NUR 2063 Essentials of Pathophysiology Exam 1
2026/2027 Actual Exam | 150 Real Exam Questions &
Correct Verified Answers with Detailed Rationales |
Rasmussen | Pass Guaranteed - A+ Graded
1. A researcher is investigating a novel drug that inhibits the activity of hypoxia-inducible factor 1
(HIF-1). Which of the following cellular responses would be most directly impaired by this drug?
A. Increased glycolysis and erythropoietin production under low oxygen
B. Upregulation of p53-mediated apoptosis in response to DNA damage
C. Activation of the unfolded protein response during endoplasmic reticulum stress
D. Induction of heat shock proteins following thermal injury
Answer: A
Rationale: HIF-1± is a transcription factor that stabilizes under hypoxia and promotes expression of
genes for glycolysis (e.g., GLUT1, PFK) and erythropoietin to enhance oxygen delivery. Inhibiting
HIF-1 impairs these adaptive responses. p53, unfolded protein response, and heat shock proteins are
regulated by different pathways.
2. In a patient with chronic inflammation, which of the following cellular changes is most likely to
contribute to the transition from acute to persistent inflammation?
A. Neutrophil apoptosis and clearance by macrophages
B. Shift from a Th1 to a Th2 cytokine profile
C. Macrophage polarization from M1 to M2 phenotype
D. Increased vascular permeability mediated by histamine
Answer: C
Rationale: M2 macrophages promote tissue repair and fibrosis but also sustain chronic inflammation by
secreting anti-inflammatory cytokines like IL-10 and TGF-, which can lead to persistent activation of
fibroblasts. Neutrophil apoptosis typically resolves inflammation. Th1 to Th2 shift may occur but is not
the primary driver. Histamine is a mediator of acute inflammation.
3. A patient with syndrome of inappropriate antidiuretic hormone (SIADH) is admitted with
hyponatremia. Which of the following intravenous fluid prescriptions would be most appropriate
to correct the electrolyte imbalance without causing osmotic demyelination?
A. 0.9% normal saline at 150 mL/hour
B. 3% hypertonic saline at a rate to increase serum sodium by 1 mEq/L/hour
C. Lactated Ringer's solution at maintenance rate
D. D5W (5% dextrose in water) at 100 mL/hour
Answer: B
Page 1
,Rationale: In SIADH, hyponatremia is due to water retention; free water restriction is first-line, but if severe symptoms,
hypertonic saline (3%) is used with a slow correction rate (8-10 mEq/L in 24 hours) to avoid osmotic demyelination. Normal
saline may worsen hyponatremia because it contains sodium but the patient's urine is concentrated. Lactated Ringer's and
D5W are hypotonic and would worsen hyponatremia.
4. A patient with chronic obstructive pulmonary disease (COPD) has arterial blood gas values: pH
7.32, PaCO2 60 mm Hg, HCO3- 30 mEq/L. Which of the following best describes the acid-base
status?
A. Uncompensated respiratory acidosis
B. Partially compensated respiratory acidosis
C. Fully compensated respiratory acidosis
D. Metabolic alkalosis with respiratory compensation
Answer: B
Rationale: The pH is acidic (7.32), PaCO2 is elevated (60 mm Hg), indicating respiratory acidosis. The
HCO3- is elevated (30 mEq/L) above normal, suggesting metabolic compensation. Since the pH remains
acidic, compensation is partial. Full compensation would normalize pH (7.35-7.45). Metabolic alkalosis
would have an alkaline pH.
5. A 48-year-old patient presents with jaundice and hepatomegaly. Liver biopsy shows hepatocytes
with pale, swollen cytoplasm and a 'feathery' appearance. Which of the following cellular
adaptations is most consistent with these findings?
A. Hydropic change due to sodium-potassium ATPase pump failure
B. Glycogen accumulation due to defective glycogenolysis
C. Steatosis due to impaired lipid metabolism
D. Intracellular accumulation of bile salts due to cholestasis
Answer: C
Rationale: Feathery degeneration in hepatocytes is characteristic of steatosis (fatty change), often due to
alcohol or metabolic syndrome. The pale, swollen cytoplasm results from triglyceride accumulation.
