NURS 5315 — UTA GRADUATE NURSING EXAM 2 EXAM 2
QUESTIONS AND VERIFIED ANSWERS MOST RECENT EDITION
(2026/2027) PASS GUARANTEE
Advanced Pathophysiology, Pharmacology & Clinical Applications
Q1. What is the primary mechanism of action of ACE inhibitors in heart failure?
ANSWER ACE inhibitors block the conversion of angiotensin I to angiotensin II,
reducing vasoconstriction and aldosterone secretion, thereby decreasing preload and
afterload, reducing cardiac workload, and slowing ventricular remodeling.
Q2. What are the classic signs and symptoms of left-sided heart failure?
ANSWER Dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, pulmonary
edema, S3 gallop, crackles (rales) in lung bases, fatigue, and decreased exercise tolerance
due to pulmonary venous congestion.
Q3. How does right-sided heart failure differ from left-sided heart failure in clinical
presentation?
ANSWER Right-sided HF presents with peripheral edema (pitting), jugular venous
distension (JVD), hepatomegaly, ascites, and weight gain from fluid retention. Left-sided
HF primarily causes pulmonary congestion with dyspnea, crackles, and orthopnea.
Q4. What is the Frank-Starling mechanism and its relevance in heart failure?
ANSWER The Frank-Starling mechanism states that increased ventricular filling
(preload) leads to increased stroke volume up to a point. In heart failure, the curve is
depressed, meaning the heart cannot increase stroke volume adequately despite increased
preload, leading to congestion.
Q5. Define ejection fraction (EF) and its clinical significance in HFrEF vs HFpEF.
ANSWER EF is the percentage of blood ejected from the left ventricle per beat (normal
55-70%). HFrEF (EF <40%) involves systolic dysfunction with reduced contractility.
HFpEF (EF ≥50%) involves diastolic dysfunction with impaired relaxation and filling,
but preserved contractility.
Q6. What is the pathophysiology of cardiogenic shock?
ANSWER Cardiogenic shock results from severe cardiac dysfunction (often massive
MI) causing markedly reduced cardiac output, leading to systemic hypoperfusion.
Compensatory mechanisms worsen the condition: increased SVR increases afterload, and
neurohormonal activation causes fluid retention, further stressing the failing heart.
NURS 5315 UTA | Exam 2 Study Guide | Page 1 of 51
,Q7. Describe the compensatory neurohormonal mechanisms activated in heart
failure.
ANSWER The SNS activates to increase heart rate and contractility. RAAS activates to
retain sodium and water, increasing preload. ADH is released, causing water retention.
BNP is released from ventricular walls to promote natriuresis. These are initially
compensatory but chronically detrimental, causing remodeling.
Q8. What is ventricular remodeling and why is it harmful in heart failure?
ANSWER Ventricular remodeling is the progressive structural change of the heart
including hypertrophy, dilation, and changes in shape (from elliptical to spherical). It
impairs mechanical efficiency, increases wall stress, causes mitral regurgitation,
promotes arrhythmias, and accelerates disease progression.
Q9. What is the mechanism by which beta-blockers improve outcomes in heart
failure?
ANSWER Beta-blockers block chronic SNS activation, reducing heart rate, myocardial
oxygen demand, and ventricular remodeling. They improve LVEF over time, decrease
arrhythmias, and reduce sudden cardiac death. Must be started at low doses and titrated
slowly in stable patients.
Q10. What is the pathophysiology of hypertensive heart disease?
ANSWER Chronic systemic hypertension increases afterload, causing compensatory
concentric left ventricular hypertrophy (LVH). LVH increases myocardial oxygen
demand, impairs diastolic filling, and predisposes to arrhythmias, ischemia, and eventual
transition to dilated cardiomyopathy with systolic dysfunction.
Q11. Describe the pathophysiology of coronary artery disease (CAD).
ANSWER CAD involves endothelial dysfunction, lipid deposition, oxidized LDL
uptake by macrophages forming foam cells, and atherosclerotic plaque formation in
coronary arteries. Plaques narrow the lumen causing stable angina, or rupture triggering
thrombosis and ACS (unstable angina or MI).
Q12. What distinguishes STEMI from NSTEMI?
