NURS 611 EXAM 1 PATHO KEY POINTS
ACTUAL EXAM TEST BANK COMPLETE
180+ QUESTIONS AND CORRECT
DETAILED ANSWERS WITH RATIONALE
SECTION 1: CELL INJURY & ADAPTATION
1. What is the primary difference between apoptosis and necrosis?
• answer:-Apoptosis is programmed cell death that is energy-dependent
and does not trigger inflammation, while necrosis is unprogrammed cell
death caused by injury that releases cellular contents and triggers
inflammation
• Rationale: Apoptosis is a regulated, ATP-dependent process that eliminates
damaged or unwanted cells without eliciting an inflammatory response.
Necrosis results from acute cellular injury, leading to membrane rupture,
release of damage-associated molecular patterns (DAMPs), and subsequent
inflammation.
2. Which type of cellular adaptation involves a decrease in cell size and
metabolic activity?
• answer:-Atrophy
• Rationale: Atrophy is characterized by reduced cell size and function, often
due to disuse, denervation, decreased blood supply, inadequate nutrition, or
hormonal changes. Cells shrink via ubiquitin-proteasome degradation of
cellular proteins and autophagy.
3. A patient with chronic hypertension develops thickening of the left
ventricular wall. This represents which type of cellular adaptation?
, • answer:-Hyperplasia (specifically pathologic hyperplasia - though some
texts call this concentric hypertrophy)
• Corrected answer:-Hypertrophy - Rationale: Cardiomyocytes have limited
replicative capacity; therefore, the heart responds to increased workload
(afterload from hypertension) through hypertrophy (increase in cell size), not
hyperplasia. The left ventricular wall thickens due to increased size of
individual myocytes.
4. Which of the following is an example of physiologic hyperplasia?
• answer:-Uterine enlargement during pregnancy
• Rationale: Physiologic hyperplasia occurs in response to normal stimuli.
During pregnancy, estrogen stimulates endometrial and myometrial cell
division (hyperplasia) in the uterus, followed by some hypertrophy. Other
examples include breast tissue proliferation during lactation and liver
regeneration after partial hepatectomy.
5. Metaplasia is best described as:
• answer:-Reversible replacement of one differentiated cell type with
another, often in response to chronic irritation
• Rationale: Metaplasia represents an adaptive substitution of cells that are
better suited to withstand adverse environmental conditions. Classic
examples include columnar to squamous metaplasia in the respiratory tract
of smokers and squamous to columnar (Barrett esophagus) from chronic
GERD.
6. Which cellular change is considered a hallmark of irreversible cell injury?
• answer:-Severe mitochondrial dysfunction with loss of membrane
integrity and nuclear changes (pyknosis, karyorrhexis, karyolysis)
• Rationale: Irreversible cell injury is characterized by inability to restore
mitochondrial function, loss of plasma membrane integrity (allowing influx
of calcium and leakage of enzymes), and pronounced nuclear changes
, including pyknosis (nuclear shrinkage), karyorrhexis (nuclear
fragmentation), and karyolysis (nuclear dissolution).
7. Free radical-induced cell damage is primarily caused by:
• answer:-Lipid peroxidation of cell membranes, oxidative modification of
proteins, and DNA strand breaks
• Rationale: Reactive oxygen species (ROS) initiate chain reactions of lipid
peroxidation, damaging membrane phospholipids. They also oxidize amino
acid residues, inactivating enzymes, and cause single/double-strand DNA
breaks. Antioxidants like glutathione, vitamins E/C, and enzymes (SOD,
catalase) normally neutralize these effects.
8. What is the role of cytochrome c in apoptosis?
• answer:-Cytochrome c is released from mitochondria into the cytoplasm
where it binds Apaf-1 to form the apoptosome, activating caspase-9 and
initiating the intrinsic apoptotic pathway
• Rationale: Mitochondrial membrane permeabilization (regulated by Bcl-2
family proteins) allows cytochrome c efflux. In the cytosol, it forms the
apoptosome with apoptotic protease activating factor-1 (Apaf-1) and dATP,
which cleaves procaspase-9 to active caspase-9, triggering downstream
effector caspases (caspase-3, -6, -7).