Hydropic change shows clear vacuoles but not feathery appearance. Glycogen accumulation is seen in
glycogen storage diseases. Bile salt accumulation causes cholate stasis but not feathery change.
6. A researcher is studying a tumor suppressor gene that is inactivated via promoter
hypermethylation in several cancers. Which of the following epigenetic mechanisms is responsible
for this inactivation?
A. Histone acetylation leading to open chromatin
B. DNA methylation of CpG islands preventing transcription factor binding
C. MicroRNA-mediated degradation of mRNA transcripts
D. Chromatin remodeling by SWI/SNF complexes
Answer: B
Rationale: Promoter hypermethylation of CpG islands is a common epigenetic silencing mechanism for
tumor suppressor genes (e.g., p16, BRCA1). This methylation recruits methyl-binding proteins and
compacts chromatin, inhibiting transcription. Histone acetylation activates genes. MicroRNA degrades
mRNA post-transcriptionally. SWI/SNF complexes remodel nucleosomes but are not
methylation-specific.
Page 2
,7. A patient with type 1 diabetes mellitus develops diabetic ketoacidosis (DKA). Which of the
following combinations of laboratory findings is most consistent with DKA?
A. pH 7.25, PaCO2 30 mm Hg, HCO3- 14 mEq/L, anion gap 18, glucose 450 mg/dL
B. pH 7.50, PaCO2 48 mm Hg, HCO3- 36 mEq/L, anion gap 8, glucose 200 mg/dL
C. pH 7.35, PaCO2 40 mm Hg, HCO3- 24 mEq/L, anion gap 10, glucose 100 mg/dL
D. pH 7.30, PaCO2 50 mm Hg, HCO3- 24 mEq/L, anion gap 12, glucose 300 mg/dL
Answer: A
Rationale: DKA presents with metabolic acidosis (low pH, low HCO3-), compensatory respiratory
alkalosis (low PaCO2), high anion gap from ketone bodies, and hyperglycemia. Option A shows pH 7.25
(acidosis), low HCO3- (14), low PaCO2 (30) as compensation, elevated anion gap (18), and high
glucose. Option B suggests metabolic alkalosis. Option C is normal. Option D shows respiratory
acidosis with normal HCO3-.
8. A patient with chronic kidney disease has a serum potassium of 6.8 mEq/L and an ECG showing
peaked T waves. Which of the following treatments would most rapidly reduce the risk of cardiac
arrhythmias?
A. Intravenous calcium gluconate
B. Intravenous regular insulin with glucose
C. Oral sodium polystyrene sulfonate
D. Hemodialysis
Answer: A
Rationale: Calcium gluconate stabilizes the cardiac membrane by antagonizing the effects of
hyperkalemia on conduction, reducing arrhythmia risk within minutes. Insulin with glucose shifts
potassium intracellularly but takes 30-60 minutes. Sodium polystyrene sulfonate works slowly over
hours. Hemodialysis is effective but requires time for setup. Therefore, calcium is first-line for
life-threatening hyperkalemia.
9. A patient with a history of chronic alcohol abuse develops acute pancreatitis. Which of the
following pathophysiological mechanisms best explains the initiation of pancreatic injury in this
setting?
A. Direct toxic effect of ethanol on pancreatic acinar cells causing necrosis
B. Premature activation of trypsinogen within pancreatic acinar cells
C. Obstruction of the pancreatic duct by protein plugs
D. Ischemia-reperfusion injury due to splanchnic vasoconstriction
Answer: B
Rationale: Alcohol and its metabolites (e.g., fatty acid ethyl esters) increase the sensitivity of acinar cells
to cholecystokinin, leading to premature activation of trypsinogen to trypsin inside the cell, triggering
autodigestion. This is the central initiating event. Direct toxicity, duct obstruction, and ischemia are
contributory but not primary.
Page 3
, 10. A researcher is analyzing a signaling pathway where a ligand binds to a receptor tyrosine
kinase (RTK), leading to activation of Ras and subsequent MAP kinase cascade. Which of the
following mutations would most likely result in constitutive activation of this pathway independent
of ligand?
