NSG 5140 Midterm and Final Exam Review
Adv Pathophysiology South College NSG 5140
Advanced Pathophysiology Exam Questions
and Answers | 100% Pass Guaranteed |
Graded A+ | This content is designed to
reflect graduate-level material and exam
standards
1. A 55-year-old patient with chronic alcohol use disorder has
biopsy showing hepatocytes with enlarged, pink cytoplasmic
inclusions (Mallory bodies). This finding is characteristic of which
type of cellular injury?
A. Apoptosis
B. Hydropic degeneration
C. Alcoholic liver disease with cytoskeletal damage
D. Glycogen accumulation
Correct ,,,answer,,,,: C
Rationale: Mallory bodies (hyaline inclusions) are aggregates of
intermediate filaments (cytokeratins) seen in alcoholic liver disease
and other liver injuries. They represent cytoskeletal damage.
Hydropic swelling is reversible injury; apoptosis is programmed cell
death.
2. Which of the following best describes the mechanism of
reperfusion injury following myocardial infarction?
,A. Prolonged ATP depletion leading to irreversible necrosis
B. Restoration of oxygen leading to reactive oxygen species (ROS)
and calcium overload
C. Activation of the intrinsic apoptotic pathway only
D. Loss of growth factor signaling
Correct ,,,answer,,,,: B
Rationale: Reperfusion after ischemia paradoxically causes
additional injury via ROS generation (oxidative stress),
mitochondrial permeability transition, and intracellular calcium
overload. This can cause arrhythmias, myocardial stunning, and cell
death beyond the original ischemic injury.
3. A biopsy of a breast tumor shows cells with large, hyperchromatic
nuclei, prominent nucleoli, and atypical mitotic figures. This
histologic description is most consistent with:
A. Benign hyperplasia
B. Well-differentiated adenocarcinoma
C. Anaplasia (poorly differentiated malignancy)
D. Chronic inflammation
Correct ,,,answer,,,,: C
Rationale: Anaplasia is a hallmark of malignancy characterized by
pleomorphism (variation in size/shape), hyperchromatic nuclei,
high nuclear-to-cytoplasmic ratio, and atypical mitoses. Well-
differentiated tumors resemble normal tissue; benign tumors lack
these features.
4. A patient with chronic ischemia to the lower extremity develops
muscle atrophy. At the cellular level, atrophy is mediated primarily
by:
A. Increased protein synthesis via mTOR
,B. Ubiquitin-proteasome pathway and autophagy
C. Inhibition of caspases
D. Telomerase activation
Correct ,,,answer,,,,: B
Rationale: Atrophy results from increased protein degradation via
the ubiquitin-proteasome pathway and autophagy (lysosomal
degradation). Reduced protein synthesis also contributes. The
mTOR pathway is anabolic (promotes growth).
5. Which of the following is an example of pathologic hyperplasia?
A. Uterine enlargement during pregnancy
B. Breast tissue enlargement during lactation
C. Benign prostatic hyperplasia (BPH)
D. Liver regeneration after partial hepatectomy
Correct ,,,answer,,,,: C
Rationale: BPH is pathologic hyperplasia due to hormonal
imbalances (androgen/estrogen ratio). Pregnancy, lactation, and
liver regeneration are physiologic (compensatory) hyperplasia.
6. A patient with prolonged hypertension develops left ventricular
hypertrophy. The molecular mechanism driving this adaptation
involves:
A. Increased cell number (hyperplasia)
B. Activation of mechanosensitive signaling pathways (e.g., MAPK,
calcineurin) leading to increased protein synthesis
C. Apoptosis of cardiac myocytes
D. Metaplasia to smooth muscle
Correct ,,,answer,,,,: B
Rationale: Pressure overload activates mechanotransducers
(integrins, stretch-activated channels) and signaling pathways
, (MAPK, calcineurin-NFAT), leading to increased protein synthesis
and myocyte hypertrophy. Cardiac myocytes do not divide in adults
(no hyperplasia).
7. In ischemia-reperfusion injury, which of the following contributes
most to mitochondrial dysfunction?
A. Decreased cytosolic calcium
B. Opening of the mitochondrial permeability transition pore
(mPTP)
C. Increased ATP synthesis
D. Inhibition of ROS production
Correct ,,,answer,,,,: B
Rationale: During reperfusion, calcium overload and ROS cause
opening of mPTP, leading to loss of mitochondrial membrane
potential, cessation of ATP synthesis, and release of pro-apoptotic
factors (cytochrome c). This commits the cell to death.
8. A patient with a mutation in the gene encoding dystrophin
develops Duchenne muscular dystrophy. Which cellular structure is
primarily affected?
A. Gap junctions
B. Cytoskeleton-membrane linkage (dystrophin-glycoprotein
complex)
C. Mitochondrial membrane
D. Nuclear envelope
Correct ,,,answer,,,,: B
Rationale: Dystrophin links the actin cytoskeleton to the
extracellular matrix via the dystrophin-glycoprotein complex. Its
absence causes membrane fragility and myocyte necrosis. This is a
classic example of a genetic defect causing cell injury.
