Pathophysiology Exam
Comprehensive Nursing Review
Examination Booklet | 120 Items
Instructions: Select the single best answer for each item. Correct responses and rationales appear immediately beneath each
question.
1. A 58-year-old heavy smoker has squamous metaplasia of the bronchial epithelium. Which cellular
adaptation mechanism is this finding most consistent with?
A. Hypertrophy of columnar epithelium converting to goblet cells
B. Reversible replacement of one adult cell type by another adult cell type [CORRECT]
C. Hyperplasia induced by chronic irritation alone with no cell-type change
D. Dysplastic transformation indicating irreversible neoplastic change
Correct Answer: B
Rationale: Correct because metaplasia is the reversible substitution of one differentiated adult cell type
(columnar) for another (squamous) in response to chronic injury such as smoking. This matches the textbook
definition of adaptive metaplasia, not dysplasia or hypertrophy.
2. A 72-year-old with chronic heart failure presents with bilateral crackles, JVD, and 3+ pitting
edema. Which hemodynamic mechanism is the primary driver of these findings?
A. Decreased afterload causing excessive forward cardiac output
B. Pure right-sided failure with no pulmonary congestion component
C. Reduced systemic vascular resistance improving renal perfusion
D. Increased preload with backward failure into both pulmonary and systemic venous circuits
[CORRECT]
Correct Answer: D
Rationale: Correct because chronic heart failure produces backward congestion: left-sided failure raises
pulmonary venous pressure (crackles), while right-sided failure raises systemic venous pressure (JVD,
edema). Priority is recognizing biventricular backward failure as the unifying mechanism.
3. Arterial blood gas: pH 7.30, PaCO2 32 mmHg, HCO3 18 mEq/L. Which acid-base imbalance is
present?
A. Respiratory acidosis with partial renal compensation
B. Metabolic alkalosis with respiratory compensation
C. Partially compensated metabolic acidosis [CORRECT]
D. Mixed respiratory and metabolic alkalosis
Correct Answer: C
Rationale: Correct because low pH with low HCO3 indicates metabolic acidosis, and the low PaCO2 reflects
respiratory compensation. This matches the expected compensation pattern of Kussmaul respirations
blowing off CO2.
,4. A patient with urosepsis meets SIRS criteria with fever, tachycardia, tachypnea, and WBC 18,000.
Which pathophysiologic process best explains the vasodilation and hypotension seen in septic shock?
A. Direct myocardial depression from endotoxin alone
B. Sympathetic-mediated vasoconstriction causing afterload rise
C. Acute adrenal insufficiency producing mineralocorticoid deficit
D. Massive release of inflammatory mediators (TNF, IL-1, NO) causing distributive vasodilation
[CORRECT]
Correct Answer: D
Rationale: Correct because septic shock is a distributive shock driven by cytokines (TNF-alpha, IL-1) and
nitric oxide that produce profound systemic vasodilation and capillary leak. This matches the
pathophysiology of warm shock seen early in sepsis.
5. A 19-year-old with new type 1 diabetes has fruity breath, Kussmaul respirations, and glucose 612
mg/dL. Which metabolic derangement explains the deep, rapid breathing?
A. Primary respiratory alkalosis from anxiety-induced hyperventilation
B. CNS depression from severe hyperglycemia causing Cheyne-Stokes
C. Compensatory hyperventilation for metabolic acidosis caused by ketoacid accumulation
[CORRECT]
D. Hypoxemia from non-cardiogenic pulmonary edema
Correct Answer: C
Rationale: Correct because DKA produces a high-anion-gap metabolic acidosis from ketone bodies;
Kussmaul respirations are the respiratory compensation to blow off CO2 and raise pH. Priority is
recognizing the compensatory mechanism, not a primary lung problem.
6. A 40-year-old sustained second- and third-degree burns over 35% TBSA. During the emergent
phase, which fluid shift is most likely?
A. Intracellular to extracellular movement causing hypervolemia
B. Interstitial to vascular space causing hypertension
C. Plasma to interstitial space causing edema and hypovolemia [CORRECT]
D. No significant fluid shift during the first 24 hours
Correct Answer: C
Rationale: Correct because burn injury increases capillary permeability, allowing plasma proteins and fluid
to shift into the interstitial space, producing edema and hypovolemic shock. This matches the rationale for
Parkland fluid resuscitation in the first 24 hours.