A. Loss-of-function mutation in the GTPase-activating protein (GAP) for Ras
B. Overexpression of a phosphatase that dephosphorylates the RTK
C. Mutation in the SH2 domain of an adaptor protein preventing binding to phosphotyrosine
D. Increased expression of a ubiquitin ligase that targets Ras for degradation
Answer: A
Rationale: GAPs promote the intrinsic GTPase activity of Ras, converting it to the inactive GDP-bound
form. Loss-of-function GAP mutation would prevent Ras inactivation, keeping it in the active
GTP-bound state and constitutively signaling. Overexpression of phosphatase would reduce RTK
activation. SH2 mutation would impair signaling. Increased ubiquitin ligase would reduce Ras levels,
not activate.
11. A researcher is investigating the role of a specific microRNA in the regulation of the p53
pathway during cellular stress. Which of the following mechanisms best explains how a microRNA
can suppress p53 function without altering the p53 gene sequence?
A. Binding to the p53 promoter and recruiting histone deacetylases to silence transcription
B. Base-pairing with p53 mRNA and promoting its degradation or inhibiting translation
C. Competing with p53 for binding to the ribosome, thereby reducing protein synthesis
D. Interacting with p53 protein and inducing a conformational change that inactivates it
Answer: B
Rationale: MicroRNAs typically exert post-transcriptional regulation by binding to complementary
sequences on target mRNAs, leading to mRNA degradation or translational repression. Option B
correctly describes this mechanism. Option A describes transcriptional silencing, not microRNA
function. Option C is not a known mechanism for microRNAs. Option D describes direct protein-protein
interaction, which is not typical for microRNAs.
12. During a prolonged ischemic event, the accumulation of which metabolic byproduct directly
contributes to the activation of the intrinsic pathway of apoptosis?
A. Lactate
B. Reactive oxygen species
C. Cytochrome c
D. ATP
Answer: B
Rationale: Reactive oxygen species (ROS) accumulate during ischemia-reperfusion and can cause
mitochondrial membrane permeabilization, leading to release of cytochrome c and activation of the
intrinsic apoptotic pathway. Lactate is a byproduct of anaerobic metabolism but does not directly
trigger apoptosis. Cytochrome c release is a consequence, not a cause. ATP depletion contributes to
necrosis, not apoptosis.
Page 4
2026/2027 Actual Exam | 150 Real Exam Questions &
Correct Verified Answers with Detailed Rationales |
Rasmussen | Pass Guaranteed - A+ Graded
1. A researcher is investigating a novel drug that inhibits the activity of hypoxia-inducible factor 1
(HIF-1). Which of the following cellular responses would be most directly impaired by this drug?
A. Increased glycolysis and erythropoietin production under low oxygen
B. Upregulation of p53-mediated apoptosis in response to DNA damage
C. Activation of the unfolded protein response during endoplasmic reticulum stress
D. Induction of heat shock proteins following thermal injury
Answer: A
Rationale: HIF-1± is a transcription factor that stabilizes under hypoxia and promotes expression of
genes for glycolysis (e.g., GLUT1, PFK) and erythropoietin to enhance oxygen delivery. Inhibiting
HIF-1 impairs these adaptive responses. p53, unfolded protein response, and heat shock proteins are
regulated by different pathways.
2. In a patient with chronic inflammation, which of the following cellular changes is most likely to
contribute to the transition from acute to persistent inflammation?
A. Neutrophil apoptosis and clearance by macrophages
B. Shift from a Th1 to a Th2 cytokine profile
C. Macrophage polarization from M1 to M2 phenotype
D. Increased vascular permeability mediated by histamine
Answer: C
Rationale: M2 macrophages promote tissue repair and fibrosis but also sustain chronic inflammation by
secreting anti-inflammatory cytokines like IL-10 and TGF-, which can lead to persistent activation of
fibroblasts. Neutrophil apoptosis typically resolves inflammation. Th1 to Th2 shift may occur but is not
the primary driver. Histamine is a mediator of acute inflammation.
3. A patient with syndrome of inappropriate antidiuretic hormone (SIADH) is admitted with
hyponatremia. Which of the following intravenous fluid prescriptions would be most appropriate
to correct the electrolyte imbalance without causing osmotic demyelination?
