NURS 611 Exam 4 — Pathophysiology — 2026/2027 Complete Maryville University | A+ Verified
NURS 611 EXAM 4 PATHO ACTUAL EXAM 2026/2027 COMPLETE
100 Questions and Correct Detailed Answers with Rationales | Already Graded A+
Maryville University · Graduate Nursing · Advanced Pathophysiology · Exam 4
Aligned with 2026-2027 Advanced Practice Nursing Pathophysiology Standards
Total Questions 100 (EXACT) Cognitive Distribution 30% Recall | 50% Application | 20% Analysis
Sections 7 Body System Domains Question Style 75% Scenario-based | 25% Direct Mechanism Recall
Format MCQ, 4 options (A-D) Rationale Depth Mechanistic + Clinical Correlation
Verified Grade A+ Passing Standard Advanced Practice Nursing Level
Section 1: Cardiovascular Pathophysiology
Atherosclerosis, Hypertension, Heart Failure, Ischemic Heart Disease, & Dysrhythmias (Q1-18)
Q1: A 58-year-old male with a 20-pack-year smoking history and LDL of 178 mg/dL presents with stable angina.
Endothelial biopsy of his coronary arteries reveals decreased nitric oxide (NO) synthase activity, increased
VCAM-1 expression, and macrophage infiltration into the tunica intima. Which cellular event most directly
initiates the formation of the fatty streak that precedes atherosclerotic plaque development?
A. Smooth muscle cell migration from the tunica media into the intima driven by PDGF
B. Oxidative modification of LDL within the intima followed by macrophage scavenger receptor-mediated
uptake [CORRECT]
C. Calcification of the fibrous cap mediated by osteoblast-like vascular cells
D. Platelet aggregation at sites of endothelial denudation with thrombin generation
Correct Answer: B
Rationale: Atherogenesis begins with endothelial injury/dysfunction that permits LDL infiltration into the intima, where it
undergoes oxidative modification. Modified LDL is taken up by macrophage scavenger receptors (SR-A, CD36) in an
unregulated fashion, converting macrophages into lipid-laden foam cells that constitute the fatty streak. Smooth muscle
migration (A) occurs later during fibrous plaque formation, calcification (C) is a late feature of complex plaques, and
platelet aggregation (D) characterizes plaque rupture/ACS rather than initiation.
Q2: A 67-year-old female with essential hypertension has a serum renin level that is low, aldosterone that is
high-normal, and urinary sodium excretion that is elevated. Her BP is 168/96 mmHg despite two antihypertensives.
Which mechanism best explains the maintenance of her elevated systemic vascular resistance (SVR)?
A. Persistent activation of the renin-angiotensin-aldosterone system (RAAS) by juxtaglomerular cells
B. Reduced bioavailability of nitric oxide with concurrent upregulation of endothelin-1 and oxidative stress
from NADPH oxidase [CORRECT]
C. Volume overload alone from primary renal sodium retention without vascular remodeling
D. Direct beta-1 adrenergic receptor stimulation increasing cardiac output as the dominant mechanism
Correct Answer: B
Rationale: In established essential hypertension, the elevated SVR is sustained not by high renin (which is typically
normal or low) but by endothelial dysfunction: decreased NO bioavailability, increased endothelin-1, and ROS-mediated
vasoconstriction and vascular remodeling. RAAS activation (A) is more prominent in secondary renovascular
hypertension. Pure volume overload (C) ignores the vascular component, and beta-1 stimulation (D) primarily affects
cardiac output, not chronic SVR elevation.
Page 1
,NURS 611 Exam 4 — Pathophysiology — 2026/2027 Complete Maryville University | A+ Verified
Q3: A 72-year-old male with chronic hypertension presents with dyspnea on exertion, bilateral crackles, and an S3
gallop. Echocardiography shows LVEF 35%, LV end-diastolic dimension 6.4 cm, and global hypokinesis. Which
neurohormonal cascade most directly contributes to progressive ventricular remodeling in this patient?
