NUR 2063 Exam 2: Essentials of Pathophysiology - Complete Questions & Answers
Exam 2 - NUR2063 / NUR 2063
Essentials of Pathophysiology
Rasmussen
Latest Update
Mechanism-focused pathophysiology with clinical correlations and lab value interpretation
Total Questions Sections Options per Q Cognitive Mix
130 8 4 (A-D) 30% Recall / 50% App / 20% Analysis
This comprehensive exam preparation document covers the full breadth of NUR 2063 Exam 2 at Rasmussen
University, focusing on pathophysiologic mechanisms across all major body systems: cardiovascular, respiratory,
renal/urinary, fluid/electrolyte/acid-base, endocrine, gastrointestinal/hepatic, hematologic, and neurologic. Each
question is mechanism-focused, requiring explanation of pathophysiologic processes rather than symptom recall.
Detailed rationales serve as study content with clinical correlations, lab value interpretation, compensation reasoning,
and comparison of similar pathophysiologic states.
Exam Structure
Section Topic Questions
Section 1: Cardiovascular Pathophysiology - Heart Failure, Ischemia/Infarction,
Q1-Q20 20
Dysrhythmia Mechanisms, Valvular Disease, and Vascular Disorders
Section 2: Respiratory Pathophysiology - Obstructive/Restrictive Disease, Gas
Q21-Q37 17
Exchange, ARDS, PE, and Respiratory Failure
Section 3: Renal and Urinary Pathophysiology - AKI, CKD, Glomerulonephritis,
Q38-Q53 16
Nephrotic Syndrome, and UTIs
Section 4: Fluid, Electrolyte, and Acid-Base Alterations in Disease - Complex
Q54-Q67 14
Imbalances, Compensation, and Mixed Disorders
Section 5: Endocrine Pathophysiology - Diabetes, DKA/HHS, Thyroid, Adrenal,
Q68-Q85 18
Pituitary, and Parathyroid Disorders
Section 6: Gastrointestinal and Hepatic Pathophysiology - PUD, IBD, Obstruction,
Q86-Q101 16
Pancreatitis, Cirrhosis, and Hepatitis
Section 7: Hematologic Pathophysiology - Anemias, Leukemias, Lymphomas,
Q102-Q116 15
Coagulopathies, and DIC
Page 1
,NUR 2063 Exam 2: Essentials of Pathophysiology - Complete Questions & Answers
Section 8: Neurologic Pathophysiology - Stroke, Increased ICP, Seizures,
Q117-Q130 14
Neurodegenerative Disease, and Spinal Cord Injury
Section 1: Cardiovascular Pathophysiology
Heart Failure, Ischemia/Infarction, Dysrhythmia Mechanisms, Valvular Disease, and Vascular Disorders
Q1: A 68-year-old client with chronic hypertension develops exertional dyspnea, bilateral crackles, and
an S3 heart sound. Echocardiography reveals left ventricular ejection fraction of 30%. Which
pathophysiologic mechanism BEST explains this presentation?
A. Diastolic heart failure with preserved EF
B. Systolic heart failure with reduced EF — impaired contractility leads to decreased stroke volume, increased
end-diastolic volume, pulmonary venous congestion, and neurohormonal activation (RAAS, sympathetic)
[CORRECT]
C. Right-sided heart failure from cor pulmonale
D. Valvular stenosis causing outflow obstruction
Correct Answer: B. Systolic heart failure with reduced EF — impaired contractility leads to decreased stroke
volume, increased end-diastolic volume, pulmonary venous congestion, and neurohormonal activation (RAAS,
sympathetic)
Rationale: Systolic heart failure (HFrEF — EF ≤40%) results from impaired contractility (ischemia, MI, dilated
cardiomyopathy, myocarditis). Decreased stroke volume → decreased cardiac output → decreased renal perfusion →
RAAS activation (renin → Ang II → aldosterone) causing sodium/water retention, vasoconstriction, and sympathetic
activation → increased afterload and preload → further LV dilation and remodeling (eccentric hypertrophy, fibrosis,
apoptosis). Backward failure to lungs: increased LVEDP → increased LA pressure → pulmonary venous hypertension →
transudation of fluid into alveoli → pulmonary edema (crackles, S3 from volume overload, dyspnea). BNP released from
ventricular myocardium in response to wall stress — diagnostic marker. Treatment: ACEi/ARB/ARNI, beta-blockers,
aldosterone antagonists, SGLT2 inhibitors, diuretics, ICD/CRT.