A. 0.9% normal saline at 150 mL/hour
B. 3% hypertonic saline at a rate to increase serum sodium by 1 mEq/L/hour
C. Lactated Ringer's solution at maintenance rate
D. D5W (5% dextrose in water) at 100 mL/hour
Answer: B
Page 1
,Rationale: In SIADH, hyponatremia is due to water retention; free water restriction is first-line, but if severe symptoms,
hypertonic saline (3%) is used with a slow correction rate (8-10 mEq/L in 24 hours) to avoid osmotic demyelination. Normal
saline may worsen hyponatremia because it contains sodium but the patient's urine is concentrated. Lactated Ringer's and
D5W are hypotonic and would worsen hyponatremia.
4. A patient with chronic obstructive pulmonary disease (COPD) has arterial blood gas values: pH
7.32, PaCO2 60 mm Hg, HCO3- 30 mEq/L. Which of the following best describes the acid-base
status?
A. Uncompensated respiratory acidosis
B. Partially compensated respiratory acidosis
C. Fully compensated respiratory acidosis
D. Metabolic alkalosis with respiratory compensation
Answer: B
Rationale: The pH is acidic (7.32), PaCO2 is elevated (60 mm Hg), indicating respiratory acidosis. The
HCO3- is elevated (30 mEq/L) above normal, suggesting metabolic compensation. Since the pH remains
acidic, compensation is partial. Full compensation would normalize pH (7.35-7.45). Metabolic alkalosis
would have an alkaline pH.
5. A 48-year-old patient presents with jaundice and hepatomegaly. Liver biopsy shows hepatocytes
with pale, swollen cytoplasm and a 'feathery' appearance. Which of the following cellular
adaptations is most consistent with these findings?
A. Hydropic change due to sodium-potassium ATPase pump failure
B. Glycogen accumulation due to defective glycogenolysis
C. Steatosis due to impaired lipid metabolism
D. Intracellular accumulation of bile salts due to cholestasis
Answer: C
Rationale: Feathery degeneration in hepatocytes is characteristic of steatosis (fatty change), often due to
alcohol or metabolic syndrome. The pale, swollen cytoplasm results from triglyceride accumulation.
Hydropic change shows clear vacuoles but not feathery appearance. Glycogen accumulation is seen in
glycogen storage diseases. Bile salt accumulation causes cholate stasis but not feathery change.
6. A researcher is studying a tumor suppressor gene that is inactivated via promoter
hypermethylation in several cancers. Which of the following epigenetic mechanisms is responsible
for this inactivation?
A. Histone acetylation leading to open chromatin
B. DNA methylation of CpG islands preventing transcription factor binding
C. MicroRNA-mediated degradation of mRNA transcripts
D. Chromatin remodeling by SWI/SNF complexes
Answer: B
Rationale: Promoter hypermethylation of CpG islands is a common epigenetic silencing mechanism for
tumor suppressor genes (e.g., p16, BRCA1). This methylation recruits methyl-binding proteins and
compacts chromatin, inhibiting transcription. Histone acetylation activates genes. MicroRNA degrades
mRNA post-transcriptionally. SWI/SNF complexes remodel nucleosomes but are not
methylation-specific.
Page 2
,7. A patient with type 1 diabetes mellitus develops diabetic ketoacidosis (DKA). Which of the
following combinations of laboratory findings is most consistent with DKA?
A. pH 7.25, PaCO2 30 mm Hg, HCO3- 14 mEq/L, anion gap 18, glucose 450 mg/dL
B. pH 7.50, PaCO2 48 mm Hg, HCO3- 36 mEq/L, anion gap 8, glucose 200 mg/dL
C. pH 7.35, PaCO2 40 mm Hg, HCO3- 24 mEq/L, anion gap 10, glucose 100 mg/dL
D. pH 7.30, PaCO2 50 mm Hg, HCO3- 24 mEq/L, anion gap 12, glucose 300 mg/dL
Answer: A
Rationale: DKA presents with metabolic acidosis (low pH, low HCO3-), compensatory respiratory
alkalosis (low PaCO2), high anion gap from ketone bodies, and hyperglycemia. Option A shows pH 7.25
(acidosis), low HCO3- (14), low PaCO2 (30) as compensation, elevated anion gap (18), and high
glucose. Option B suggests metabolic alkalosis. Option C is normal. Option D shows respiratory
acidosis with normal HCO3-.
