NUR 5240 Advanced Pathophysiology Final Exam | Complete
Practice QUESTIONs, Verified Answers & Detailed Rationales |
Latest 2026/2027 Edition
QUESTION 1
Which of the following describes the initial step in the intrinsic
(mitochondrial) pathway of apoptosis?
• A. Activation of extracellular death receptors such as Fas (CD95)
• B. Increased permeability of the mitochondrial outer membrane
mediated by pro-apoptotic proteins like Bax and Bak, leading to
cytochrome c release
• C. Direct proteolytic cleavage of structural actin filaments by
executioner caspases without mitochondrial involvement
• D. Uncontrolled ATP depletion leading to accidental cell lysis and
plasma membrane rupture
Correct Answer: B. Increased permeability of the mitochondrial outer
membrane mediated by pro-apoptotic proteins like Bax and Bak,
leading to cytochrome c release
Detailed Rationale: The intrinsic pathway is governed by the
mitochondria. When internal cellular stress occurs, pro-apoptotic
proteins (Bax, Bak) oligomerize on the mitochondrial membrane,
increasing permeability and releasing cytochrome c into the cytoplasm
to activate the caspase cascade.
QUESTION 2
,Pathological myocardial hypertrophy in response to chronic
hemodynamic overload is primarily driven by which of the following
cellular mechanisms?
• A. Proliferation and rapid mitotic division of mature adult
cardiomyocytes
• B. Upregulation of fetal gene programs, increased protein
synthesis, and enhanced sarcomere assembly without cellular
division
• C. Massive infiltration of neutrophils replacing contractile tissue
with scar matrix
• D. Permanent downregulation of cellular transcription factors to
conserve metabolic energy
Correct Answer: B. Upregulation of fetal gene programs, increased
protein synthesis, and enhanced sarcomere assembly without cellular
division
Detailed Rationale: Adult cardiomyocytes are terminally differentiated
and cannot divide (hyperplasia). Instead, they adapt to increased
workload via hypertrophy—increasing in size through augmented
protein synthesis and reactivation of genes normally active during
embryonic development.
QUESTION 3
A patient presents with severe polyuria, hypernatremia, and high serum
osmolality coupled with a very low urine osmolality that fails to correct
following the administration of exogenous desmopressin (ADH). This
confirms:
, • A. Central Diabetes Insipidus
• B. Nephrogenic Diabetes Insipidus
• C. Syndrome of Inappropriate Antidiuretic Hormone Secretion
(SIADH)
• D. Primary Polydipsia
Correct Answer: B. Nephrogenic Diabetes Insipidus
Detailed Rationale: Nephrogenic diabetes insipidus occurs when the
renal tubules are unresponsive to antidiuretic hormone (ADH), often
due to receptor mutations or drug toxicity. Unlike central DI, exogenous
desmopressin will not concentrate the urine.
QUESTION 4
Myasthenia Gravis is characterized by muscle weakness that worsens
with use. This condition represents which type of hypersensitivity
reaction?
• A. Type I IgE-mediated hypersensitivity
• B. Type II antibody-mediated cytotoxic hypersensitivity
• C. Type III immune complex-mediated hypersensitivity
• D. Type IV cell-mediated delayed hypersensitivity
Correct Answer: B. Type II antibody-mediated cytotoxic hypersensitivity
Detailed Rationale: Myasthenia gravis is a Type II hypersensitivity
disorder where autoantibodies bind to postsynaptic nicotinic
acetylcholine receptors at the neuromuscular junction, blocking neural
transmission and causing receptor destruction via complement
activation and endocytosis.
, QUESTION 5
The tumor suppressor gene TP53 is often referred to as the "guardian of
the genome." What is its primary role following DNA damage?
• A. Inducing rapid mutations to promote cellular evolution and
adaptation
• B. Halting the cell cycle at the G1/S checkpoint to allow DNA
repair, or triggering apoptosis if damage is irreparable
• C. Promoting unregulated angiogenesis to supply the damaged
tissue with nutrients
*D. Directly replicating damaged nucleotide sequences without
proofreading
Correct Answer: B. Halting the cell cycle at the G1/S checkpoint to allow
DNA repair, or triggering apoptosis if damage is irreparable
Detailed Rationale: The p53 protein acts as a critical transcription factor
that senses cellular DNA damage. It arrests the cell cycle to allow DNA
repair enzymes to work or, if the damage is too severe, directs the cell
into programmed cell death (apoptosis).
QUESTION 6
Heart Failure with Preserved Ejection Fraction (HFpEF) differs
fundamentally from HFrEF because it is characterized by:
• A. Severe left ventricular systolic dilation and reduced contractility
• B. Impaired ventricular relaxation and increased chamber
stiffness, leading to elevated filling pressures despite a normal
ejection fraction (≥ 50%)
Practice QUESTIONs, Verified Answers & Detailed Rationales |
Latest 2026/2027 Edition
QUESTION 1
Which of the following describes the initial step in the intrinsic
(mitochondrial) pathway of apoptosis?