Q2: A 72-year-old female client presents with exertional dyspnea and fatigue. Echocardiogram shows
preserved ejection fraction (EF 65%) but impaired ventricular relaxation with elevated left ventricular
end-diastolic pressure. Which pathophysiologic mechanism BEST explains this condition?
A. Systolic heart failure from impaired contractility
B. Diastolic heart failure (HFpEF) — impaired ventricular relaxation and decreased compliance (stiff ventricle)
→ elevated LVEDP → pulmonary venous congestion despite preserved EF; common in elderly women with
HTN, diabetes [CORRECT]
C. Right ventricular infarction
D. Mitral stenosis
Correct Answer: B. Diastolic heart failure (HFpEF) — impaired ventricular relaxation and decreased
compliance (stiff ventricle) → elevated LVEDP → pulmonary venous congestion despite preserved EF;
common in elderly women with HTN, diabetes
Rationale: Diastolic heart failure (HFpEF — EF ≥50%) results from impaired ventricular RELAXATION (active,
ATP-dependent) and/or decreased compliance (stiff ventricle from fibrosis, hypertrophy). Causes: chronic hypertension
(LVH — stiff ventricle), restrictive cardiomyopathy (amyloidosis), aging, diabetes, obesity. Pathophysiology: stiff
ventricle requires higher filling pressures → elevated LVEDP → increased LA pressure → pulmonary venous congestion
(dyspnea, orthopnea). EF preserved (normal stroke volume) but filling impaired. Clinical: elderly women, HTN, diabetes,
obesity, CKD, AF. Diagnosis: echo (EF ≥50%, E/A ratio reversal, elevated E/e', LA enlargement, LVH, diastolic
dysfunction grade), BNP may be elevated. Treatment: control BP, rate control (AF), diuretics (cautiously —
preload-dependent), SGLT2 inhibitors (EMPEROR-Preserved). No clear mortality benefit from
ACEi/ARB/beta-blockers in HFpEF.
Page 2
,NUR 2063 Exam 2: Essentials of Pathophysiology - Complete Questions & Answers
Q3: A 65-year-old client presents with right-sided heart failure: peripheral edema, jugular venous
distension, hepatomegaly, and ascites. Which pathophysiologic mechanism BEST explains these
manifestations?
A. Left ventricular failure causing pulmonary congestion
B. Right ventricular failure — backward failure to systemic venous system: increased right atrial pressure,
systemic venous congestion, edema, hepatomegaly, JVD; often secondary to left HF (most common) or
pulmonary HTN (cor pulmonale) [CORRECT]
C. Pericardial tamponade
D. Mitral regurgitation
Correct Answer: B. Right ventricular failure — backward failure to systemic venous system: increased right
atrial pressure, systemic venous congestion, edema, hepatomegaly, JVD; often secondary to left HF (most
common) or pulmonary HTN (cor pulmonale)
Rationale: Right heart failure pathophysiology: RV cannot effectively pump blood to lungs → backward failure to
systemic venous circulation → increased right atrial pressure → systemic venous congestion → peripheral edema
(dependent, pitting), JVD (jugular venous distension), hepatomegaly (congestive hepatopathy — 'nutmeg liver'), ascites,
pleural effusion, GI congestion (anorexia, nausea). Decreased RV output → decreased LV preload → decreased cardiac
output → fatigue, decreased renal perfusion → RAAS activation → sodium/water retention → worsening edema. CAUSES:
(1) Left HF (most common — pulmonary venous HTN → pulmonary arterial HTN → RV overload); (2) Pulmonary HTN
(primary, secondary — COPD, ILD, sleep apnea — 'cor pulmonale'); (3) RV MI; (4) Pulmonary embolism (acute RV
overload); (5) Tricuspid regurgitation; (6) Arrhythmogenic RV cardiomyopathy. Treatment: treat underlying cause;
diuretics; oxygen (if hypoxemic); pulmonary vasodilators if PAH.