A. Activation of the parasympathetic nervous system with vagally mediated bradycardia
B. Release of brain natriuretic peptide (BNP) that promotes vasoconstriction and fluid retention
C. Chronic sympathetic nervous system activation and angiotensin II signaling through AT1 receptors
promoting myocyte apoptosis, fibrosis, and hypertrophy [CORRECT]
D. Increased insulin-like growth factor-1 (IGF-1) driving physiologic compensatory hypertrophy without fibrosis
Correct Answer: C
Rationale: Heart failure with reduced EF is driven by maladaptive neurohormonal activation: sympathetic overload and
RAAS activation. Angiotensin II acting on AT1 receptors stimulates myocyte apoptosis, fibroblast proliferation, and
pathologic hypertrophy, accelerating remodeling. BNP (B) is actually counter-regulatory (natriuretic, vasodilatory), the
parasympathetic system (A) is blunted rather than overactive, and IGF-1 (D) is associated with physiologic, not
pathologic, hypertrophy.
Q4: A 65-year-old female presents with acute pulmonary edema. Echocardiography shows LVEF 65%, preserved
systolic function, LV wall thickness 14 mm, E/A ratio >2, and deceleration time 150 ms. Which pathophysiologic
mechanism best accounts for her symptoms?
A. Loss of cardiomyocytes with subsequent eccentric hypertrophy and chamber dilation
B. Increased LV chamber stiffness and impaired active relaxation (lusitropy) leading to elevated left atrial and
pulmonary venous pressures [CORRECT]
C. Acute papillary muscle rupture causing torrential mitral regurgitation
D. Pericardial constriction impairing RV filling during diastole
Correct Answer: B
Rationale: Heart failure with preserved EF (HFpEF) is characterized by diastolic dysfunction: increased chamber stiffness
from interstitial fibrosis and impaired active relaxation (calcium reuptake dysfunction in sarcoplasmic reticulum). This
produces elevated filling pressures that transmit retrograde to the pulmonary vasculature. Eccentric hypertrophy with
chamber dilation (A) defines HFrEF. Papillary muscle rupture (C) is mechanical, not diastolic. Constriction (D) affects
both ventricles with equalization of diastolic pressures.
Q5: A 55-year-old male presents with crushing substernal chest pressure for 90 minutes. ECG shows ST-segment
elevation in leads II, III, and aVF. Troponin I is 12.8 ng/mL (reference <0.04). Which pathophysiologic sequence
most accurately describes the progression from coronary plaque rupture to myocyte necrosis?
A. Endothelial erosion → vasoconstriction → stable plaque growth → transient ischemia
B. Plaque rupture with exposed lipid core → tissue factor exposure → platelet adhesion/aggregation →
thrombin generation and fibrin formation → complete coronary occlusion → ischemia then necrosis
[CORRECT]
C. Vasospasm of a coronary artery without plaque disruption → reversible ischemia only
D. Microvascular disease with capillary rarefaction causing chronic low-grade myocyte loss
Correct Answer: B
Rationale: ST-elevation MI arises from plaque rupture (or erosion) exposing the lipid core and tissue factor to circulating
blood. This initiates platelet adhesion (via vWF-GPIb), aggregation (GPIIb/IIIa-fibrinogen), and the coagulation cascade
generating thrombin and fibrin. Complete coronary occlusion results in ischemia within seconds, ATP depletion,
membrane failure, and myocyte necrosis within ~20-30 minutes of severe ischemia. Choice A describes stable angina
progression; C describes Prinzmetal angina; D describes chronic ischemic cardiomyopathy.
Page 2
,NURS 611 Exam 4 — Pathophysiology — 2026/2027 Complete Maryville University | A+ Verified
Q6: A 60-year-old female is admitted with chest pain and an initial troponin of 0.06 ng/mL that rises to 0.8 ng/mL
at 6 hours, then to 1.5 ng/mL at 12 hours. ECG shows T-wave inversions in V2-V4 without ST elevation. Cardiac
biomarker kinetics in this patient are best explained by which mechanism?
A. Release of myoglobin from cytoplasm due to reversible ischemia without cell death
B. Necrosis of myocytes with release of troponin from the cytosolic pool followed by the structural
(myofibril-bound) pool as degradation occurs [CORRECT]
C. Renal failure causing decreased clearance of troponin fragments producing a false positive
D. Skeletal muscle injury releasing cardiac troponin due to cross-reactivity with skeletal isoforms
Correct Answer: B
Rationale: Cardiac troponin elevation in NSTEMI reflects myocyte necrosis. The early rise (3-6 hr) comes from the small
free cytosolic pool; the prolonged elevation (peak at 18-24 hr, persistent for 7-10 days) reflects release from the
myofibril-bound structural pool as contractile proteins degrade. Myoglobin (A) is nonspecific and rises earlier but is not
the biomarker used here. Renal failure (C) can mildly elevate troponin but not with the typical rise/fall pattern of acute
injury. Cardiac troponin isoforms (D) are not expressed in skeletal muscle, so cross-reactivity is not the cause.