Adv Pathophysiology South College NSG 5140
Advanced Pathophysiology Exam Questions
and Answers | 100% Pass Guaranteed |
Graded A+ | This content is designed to
reflect graduate-level material and exam
standards
1. A 55-year-old patient with chronic alcohol use disorder has
biopsy showing hepatocytes with enlarged, pink cytoplasmic
inclusions (Mallory bodies). This finding is characteristic of which
type of cellular injury?
A. Apoptosis
B. Hydropic degeneration
C. Alcoholic liver disease with cytoskeletal damage
D. Glycogen accumulation
Correct ,,,answer,,,,: C
Rationale: Mallory bodies (hyaline inclusions) are aggregates of
intermediate filaments (cytokeratins) seen in alcoholic liver disease
and other liver injuries. They represent cytoskeletal damage.
Hydropic swelling is reversible injury; apoptosis is programmed cell
death.
2. Which of the following best describes the mechanism of
reperfusion injury following myocardial infarction?
,A. Prolonged ATP depletion leading to irreversible necrosis
B. Restoration of oxygen leading to reactive oxygen species (ROS)
and calcium overload
C. Activation of the intrinsic apoptotic pathway only
D. Loss of growth factor signaling
Correct ,,,answer,,,,: B
Rationale: Reperfusion after ischemia paradoxically causes
additional injury via ROS generation (oxidative stress),
mitochondrial permeability transition, and intracellular calcium
overload. This can cause arrhythmias, myocardial stunning, and cell
death beyond the original ischemic injury.
3. A biopsy of a breast tumor shows cells with large, hyperchromatic
nuclei, prominent nucleoli, and atypical mitotic figures. This
histologic description is most consistent with:
A. Benign hyperplasia
B. Well-differentiated adenocarcinoma
C. Anaplasia (poorly differentiated malignancy)
D. Chronic inflammation
Correct ,,,answer,,,,: C
Rationale: Anaplasia is a hallmark of malignancy characterized by
pleomorphism (variation in size/shape), hyperchromatic nuclei,
high nuclear-to-cytoplasmic ratio, and atypical mitoses. Well-
differentiated tumors resemble normal tissue; benign tumors lack
these features.
4. A patient with chronic ischemia to the lower extremity develops
muscle atrophy. At the cellular level, atrophy is mediated primarily
by:
A. Increased protein synthesis via mTOR
,B. Ubiquitin-proteasome pathway and autophagy
C. Inhibition of caspases
D. Telomerase activation
Correct ,,,answer,,,,: B
Rationale: Atrophy results from increased protein degradation via
the ubiquitin-proteasome pathway and autophagy (lysosomal
degradation). Reduced protein synthesis also contributes. The
mTOR pathway is anabolic (promotes growth).
5. Which of the following is an example of pathologic hyperplasia?
A. Uterine enlargement during pregnancy
B. Breast tissue enlargement during lactation
C. Benign prostatic hyperplasia (BPH)
D. Liver regeneration after partial hepatectomy
Correct ,,,answer,,,,: C
Rationale: BPH is pathologic hyperplasia due to hormonal
imbalances (androgen/estrogen ratio). Pregnancy, lactation, and
liver regeneration are physiologic (compensatory) hyperplasia.
6. A patient with prolonged hypertension develops left ventricular
hypertrophy. The molecular mechanism driving this adaptation
involves:
A. Increased cell number (hyperplasia)
B. Activation of mechanosensitive signaling pathways (e.g., MAPK,
calcineurin) leading to increased protein synthesis
C. Apoptosis of cardiac myocytes
D. Metaplasia to smooth muscle
Correct ,,,answer,,,,: B
Rationale: Pressure overload activates mechanotransducers
(integrins, stretch-activated channels) and signaling pathways
, (MAPK, calcineurin-NFAT), leading to increased protein synthesis
and myocyte hypertrophy. Cardiac myocytes do not divide in adults
(no hyperplasia).
7. In ischemia-reperfusion injury, which of the following contributes
most to mitochondrial dysfunction?
A. Decreased cytosolic calcium
B. Opening of the mitochondrial permeability transition pore
(mPTP)
C. Increased ATP synthesis
D. Inhibition of ROS production
Correct ,,,answer,,,,: B
Rationale: During reperfusion, calcium overload and ROS cause
opening of mPTP, leading to loss of mitochondrial membrane
potential, cessation of ATP synthesis, and release of pro-apoptotic
factors (cytochrome c). This commits the cell to death.
8. A patient with a mutation in the gene encoding dystrophin
develops Duchenne muscular dystrophy. Which cellular structure is
primarily affected?
A. Gap junctions
B. Cytoskeleton-membrane linkage (dystrophin-glycoprotein
complex)
C. Mitochondrial membrane
D. Nuclear envelope
Correct ,,,answer,,,,: B
Rationale: Dystrophin links the actin cytoskeleton to the
extracellular matrix via the dystrophin-glycoprotein complex. Its
absence causes membrane fragility and myocyte necrosis. This is a
classic example of a genetic defect causing cell injury.