Q4: A 55-year-old client presents with acute substernal chest pain for 2 hours. ECG shows ST elevation
in leads II, III, aVF. Which coronary artery is MOST likely occluded?
A. Left anterior descending (LAD)
B. Right coronary artery (RCA) — supplies inferior wall (II, III, aVF); also SA node (55%), AV node (90%)
[CORRECT]
C. Left circumflex (LCx)
D. Left main coronary artery
Correct Answer: B. Right coronary artery (RCA) — supplies inferior wall (II, III, aVF); also SA node (55%),
AV node (90%)
Rationale: ECG lead-to-coronary artery correlation: II, III, aVF = INFERIOR wall = RIGHT CORONARY ARTERY
(RCA); V1-V4 = ANTERIOR wall = LEFT ANTERIOR DESCENDING (LAD); I, aVL, V5-V6 = LATERAL wall =
LEFT CIRCUMFLEX (LCx) or LAD diagonal branches; V7-V9 = POSTERIOR wall = RCA or LCx; V1-V2 (tall R, ST
depression) = RECIPROCAL posterior = RCA or LCx. RCA also supplies SA node (55% — bradycardia with inferior
MI), AV node (90% — complete heart block with inferior MI, usually transient). Treatment: immediate reperfusion —
PCI within 90 min (door-to-balloon) preferred; thrombolytics (alteplase) within 12 hr if PCI unavailable; dual antiplatelet
therapy (aspirin + P2Y12 — clopidogrel/ticagrelor), anticoagulation (heparin/enoxaparin/bivalirudin), statin,
beta-blocker, ACEi/ARB, nitroglycerin, morphine, oxygen if hypoxemic.
Q5: A client who received thrombolytic therapy for STEMI 2 hours ago now develops reperfusion injury.
Which pathophysiologic mechanism is PRIMARILY responsible for this paradoxical tissue damage?
A. Resolution of intracellular acidosis
B. Generation of reactive oxygen species (ROS) via xanthine oxidase and mitochondrial dysfunction —
superoxide, hydrogen peroxide, hydroxyl radicals damage lipids, proteins, DNA; calcium overload; neutrophil
infiltration [CORRECT]
C. Re-establishment of ATP production
D. Restoration of normal sodium gradient
Correct Answer: B. Generation of reactive oxygen species (ROS) via xanthine oxidase and mitochondrial
dysfunction — superoxide, hydrogen peroxide, hydroxyl radicals damage lipids, proteins, DNA; calcium
overload; neutrophil infiltration
Page 3
, NUR 2063 Exam 2: Essentials of Pathophysiology - Complete Questions & Answers
Rationale: Reperfusion injury — paradoxical worsening after blood flow restoration. Mechanisms: (1) ROS generation
— during ischemia, ATP → hypoxanthine; xanthine dehydrogenase converted to xanthine oxidase; on reperfusion with
O2, xanthine oxidase converts hypoxanthine + O2 → xanthine + superoxide → cascade of ROS → lipid peroxidation,
protein denaturation, DNA damage; (2) Mitochondrial dysfunction → further ROS, opening of mitochondrial
permeability transition pore (mPTP) → cytochrome c release → apoptosis; (3) Calcium overload — Na/Ca exchanger
reverse flow, sarcoplasmic reticulum release → activates proteases, lipases, endonucleases; (4) Complement activation; (5)
Neutrophil infiltration → additional ROS, proteases; (6) Microvascular 'no-reflow' (endothelial swelling, neutrophil
plugging). Clinical: arrhythmias (reperfusion VT/VF), chest pain recurrence, ST re-elevation, CK-MB/troponin washout
(marker rise), transient LV dysfunction (stunning). Treatment under investigation — ischemic preconditioning,
cyclosporine (mPTP inhibitor), antioxidants.
Q6: A client with atrial fibrillation develops a rapid ventricular response. Which electrophysiologic
mechanism is the PRIMARY cause of atrial fibrillation?
A. Enhanced automaticity in the SA node
B. Multiple reentrant wavelets in atrial myocardium — chaotic atrial depolarization with loss of coordinated
atrial contraction ('atrial kick'); AV node receives rapid, irregular input → irregularly irregular ventricular
response [CORRECT]
C. Triggered activity from afterdepolarizations
D. Reentry within the AV node
Correct Answer: B. Multiple reentrant wavelets in atrial myocardium — chaotic atrial depolarization with
loss of coordinated atrial contraction ('atrial kick'); AV node receives rapid, irregular input → irregularly
irregular ventricular response
Rationale: Atrial fibrillation (AF) mechanisms: (1) Multiple reentrant wavelets (Moe's multiple wavelet hypothesis) —
circus movement of electrical impulses through atrial tissue; (2) Focal triggers from pulmonary vein ostia (90% — ectopic
foci fire rapidly; basis for pulmonary vein isolation ablation). Pathophysiology: chaotic atrial depolarization → no
effective atrial contraction → loss of 'atrial kick' (15-25% of cardiac output — significant in stiff ventricles), blood stasis
in left atrial appendage → thrombus formation → embolic stroke (5x risk). ECG: no P waves (replaced by fibrillatory
waves at 350-600 bpm), irregularly irregular R-R intervals (AV node conduction varies), narrow QRS. Risk factors: age,
HTN (most common cause), coronary disease, HF, valvular disease (mitral), hyperthyroidism, alcohol ('holiday heart'),
sleep apnea. Treatment: rate control (beta-blockers, CCB), rhythm control (antiarrhythmics, cardioversion, ablation),
anticoagulation (CHA2DS2-VASc — DOAC preferred unless mechanical valve/moderate-severe MS).
Q7: A 70-year-old client with chronic hypertension develops aortic regurgitation. Which
pathophysiologic hemodynamic change occurs during diastole?
A. Increased afterload from outflow obstruction
B. Diastolic backflow from aorta into LV — volume overload, eccentric hypertrophy (sarcomeres in series),
widened pulse pressure, low diastolic pressure; high systolic (large stroke volume) [CORRECT]
C. Systolic pressure overload on LV
D. Coronary artery compression during systole
Correct Answer: B. Diastolic backflow from aorta into LV — volume overload, eccentric hypertrophy
(sarcomeres in series), widened pulse pressure, low diastolic pressure; high systolic (large stroke volume)
Rationale: Aortic regurgitation (AR) hemodynamics: (1) During DIASTOLE — aortic valve incompetent → blood flows
BACK from aorta into LV → diastolic volume overload on LV (both normal filling from LA + regurgitant volume); (2)
LV dilates to accommodate increased volume → ECCENTRIC HYPERTROPHY (sarcomeres in series, chamber
dilation); (3) Increased total stroke volume (forward + regurgitant) → high systolic BP; (4) Rapid diastolic runoff from
aorta into LV → low diastolic BP; (5) WIDENED PULSE PRESSURE (systolic - diastolic); (6) Hyperdynamic circulation
— bounding pulses (Corrigan's pulse, water-hammer pulse), head bobbing (de Musset's sign), pistol-shot femoral pulses
(Duroziez's sign), nailbed pulsation (Quincke's sign); (7) S3 (volume overload), S4 (if LVH); diastolic blowing
decrescendo murmur at left sternal border (Austin Flint murmur — mitral rumble from mitral valve vibration). Chronic
AR: LV compensates for years (eccentric + some concentric hypertrophy); acute AR (endocarditis, dissection) — sudden
volume overload, pulmonary edema, cardiogenic shock.