Q7: A 70-year-old male with no cardiac history presents with sudden palpitations. ECG shows a regular
wide-complex tachycardia at 180 bpm with concordance in precordial leads and AV dissociation. Which
electrophysiologic mechanism best explains this rhythm?
A. Reentry through an accessory pathway connecting atria and ventricles
B. Enhanced automaticity from a ventricular ectopic focus firing faster than the sinus node [CORRECT]
C. Triggered activity from delayed afterdepolarizations due to intracellular calcium overload
D. Reentry within the AV node producing a narrow QRS tachycardia
Correct Answer: B
Rationale: A regular wide-complex tachycardia with AV dissociation and precordial concordance is most consistent with
ventricular tachycardia originating from an ectopic ventricular focus exhibiting enhanced automaticity. Reentry through an
accessory pathway (A) typically produces pre-excited tachycardias like orthodromic AVRT with narrow QRS. Delayed
afterdepolarizations (C) are the mechanism of torsades de pointes and digoxin toxicity. AV node reentry (D) produces a
narrow QRS tachycardia, not wide.
Q8: A 68-year-old female on furosemide for heart failure develops palpitations. ECG shows prolonged QT interval,
prominent U waves, and premature ventricular contractions. Which electrolyte disturbance most directly accounts
for her dysrhythmia through prolongation of the action potential?
A. Hypomagnesemia alone, as magnesium does not directly affect the cardiac action potential
B. Hypokalemia prolonging phase 3 repolarization by delaying K+ efflux through delayed rectifier channels
(IKr) [CORRECT]
C. Hypercalcemia shortening the action potential by enhancing Ca2+ influx during phase 2
D. Hyponatremia slowing phase 0 depolarization of ventricular myocytes
Correct Answer: B
Rationale: Hypokalemia (often from loop diuretics) impairs IKr (rapid component of delayed rectifier K+ current),
prolonging phase 3 repolarization and the QT interval, with U-wave prominence and risk of torsades. Hypomagnesemia
(A) frequently coexists and worsens hypokalemia. Hypercalcemia (C) shortens the QT, the opposite of what is described.
Hyponatremia (D) does not significantly affect the ventricular action potential phase 0 (which is largely Na-driven in
Purkinje/myocytes but is not the issue here).
Page 3
, NURS 611 Exam 4 — Pathophysiology — 2026/2027 Complete Maryville University | A+ Verified
Q9: A 62-year-old male with a history of MI presents with sudden syncope. ECG shows a regular rhythm with
absent P waves, normal QRS, and rate of 40 bpm. His medication list includes metoprolol and amiodarone. Which
mechanism most likely produced this rhythm?
A. Reentrant circuit within the Bundle of His producing atrial tachycardia with block
B. Complete conduction block at the AV node with escape rhythm originating from the His-Purkinje system
[CORRECT]
C. Sinus node dysfunction with atrial standstill from amyloid infiltration
D. Vagal-mediated bradycardia from carotid sinus hypersensitivity
Correct Answer: B
Rationale: Third-degree (complete) AV block produces AV dissociation with a junctional or His-Purkinje escape rhythm.
In a patient on AV nodal-blocking agents (beta-blocker, amiodarone) with prior MI, conduction failure at or below the AV
node is most likely, with a narrow-QRS escape (rate 40-60) if junctional and wide if ventricular. Reentrant atrial
tachycardia (A) would show P waves. Sinus node dysfunction (C) would not produce AV dissociation. Vagal
hypersensitivity (D) typically produces sinus slowing or transient AV block, not stable complete block.
Q10: A 49-year-old male with hypertension and chronic kidney disease stage 3 has a BP of 162/98 mmHg despite
amlodipine 10 mg daily. His plasma renin activity is 14 ng/mL/hr (normal 0.6-4.3). CT angiography reveals a
stenotic lesion in the proximal right renal artery with post-stenotic dilation. Which mechanism most directly links
the renal artery stenosis to his hypertension?
A. Decreased GFR leading to volume expansion and primary suppression of renin
B. Decreased perfusion pressure sensed by juxtaglomerular cells triggering renin release, angiotensin
II-mediated vasoconstriction, and aldosterone-mediated sodium retention [CORRECT]
C. Direct compression of renal sympathetic nerves causing unopposed alpha-1 vasoconstriction
D. Loss of renal parenchymal mass reducing medullary lipases that generate antihypertensive vasodilators
Correct Answer: B
Rationale: Renovascular hypertension is driven by underperfusion of the juxtaglomerular apparatus, which triggers
baroreceptor-mediated renin release. Renin converts angiotensinogen to angiotensin I, then ACE generates angiotensin II
(vasoconstriction, efferent arteriolar constriction) and aldosterone (sodium retention). High renin is the hallmark,
distinguishing this from primary HTN. Choice A incorrectly suppresses renin. C and D are not recognized mechanisms of
renovascular hypertension.
Q11: A 75-year-old male with long-standing hypertension has an echocardiogram showing concentric LV
hypertrophy (wall thickness 16 mm) with preserved EF. Left atrial volume index is 48 mL/m² (normal <34). Which
cellular adaptation most directly explains the LV wall changes, and what is its long-term consequence?
A. Hyperplasia of cardiomyocytes increasing cell number to normalize wall stress
B. Compensatory hypertrophy of terminally differentiated cardiomyocytes (increased cell size) with eventual
interstitial fibrosis, diastolic dysfunction, and progression to HFpEF or HFrEF [CORRECT]
C. Metaplasia of cardiomyocytes to smooth muscle cells reducing contractile efficiency
D. Physiologic hypertrophy mediated by IGF-1 with proportional capillary growth and no long-term consequence
Correct Answer: B
Rationale: Cardiomyocytes are terminally differentiated and respond to pressure overload (high afterload) by hypertrophy
(increased cell size, not number — A is wrong). This concentric hypertrophy initially normalizes wall stress (Laplace's
law) but progresses to interstitial fibrosis, impaired relaxation, increased left atrial pressure (dilated LA), and eventual
diastolic or systolic failure. Pathologic hypertrophy (B) differs from physiologic (D) by reduced capillary density and
fibrosis. Metaplasia (C) does not occur in adult myocardium.
Page 4
NURS 611 EXAM 4 PATHO ACTUAL EXAM 2026/2027 COMPLETE
100 Questions and Correct Detailed Answers with Rationales | Already Graded A+
Maryville University · Graduate Nursing · Advanced Pathophysiology · Exam 4
Aligned with 2026-2027 Advanced Practice Nursing Pathophysiology Standards
Total Questions 100 (EXACT) Cognitive Distribution 30% Recall | 50% Application | 20% Analysis
Sections 7 Body System Domains Question Style 75% Scenario-based | 25% Direct Mechanism Recall
Format MCQ, 4 options (A-D) Rationale Depth Mechanistic + Clinical Correlation
Verified Grade A+ Passing Standard Advanced Practice Nursing Level
Section 1: Cardiovascular Pathophysiology
Atherosclerosis, Hypertension, Heart Failure, Ischemic Heart Disease, & Dysrhythmias (Q1-18)
Q1: A 58-year-old male with a 20-pack-year smoking history and LDL of 178 mg/dL presents with stable angina.
Endothelial biopsy of his coronary arteries reveals decreased nitric oxide (NO) synthase activity, increased
VCAM-1 expression, and macrophage infiltration into the tunica intima. Which cellular event most directly
initiates the formation of the fatty streak that precedes atherosclerotic plaque development?
A. Smooth muscle cell migration from the tunica media into the intima driven by PDGF
B. Oxidative modification of LDL within the intima followed by macrophage scavenger receptor-mediated
uptake [CORRECT]
C. Calcification of the fibrous cap mediated by osteoblast-like vascular cells
D. Platelet aggregation at sites of endothelial denudation with thrombin generation
Correct Answer: B
Rationale: Atherogenesis begins with endothelial injury/dysfunction that permits LDL infiltration into the intima, where it
undergoes oxidative modification. Modified LDL is taken up by macrophage scavenger receptors (SR-A, CD36) in an
unregulated fashion, converting macrophages into lipid-laden foam cells that constitute the fatty streak. Smooth muscle
migration (A) occurs later during fibrous plaque formation, calcification (C) is a late feature of complex plaques, and
platelet aggregation (D) characterizes plaque rupture/ACS rather than initiation.