7. A 65-year-old with COPD has chronic CO2 retention with baseline PaCO2 60 mmHg. Which
acid-base compensation is expected?
A. Respiratory alkalosis as the primary disorder
B. Compensated respiratory acidosis with elevated HCO3 from renal retention [CORRECT]
C. Acute uncompensated respiratory acidosis
D. Metabolic acidosis from chronic hypoxemia
Correct Answer: B
Rationale: Correct because chronic CO2 retention in COPD triggers renal compensation: bicarbonate is
retained to normalize pH. This matches the classic compensated respiratory acidosis ABG pattern of
elevated PaCO2 with proportionally elevated HCO3.
,8. A 68-year-old suddenly develops right-sided hemiparesis and aphasia. CT shows no hemorrhage.
Which pathophysiologic mechanism is most likely?
A. Hemorrhagic stroke from ruptured cerebral aneurysm
B. Lacunar infarct from hypertensive small-vessel disease producing ataxia
C. Subarachnoid hemorrhage with thunderclap headache
D. Embolic occlusion of the left middle cerebral artery [CORRECT]
Correct Answer: D
Rationale: Correct because sudden focal neurologic deficits with aphasia and right hemiparesis localize to
the dominant (left) middle cerebral artery territory. This matches the most common ischemic stroke pattern;
CT without hemorrhage supports ischemic etiology.
9. During the acute inflammatory response, which cell is the first to arrive at the site of bacterial
injury within 30-60 minutes?
A. Lymphocyte arriving for adaptive response
B. Eosinophil mediating parasitic defense
C. Macrophage derived from circulating monocytes
D. Neutrophil performing early phagocytosis [CORRECT]
Correct Answer: D
Rationale: Correct because neutrophils are the predominant early effector cell in acute bacterial
inflammation, arriving within 30-60 minutes via margination and diapedesis. This matches the classic acute
inflammation cellular timeline.
10. A child develops urticaria, wheezing, and hypotension within minutes of a bee sting. Which
immune mechanism is responsible?
A. Type I IgE-mediated mast cell degranulation releasing histamine [CORRECT]
B. IgG-mediated cytotoxic reaction against erythrocytes
C. Type III immune complex deposition in glomeruli
D. Type IV delayed T-cell-mediated tuberculin reaction
Correct Answer: A
Rationale: Correct because anaphylaxis is a Type I hypersensitivity reaction: IgE binds mast cells, and
re-exposure triggers degranulation with histamine release causing urticaria, bronchospasm, and shock. This
matches the rapid timeline and classic mediator.
11. A patient with acute kidney injury has potassium 6.8 mEq/L. Which ECG finding is the most
dangerous and indicates the need for immediate intervention?
A. Peaked T waves progressing to widened QRS [CORRECT]
B. Sinus bradycardia alone with no waveform change
C. Prolonged QT interval from hypocalcemia
D. ST elevation in anterior leads suggesting MI
Correct Answer: A
Rationale: Correct because hyperkalemia alters myocardial repolarization: tall peaked T waves appear first,
followed by widened QRS, then sine-wave and arrest. This matches the progression that mandates
immediate calcium gluconate and potassium-lowering therapy.
, 12. A 55-year-old with essential hypertension has left ventricular hypertrophy on ECG. Which
mechanism best explains this cardiac adaptation?
A. Pressure overload producing concentric hypertrophy [CORRECT]
B. Volume overload producing eccentric hypertrophy
C. Myocardial ischemia causing dilated cardiomyopathy
D. Inflammatory myocarditis causing interstitial fibrosis
Correct Answer: A
Rationale: Correct because chronic pressure overload from hypertension produces concentric hypertrophy
(parallel sarcomere deposition) as the ventricle works against elevated afterload. This matches the
pathophysiology differentiating it from eccentric hypertrophy seen in volume overload.
13. A patient with sepsis develops oozing from IV sites, petechiae, and prolonged PT/PTT with low
platelets and low fibrinogen. Which pathophysiologic process is occurring?