9. Which laboratory finding is most consistent with extensive necrosis?
• answer:-Elevated serum lactate dehydrogenase (LDH) and cell-type-
specific enzymes (AST, ALT, CK, troponin)
• Rationale: Necrotic cells release intracellular enzymes into the bloodstream.
LDH is a nonspecific marker. Hepatocellular necrosis elevates AST/ALT.
Cardiac myocyte necrosis elevates CK-MB and troponins. Pancreatic
necrosis elevates amylase/lipase.
, 10. Dystrophic calcification occurs in:
• answer:-Previously damaged or necrotic tissue despite normal serum
calcium levels
• Rationale: Dystrophic calcification deposits calcium complexes in dead or
degenerated tissues (e.g., atherosclerotic plaques, damaged heart valves,
caseous granulomas of tuberculosis). Serum calcium is normal. This
contrasts with metastatic calcification, which occurs in normal tissues due to
hypercalcemia.
11. A patient with chronic alcoholism develops liver disease characterized by
Mallory bodies (hyaline inclusions). These represent:
• answer:-Aggregates of intermediate filaments (cytokeratins) and
ubiquitin within hepatocytes, indicating cellular injury
• Rationale: Mallory bodies (Mallory-Denk bodies) are eosinophilic
cytoplasmic inclusions seen in alcoholic and non-alcoholic steatohepatitis.
They represent misfolded keratin intermediate filaments and other proteins
that have undergone ubiquitination, reflecting chronic hepatocellular injury
and oxidative stress.
12. Which statement best describes the ischemic cascade?
• answer:-Progressive sequence of ATP depletion, ion pump failure
(Na+/K+ ATPase), calcium influx, mitochondrial dysfunction, and
eventual cell death following interruption of blood flow
• Rationale: Ischemia causes oxygen/nutrient deprivation → reduced oxidative
phosphorylation → ATP depletion → Na+/K+ pump failure → cellular
swelling. Anaerobic glycolysis generates lactate, lowering pH. Calcium
accumulates, activating destructive enzymes (phospholipases, proteases,
endonucleases), culminating in irreversible injury.
13. Reperfusion injury is primarily mediated by:
ACTUAL EXAM TEST BANK COMPLETE
180+ QUESTIONS AND CORRECT
DETAILED ANSWERS WITH RATIONALE
SECTION 1: CELL INJURY & ADAPTATION
1. What is the primary difference between apoptosis and necrosis?
• answer:-Apoptosis is programmed cell death that is energy-dependent
and does not trigger inflammation, while necrosis is unprogrammed cell
death caused by injury that releases cellular contents and triggers
inflammation
• Rationale: Apoptosis is a regulated, ATP-dependent process that eliminates
damaged or unwanted cells without eliciting an inflammatory response.
Necrosis results from acute cellular injury, leading to membrane rupture,
release of damage-associated molecular patterns (DAMPs), and subsequent
inflammation.
2. Which type of cellular adaptation involves a decrease in cell size and
metabolic activity?
• answer:-Atrophy
• Rationale: Atrophy is characterized by reduced cell size and function, often
due to disuse, denervation, decreased blood supply, inadequate nutrition, or
hormonal changes. Cells shrink via ubiquitin-proteasome degradation of
cellular proteins and autophagy.
3. A patient with chronic hypertension develops thickening of the left
ventricular wall. This represents which type of cellular adaptation?
, • answer:-Hyperplasia (specifically pathologic hyperplasia - though some
texts call this concentric hypertrophy)
• Corrected answer:-Hypertrophy - Rationale: Cardiomyocytes have limited
replicative capacity; therefore, the heart responds to increased workload
(afterload from hypertension) through hypertrophy (increase in cell size), not
hyperplasia. The left ventricular wall thickens due to increased size of
individual myocytes.
4. Which of the following is an example of physiologic hyperplasia?
• answer:-Uterine enlargement during pregnancy
• Rationale: Physiologic hyperplasia occurs in response to normal stimuli.
During pregnancy, estrogen stimulates endometrial and myometrial cell
division (hyperplasia) in the uterus, followed by some hypertrophy. Other
examples include breast tissue proliferation during lactation and liver
regeneration after partial hepatectomy.
