1
NURS 6501 Advanced Pathophysiology
Midterm Exam Questions (Walden
University, 2025/2026 Edition) – complete
exam material with answers
Cellular and Molecular Pathophysiology (Questions 1-10)
1. In the context of cellular injury due to hypoxia, which
mechanism primarily leads to ATP depletion and subsequent
Na+/K+ ATPase pump failure? A. Increased oxidative
phosphorylation B. Impaired mitochondrial electron transport
chain C. Enhanced glycolysis under anaerobic conditions D.
Activation of lysosomal enzymes
B. Impaired mitochondrial electron transport chain
Rationale: Hypoxia disrupts oxygen delivery to mitochondria,
halting the electron transport chain and oxidative phosphorylation,
which accounts for 90% of ATP production. This leads to rapid
ATP depletion (<2 minutes), causing Na+/K+ ATPase failure,
cellular swelling, and bleb formation. Distractor A is incorrect as
oxidative phosphorylation decreases; C is a compensatory but
inefficient pathway producing only 2 ATP per glucose; D relates to
later necrosis stages, not primary ATP loss (McCance & Huether,
2023).
2. Which epigenetic modification is most associated with gene
silencing in cancer pathogenesis, such as in promoter regions of
tumor suppressor genes? A. Histone acetylation B. DNA
hypomethylation C. DNA hypermethylation D. Histone
phosphorylation
C. DNA hypermethylation
Rationale: DNA hypermethylation at CpG islands in promoter
regions silences tumor suppressor genes (e.g., BRCA1 in breast
cancer) by inhibiting transcription factor binding, a hallmark of
, 2
epigenetic dysregulation in oncogenesis (updated 2024 NCCN
guidelines). A promotes gene activation; B leads to oncogene
activation; D is involved in transient signaling, not stable silencing.
3. During apoptosis, which caspase cascade is initiated by
intrinsic mitochondrial pathways triggered by DNA damage?
A. Caspase-8 activation via death receptors B. Caspase-9
activation by cytochrome c release C. Caspase-3 inhibition by Bcl-
2 family proteins D. Caspase-1 activation in inflammasomes
B. Caspase-9 activation by cytochrome c release
Rationale: Intrinsic apoptosis involves mitochondrial outer
membrane permeabilization, releasing cytochrome c to form the
apoptosome with Apaf-1, activating initiator caspase-9, which
cleaves effector caspases like 3/7 for DNA fragmentation. This is
key in p53-mediated responses to genotoxic stress (2023 updates in
cell death research). A is extrinsic pathway; C is anti-apoptotic; D
is pyroptosis-related.
4. In reversible cellular adaptation, what is the primary stimulus
for cellular hypertrophy in cardiac myocytes? A. Nutritional
deficiency B. Increased functional demand (e.g., pressure
overload) C. Hypoxia-induced atrophy D. Hyperplasia from
hormonal stimulation
B. Increased functional demand (e.g., pressure overload)
Rationale: Hypertrophy involves increased cell size via enhanced
protein synthesis (e.g., actin/myosin) in response to workload, as in
hypertension-induced left ventricular hypertrophy. It's adaptive
initially but progresses to failure (AHA 2024 guidelines). A causes
atrophy; C is atrophy; D is cell number increase, seen in
endometrial hyperplasia.
5. Which free radical species is most implicated in lipid
peroxidation during ischemia-reperfusion injury? A.
Superoxide anion (O2•−) B. Hydroxyl radical (•OH) C. Nitric
oxide (NO•) D. Singlet oxygen (1O2)
, 3
B. Hydroxyl radical (•OH)
Rationale: •OH, formed via Fenton reaction from H2O2 and Fe2+,
is highly reactive and initiates polyunsaturated fatty acid
peroxidation in membranes, leading to membrane disruption in
post-ischemic tissues (e.g., myocardial infarction). Recent 2025
ROS research emphasizes its role over less reactive species like A
or C, which contribute upstream; D is photosensitization-specific.
6. What is the hallmark morphologic feature of necrosis in tissues
exposed to severe bacterial toxins? A. Karyorrhexis and pyknosis
B. Coagulative necrosis with preserved architecture C.
Liquefactive necrosis with pus formation D. Caseous necrosis with
granular debris
C. Liquefactive necrosis with pus formation
Rationale: Bacterial toxins (e.g., in abscesses) cause enzymatic
digestion by neutrophils, resulting in liquefactive necrosis with
creamy pus. This is common in CNS or lung infections (updated
IDSA 2024). A is apoptosis; B is ischemic (e.g., heart); D is
granulomatous (e.g., TB).
7. In protein misfolding disorders like Alzheimer's, which cellular
process is primarily impaired by amyloid-beta aggregates? A.
Autophagy-lysosomal degradation B. Ubiquitin-proteasome
pathway C. Mitochondrial fission D. Golgi apparatus trafficking
A. Autophagy-lysosomal degradation
Rationale: Amyloid-beta impairs macroautophagy, leading to
accumulation of aggregates and impaired clearance, a key 2024
AD pathogenesis update linking to tau hyperphosphorylation. B
handles short-lived proteins; C/D are mitochondrial/Golgi-specific,
secondary effects.
8. Which ion channel dysfunction is central to the
pathophysiology of long QT syndrome type 2? A. Loss-of-
function in KCNQ1 (IKs channel) B. Gain-of-function in SCN5A
NURS 6501 Advanced Pathophysiology
Midterm Exam Questions (Walden
University, 2025/2026 Edition) – complete
exam material with answers
Cellular and Molecular Pathophysiology (Questions 1-10)
1. In the context of cellular injury due to hypoxia, which
mechanism primarily leads to ATP depletion and subsequent
Na+/K+ ATPase pump failure? A. Increased oxidative
phosphorylation B. Impaired mitochondrial electron transport
chain C. Enhanced glycolysis under anaerobic conditions D.
Activation of lysosomal enzymes
B. Impaired mitochondrial electron transport chain
Rationale: Hypoxia disrupts oxygen delivery to mitochondria,
halting the electron transport chain and oxidative phosphorylation,
which accounts for 90% of ATP production. This leads to rapid
ATP depletion (<2 minutes), causing Na+/K+ ATPase failure,
cellular swelling, and bleb formation. Distractor A is incorrect as
oxidative phosphorylation decreases; C is a compensatory but
inefficient pathway producing only 2 ATP per glucose; D relates to
later necrosis stages, not primary ATP loss (McCance & Huether,
2023).
2. Which epigenetic modification is most associated with gene
silencing in cancer pathogenesis, such as in promoter regions of
tumor suppressor genes? A. Histone acetylation B. DNA
hypomethylation C. DNA hypermethylation D. Histone
phosphorylation
C. DNA hypermethylation
Rationale: DNA hypermethylation at CpG islands in promoter
regions silences tumor suppressor genes (e.g., BRCA1 in breast
cancer) by inhibiting transcription factor binding, a hallmark of
, 2
epigenetic dysregulation in oncogenesis (updated 2024 NCCN
guidelines). A promotes gene activation; B leads to oncogene
activation; D is involved in transient signaling, not stable silencing.
3. During apoptosis, which caspase cascade is initiated by
intrinsic mitochondrial pathways triggered by DNA damage?
A. Caspase-8 activation via death receptors B. Caspase-9
activation by cytochrome c release C. Caspase-3 inhibition by Bcl-
2 family proteins D. Caspase-1 activation in inflammasomes
B. Caspase-9 activation by cytochrome c release
Rationale: Intrinsic apoptosis involves mitochondrial outer
membrane permeabilization, releasing cytochrome c to form the
apoptosome with Apaf-1, activating initiator caspase-9, which
cleaves effector caspases like 3/7 for DNA fragmentation. This is
key in p53-mediated responses to genotoxic stress (2023 updates in
cell death research). A is extrinsic pathway; C is anti-apoptotic; D
is pyroptosis-related.
4. In reversible cellular adaptation, what is the primary stimulus
for cellular hypertrophy in cardiac myocytes? A. Nutritional
deficiency B. Increased functional demand (e.g., pressure
overload) C. Hypoxia-induced atrophy D. Hyperplasia from
hormonal stimulation
B. Increased functional demand (e.g., pressure overload)
Rationale: Hypertrophy involves increased cell size via enhanced
protein synthesis (e.g., actin/myosin) in response to workload, as in
hypertension-induced left ventricular hypertrophy. It's adaptive
initially but progresses to failure (AHA 2024 guidelines). A causes
atrophy; C is atrophy; D is cell number increase, seen in
endometrial hyperplasia.
5. Which free radical species is most implicated in lipid
peroxidation during ischemia-reperfusion injury? A.
Superoxide anion (O2•−) B. Hydroxyl radical (•OH) C. Nitric
oxide (NO•) D. Singlet oxygen (1O2)
, 3
B. Hydroxyl radical (•OH)
Rationale: •OH, formed via Fenton reaction from H2O2 and Fe2+,
is highly reactive and initiates polyunsaturated fatty acid
peroxidation in membranes, leading to membrane disruption in
post-ischemic tissues (e.g., myocardial infarction). Recent 2025
ROS research emphasizes its role over less reactive species like A
or C, which contribute upstream; D is photosensitization-specific.
6. What is the hallmark morphologic feature of necrosis in tissues
exposed to severe bacterial toxins? A. Karyorrhexis and pyknosis
B. Coagulative necrosis with preserved architecture C.
Liquefactive necrosis with pus formation D. Caseous necrosis with
granular debris
C. Liquefactive necrosis with pus formation
Rationale: Bacterial toxins (e.g., in abscesses) cause enzymatic
digestion by neutrophils, resulting in liquefactive necrosis with
creamy pus. This is common in CNS or lung infections (updated
IDSA 2024). A is apoptosis; B is ischemic (e.g., heart); D is
granulomatous (e.g., TB).
7. In protein misfolding disorders like Alzheimer's, which cellular
process is primarily impaired by amyloid-beta aggregates? A.
Autophagy-lysosomal degradation B. Ubiquitin-proteasome
pathway C. Mitochondrial fission D. Golgi apparatus trafficking
A. Autophagy-lysosomal degradation
Rationale: Amyloid-beta impairs macroautophagy, leading to
accumulation of aggregates and impaired clearance, a key 2024
AD pathogenesis update linking to tau hyperphosphorylation. B
handles short-lived proteins; C/D are mitochondrial/Golgi-specific,
secondary effects.
8. Which ion channel dysfunction is central to the
pathophysiology of long QT syndrome type 2? A. Loss-of-
function in KCNQ1 (IKs channel) B. Gain-of-function in SCN5A