Page 4
Exam 2 - NUR2063 / NUR 2063
Essentials of Pathophysiology
Rasmussen
Latest Update
Mechanism-focused pathophysiology with clinical correlations and lab value interpretation
Total Questions Sections Options per Q Cognitive Mix
130 8 4 (A-D) 30% Recall / 50% App / 20% Analysis
This comprehensive exam preparation document covers the full breadth of NUR 2063 Exam 2 at Rasmussen
University, focusing on pathophysiologic mechanisms across all major body systems: cardiovascular, respiratory,
renal/urinary, fluid/electrolyte/acid-base, endocrine, gastrointestinal/hepatic, hematologic, and neurologic. Each
question is mechanism-focused, requiring explanation of pathophysiologic processes rather than symptom recall.
Detailed rationales serve as study content with clinical correlations, lab value interpretation, compensation reasoning,
and comparison of similar pathophysiologic states.
Exam Structure
Section Topic Questions
Section 1: Cardiovascular Pathophysiology - Heart Failure, Ischemia/Infarction,
Q1-Q20 20
Dysrhythmia Mechanisms, Valvular Disease, and Vascular Disorders
Section 2: Respiratory Pathophysiology - Obstructive/Restrictive Disease, Gas
Q21-Q37 17
Exchange, ARDS, PE, and Respiratory Failure
Section 3: Renal and Urinary Pathophysiology - AKI, CKD, Glomerulonephritis,
Q38-Q53 16
Nephrotic Syndrome, and UTIs
Section 4: Fluid, Electrolyte, and Acid-Base Alterations in Disease - Complex
Q54-Q67 14
Imbalances, Compensation, and Mixed Disorders
Section 5: Endocrine Pathophysiology - Diabetes, DKA/HHS, Thyroid, Adrenal,
Q68-Q85 18
Pituitary, and Parathyroid Disorders
Section 6: Gastrointestinal and Hepatic Pathophysiology - PUD, IBD, Obstruction,
Q86-Q101 16
Pancreatitis, Cirrhosis, and Hepatitis
Section 7: Hematologic Pathophysiology - Anemias, Leukemias, Lymphomas,
Q102-Q116 15
Coagulopathies, and DIC
Page 1
,NUR 2063 Exam 2: Essentials of Pathophysiology - Complete Questions & Answers
Section 8: Neurologic Pathophysiology - Stroke, Increased ICP, Seizures,
Q117-Q130 14
Neurodegenerative Disease, and Spinal Cord Injury
Section 1: Cardiovascular Pathophysiology
Heart Failure, Ischemia/Infarction, Dysrhythmia Mechanisms, Valvular Disease, and Vascular Disorders
Q1: A 68-year-old client with chronic hypertension develops exertional dyspnea, bilateral crackles, and
an S3 heart sound. Echocardiography reveals left ventricular ejection fraction of 30%. Which
pathophysiologic mechanism BEST explains this presentation?
A. Diastolic heart failure with preserved EF
B. Systolic heart failure with reduced EF — impaired contractility leads to decreased stroke volume, increased
end-diastolic volume, pulmonary venous congestion, and neurohormonal activation (RAAS, sympathetic)
[CORRECT]
C. Right-sided heart failure from cor pulmonale
D. Valvular stenosis causing outflow obstruction
Correct Answer: B. Systolic heart failure with reduced EF — impaired contractility leads to decreased stroke
volume, increased end-diastolic volume, pulmonary venous congestion, and neurohormonal activation (RAAS,
sympathetic)
Rationale: Systolic heart failure (HFrEF — EF ≤40%) results from impaired contractility (ischemia, MI, dilated
cardiomyopathy, myocarditis). Decreased stroke volume → decreased cardiac output → decreased renal perfusion →
RAAS activation (renin → Ang II → aldosterone) causing sodium/water retention, vasoconstriction, and sympathetic
activation → increased afterload and preload → further LV dilation and remodeling (eccentric hypertrophy, fibrosis,
apoptosis). Backward failure to lungs: increased LVEDP → increased LA pressure → pulmonary venous hypertension →
transudation of fluid into alveoli → pulmonary edema (crackles, S3 from volume overload, dyspnea). BNP released from
ventricular myocardium in response to wall stress — diagnostic marker. Treatment: ACEi/ARB/ARNI, beta-blockers,
aldosterone antagonists, SGLT2 inhibitors, diuretics, ICD/CRT.