• A. Activation of extracellular death receptors such as Fas (CD95)
• B. Increased permeability of the mitochondrial outer membrane
mediated by pro-apoptotic proteins like Bax and Bak, leading to
cytochrome c release
• C. Direct proteolytic cleavage of structural actin filaments by
executioner caspases without mitochondrial involvement
• D. Uncontrolled ATP depletion leading to accidental cell lysis and
plasma membrane rupture
Correct Answer: B. Increased permeability of the mitochondrial outer
membrane mediated by pro-apoptotic proteins like Bax and Bak,
leading to cytochrome c release
Detailed Rationale: The intrinsic pathway is governed by the
mitochondria. When internal cellular stress occurs, pro-apoptotic
proteins (Bax, Bak) oligomerize on the mitochondrial membrane,
increasing permeability and releasing cytochrome c into the cytoplasm
to activate the caspase cascade.
QUESTION 2
,Pathological myocardial hypertrophy in response to chronic
hemodynamic overload is primarily driven by which of the following
cellular mechanisms?
• A. Proliferation and rapid mitotic division of mature adult
cardiomyocytes
• B. Upregulation of fetal gene programs, increased protein
synthesis, and enhanced sarcomere assembly without cellular
division
• C. Massive infiltration of neutrophils replacing contractile tissue
with scar matrix
• D. Permanent downregulation of cellular transcription factors to
conserve metabolic energy
Correct Answer: B. Upregulation of fetal gene programs, increased
protein synthesis, and enhanced sarcomere assembly without cellular
division
Detailed Rationale: Adult cardiomyocytes are terminally differentiated
and cannot divide (hyperplasia). Instead, they adapt to increased
workload via hypertrophy—increasing in size through augmented
protein synthesis and reactivation of genes normally active during
embryonic development.
QUESTION 3
A patient presents with severe polyuria, hypernatremia, and high serum
osmolality coupled with a very low urine osmolality that fails to correct
following the administration of exogenous desmopressin (ADH). This
confirms:
, • A. Central Diabetes Insipidus
• B. Nephrogenic Diabetes Insipidus
• C. Syndrome of Inappropriate Antidiuretic Hormone Secretion
(SIADH)
• D. Primary Polydipsia
Correct Answer: B. Nephrogenic Diabetes Insipidus
Detailed Rationale: Nephrogenic diabetes insipidus occurs when the
renal tubules are unresponsive to antidiuretic hormone (ADH), often
due to receptor mutations or drug toxicity. Unlike central DI, exogenous
desmopressin will not concentrate the urine.
QUESTION 4
Myasthenia Gravis is characterized by muscle weakness that worsens
with use. This condition represents which type of hypersensitivity
reaction?
• A. Type I IgE-mediated hypersensitivity
• B. Type II antibody-mediated cytotoxic hypersensitivity
• C. Type III immune complex-mediated hypersensitivity
• D. Type IV cell-mediated delayed hypersensitivity
Correct Answer: B. Type II antibody-mediated cytotoxic hypersensitivity
Detailed Rationale: Myasthenia gravis is a Type II hypersensitivity
disorder where autoantibodies bind to postsynaptic nicotinic
acetylcholine receptors at the neuromuscular junction, blocking neural
transmission and causing receptor destruction via complement
activation and endocytosis.
, QUESTION 5
The tumor suppressor gene TP53 is often referred to as the "guardian of
the genome." What is its primary role following DNA damage?
• A. Inducing rapid mutations to promote cellular evolution and
adaptation
• B. Halting the cell cycle at the G1/S checkpoint to allow DNA
repair, or triggering apoptosis if damage is irreparable
• C. Promoting unregulated angiogenesis to supply the damaged
tissue with nutrients
*D. Directly replicating damaged nucleotide sequences without
proofreading
Correct Answer: B. Halting the cell cycle at the G1/S checkpoint to allow
DNA repair, or triggering apoptosis if damage is irreparable
Detailed Rationale: The p53 protein acts as a critical transcription factor
that senses cellular DNA damage. It arrests the cell cycle to allow DNA
repair enzymes to work or, if the damage is too severe, directs the cell
into programmed cell death (apoptosis).
QUESTION 6
Heart Failure with Preserved Ejection Fraction (HFpEF) differs
fundamentally from HFrEF because it is characterized by:
• A. Severe left ventricular systolic dilation and reduced contractility
• B. Impaired ventricular relaxation and increased chamber
stiffness, leading to elevated filling pressures despite a normal
ejection fraction (≥ 50%)