Q2: A 67-year-old female with essential hypertension has a serum renin level that is low, aldosterone that is
high-normal, and urinary sodium excretion that is elevated. Her BP is 168/96 mmHg despite two antihypertensives.
Which mechanism best explains the maintenance of her elevated systemic vascular resistance (SVR)?
A. Persistent activation of the renin-angiotensin-aldosterone system (RAAS) by juxtaglomerular cells
B. Reduced bioavailability of nitric oxide with concurrent upregulation of endothelin-1 and oxidative stress
from NADPH oxidase [CORRECT]
C. Volume overload alone from primary renal sodium retention without vascular remodeling
D. Direct beta-1 adrenergic receptor stimulation increasing cardiac output as the dominant mechanism
Correct Answer: B
Rationale: In established essential hypertension, the elevated SVR is sustained not by high renin (which is typically
normal or low) but by endothelial dysfunction: decreased NO bioavailability, increased endothelin-1, and ROS-mediated
vasoconstriction and vascular remodeling. RAAS activation (A) is more prominent in secondary renovascular
hypertension. Pure volume overload (C) ignores the vascular component, and beta-1 stimulation (D) primarily affects
cardiac output, not chronic SVR elevation.
Page 1
,NURS 611 Exam 4 — Pathophysiology — 2026/2027 Complete Maryville University | A+ Verified
Q3: A 72-year-old male with chronic hypertension presents with dyspnea on exertion, bilateral crackles, and an S3
gallop. Echocardiography shows LVEF 35%, LV end-diastolic dimension 6.4 cm, and global hypokinesis. Which
neurohormonal cascade most directly contributes to progressive ventricular remodeling in this patient?
A. Activation of the parasympathetic nervous system with vagally mediated bradycardia
B. Release of brain natriuretic peptide (BNP) that promotes vasoconstriction and fluid retention
C. Chronic sympathetic nervous system activation and angiotensin II signaling through AT1 receptors
promoting myocyte apoptosis, fibrosis, and hypertrophy [CORRECT]
D. Increased insulin-like growth factor-1 (IGF-1) driving physiologic compensatory hypertrophy without fibrosis
Correct Answer: C
Rationale: Heart failure with reduced EF is driven by maladaptive neurohormonal activation: sympathetic overload and
RAAS activation. Angiotensin II acting on AT1 receptors stimulates myocyte apoptosis, fibroblast proliferation, and
pathologic hypertrophy, accelerating remodeling. BNP (B) is actually counter-regulatory (natriuretic, vasodilatory), the
parasympathetic system (A) is blunted rather than overactive, and IGF-1 (D) is associated with physiologic, not
pathologic, hypertrophy.
Q4: A 65-year-old female presents with acute pulmonary edema. Echocardiography shows LVEF 65%, preserved
systolic function, LV wall thickness 14 mm, E/A ratio >2, and deceleration time 150 ms. Which pathophysiologic
mechanism best accounts for her symptoms?
A. Loss of cardiomyocytes with subsequent eccentric hypertrophy and chamber dilation
B. Increased LV chamber stiffness and impaired active relaxation (lusitropy) leading to elevated left atrial and
pulmonary venous pressures [CORRECT]
C. Acute papillary muscle rupture causing torrential mitral regurgitation
D. Pericardial constriction impairing RV filling during diastole
Correct Answer: B
Rationale: Heart failure with preserved EF (HFpEF) is characterized by diastolic dysfunction: increased chamber stiffness
from interstitial fibrosis and impaired active relaxation (calcium reuptake dysfunction in sarcoplasmic reticulum). This
produces elevated filling pressures that transmit retrograde to the pulmonary vasculature. Eccentric hypertrophy with
chamber dilation (A) defines HFrEF. Papillary muscle rupture (C) is mechanical, not diastolic. Constriction (D) affects
both ventricles with equalization of diastolic pressures.
Q5: A 55-year-old male presents with crushing substernal chest pressure for 90 minutes. ECG shows ST-segment
elevation in leads II, III, and aVF. Troponin I is 12.8 ng/mL (reference <0.04). Which pathophysiologic sequence
most accurately describes the progression from coronary plaque rupture to myocyte necrosis?
