, NURS 611 EXAM 1 PATHO ACTUAL EXAM 2024 NEWEST
EXAM COMPLETE AND CORRECT DETAILED ANSWERS
|ALREADY GRADED A+ (MARYVILLE UNIVERSITY) - 149
Questions
Section 1: Cellular Adaptation and Injury (Questions 1-15)
1 A researcher studying myocardial ischemia observes that after 30 minutes of oxygen deprivation,
cardiomyocytes exhibit swelling of mitochondria and loss of microvilli, but the nuclei remain normal. Upon
reoxygenation, the cells recover. Which of the following best characterizes the cellular state during the ischemic
period?
A) Necrosis with karyolysis
B) Reversible cell injury
C) Apoptosis with caspase activation
D) Sublethal injury with DNA fragmentation
Answer: B
Rationale: The morphological changes described (mitochondrial swelling, loss of microvilli) are characteristic of
reversible cell injury. The absence of nuclear changes and the ability to recover upon reperfusion confirm
reversibility. Necrosis would show nuclear pyknosis, karyolysis, or karyorrhexis. Apoptosis involves caspase
activation and DNA fragmentation, not reversible swelling.
2 In a patient with chronic iron overload, hepatocytes accumulate excess iron in the form of hemosiderin. This
represents which type of cellular adaptation?
A) Metaplasia
B) Dysplasia
C) Pathologic calcification
D) Intracellular accumulation
Answer: D
Rationale: Hemosiderin accumulation is a form of intracellular accumulation of abnormal substances, not an
adaptive change in cell size, number, or differentiation. Metaplasia is a reversible change where one adult cell type
is replaced by another. Dysplasia refers to abnormal growth. Pathologic calcification involves calcium salt
deposition in tissues.
3 A 45-year-old individual with a history of chronic gastritis undergoes an endoscopic biopsy. Histologic
examination reveals replacement of gastric foveolar cells by intestinal-type columnar cells with goblet cells.
This finding is most consistent with which adaptive process?
A) Hyperplasia
B) Metaplasia
C) Dysplasia
D) Atrophy
Answer: B
Rationale: The replacement of one mature cell type (gastric foveolar) by another (intestinal epithelium with goblet
cells) is classic intestinal metaplasia, often a response to chronic irritation. Hyperplasia is an increase in cell
number. Dysplasia shows disordered growth and cytologic atypia. Atrophy is a decrease in cell size or number.
,4 Which of the following best explains why cells undergoing apoptosis do not elicit an inflammatory response?
A) Caspases degrade pro-inflammatory cytokines
B) Apoptotic cells release IL-10 to suppress inflammation
C) Cellular contents are retained within membrane-bound apoptotic bodies that are rapidly phagocytosed
D) Apoptosis requires ATP, which is depleted in inflammation
Answer: C
Rationale: Apoptotic cells maintain membrane integrity and fragment into apoptotic bodies that are quickly engulfed
by phagocytes without releasing intracellular contents. This prevents activation of the inflammatory response.
Caspases do not degrade cytokines; IL-10 is not specifically released. ATP depletion is a feature of necrosis, not
apoptosis.
5 A laboratory experiment exposes cultured hepatocytes to a toxin that inhibits mitochondrial ATP synthase.
Within minutes, cells show swelling of the endoplasmic reticulum and blebbing of the plasma membrane.
Which of the following is the most likely immediate consequence of ATP depletion?
A) Increased activity of the Na+/K+ ATPase
B) Failure of the Na+/Ca2+ exchanger leading to calcium influx
C) Activation of caspases
D) Upregulation of heat shock proteins
Answer: B
Rationale: ATP depletion impairs the Na+/K+ pump, causing sodium and water accumulation (swelling). It also
reduces function of the Na+/Ca2+ exchanger, leading to intracellular calcium accumulation. Calcium overload
activates enzymes that damage membranes. Caspase activation is ATP-dependent and occurs in apoptosis, not early
injury. Heat shock proteins are upregulated later as a protective response.
6 Which of the following cellular changes is most indicative of irreversible cell injury?
A) Cellular swelling
B) Formation of blebs
C) Flocculent densities in mitochondria
D) Dilation of the endoplasmic reticulum
Answer: C
Rationale: Flocculent densities (amorphous densities) in mitochondria are a hallmark of irreversible injury,
representing denatured proteins and lipids. Cellular swelling, bleb formation, and ER dilation are reversible
changes. Irreversible injury is characterized by severe mitochondrial damage and loss of membrane integrity.
7 A patient with a hormone-secreting adrenal adenoma has elevated cortisol levels. The contralateral adrenal
cortex shows decreased cell size and reduced number of cells. This adaptation is best described as:
A) Pathologic atrophy due to decreased workload
B) Compensatory atrophy due to loss of trophic stimulation
C) Atrophy due to ischemia
D) Apoptosis induced by glucocorticoid excess
Answer: B
Rationale: Elevated cortisol from the adenoma suppresses ACTH secretion via negative feedback, leading to loss of
trophic stimulation to the contralateral adrenal cortex, causing atrophy. This is not due to decreased workload
(disuse) or ischemia. While apoptosis may contribute, the primary process is atrophy from reduced trophic support.
8 In a study of cardiac hypertrophy, which of the following molecular events is most directly responsible for the
transition from compensatory hypertrophy to heart failure?
, A) Activation of the PI3K/Akt pathway
B) Increased expression of fetal genes such as ANP and BNP
C) Mitochondrial dysfunction and oxidative stress
D) Enhanced calcium handling by the sarcoplasmic reticulum
Answer: C
Rationale: While hypertrophy initially compensates for increased workload, sustained stress leads to mitochondrial
dysfunction, oxidative stress, and energy deficit, contributing to failure. PI3K/Akt activation is protective. Fetal
gene expression is a marker of hypertrophy but not the cause of failure. Enhanced calcium handling would be
beneficial, not detrimental.
9 Which of the following best describes the role of p53 in cellular response to DNA damage?
A) It promotes cell cycle progression to allow DNA repair
B) It induces apoptosis if DNA damage is irreparable
C) It activates caspases directly
D) It inhibits the production of reactive oxygen species
Answer: B
Rationale: p53 is a tumor suppressor that, in response to DNA damage, can arrest the cell cycle to allow repair or, if
damage is severe, induce apoptosis by upregulating pro-apoptotic genes like Bax. It does not promote cell cycle
progression; it inhibits it. p53 does not directly activate caspases or inhibit ROS production.
10 A researcher treats cells with a drug that inhibits the proteasome. Which of the following is the most likely
consequence?
A) Increased degradation of misfolded proteins
B) Accumulation of ubiquitinated proteins and ER stress
C) Enhanced autophagy
D) Activation of the unfolded protein response (UPR) leading to adaptation
Answer: B
Rationale: Proteasome inhibition prevents degradation of ubiquitinated proteins, leading to their accumulation and
ER stress. This can trigger the UPR, but if severe, it leads to apoptosis. Misfolded proteins are not degraded more;
they accumulate. Autophagy is a separate pathway that may be induced but is not the direct consequence.
11 A researcher exposes cultured hepatocytes to a sublethal dose of carbon tetrachloride, a known inducer of
oxidative stress. After 24 hours, the cells exhibit a marked increase in smooth endoplasmic reticulum (SER)
and upregulation of cytochrome P450 enzymes. Which of the following best describes this cellular response?
A) Atrophy due to decreased functional demand
B) Metaplasia with transformation to a more resistant cell type
C) Hypertrophy resulting from increased workload
D) Hyperplasia with increased cell number
Answer: B
Rationale: The increase in SER and cytochrome P450 represents a classic adaptive response to chemical injury,
where cells undergo metaplasia to a phenotype better suited to metabolize toxins. Atrophy (A) involves shrinkage,
not SER proliferation. Hypertrophy (C) involves increased cell size from workload, not detoxification. Hyperplasia
(D) involves increased cell number, not organelle changes.
12 In a patient with chronic gastroesophageal reflux disease, the squamous epithelium of the lower esophagus is
replaced by columnar epithelium resembling that of the stomach and intestines. This change is most likely
mediated by which of the following mechanisms?
EXAM COMPLETE AND CORRECT DETAILED ANSWERS
|ALREADY GRADED A+ (MARYVILLE UNIVERSITY) - 149
Questions
Section 1: Cellular Adaptation and Injury (Questions 1-15)
1 A researcher studying myocardial ischemia observes that after 30 minutes of oxygen deprivation,
cardiomyocytes exhibit swelling of mitochondria and loss of microvilli, but the nuclei remain normal. Upon
reoxygenation, the cells recover. Which of the following best characterizes the cellular state during the ischemic
period?
A) Necrosis with karyolysis
B) Reversible cell injury
C) Apoptosis with caspase activation
D) Sublethal injury with DNA fragmentation
Answer: B
Rationale: The morphological changes described (mitochondrial swelling, loss of microvilli) are characteristic of
reversible cell injury. The absence of nuclear changes and the ability to recover upon reperfusion confirm
reversibility. Necrosis would show nuclear pyknosis, karyolysis, or karyorrhexis. Apoptosis involves caspase
activation and DNA fragmentation, not reversible swelling.
2 In a patient with chronic iron overload, hepatocytes accumulate excess iron in the form of hemosiderin. This
represents which type of cellular adaptation?
A) Metaplasia
B) Dysplasia
C) Pathologic calcification
D) Intracellular accumulation
Answer: D
Rationale: Hemosiderin accumulation is a form of intracellular accumulation of abnormal substances, not an
adaptive change in cell size, number, or differentiation. Metaplasia is a reversible change where one adult cell type
is replaced by another. Dysplasia refers to abnormal growth. Pathologic calcification involves calcium salt
deposition in tissues.
3 A 45-year-old individual with a history of chronic gastritis undergoes an endoscopic biopsy. Histologic
examination reveals replacement of gastric foveolar cells by intestinal-type columnar cells with goblet cells.
This finding is most consistent with which adaptive process?
A) Hyperplasia
B) Metaplasia
C) Dysplasia
D) Atrophy
Answer: B
Rationale: The replacement of one mature cell type (gastric foveolar) by another (intestinal epithelium with goblet
cells) is classic intestinal metaplasia, often a response to chronic irritation. Hyperplasia is an increase in cell
number. Dysplasia shows disordered growth and cytologic atypia. Atrophy is a decrease in cell size or number.
,4 Which of the following best explains why cells undergoing apoptosis do not elicit an inflammatory response?
A) Caspases degrade pro-inflammatory cytokines
B) Apoptotic cells release IL-10 to suppress inflammation
C) Cellular contents are retained within membrane-bound apoptotic bodies that are rapidly phagocytosed
D) Apoptosis requires ATP, which is depleted in inflammation
Answer: C
Rationale: Apoptotic cells maintain membrane integrity and fragment into apoptotic bodies that are quickly engulfed
by phagocytes without releasing intracellular contents. This prevents activation of the inflammatory response.
Caspases do not degrade cytokines; IL-10 is not specifically released. ATP depletion is a feature of necrosis, not
apoptosis.
5 A laboratory experiment exposes cultured hepatocytes to a toxin that inhibits mitochondrial ATP synthase.
Within minutes, cells show swelling of the endoplasmic reticulum and blebbing of the plasma membrane.
Which of the following is the most likely immediate consequence of ATP depletion?
A) Increased activity of the Na+/K+ ATPase
B) Failure of the Na+/Ca2+ exchanger leading to calcium influx
C) Activation of caspases
D) Upregulation of heat shock proteins
Answer: B
Rationale: ATP depletion impairs the Na+/K+ pump, causing sodium and water accumulation (swelling). It also
reduces function of the Na+/Ca2+ exchanger, leading to intracellular calcium accumulation. Calcium overload
activates enzymes that damage membranes. Caspase activation is ATP-dependent and occurs in apoptosis, not early
injury. Heat shock proteins are upregulated later as a protective response.