Q2: A 72-year-old female client presents with exertional dyspnea and fatigue. Echocardiogram shows
preserved ejection fraction (EF 65%) but impaired ventricular relaxation with elevated left ventricular
end-diastolic pressure. Which pathophysiologic mechanism BEST explains this condition?
A. Systolic heart failure from impaired contractility
B. Diastolic heart failure (HFpEF) — impaired ventricular relaxation and decreased compliance (stiff ventricle)
→ elevated LVEDP → pulmonary venous congestion despite preserved EF; common in elderly women with
HTN, diabetes [CORRECT]
C. Right ventricular infarction
D. Mitral stenosis
Correct Answer: B. Diastolic heart failure (HFpEF) — impaired ventricular relaxation and decreased
compliance (stiff ventricle) → elevated LVEDP → pulmonary venous congestion despite preserved EF;
common in elderly women with HTN, diabetes
Rationale: Diastolic heart failure (HFpEF — EF ≥50%) results from impaired ventricular RELAXATION (active,
ATP-dependent) and/or decreased compliance (stiff ventricle from fibrosis, hypertrophy). Causes: chronic hypertension
(LVH — stiff ventricle), restrictive cardiomyopathy (amyloidosis), aging, diabetes, obesity. Pathophysiology: stiff
ventricle requires higher filling pressures → elevated LVEDP → increased LA pressure → pulmonary venous congestion
(dyspnea, orthopnea). EF preserved (normal stroke volume) but filling impaired. Clinical: elderly women, HTN, diabetes,
obesity, CKD, AF. Diagnosis: echo (EF ≥50%, E/A ratio reversal, elevated E/e', LA enlargement, LVH, diastolic
dysfunction grade), BNP may be elevated. Treatment: control BP, rate control (AF), diuretics (cautiously —
preload-dependent), SGLT2 inhibitors (EMPEROR-Preserved). No clear mortality benefit from
ACEi/ARB/beta-blockers in HFpEF.
Page 2
,NUR 2063 Exam 2: Essentials of Pathophysiology - Complete Questions & Answers
Q3: A 65-year-old client presents with right-sided heart failure: peripheral edema, jugular venous
distension, hepatomegaly, and ascites. Which pathophysiologic mechanism BEST explains these
manifestations?
A. Left ventricular failure causing pulmonary congestion
B. Right ventricular failure — backward failure to systemic venous system: increased right atrial pressure,
systemic venous congestion, edema, hepatomegaly, JVD; often secondary to left HF (most common) or
pulmonary HTN (cor pulmonale) [CORRECT]
C. Pericardial tamponade
D. Mitral regurgitation
Correct Answer: B. Right ventricular failure — backward failure to systemic venous system: increased right
atrial pressure, systemic venous congestion, edema, hepatomegaly, JVD; often secondary to left HF (most
common) or pulmonary HTN (cor pulmonale)
Rationale: Right heart failure pathophysiology: RV cannot effectively pump blood to lungs → backward failure to
systemic venous circulation → increased right atrial pressure → systemic venous congestion → peripheral edema
(dependent, pitting), JVD (jugular venous distension), hepatomegaly (congestive hepatopathy — 'nutmeg liver'), ascites,
pleural effusion, GI congestion (anorexia, nausea). Decreased RV output → decreased LV preload → decreased cardiac
output → fatigue, decreased renal perfusion → RAAS activation → sodium/water retention → worsening edema. CAUSES:
(1) Left HF (most common — pulmonary venous HTN → pulmonary arterial HTN → RV overload); (2) Pulmonary HTN
(primary, secondary — COPD, ILD, sleep apnea — 'cor pulmonale'); (3) RV MI; (4) Pulmonary embolism (acute RV
overload); (5) Tricuspid regurgitation; (6) Arrhythmogenic RV cardiomyopathy. Treatment: treat underlying cause;
diuretics; oxygen (if hypoxemic); pulmonary vasodilators if PAH.
Q4: A 55-year-old client presents with acute substernal chest pain for 2 hours. ECG shows ST elevation
in leads II, III, aVF. Which coronary artery is MOST likely occluded?
A. Left anterior descending (LAD)
B. Right coronary artery (RCA) — supplies inferior wall (II, III, aVF); also SA node (55%), AV node (90%)
[CORRECT]
C. Left circumflex (LCx)
D. Left main coronary artery
Correct Answer: B. Right coronary artery (RCA) — supplies inferior wall (II, III, aVF); also SA node (55%),
AV node (90%)
Rationale: ECG lead-to-coronary artery correlation: II, III, aVF = INFERIOR wall = RIGHT CORONARY ARTERY
(RCA); V1-V4 = ANTERIOR wall = LEFT ANTERIOR DESCENDING (LAD); I, aVL, V5-V6 = LATERAL wall =
LEFT CIRCUMFLEX (LCx) or LAD diagonal branches; V7-V9 = POSTERIOR wall = RCA or LCx; V1-V2 (tall R, ST
depression) = RECIPROCAL posterior = RCA or LCx. RCA also supplies SA node (55% — bradycardia with inferior
MI), AV node (90% — complete heart block with inferior MI, usually transient). Treatment: immediate reperfusion —
PCI within 90 min (door-to-balloon) preferred; thrombolytics (alteplase) within 12 hr if PCI unavailable; dual antiplatelet
therapy (aspirin + P2Y12 — clopidogrel/ticagrelor), anticoagulation (heparin/enoxaparin/bivalirudin), statin,
beta-blocker, ACEi/ARB, nitroglycerin, morphine, oxygen if hypoxemic.
Q5: A client who received thrombolytic therapy for STEMI 2 hours ago now develops reperfusion injury.
Which pathophysiologic mechanism is PRIMARILY responsible for this paradoxical tissue damage?
A. Resolution of intracellular acidosis
B. Generation of reactive oxygen species (ROS) via xanthine oxidase and mitochondrial dysfunction —
superoxide, hydrogen peroxide, hydroxyl radicals damage lipids, proteins, DNA; calcium overload; neutrophil
infiltration [CORRECT]
C. Re-establishment of ATP production
D. Restoration of normal sodium gradient
Correct Answer: B. Generation of reactive oxygen species (ROS) via xanthine oxidase and mitochondrial
dysfunction — superoxide, hydrogen peroxide, hydroxyl radicals damage lipids, proteins, DNA; calcium
overload; neutrophil infiltration
Page 3
, NUR 2063 Exam 2: Essentials of Pathophysiology - Complete Questions & Answers
Rationale: Reperfusion injury — paradoxical worsening after blood flow restoration. Mechanisms: (1) ROS generation
— during ischemia, ATP → hypoxanthine; xanthine dehydrogenase converted to xanthine oxidase; on reperfusion with
O2, xanthine oxidase converts hypoxanthine + O2 → xanthine + superoxide → cascade of ROS → lipid peroxidation,
protein denaturation, DNA damage; (2) Mitochondrial dysfunction → further ROS, opening of mitochondrial
permeability transition pore (mPTP) → cytochrome c release → apoptosis; (3) Calcium overload — Na/Ca exchanger
reverse flow, sarcoplasmic reticulum release → activates proteases, lipases, endonucleases; (4) Complement activation; (5)
Neutrophil infiltration → additional ROS, proteases; (6) Microvascular 'no-reflow' (endothelial swelling, neutrophil
plugging). Clinical: arrhythmias (reperfusion VT/VF), chest pain recurrence, ST re-elevation, CK-MB/troponin washout
(marker rise), transient LV dysfunction (stunning). Treatment under investigation — ischemic preconditioning,
cyclosporine (mPTP inhibitor), antioxidants.
Q6: A client with atrial fibrillation develops a rapid ventricular response. Which electrophysiologic
mechanism is the PRIMARY cause of atrial fibrillation?
A. Enhanced automaticity in the SA node
B. Multiple reentrant wavelets in atrial myocardium — chaotic atrial depolarization with loss of coordinated
atrial contraction ('atrial kick'); AV node receives rapid, irregular input → irregularly irregular ventricular
response [CORRECT]
C. Triggered activity from afterdepolarizations
D. Reentry within the AV node
Correct Answer: B. Multiple reentrant wavelets in atrial myocardium — chaotic atrial depolarization with
loss of coordinated atrial contraction ('atrial kick'); AV node receives rapid, irregular input → irregularly
irregular ventricular response
Rationale: Atrial fibrillation (AF) mechanisms: (1) Multiple reentrant wavelets (Moe's multiple wavelet hypothesis) —
circus movement of electrical impulses through atrial tissue; (2) Focal triggers from pulmonary vein ostia (90% — ectopic
foci fire rapidly; basis for pulmonary vein isolation ablation). Pathophysiology: chaotic atrial depolarization → no
effective atrial contraction → loss of 'atrial kick' (15-25% of cardiac output — significant in stiff ventricles), blood stasis
in left atrial appendage → thrombus formation → embolic stroke (5x risk). ECG: no P waves (replaced by fibrillatory
waves at 350-600 bpm), irregularly irregular R-R intervals (AV node conduction varies), narrow QRS. Risk factors: age,
HTN (most common cause), coronary disease, HF, valvular disease (mitral), hyperthyroidism, alcohol ('holiday heart'),
sleep apnea. Treatment: rate control (beta-blockers, CCB), rhythm control (antiarrhythmics, cardioversion, ablation),
anticoagulation (CHA2DS2-VASc — DOAC preferred unless mechanical valve/moderate-severe MS).
Q7: A 70-year-old client with chronic hypertension develops aortic regurgitation. Which
pathophysiologic hemodynamic change occurs during diastole?
A. Increased afterload from outflow obstruction
B. Diastolic backflow from aorta into LV — volume overload, eccentric hypertrophy (sarcomeres in series),
widened pulse pressure, low diastolic pressure; high systolic (large stroke volume) [CORRECT]
C. Systolic pressure overload on LV
D. Coronary artery compression during systole
Correct Answer: B. Diastolic backflow from aorta into LV — volume overload, eccentric hypertrophy
(sarcomeres in series), widened pulse pressure, low diastolic pressure; high systolic (large stroke volume)
Rationale: Aortic regurgitation (AR) hemodynamics: (1) During DIASTOLE — aortic valve incompetent → blood flows
BACK from aorta into LV → diastolic volume overload on LV (both normal filling from LA + regurgitant volume); (2)
LV dilates to accommodate increased volume → ECCENTRIC HYPERTROPHY (sarcomeres in series, chamber
dilation); (3) Increased total stroke volume (forward + regurgitant) → high systolic BP; (4) Rapid diastolic runoff from
aorta into LV → low diastolic BP; (5) WIDENED PULSE PRESSURE (systolic - diastolic); (6) Hyperdynamic circulation
— bounding pulses (Corrigan's pulse, water-hammer pulse), head bobbing (de Musset's sign), pistol-shot femoral pulses
(Duroziez's sign), nailbed pulsation (Quincke's sign); (7) S3 (volume overload), S4 (if LVH); diastolic blowing
decrescendo murmur at left sternal border (Austin Flint murmur — mitral rumble from mitral valve vibration). Chronic
AR: LV compensates for years (eccentric + some concentric hypertrophy); acute AR (endocarditis, dissection) — sudden
volume overload, pulmonary edema, cardiogenic shock.
Page 4