A. Primary immune thrombocytopenia from autoantibodies
B. Widespread microvascular coagulation with consumption of clotting factors and platelets
[CORRECT]
C. Vitamin K deficiency causing factor depletion
D. Heparin-induced thrombocytopenia with thrombosis
Correct Answer: B
Rationale: Correct because DIC triggers widespread thrombin activation, consuming platelets and clotting
factors, which paradoxically causes bleeding. This matches the classic lab pattern of prolonged PT/PTT, low
fibrinogen, and thrombocytopenia in sepsis.
14. An 11-year-old with asthma has wheezing, prolonged exhalation, and hyperinflation on chest
X-ray. Which pathophysiologic triad drives these findings?
A. Alveolar destruction, fibrosis, and loss of elastic recoil
B. Pulmonary vascular remodeling causing right heart strain
C. Bronchoconstriction, mucosal edema, and mucus plugs [CORRECT]
D. Pleural effusion compressing lung parenchyma
Correct Answer: C
Rationale: Correct because asthma exacerbation involves three reversible airway changes: smooth muscle
bronchoconstriction, inflammatory mucosal edema, and tenacious mucus plugs. This matches the
pathophysiology that responds to bronchodilators and corticosteroids.
MINI-CASE: A 48-year-old accountant reports burning epigastric pain that worsens with meals and is relieved by
antacids. H. pylori stool antigen is positive. Endoscopy reveals a duodenal ulcer.
15. Which pathophysiologic mechanism best explains this patient's duodenal ulcer?
A. Excessive somatostatin secretion suppressing acid production
B. Helicobacter pylori urease and cytokines disrupting mucosal defenses with hypergastrinemia
[CORRECT]
C. Autoimmune destruction of parietal cells causing achlorhydria
D. Zollinger-Ellison syndrome with gastrinoma of the pancreas
Correct Answer: B
Rationale: Correct because H. pylori colonizes the duodenal gastric metaplasia, secretes urease that
neutralizes acid locally, and induces inflammation that disrupts mucosal defenses while increasing gastrin.
This matches the dominant cause of duodenal ulcers worldwide.
Comprehensive Nursing Review
Examination Booklet | 120 Items
Instructions: Select the single best answer for each item. Correct responses and rationales appear immediately beneath each
question.
1. A 58-year-old heavy smoker has squamous metaplasia of the bronchial epithelium. Which cellular
adaptation mechanism is this finding most consistent with?
A. Hypertrophy of columnar epithelium converting to goblet cells
B. Reversible replacement of one adult cell type by another adult cell type [CORRECT]
C. Hyperplasia induced by chronic irritation alone with no cell-type change
D. Dysplastic transformation indicating irreversible neoplastic change
Correct Answer: B
Rationale: Correct because metaplasia is the reversible substitution of one differentiated adult cell type
(columnar) for another (squamous) in response to chronic injury such as smoking. This matches the textbook
definition of adaptive metaplasia, not dysplasia or hypertrophy.
2. A 72-year-old with chronic heart failure presents with bilateral crackles, JVD, and 3+ pitting
edema. Which hemodynamic mechanism is the primary driver of these findings?
A. Decreased afterload causing excessive forward cardiac output
B. Pure right-sided failure with no pulmonary congestion component
C. Reduced systemic vascular resistance improving renal perfusion
D. Increased preload with backward failure into both pulmonary and systemic venous circuits
[CORRECT]
Correct Answer: D
Rationale: Correct because chronic heart failure produces backward congestion: left-sided failure raises
pulmonary venous pressure (crackles), while right-sided failure raises systemic venous pressure (JVD,
edema). Priority is recognizing biventricular backward failure as the unifying mechanism.
3. Arterial blood gas: pH 7.30, PaCO2 32 mmHg, HCO3 18 mEq/L. Which acid-base imbalance is
present?
A. Respiratory acidosis with partial renal compensation
B. Metabolic alkalosis with respiratory compensation
C. Partially compensated metabolic acidosis [CORRECT]
D. Mixed respiratory and metabolic alkalosis
Correct Answer: C
Rationale: Correct because low pH with low HCO3 indicates metabolic acidosis, and the low PaCO2 reflects
respiratory compensation. This matches the expected compensation pattern of Kussmaul respirations
blowing off CO2.
,4. A patient with urosepsis meets SIRS criteria with fever, tachycardia, tachypnea, and WBC 18,000.
Which pathophysiologic process best explains the vasodilation and hypotension seen in septic shock?
A. Direct myocardial depression from endotoxin alone
B. Sympathetic-mediated vasoconstriction causing afterload rise
C. Acute adrenal insufficiency producing mineralocorticoid deficit
D. Massive release of inflammatory mediators (TNF, IL-1, NO) causing distributive vasodilation
[CORRECT]
Correct Answer: D
Rationale: Correct because septic shock is a distributive shock driven by cytokines (TNF-alpha, IL-1) and
nitric oxide that produce profound systemic vasodilation and capillary leak. This matches the
pathophysiology of warm shock seen early in sepsis.
5. A 19-year-old with new type 1 diabetes has fruity breath, Kussmaul respirations, and glucose 612
mg/dL. Which metabolic derangement explains the deep, rapid breathing?
A. Primary respiratory alkalosis from anxiety-induced hyperventilation
B. CNS depression from severe hyperglycemia causing Cheyne-Stokes
C. Compensatory hyperventilation for metabolic acidosis caused by ketoacid accumulation
[CORRECT]
D. Hypoxemia from non-cardiogenic pulmonary edema
Correct Answer: C
Rationale: Correct because DKA produces a high-anion-gap metabolic acidosis from ketone bodies;
Kussmaul respirations are the respiratory compensation to blow off CO2 and raise pH. Priority is
recognizing the compensatory mechanism, not a primary lung problem.
6. A 40-year-old sustained second- and third-degree burns over 35% TBSA. During the emergent
phase, which fluid shift is most likely?
A. Intracellular to extracellular movement causing hypervolemia
B. Interstitial to vascular space causing hypertension
C. Plasma to interstitial space causing edema and hypovolemia [CORRECT]
D. No significant fluid shift during the first 24 hours
Correct Answer: C
Rationale: Correct because burn injury increases capillary permeability, allowing plasma proteins and fluid
to shift into the interstitial space, producing edema and hypovolemic shock. This matches the rationale for
Parkland fluid resuscitation in the first 24 hours.
7. A 65-year-old with COPD has chronic CO2 retention with baseline PaCO2 60 mmHg. Which
acid-base compensation is expected?
A. Respiratory alkalosis as the primary disorder
B. Compensated respiratory acidosis with elevated HCO3 from renal retention [CORRECT]
C. Acute uncompensated respiratory acidosis
D. Metabolic acidosis from chronic hypoxemia
Correct Answer: B
Rationale: Correct because chronic CO2 retention in COPD triggers renal compensation: bicarbonate is
retained to normalize pH. This matches the classic compensated respiratory acidosis ABG pattern of
elevated PaCO2 with proportionally elevated HCO3.
,8. A 68-year-old suddenly develops right-sided hemiparesis and aphasia. CT shows no hemorrhage.
Which pathophysiologic mechanism is most likely?
A. Hemorrhagic stroke from ruptured cerebral aneurysm
B. Lacunar infarct from hypertensive small-vessel disease producing ataxia
C. Subarachnoid hemorrhage with thunderclap headache
D. Embolic occlusion of the left middle cerebral artery [CORRECT]
Correct Answer: D
Rationale: Correct because sudden focal neurologic deficits with aphasia and right hemiparesis localize to
the dominant (left) middle cerebral artery territory. This matches the most common ischemic stroke pattern;
CT without hemorrhage supports ischemic etiology.
9. During the acute inflammatory response, which cell is the first to arrive at the site of bacterial
injury within 30-60 minutes?
A. Lymphocyte arriving for adaptive response
B. Eosinophil mediating parasitic defense
C. Macrophage derived from circulating monocytes
D. Neutrophil performing early phagocytosis [CORRECT]
Correct Answer: D
Rationale: Correct because neutrophils are the predominant early effector cell in acute bacterial
inflammation, arriving within 30-60 minutes via margination and diapedesis. This matches the classic acute
inflammation cellular timeline.