A. Endothelial erosion → vasoconstriction → stable plaque growth → transient ischemia
B. Plaque rupture with exposed lipid core → tissue factor exposure → platelet adhesion/aggregation →
thrombin generation and fibrin formation → complete coronary occlusion → ischemia then necrosis
[CORRECT]
C. Vasospasm of a coronary artery without plaque disruption → reversible ischemia only
D. Microvascular disease with capillary rarefaction causing chronic low-grade myocyte loss
Correct Answer: B
Rationale: ST-elevation MI arises from plaque rupture (or erosion) exposing the lipid core and tissue factor to circulating
blood. This initiates platelet adhesion (via vWF-GPIb), aggregation (GPIIb/IIIa-fibrinogen), and the coagulation cascade
generating thrombin and fibrin. Complete coronary occlusion results in ischemia within seconds, ATP depletion,
membrane failure, and myocyte necrosis within ~20-30 minutes of severe ischemia. Choice A describes stable angina
progression; C describes Prinzmetal angina; D describes chronic ischemic cardiomyopathy.
Page 2
,NURS 611 Exam 4 — Pathophysiology — 2026/2027 Complete Maryville University | A+ Verified
Q6: A 60-year-old female is admitted with chest pain and an initial troponin of 0.06 ng/mL that rises to 0.8 ng/mL
at 6 hours, then to 1.5 ng/mL at 12 hours. ECG shows T-wave inversions in V2-V4 without ST elevation. Cardiac
biomarker kinetics in this patient are best explained by which mechanism?
A. Release of myoglobin from cytoplasm due to reversible ischemia without cell death
B. Necrosis of myocytes with release of troponin from the cytosolic pool followed by the structural
(myofibril-bound) pool as degradation occurs [CORRECT]
C. Renal failure causing decreased clearance of troponin fragments producing a false positive
D. Skeletal muscle injury releasing cardiac troponin due to cross-reactivity with skeletal isoforms
Correct Answer: B
Rationale: Cardiac troponin elevation in NSTEMI reflects myocyte necrosis. The early rise (3-6 hr) comes from the small
free cytosolic pool; the prolonged elevation (peak at 18-24 hr, persistent for 7-10 days) reflects release from the
myofibril-bound structural pool as contractile proteins degrade. Myoglobin (A) is nonspecific and rises earlier but is not
the biomarker used here. Renal failure (C) can mildly elevate troponin but not with the typical rise/fall pattern of acute
injury. Cardiac troponin isoforms (D) are not expressed in skeletal muscle, so cross-reactivity is not the cause.
Q7: A 70-year-old male with no cardiac history presents with sudden palpitations. ECG shows a regular
wide-complex tachycardia at 180 bpm with concordance in precordial leads and AV dissociation. Which
electrophysiologic mechanism best explains this rhythm?
A. Reentry through an accessory pathway connecting atria and ventricles
B. Enhanced automaticity from a ventricular ectopic focus firing faster than the sinus node [CORRECT]
C. Triggered activity from delayed afterdepolarizations due to intracellular calcium overload
D. Reentry within the AV node producing a narrow QRS tachycardia
Correct Answer: B
Rationale: A regular wide-complex tachycardia with AV dissociation and precordial concordance is most consistent with
ventricular tachycardia originating from an ectopic ventricular focus exhibiting enhanced automaticity. Reentry through an
accessory pathway (A) typically produces pre-excited tachycardias like orthodromic AVRT with narrow QRS. Delayed
afterdepolarizations (C) are the mechanism of torsades de pointes and digoxin toxicity. AV node reentry (D) produces a
narrow QRS tachycardia, not wide.
Q8: A 68-year-old female on furosemide for heart failure develops palpitations. ECG shows prolonged QT interval,
prominent U waves, and premature ventricular contractions. Which electrolyte disturbance most directly accounts
for her dysrhythmia through prolongation of the action potential?
A. Hypomagnesemia alone, as magnesium does not directly affect the cardiac action potential
B. Hypokalemia prolonging phase 3 repolarization by delaying K+ efflux through delayed rectifier channels
(IKr) [CORRECT]
C. Hypercalcemia shortening the action potential by enhancing Ca2+ influx during phase 2
D. Hyponatremia slowing phase 0 depolarization of ventricular myocytes
Correct Answer: B
Rationale: Hypokalemia (often from loop diuretics) impairs IKr (rapid component of delayed rectifier K+ current),
prolonging phase 3 repolarization and the QT interval, with U-wave prominence and risk of torsades. Hypomagnesemia
(A) frequently coexists and worsens hypokalemia. Hypercalcemia (C) shortens the QT, the opposite of what is described.
Hyponatremia (D) does not significantly affect the ventricular action potential phase 0 (which is largely Na-driven in
Purkinje/myocytes but is not the issue here).
Page 3
, NURS 611 Exam 4 — Pathophysiology — 2026/2027 Complete Maryville University | A+ Verified
Q9: A 62-year-old male with a history of MI presents with sudden syncope. ECG shows a regular rhythm with
absent P waves, normal QRS, and rate of 40 bpm. His medication list includes metoprolol and amiodarone. Which
mechanism most likely produced this rhythm?
A. Reentrant circuit within the Bundle of His producing atrial tachycardia with block
B. Complete conduction block at the AV node with escape rhythm originating from the His-Purkinje system
[CORRECT]
C. Sinus node dysfunction with atrial standstill from amyloid infiltration
D. Vagal-mediated bradycardia from carotid sinus hypersensitivity
Correct Answer: B
Rationale: Third-degree (complete) AV block produces AV dissociation with a junctional or His-Purkinje escape rhythm.
In a patient on AV nodal-blocking agents (beta-blocker, amiodarone) with prior MI, conduction failure at or below the AV
node is most likely, with a narrow-QRS escape (rate 40-60) if junctional and wide if ventricular. Reentrant atrial
tachycardia (A) would show P waves. Sinus node dysfunction (C) would not produce AV dissociation. Vagal
hypersensitivity (D) typically produces sinus slowing or transient AV block, not stable complete block.
Q10: A 49-year-old male with hypertension and chronic kidney disease stage 3 has a BP of 162/98 mmHg despite
amlodipine 10 mg daily. His plasma renin activity is 14 ng/mL/hr (normal 0.6-4.3). CT angiography reveals a
stenotic lesion in the proximal right renal artery with post-stenotic dilation. Which mechanism most directly links
the renal artery stenosis to his hypertension?
A. Decreased GFR leading to volume expansion and primary suppression of renin
B. Decreased perfusion pressure sensed by juxtaglomerular cells triggering renin release, angiotensin
II-mediated vasoconstriction, and aldosterone-mediated sodium retention [CORRECT]
C. Direct compression of renal sympathetic nerves causing unopposed alpha-1 vasoconstriction
D. Loss of renal parenchymal mass reducing medullary lipases that generate antihypertensive vasodilators
Correct Answer: B
Rationale: Renovascular hypertension is driven by underperfusion of the juxtaglomerular apparatus, which triggers
baroreceptor-mediated renin release. Renin converts angiotensinogen to angiotensin I, then ACE generates angiotensin II
(vasoconstriction, efferent arteriolar constriction) and aldosterone (sodium retention). High renin is the hallmark,
distinguishing this from primary HTN. Choice A incorrectly suppresses renin. C and D are not recognized mechanisms of
renovascular hypertension.
Q11: A 75-year-old male with long-standing hypertension has an echocardiogram showing concentric LV
hypertrophy (wall thickness 16 mm) with preserved EF. Left atrial volume index is 48 mL/m² (normal <34). Which
cellular adaptation most directly explains the LV wall changes, and what is its long-term consequence?
A. Hyperplasia of cardiomyocytes increasing cell number to normalize wall stress
B. Compensatory hypertrophy of terminally differentiated cardiomyocytes (increased cell size) with eventual
interstitial fibrosis, diastolic dysfunction, and progression to HFpEF or HFrEF [CORRECT]
C. Metaplasia of cardiomyocytes to smooth muscle cells reducing contractile efficiency
D. Physiologic hypertrophy mediated by IGF-1 with proportional capillary growth and no long-term consequence
Correct Answer: B
Rationale: Cardiomyocytes are terminally differentiated and respond to pressure overload (high afterload) by hypertrophy
(increased cell size, not number — A is wrong). This concentric hypertrophy initially normalizes wall stress (Laplace's
law) but progresses to interstitial fibrosis, impaired relaxation, increased left atrial pressure (dilated LA), and eventual
diastolic or systolic failure. Pathologic hypertrophy (B) differs from physiologic (D) by reduced capillary density and
fibrosis. Metaplasia (C) does not occur in adult myocardium.
Page 4