8. A patient with chronic kidney disease has a serum potassium of 6.8 mEq/L and an ECG showing
peaked T waves. Which of the following treatments would most rapidly reduce the risk of cardiac
arrhythmias?
A. Intravenous calcium gluconate
B. Intravenous regular insulin with glucose
C. Oral sodium polystyrene sulfonate
D. Hemodialysis
Answer: A
Rationale: Calcium gluconate stabilizes the cardiac membrane by antagonizing the effects of
hyperkalemia on conduction, reducing arrhythmia risk within minutes. Insulin with glucose shifts
potassium intracellularly but takes 30-60 minutes. Sodium polystyrene sulfonate works slowly over
hours. Hemodialysis is effective but requires time for setup. Therefore, calcium is first-line for
life-threatening hyperkalemia.
9. A patient with a history of chronic alcohol abuse develops acute pancreatitis. Which of the
following pathophysiological mechanisms best explains the initiation of pancreatic injury in this
setting?
A. Direct toxic effect of ethanol on pancreatic acinar cells causing necrosis
B. Premature activation of trypsinogen within pancreatic acinar cells
C. Obstruction of the pancreatic duct by protein plugs
D. Ischemia-reperfusion injury due to splanchnic vasoconstriction
Answer: B
Rationale: Alcohol and its metabolites (e.g., fatty acid ethyl esters) increase the sensitivity of acinar cells
to cholecystokinin, leading to premature activation of trypsinogen to trypsin inside the cell, triggering
autodigestion. This is the central initiating event. Direct toxicity, duct obstruction, and ischemia are
contributory but not primary.
Page 3
, 10. A researcher is analyzing a signaling pathway where a ligand binds to a receptor tyrosine
kinase (RTK), leading to activation of Ras and subsequent MAP kinase cascade. Which of the
following mutations would most likely result in constitutive activation of this pathway independent
of ligand?
A. Loss-of-function mutation in the GTPase-activating protein (GAP) for Ras
B. Overexpression of a phosphatase that dephosphorylates the RTK
C. Mutation in the SH2 domain of an adaptor protein preventing binding to phosphotyrosine
D. Increased expression of a ubiquitin ligase that targets Ras for degradation
Answer: A
Rationale: GAPs promote the intrinsic GTPase activity of Ras, converting it to the inactive GDP-bound
form. Loss-of-function GAP mutation would prevent Ras inactivation, keeping it in the active
GTP-bound state and constitutively signaling. Overexpression of phosphatase would reduce RTK
activation. SH2 mutation would impair signaling. Increased ubiquitin ligase would reduce Ras levels,
not activate.
11. A researcher is investigating the role of a specific microRNA in the regulation of the p53
pathway during cellular stress. Which of the following mechanisms best explains how a microRNA
can suppress p53 function without altering the p53 gene sequence?
A. Binding to the p53 promoter and recruiting histone deacetylases to silence transcription
B. Base-pairing with p53 mRNA and promoting its degradation or inhibiting translation
C. Competing with p53 for binding to the ribosome, thereby reducing protein synthesis
D. Interacting with p53 protein and inducing a conformational change that inactivates it
Answer: B
Rationale: MicroRNAs typically exert post-transcriptional regulation by binding to complementary
sequences on target mRNAs, leading to mRNA degradation or translational repression. Option B
correctly describes this mechanism. Option A describes transcriptional silencing, not microRNA
function. Option C is not a known mechanism for microRNAs. Option D describes direct protein-protein
interaction, which is not typical for microRNAs.
12. During a prolonged ischemic event, the accumulation of which metabolic byproduct directly
contributes to the activation of the intrinsic pathway of apoptosis?
A. Lactate
B. Reactive oxygen species
C. Cytochrome c
D. ATP
Answer: B
Rationale: Reactive oxygen species (ROS) accumulate during ischemia-reperfusion and can cause
mitochondrial membrane permeabilization, leading to release of cytochrome c and activation of the
intrinsic apoptotic pathway. Lactate is a byproduct of anaerobic metabolism but does not directly
trigger apoptosis. Cytochrome c release is a consequence, not a cause. ATP depletion contributes to
necrosis, not apoptosis.
Page 4