10. A child develops urticaria, wheezing, and hypotension within minutes of a bee sting. Which
immune mechanism is responsible?
A. Type I IgE-mediated mast cell degranulation releasing histamine [CORRECT]
B. IgG-mediated cytotoxic reaction against erythrocytes
C. Type III immune complex deposition in glomeruli
D. Type IV delayed T-cell-mediated tuberculin reaction
Correct Answer: A
Rationale: Correct because anaphylaxis is a Type I hypersensitivity reaction: IgE binds mast cells, and
re-exposure triggers degranulation with histamine release causing urticaria, bronchospasm, and shock. This
matches the rapid timeline and classic mediator.
11. A patient with acute kidney injury has potassium 6.8 mEq/L. Which ECG finding is the most
dangerous and indicates the need for immediate intervention?
A. Peaked T waves progressing to widened QRS [CORRECT]
B. Sinus bradycardia alone with no waveform change
C. Prolonged QT interval from hypocalcemia
D. ST elevation in anterior leads suggesting MI
Correct Answer: A
Rationale: Correct because hyperkalemia alters myocardial repolarization: tall peaked T waves appear first,
followed by widened QRS, then sine-wave and arrest. This matches the progression that mandates
immediate calcium gluconate and potassium-lowering therapy.
, 12. A 55-year-old with essential hypertension has left ventricular hypertrophy on ECG. Which
mechanism best explains this cardiac adaptation?
A. Pressure overload producing concentric hypertrophy [CORRECT]
B. Volume overload producing eccentric hypertrophy
C. Myocardial ischemia causing dilated cardiomyopathy
D. Inflammatory myocarditis causing interstitial fibrosis
Correct Answer: A
Rationale: Correct because chronic pressure overload from hypertension produces concentric hypertrophy
(parallel sarcomere deposition) as the ventricle works against elevated afterload. This matches the
pathophysiology differentiating it from eccentric hypertrophy seen in volume overload.
13. A patient with sepsis develops oozing from IV sites, petechiae, and prolonged PT/PTT with low
platelets and low fibrinogen. Which pathophysiologic process is occurring?
A. Primary immune thrombocytopenia from autoantibodies
B. Widespread microvascular coagulation with consumption of clotting factors and platelets
[CORRECT]
C. Vitamin K deficiency causing factor depletion
D. Heparin-induced thrombocytopenia with thrombosis
Correct Answer: B
Rationale: Correct because DIC triggers widespread thrombin activation, consuming platelets and clotting
factors, which paradoxically causes bleeding. This matches the classic lab pattern of prolonged PT/PTT, low
fibrinogen, and thrombocytopenia in sepsis.
14. An 11-year-old with asthma has wheezing, prolonged exhalation, and hyperinflation on chest
X-ray. Which pathophysiologic triad drives these findings?
A. Alveolar destruction, fibrosis, and loss of elastic recoil
B. Pulmonary vascular remodeling causing right heart strain
C. Bronchoconstriction, mucosal edema, and mucus plugs [CORRECT]
D. Pleural effusion compressing lung parenchyma
Correct Answer: C
Rationale: Correct because asthma exacerbation involves three reversible airway changes: smooth muscle
bronchoconstriction, inflammatory mucosal edema, and tenacious mucus plugs. This matches the
pathophysiology that responds to bronchodilators and corticosteroids.
MINI-CASE: A 48-year-old accountant reports burning epigastric pain that worsens with meals and is relieved by
antacids. H. pylori stool antigen is positive. Endoscopy reveals a duodenal ulcer.
15. Which pathophysiologic mechanism best explains this patient's duodenal ulcer?
A. Excessive somatostatin secretion suppressing acid production
B. Helicobacter pylori urease and cytokines disrupting mucosal defenses with hypergastrinemia
[CORRECT]
C. Autoimmune destruction of parietal cells causing achlorhydria
D. Zollinger-Ellison syndrome with gastrinoma of the pancreas
Correct Answer: B
Rationale: Correct because H. pylori colonizes the duodenal gastric metaplasia, secretes urease that
neutralizes acid locally, and induces inflammation that disrupts mucosal defenses while increasing gastrin.
This matches the dominant cause of duodenal ulcers worldwide.