6 Which of the following cellular changes is most indicative of irreversible cell injury?
A) Cellular swelling
B) Formation of blebs
C) Flocculent densities in mitochondria
D) Dilation of the endoplasmic reticulum
Answer: C
Rationale: Flocculent densities (amorphous densities) in mitochondria are a hallmark of irreversible injury,
representing denatured proteins and lipids. Cellular swelling, bleb formation, and ER dilation are reversible
changes. Irreversible injury is characterized by severe mitochondrial damage and loss of membrane integrity.
7 A patient with a hormone-secreting adrenal adenoma has elevated cortisol levels. The contralateral adrenal
cortex shows decreased cell size and reduced number of cells. This adaptation is best described as:
A) Pathologic atrophy due to decreased workload
B) Compensatory atrophy due to loss of trophic stimulation
C) Atrophy due to ischemia
D) Apoptosis induced by glucocorticoid excess
Answer: B
Rationale: Elevated cortisol from the adenoma suppresses ACTH secretion via negative feedback, leading to loss of
trophic stimulation to the contralateral adrenal cortex, causing atrophy. This is not due to decreased workload
(disuse) or ischemia. While apoptosis may contribute, the primary process is atrophy from reduced trophic support.
8 In a study of cardiac hypertrophy, which of the following molecular events is most directly responsible for the
transition from compensatory hypertrophy to heart failure?
, A) Activation of the PI3K/Akt pathway
B) Increased expression of fetal genes such as ANP and BNP
C) Mitochondrial dysfunction and oxidative stress
D) Enhanced calcium handling by the sarcoplasmic reticulum
Answer: C
Rationale: While hypertrophy initially compensates for increased workload, sustained stress leads to mitochondrial
dysfunction, oxidative stress, and energy deficit, contributing to failure. PI3K/Akt activation is protective. Fetal
gene expression is a marker of hypertrophy but not the cause of failure. Enhanced calcium handling would be
beneficial, not detrimental.
9 Which of the following best describes the role of p53 in cellular response to DNA damage?
A) It promotes cell cycle progression to allow DNA repair
B) It induces apoptosis if DNA damage is irreparable
C) It activates caspases directly
D) It inhibits the production of reactive oxygen species
Answer: B
Rationale: p53 is a tumor suppressor that, in response to DNA damage, can arrest the cell cycle to allow repair or, if
damage is severe, induce apoptosis by upregulating pro-apoptotic genes like Bax. It does not promote cell cycle
progression; it inhibits it. p53 does not directly activate caspases or inhibit ROS production.
10 A researcher treats cells with a drug that inhibits the proteasome. Which of the following is the most likely
consequence?
A) Increased degradation of misfolded proteins
B) Accumulation of ubiquitinated proteins and ER stress
C) Enhanced autophagy
D) Activation of the unfolded protein response (UPR) leading to adaptation
Answer: B
Rationale: Proteasome inhibition prevents degradation of ubiquitinated proteins, leading to their accumulation and
ER stress. This can trigger the UPR, but if severe, it leads to apoptosis. Misfolded proteins are not degraded more;
they accumulate. Autophagy is a separate pathway that may be induced but is not the direct consequence.
11 A researcher exposes cultured hepatocytes to a sublethal dose of carbon tetrachloride, a known inducer of
oxidative stress. After 24 hours, the cells exhibit a marked increase in smooth endoplasmic reticulum (SER)
and upregulation of cytochrome P450 enzymes. Which of the following best describes this cellular response?
A) Atrophy due to decreased functional demand
B) Metaplasia with transformation to a more resistant cell type
C) Hypertrophy resulting from increased workload
D) Hyperplasia with increased cell number
Answer: B
Rationale: The increase in SER and cytochrome P450 represents a classic adaptive response to chemical injury,
where cells undergo metaplasia to a phenotype better suited to metabolize toxins. Atrophy (A) involves shrinkage,
not SER proliferation. Hypertrophy (C) involves increased cell size from workload, not detoxification. Hyperplasia
(D) involves increased cell number, not organelle changes.
12 In a patient with chronic gastroesophageal reflux disease, the squamous epithelium of the lower esophagus is
replaced by columnar epithelium resembling that of the stomach and intestines. This change is most likely
mediated by which of the following mechanisms?