ANSWER STEMI involves complete occlusion of a coronary artery with ST elevation
on ECG and full-thickness (transmural) myocardial necrosis. NSTEMI involves partial
occlusion with no ST elevation (may have depression/T-wave changes), subendocardial
damage, and elevated troponin without ST elevation.
Q13. What are the zones of injury in myocardial infarction?
ANSWER The zone of necrosis (central, irreversible death) is surrounded by the zone of
injury (injured but potentially salvageable myocardium, causing ST elevation) and then
the zone of ischemia (outer ring, viable but ischemic tissue causing T-wave inversions).
Q14. What is the role of troponin in diagnosing myocardial infarction?
NURS 5315 UTA | Exam 2 Study Guide | Page 2 of 51
, ANSWER Troponin I and T are cardiac-specific proteins released into circulation after
myocardial cell death. They rise within 3-6 hours of MI, peak at 18-24 hours, and remain
elevated 7-14 days. High-sensitivity troponin assays allow earlier detection and better
risk stratification.
Q15. Describe the pathophysiology of atrial fibrillation.
ANSWER AFib results from rapid, chaotic electrical impulses from multiple reentrant
circuits in the atria (often triggered near pulmonary veins). Atria quiver rather than
contract, causing irregular ventricular response, loss of atrial kick (reduces CO ~20%),
blood stasis, and thrombus formation (stroke risk).
Q16. What is the CHA2DS2-VASc score and how is it used?
ANSWER CHA2DS2-VASc scores stroke risk in AFib: Congestive HF, Hypertension,
Age ≥75 (2pts), Diabetes, Stroke/TIA (2pts), Vascular disease, Age 65-74, Sex (female).
Score ≥2 (men) or ≥3 (women) warrants anticoagulation. It guides anticoagulant therapy
decisions.
Q17. What is the difference between rate control and rhythm control strategies in
AFib management?
ANSWER Rate control slows ventricular rate using beta-blockers, CCBs, or digoxin
without converting to sinus rhythm—preferred in elderly/asymptomatic. Rhythm control
restores sinus rhythm via antiarrhythmics or cardioversion—preferred in symptomatic or
younger patients. Both strategies require anticoagulation if CHA2DS2-VASc warrants.
Q18. Describe the pathophysiology of aortic stenosis.
ANSWER Aortic stenosis involves progressive narrowing of the aortic valve orifice
(calcific, congenital, or rheumatic). The LV hypertrophies to overcome increased
afterload. Eventually LV fails, causing the classic triad: syncope, angina, and heart
failure. Valve area <1.0 cm² indicates severe AS.
Q19. What is Virchow's triad and its clinical relevance?
ANSWER Virchow's triad identifies three factors predisposing to thrombosis:
endothelial injury, hypercoagulability, and venous stasis. Clinically relevant for DVT/PE
risk assessment and prevention strategies in hospitalized, postoperative, and immobilized
patients.
Q20. What is the pathophysiology of pulmonary embolism?
ANSWER PE typically arises from DVT in leg or pelvic veins. Clot embolizes to
pulmonary vasculature, causing mechanical obstruction, increased pulmonary vascular
resistance, right heart strain/failure, V/Q mismatch leading to hypoxemia, and potential
hemodynamic collapse in massive PE.
■ RESPIRATORY SYSTEM
NURS 5315 UTA | Exam 2 Study Guide | Page 3 of 51
, Q21. What is the pathophysiology of COPD?
ANSWER COPD involves chronic airflow limitation from emphysema (destruction of
alveolar walls, loss of elastic recoil, air trapping) and/or chronic bronchitis (mucus
hypersecretion, airway inflammation, small airway remodeling). Triggered primarily by
cigarette smoke, causing irreversible, progressive obstruction.
Q22. Distinguish between obstructive and restrictive pulmonary disease using
spirometry.
ANSWER Obstructive disease (asthma, COPD): decreased FEV1, normal or increased
TLC, decreased FEV1/FVC ratio (<0.70). Restrictive disease (pulmonary fibrosis,
obesity): decreased FVC, decreased TLC, normal or increased FEV1/FVC ratio (>0.70).
Q23. What is the pathophysiology of asthma?
ANSWER Asthma involves airway hyperresponsiveness to triggers, causing
bronchoconstriction, airway edema, and mucus hypersecretion. Th2-driven inflammatory
response involves mast cells, eosinophils, and IgE. Airflow obstruction is reversible with
bronchodilators. Chronic inflammation leads to airway remodeling.
Q24. Describe the mechanism of action of short-acting beta-2 agonists (SABAs).
ANSWER SABAs (albuterol) bind beta-2 receptors on bronchial smooth muscle,
activating adenylyl cyclase, increasing cAMP, activating PKA, causing smooth muscle
relaxation and bronchodilation. Also inhibit mast cell mediator release. Onset within
minutes; duration 4-6 hours.
Q25. What is status asthmaticus and how does it cause respiratory failure?
ANSWER Status asthmaticus is a severe, prolonged asthma attack unresponsive to
initial bronchodilator therapy. Progressive bronchoconstriction causes increased work of
breathing, air trapping, hyperinflation, respiratory muscle fatigue, rising PaCO2
(hypercapnia), and eventually respiratory failure requiring intubation.
Q26. What is ARDS and what are its diagnostic criteria (Berlin Definition)?
ANSWER ARDS (Acute Respiratory Distress Syndrome) criteri ANSWER acute onset
within 1 week of insult, bilateral infiltrates on CXR/CT not explained by
effusions/atelectasis, respiratory failure not fully explained by HF, PaO2/FiO2 ratio: mild
201-300, moderate 101-200, severe ≤100 on PEEP ≥5 cmH2O.
Q27. Describe the two phases of ARDS pathophysiology.
ANSWER Exudative phase (days 1-7): diffuse alveolar damage, loss of type I
pneumocytes, hyaline membrane formation, protein-rich edema floods alveoli, causing
severe hypoxemia. Proliferative phase (days 7-21): type II pneumocyte proliferation,
fibroblast activation, potential fibrosis—leading to decreased compliance.
Q28. What is the physiological basis of V/Q mismatch and its effect on gas
exchange?
NURS 5315 UTA | Exam 2 Study Guide | Page 4 of 51
QUESTIONS AND VERIFIED ANSWERS MOST RECENT EDITION
(2026/2027) PASS GUARANTEE
Advanced Pathophysiology, Pharmacology & Clinical Applications
Q1. What is the primary mechanism of action of ACE inhibitors in heart failure?
ANSWER ACE inhibitors block the conversion of angiotensin I to angiotensin II,
reducing vasoconstriction and aldosterone secretion, thereby decreasing preload and
afterload, reducing cardiac workload, and slowing ventricular remodeling.
Q2. What are the classic signs and symptoms of left-sided heart failure?
ANSWER Dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, pulmonary
edema, S3 gallop, crackles (rales) in lung bases, fatigue, and decreased exercise tolerance
due to pulmonary venous congestion.
Q3. How does right-sided heart failure differ from left-sided heart failure in clinical
presentation?
ANSWER Right-sided HF presents with peripheral edema (pitting), jugular venous
distension (JVD), hepatomegaly, ascites, and weight gain from fluid retention. Left-sided
HF primarily causes pulmonary congestion with dyspnea, crackles, and orthopnea.
Q4. What is the Frank-Starling mechanism and its relevance in heart failure?
ANSWER The Frank-Starling mechanism states that increased ventricular filling
(preload) leads to increased stroke volume up to a point. In heart failure, the curve is
depressed, meaning the heart cannot increase stroke volume adequately despite increased
preload, leading to congestion.
Q5. Define ejection fraction (EF) and its clinical significance in HFrEF vs HFpEF.
ANSWER EF is the percentage of blood ejected from the left ventricle per beat (normal
55-70%). HFrEF (EF <40%) involves systolic dysfunction with reduced contractility.
HFpEF (EF ≥50%) involves diastolic dysfunction with impaired relaxation and filling,
but preserved contractility.
Q6. What is the pathophysiology of cardiogenic shock?
ANSWER Cardiogenic shock results from severe cardiac dysfunction (often massive
MI) causing markedly reduced cardiac output, leading to systemic hypoperfusion.
Compensatory mechanisms worsen the condition: increased SVR increases afterload, and
neurohormonal activation causes fluid retention, further stressing the failing heart.
NURS 5315 UTA | Exam 2 Study Guide | Page 1 of 51
,Q7. Describe the compensatory neurohormonal mechanisms activated in heart
failure.
ANSWER The SNS activates to increase heart rate and contractility. RAAS activates to
retain sodium and water, increasing preload. ADH is released, causing water retention.
BNP is released from ventricular walls to promote natriuresis. These are initially
compensatory but chronically detrimental, causing remodeling.
Q8. What is ventricular remodeling and why is it harmful in heart failure?
ANSWER Ventricular remodeling is the progressive structural change of the heart
including hypertrophy, dilation, and changes in shape (from elliptical to spherical). It
impairs mechanical efficiency, increases wall stress, causes mitral regurgitation,
promotes arrhythmias, and accelerates disease progression.
Q9. What is the mechanism by which beta-blockers improve outcomes in heart
failure?
ANSWER Beta-blockers block chronic SNS activation, reducing heart rate, myocardial
oxygen demand, and ventricular remodeling. They improve LVEF over time, decrease
arrhythmias, and reduce sudden cardiac death. Must be started at low doses and titrated
slowly in stable patients.
Q10. What is the pathophysiology of hypertensive heart disease?
ANSWER Chronic systemic hypertension increases afterload, causing compensatory
concentric left ventricular hypertrophy (LVH). LVH increases myocardial oxygen
demand, impairs diastolic filling, and predisposes to arrhythmias, ischemia, and eventual
transition to dilated cardiomyopathy with systolic dysfunction.
Q11. Describe the pathophysiology of coronary artery disease (CAD).
ANSWER CAD involves endothelial dysfunction, lipid deposition, oxidized LDL
uptake by macrophages forming foam cells, and atherosclerotic plaque formation in
coronary arteries. Plaques narrow the lumen causing stable angina, or rupture triggering
thrombosis and ACS (unstable angina or MI).
Q12. What distinguishes STEMI from NSTEMI?
ANSWER STEMI involves complete occlusion of a coronary artery with ST elevation
on ECG and full-thickness (transmural) myocardial necrosis. NSTEMI involves partial
occlusion with no ST elevation (may have depression/T-wave changes), subendocardial
damage, and elevated troponin without ST elevation.
Q13. What are the zones of injury in myocardial infarction?
ANSWER The zone of necrosis (central, irreversible death) is surrounded by the zone of
injury (injured but potentially salvageable myocardium, causing ST elevation) and then
the zone of ischemia (outer ring, viable but ischemic tissue causing T-wave inversions).
Q14. What is the role of troponin in diagnosing myocardial infarction?
NURS 5315 UTA | Exam 2 Study Guide | Page 2 of 51
, ANSWER Troponin I and T are cardiac-specific proteins released into circulation after
myocardial cell death. They rise within 3-6 hours of MI, peak at 18-24 hours, and remain
elevated 7-14 days. High-sensitivity troponin assays allow earlier detection and better
risk stratification.
Q15. Describe the pathophysiology of atrial fibrillation.
ANSWER AFib results from rapid, chaotic electrical impulses from multiple reentrant
circuits in the atria (often triggered near pulmonary veins). Atria quiver rather than
contract, causing irregular ventricular response, loss of atrial kick (reduces CO ~20%),
blood stasis, and thrombus formation (stroke risk).
Q16. What is the CHA2DS2-VASc score and how is it used?
ANSWER CHA2DS2-VASc scores stroke risk in AFib: Congestive HF, Hypertension,
Age ≥75 (2pts), Diabetes, Stroke/TIA (2pts), Vascular disease, Age 65-74, Sex (female).
Score ≥2 (men) or ≥3 (women) warrants anticoagulation. It guides anticoagulant therapy
decisions.
Q17. What is the difference between rate control and rhythm control strategies in
AFib management?
ANSWER Rate control slows ventricular rate using beta-blockers, CCBs, or digoxin
without converting to sinus rhythm—preferred in elderly/asymptomatic. Rhythm control
restores sinus rhythm via antiarrhythmics or cardioversion—preferred in symptomatic or
younger patients. Both strategies require anticoagulation if CHA2DS2-VASc warrants.
Q18. Describe the pathophysiology of aortic stenosis.
ANSWER Aortic stenosis involves progressive narrowing of the aortic valve orifice
(calcific, congenital, or rheumatic). The LV hypertrophies to overcome increased
afterload. Eventually LV fails, causing the classic triad: syncope, angina, and heart
failure. Valve area <1.0 cm² indicates severe AS.
Q19. What is Virchow's triad and its clinical relevance?
ANSWER Virchow's triad identifies three factors predisposing to thrombosis:
endothelial injury, hypercoagulability, and venous stasis. Clinically relevant for DVT/PE
risk assessment and prevention strategies in hospitalized, postoperative, and immobilized
patients.
Q20. What is the pathophysiology of pulmonary embolism?
ANSWER PE typically arises from DVT in leg or pelvic veins. Clot embolizes to
pulmonary vasculature, causing mechanical obstruction, increased pulmonary vascular
resistance, right heart strain/failure, V/Q mismatch leading to hypoxemia, and potential
hemodynamic collapse in massive PE.
■ RESPIRATORY SYSTEM
NURS 5315 UTA | Exam 2 Study Guide | Page 3 of 51
, Q21. What is the pathophysiology of COPD?
ANSWER COPD involves chronic airflow limitation from emphysema (destruction of
alveolar walls, loss of elastic recoil, air trapping) and/or chronic bronchitis (mucus
hypersecretion, airway inflammation, small airway remodeling). Triggered primarily by
cigarette smoke, causing irreversible, progressive obstruction.
Q22. Distinguish between obstructive and restrictive pulmonary disease using
spirometry.
ANSWER Obstructive disease (asthma, COPD): decreased FEV1, normal or increased
TLC, decreased FEV1/FVC ratio (<0.70). Restrictive disease (pulmonary fibrosis,
obesity): decreased FVC, decreased TLC, normal or increased FEV1/FVC ratio (>0.70).
Q23. What is the pathophysiology of asthma?
ANSWER Asthma involves airway hyperresponsiveness to triggers, causing
bronchoconstriction, airway edema, and mucus hypersecretion. Th2-driven inflammatory
response involves mast cells, eosinophils, and IgE. Airflow obstruction is reversible with
bronchodilators. Chronic inflammation leads to airway remodeling.
Q24. Describe the mechanism of action of short-acting beta-2 agonists (SABAs).
ANSWER SABAs (albuterol) bind beta-2 receptors on bronchial smooth muscle,
activating adenylyl cyclase, increasing cAMP, activating PKA, causing smooth muscle
relaxation and bronchodilation. Also inhibit mast cell mediator release. Onset within
minutes; duration 4-6 hours.
Q25. What is status asthmaticus and how does it cause respiratory failure?
ANSWER Status asthmaticus is a severe, prolonged asthma attack unresponsive to
initial bronchodilator therapy. Progressive bronchoconstriction causes increased work of
breathing, air trapping, hyperinflation, respiratory muscle fatigue, rising PaCO2
(hypercapnia), and eventually respiratory failure requiring intubation.
Q26. What is ARDS and what are its diagnostic criteria (Berlin Definition)?
ANSWER ARDS (Acute Respiratory Distress Syndrome) criteri ANSWER acute onset
within 1 week of insult, bilateral infiltrates on CXR/CT not explained by
effusions/atelectasis, respiratory failure not fully explained by HF, PaO2/FiO2 ratio: mild
201-300, moderate 101-200, severe ≤100 on PEEP ≥5 cmH2O.
Q27. Describe the two phases of ARDS pathophysiology.
ANSWER Exudative phase (days 1-7): diffuse alveolar damage, loss of type I
pneumocytes, hyaline membrane formation, protein-rich edema floods alveoli, causing
severe hypoxemia. Proliferative phase (days 7-21): type II pneumocyte proliferation,
fibroblast activation, potential fibrosis—leading to decreased compliance.
Q28. What is the physiological basis of V/Q mismatch and its effect on gas
exchange?
NURS 5315 UTA | Exam 2 Study Guide | Page 4 of 51