5. Metaplasia is best described as:
• answer:-Reversible replacement of one differentiated cell type with
another, often in response to chronic irritation
• Rationale: Metaplasia represents an adaptive substitution of cells that are
better suited to withstand adverse environmental conditions. Classic
examples include columnar to squamous metaplasia in the respiratory tract
of smokers and squamous to columnar (Barrett esophagus) from chronic
GERD.
6. Which cellular change is considered a hallmark of irreversible cell injury?
• answer:-Severe mitochondrial dysfunction with loss of membrane
integrity and nuclear changes (pyknosis, karyorrhexis, karyolysis)
• Rationale: Irreversible cell injury is characterized by inability to restore
mitochondrial function, loss of plasma membrane integrity (allowing influx
of calcium and leakage of enzymes), and pronounced nuclear changes
, including pyknosis (nuclear shrinkage), karyorrhexis (nuclear
fragmentation), and karyolysis (nuclear dissolution).
7. Free radical-induced cell damage is primarily caused by:
• answer:-Lipid peroxidation of cell membranes, oxidative modification of
proteins, and DNA strand breaks
• Rationale: Reactive oxygen species (ROS) initiate chain reactions of lipid
peroxidation, damaging membrane phospholipids. They also oxidize amino
acid residues, inactivating enzymes, and cause single/double-strand DNA
breaks. Antioxidants like glutathione, vitamins E/C, and enzymes (SOD,
catalase) normally neutralize these effects.
8. What is the role of cytochrome c in apoptosis?
• answer:-Cytochrome c is released from mitochondria into the cytoplasm
where it binds Apaf-1 to form the apoptosome, activating caspase-9 and
initiating the intrinsic apoptotic pathway
• Rationale: Mitochondrial membrane permeabilization (regulated by Bcl-2
family proteins) allows cytochrome c efflux. In the cytosol, it forms the
apoptosome with apoptotic protease activating factor-1 (Apaf-1) and dATP,
which cleaves procaspase-9 to active caspase-9, triggering downstream
effector caspases (caspase-3, -6, -7).
9. Which laboratory finding is most consistent with extensive necrosis?
• answer:-Elevated serum lactate dehydrogenase (LDH) and cell-type-
specific enzymes (AST, ALT, CK, troponin)
• Rationale: Necrotic cells release intracellular enzymes into the bloodstream.
LDH is a nonspecific marker. Hepatocellular necrosis elevates AST/ALT.
Cardiac myocyte necrosis elevates CK-MB and troponins. Pancreatic
necrosis elevates amylase/lipase.
, 10. Dystrophic calcification occurs in:
• answer:-Previously damaged or necrotic tissue despite normal serum
calcium levels
• Rationale: Dystrophic calcification deposits calcium complexes in dead or
degenerated tissues (e.g., atherosclerotic plaques, damaged heart valves,
caseous granulomas of tuberculosis). Serum calcium is normal. This
contrasts with metastatic calcification, which occurs in normal tissues due to
hypercalcemia.
11. A patient with chronic alcoholism develops liver disease characterized by
Mallory bodies (hyaline inclusions). These represent:
• answer:-Aggregates of intermediate filaments (cytokeratins) and
ubiquitin within hepatocytes, indicating cellular injury
• Rationale: Mallory bodies (Mallory-Denk bodies) are eosinophilic
cytoplasmic inclusions seen in alcoholic and non-alcoholic steatohepatitis.
They represent misfolded keratin intermediate filaments and other proteins
that have undergone ubiquitination, reflecting chronic hepatocellular injury
and oxidative stress.
12. Which statement best describes the ischemic cascade?
• answer:-Progressive sequence of ATP depletion, ion pump failure
(Na+/K+ ATPase), calcium influx, mitochondrial dysfunction, and
eventual cell death following interruption of blood flow
• Rationale: Ischemia causes oxygen/nutrient deprivation → reduced oxidative
phosphorylation → ATP depletion → Na+/K+ pump failure → cellular
swelling. Anaerobic glycolysis generates lactate, lowering pH. Calcium
accumulates, activating destructive enzymes (phospholipases, proteases,
endonucleases), culminating in irreversible injury.
13. Reperfusion injury is primarily mediated by:
