production.
Without sufficient ATP, the sodium-potassium pump fails, allowing sodium and
water to accumulate intracellularly, causing cellular swelling. Increased ATP
production and enhanced oxidative phosphorylation are not consequences of
hypoxia. Apoptosis is a separate process from hypoxic cellular swelling.
Q2. A 58-year-old male with long-standing hypertension develops thickening of
the left ventricular wall. Which cellular adaptation does this represent?
A) Atrophy
B) Hyperplasia
C) Hypertrophy
D) Metaplasia
Answer: C
Rationale: Hypertrophy is an increase in cell size in response to increased
workload. Cardiac myocytes enlarge to compensate for the increased pressure
load caused by hypertension. Atrophy is a decrease in cell size. Hyperplasia
1
,involves an increase in cell number. Metaplasia is the replacement of one adult
cell type with another.
Q3. What is the primary difference between necrosis and apoptosis?
A) Necrosis is programmed cell death, while apoptosis is passive cell death
B) Necrosis causes inflammation, while apoptosis does not
C) Apoptosis affects groups of cells, while necrosis affects single cells
D) Apoptosis is always pathological, while necrosis is always physiological
Answer: B
Rationale: Necrosis is passive cell death resulting from irreversible injury and
triggers an inflammatory response due to the release of cellular contents.
Apoptosis is programmed cell death that does not cause inflammation and
typically affects individual cells.
Q4. A pathologist examines a tissue section showing cells with enlarged nuclei,
prominent nucleoli, and a high nuclear-to-cytoplasmic ratio. Some cells exhibit
basophilic cytoplasmic granules and mitotic figures with abnormal spindles.
Which pattern of cellular adaptation or injury is predominantly present?
A) Metaplasia with compensatory hyperplasia
B) Dysplasia with potential for malignant transformation
C) Reversible cell injury with hydropic change
D) Apoptosis with autophagic vacuole formation
Answer: B
Rationale: Dysplasia is characterized by disordered cell growth, nuclear
pleomorphism, increased mitoses (including abnormal), and loss of uniformity.
These features are distinct from metaplasia, reversible injury, and apoptosis.
Q5. A researcher treats cultured endothelial cells with a high dose of bacterial
lipopolysaccharide (LPS) for 6 hours. Compared to controls, the treated cells show
upregulated surface expression of E-selectin, ICAM-1, and increased production of
IL-6. Which phase of the inflammatory response is predominantly activated?
A) Chronic granulomatous inflammation
B) Acute vascular permeability phase
C) Leukocyte recruitment mediated by adhesion molecules
D) Resolution phase with angiogenesis
Answer: C
2
,Rationale: LPS stimulates endothelial cells to express selectins and adhesion
molecules, which mediate leukocyte rolling and firm adhesion. This is a key step in
acute inflammation.
Q6. A patient presents with acute hemolytic anemia, thrombocytopenia, and
acute kidney injury after receiving a blood transfusion. Laboratory findings show
low haptoglobin, elevated LDH, and schistocytes on peripheral smear. Which type
of hypersensitivity mechanism is most likely responsible?
A) Type I IgE-mediated mast cell degranulation
B) Type II antibody-dependent cytotoxicity against mismatched RBC antigens
C) Type III immune complex deposition in renal glomeruli
D) Type IV delayed-type hypersensitivity mediated by cytotoxic T cells
Answer: B
Rationale: Transfusion reaction involves pre-existing antibodies binding to
incompatible RBC antigens, leading to complement activation, intravascular
hemolysis, and sequelae. This is a classic Type II hypersensitivity.
Q7. In a family with hereditary nonpolyposis colorectal cancer (Lynch syndrome),
a mutation in an MLH1 gene leads to defective mismatch repair. Which of the
following best describes the consequence for tumor suppressor gene function in
affected cells?
A) Loss of heterozygosity and accelerated accumulation of mutations
B) Enhanced apoptosis and cell cycle arrest
C) Increased DNA repair capacity and genomic stability
D) Activation of oncogenes and uncontrolled cell proliferation
Answer: A
Rationale: Defective mismatch repair leads to microsatellite instability and
accelerated accumulation of mutations in tumor suppressor genes and
oncogenes, contributing to cancer development.
Q8. In a patient with untreated type 1 diabetes mellitus, the excessive breakdown
of fatty acids leads to the production of which of the following metabolites,
resulting in a life-threatening acid-base imbalance?
A) Lactic acid
B) Pyruvic acid
C) Acetoacetic acid
D) Glucuronic acid
3
, Answer: C
Rationale: In the absence of insulin, the body shifts to fatty acid metabolism,
producing ketone bodies including acetoacetic acid, which leads to metabolic
acidosis.
Q9. Which of the following cellular adaptations is characterized by a decrease in
the size of individual cells, leading to a reduction in the overall size of an organ,
and is most commonly reversible upon removal of the stimulus?
A) Hyperplasia
B) Hypertrophy
C) Atrophy
D) Metaplasia
Answer: C
Rationale: Atrophy is a decrease in cellular size and function, which can be
physiological or pathological. It is generally reversible if the causative stimulus is
removed.
Q10. A patient presents with jaundice, dark urine, and pale stools. Laboratory
tests reveal elevated unconjugated bilirubin and normal urine urobilinogen.
Which of the following is the most likely underlying mechanism for this
presentation?
A) Intrahepatic cholestasis
B) Hemolytic anemia
C) Biliary duct obstruction
D) Hepatocellular failure
Answer: B
Rationale: In hemolytic anemia, excessive destruction of red blood cells leads to
overproduction of unconjugated bilirubin, which is water-insoluble and cannot be
excreted in urine. This results in elevated serum unconjugated bilirubin, causing
jaundice.
Q11. In the context of cellular injury, which of the following mechanisms is
primarily responsible for the irreversible stage of injury, characterized by severe
mitochondrial dysfunction and depletion of adenosine triphosphate (ATP)?
A) Loss of cell membrane integrity
B) Reversible swelling of the endoplasmic reticulum
C) ATP depletion
4
